MRS. MARGARET McTEAR v. IMPERIAL TOBACCO LIMITED
| OUTER HOUSE, COURT OF SESSION [2005] CSOH 69 |
| | OPINION OF LORD NIMMO SMITH in the cause MRS MARGARET McTEAR Pursuer; against IMPERIAL TOBACCO LIMITED Defenders: ________________ |
Pursuer: McEachran, Q.C., Divers, Locke; Drummond Miller, W.S.
Defenders: Jones, Q.C., Wolffe; McGrigor Donald
31 May 2005
List of contents
[1.1]In view of the length of this Opinion, it may be helpful if at the outset I set out a list of its contents, by reference to its paragraph numbers, as follows:
PART I: PRELIMINARIES
Introduction
[1.2]Alfred McTear died, aged 48, on 23 March 1993. He and his wife, Mrs Margaret McTear, last lived together at 20 Cherrywood Drive, Beith, Ayrshire. He was the original pursuer in this action. After his death his wife, as his executrix-dative, was sisted as the pursuer in his room and place. For convenience I shall refer to them respectively as Mr McTear and Mrs McTear.
[1.3]The defenders are Imperial Tobacco Limited, whom I shall refer to as ITL. They manufacture, market and sell tobacco products in the United Kingdom, particularly cigarettes, including the John Player brand. They supply cigarettes to retail outlets throughout Scotland for onward sale to the public, and have done so for many years.
[1.4]Mr McTear died of lung cancer. In this action Mrs McTear claims that this was caused, at least to a material extent, by his smoking, from 1964 to 1992 cigarettes manufactured by ITL, and that throughout the period during which he smoked them ITL were negligent in selling cigarettes, or in any event in selling them without appropriate warnings, and she seeks an award of damages accordingly.
What the pursuer requires to prove
[1.5]The pursuer can succeed in this case only if she proves all of the following:
(1)that cigarette smoking can cause lung cancer;
(2)that cigarette smoking caused Mr McTear's lung cancer;
(3)that Mr McTear smoked cigarettes manufactured by ITL for long enough and in sufficient quantity for his smoking of their products to have caused or materially contributed to the development of his lung cancer;
(4)that Mr McTear smoked cigarettes manufactured by ITL because ITL were in breach of a duty of care owed by them to him; and
(5)that such breach caused or materially contributed to Mr McTear's lung cancer, either by making at least a material contribution to the exposure which caused his lung cancer or by materially increasing the risk of his contracting lung cancer.
Items (1) to (4) are as formulated by Mr Jones. Mr McEachran did not take issue with them. Item (5) takes account of counsel's submissions, discussed paras.[6.2] to [6.29].
[1.6]The burden of proving each of these matters rests on the pursuer. In order to discharge that burden, she must satisfy me, on the balance of probabilities, and on the basis of the evidence led before me and the applicable law, that each of these matters is proved.
[1.7]ITL plead, among other things, that Mr McTear willingly accepted as his own any risk to his health from smoking cigarettes; in doing this, they rely on the maxim volenti non fit iniuria, which I discuss below under that heading. The burden of proving this, on the balance of probabilities, is on ITL. ITL also plead that Mr McTear's illness was caused by his own fault or was contributed to by his fault, but at the hearing on evidence, Mr Jones did not invite me to sustain either of these pleas.
[1.8]I wish to state clearly now, and shall reflect this throughout my Opinion, that:
(1)This is in no sense a public inquiry into issues relating to smoking and health; it is a proof before answer in which I have to consider, having regard to the facts and the law, whether ITL should be found liable in damages to Mrs McTear.
(2)I must base my decision about questions of fact on the evidence, and that alone.
[1.9]Under our procedure, fair notice must be given by a party in the written pleadings (the final version of which is incorporated in the Closed Record) of any matter of fact about which the party may seek to lead evidence. Subject to the court's discretion to allow amendment at any stage (which may well be refused after a proof has started if it would seriously prejudice the other party) evidence may not be admitted of any matter of fact about which fair notice has not been given in this way.
[1.10]It must be emphasized that our system is evidence-based. My duty as a fact-finder is exactly the same as that of a jury, who in terms of their oath are bound to "give a true verdict according to the evidence". This brings me to a related topic.
Judicial knowledge
[1.11]On at least two occasions Mr McEachran made reference to judicial knowledge. The first was to suggest, at a By Order hearing before the proof, that it lay within judicial knowledge that cigarette smoking could cause lung cancer. The second was a suggestion, during the discussion of an objection at the proof, that the purpose and effect of advertising lay within judicial knowledge. Judicial knowledge must be distinguished from the personal knowledge of an individual judge. It is generally taken as relating to matters which can be immediately ascertained from sources of indisputable accuracy, or which are so notorious as to be indisputable, so that the judge is bound to take notice of them. If a matter does fall within judicial knowledge, a judge may refresh his memory or supplement his knowledge regarding it by consulting recognised works of reference, such as dictionaries or textbooks. Apart from the matters which are recognised as being within judicial knowledge, it is improper for a judge to proceed upon personal knowledge of the facts in issue, or upon personal examination of passages in textbooks. For a discussion of this, and reference to authorities vouching the foregoing proposition, see Walkers on Evidence (2nd edn., 2000), pp.171-3, para.11.6.
[1.12]No doubt, where there is an issue of general public importance, a judge may have views about it in his or her private capacity. But it is an essential part of the judicial function that these views be put out of mind when hearing a case: otherwise, the judge would simply be at risk of pre-judging the very issue upon which he or she may be called to make a decision judicially. One of the fundamental issues in this case is whether cigarette smoking can cause lung cancer. This is an issue which I am duty-bound to approach with an open mind and to decide on the basis of the evidence led before me. As with all other disputed issues of fact, the burden of proof is on the party who seeks to establish this, in this instance on the pursuer.
Procedure
[1.13]It is appropriate at this stage to refer to some of the procedural events which have taken place in this action and in a related application for judicial review by Mrs McTear.
[1.14]A claim was intimated on behalf of Mr McTear in July 1992. In early January 1993 an application for legal aid on behalf of Mr McTear was submitted to the Scottish Legal Aid Board for legal aid to fund the conduct of litigation on his behalf. In the application form it was stated that legal aid was sought to raise an action against "Richard Lloyd & Sons (who manufacture Old Holborn tobacco) and John Player & Sons (who manufacture John Players [sic] cigarettes)".
[1.15]The summons in the present action was signeted on 28 January 1993, and was presumably served shortly thereafter. On 3 March 1993 an interlocutor was pronounced granting commission to Mr Bolland, Q.C. to take the evidence of Mr McTear at a time and place to be appointed by the Commissioner. On 16 March 1993 at his home address, 20 Cherrywood Drive, Beith, Ayrshire, Mr McTear was duly sworn, and was examined in chief by his senior counsel, Mr McEachran, Q.C. On the same day Mr Hodge, who acted at that time as junior counsel for ITL, began his cross-examination of Mr McTear. As subsequently reported by the Commissioner, the commission was adjourned in mid-afternoon on that day "due to a deterioration in [Mr McTear's] condition and consequent inability to deal with questions". This followed advice from Mr McTear's general medical practitioner, who examined him at lunch-time. The next day, 17 March, Mr Hodge continued his cross-examination, but after approximately an hour and a half the Commissioner adjourned the commission in order to have Mr McTear medically examined. The view was then taken that Mr McTear was unable to continue giving evidence that day. An attempt was made to reconvene the commission on 19 March, but the doctor's advice was that Mr McTear was unable to resume giving evidence that day. That remained the position until he died on 23 March. At the point when the commission was adjourned on 17 March, Mr Hodge was, as he informed the Commissioner, about to put more contentious questions designed to test credibility and reliability. In the event, these questions were never put to Mr McTear. It appears, therefore, that most of the intended cross-examination was unable to take place. In his supplementary report, the Commissioner explained that he did not consider it appropriate to offer a view on the credibility and reliability of Mr McTear in relation to part of his evidence and not the whole, so he was unable to comply with a request to do so.
[1.16]A transcript of the evidence given by Mr McTear on commission, so far as it went, is available to me and forms part of the evidence in the case. Most of his evidence in chief was read out at the beginning of the proof before me, and in due course Mr McEachran sought to rely on certain passages in it. For reasons which I discuss in detail below, Mr Jones submitted that I should find Mr McTear's evidence to have been incredible and unreliable in certain material respects. I shall therefore have to make an assessment of this evidence as best I can, bearing in mind that it was given by a dying man, and one whose demeanour I have not had the opportunity of observing for myself.
[1.17]On 24 September 1993 the action was sisted pending determination of an application by Mrs McTear to the Scottish Legal Aid Board for civil legal aid to enable her to pursue the action. The tests which required to be satisfied in order for her application to succeed were as set out in section 14 (1) of the Legal Aid (Scotland) Act 1986, which provides inter alia:
"[C]ivil legal aid shall be available to a person if, on an application made to the Board -
(a)the Board is satisfied that he has a probabilis causa litigandi; and
(b)it appears to the Board that it is reasonable in the particular circumstances of the case that he should receive legal aid."
Mrs McTear's application was refused as unreasonable by the Board. An application to the Board for review of that decision was also refused. Mrs McTear then applied to this court for judicial review of the Board's decision, alleging that it had acted unreasonably in refusing the application. After a first hearing, at which Mrs McTear and the Board were represented by counsel, the Lord Ordinary, Lord Kirkwood, by interlocutor dated 15 February 1995 dismissed the petition. There was no appeal against Lord Kirkwood's decision. The full history of the matter, including the reasons given by the Board and by Lord Kirkwood for their respective decisions, can be found in the report McTear v Scottish Legal Aid Board 1995 S.C.L.R. 611.
[1.18]At one stage of the procedural discussions before me, when preparations for the proof were being reviewed, Mr McEachran suggested that I might write to the Board, expressing the view that Mrs McTear should be granted legal aid. I declined to do this, because it is not my function to enter into such correspondence, and the appropriate occasion for the court to express its views is when disposing of an application for judicial review of a decision of the Board, as had already happened in the present case. Even then, as explained by Lord Kirkwood, the court cannot substitute its own view on the merits of the application for that reached by the Board, unless the latter had arrived at a perverse or unreasonable decision.
[1.19]As I understand it, counsel and solicitors representing Mrs McTear have conducted this action of her behalf on a speculative ("no win, no fee") basis. Reference will be made hereafter to the voluntary organisations Action on Smoking and Health (ASH) and ASH Scotland. At this stage, I should say that I believe it to be the case that ASH Scotland is in general supportive of the present action, but at no time has given any financial support for it.
[1.20]In these circumstances, ITL enrolled a motion to ordain Mrs McTear to find caution for expenses (in English procedure, security for costs) in respect of the following factors:
"(1)The nature, scale and cost of the litigation, (2) the apparent inability of the pursuer to meet the expenses liable to arise, (3) the refusal of legal aid to the pursuer, (4) the pursuer's limited prospects of success, (5) the small value of the claim, (6) the fact that the action had been raised in the interests of persons other than the pursuer, (7) the delay in arranging to take Mr McTear's evidence on commission, and (8) the unavailability to the defenders of other protective remedies."
On 9 April 1996 Lord Gill refused this motion. In his Opinion, he said that the sixth factor was the aspect of the case that had troubled him most. He referred to newspaper cuttings and broadcast transcripts. These indicated that the pursuer's Glasgow solicitors, Ross Harper who originally acted for Mr McTear, had been "fairly accessible to the media on the subject of this case". It appeared from statements made by these solicitors that they had established a special claims unit to deal with similar claims and had numerous similar actions to follow on this one. According to a broadcast transcript, a partner in the firm, Mr Cameron Fyfe, said that "the world is watching this case" and predicted that if it were to succeed it would "open the floodgates to thousands of others, not only in Scotland, but interestingly in the western world". In addition, Lord Gill said, there had been numerous reports that the present action was being "backed" by an "anti-smoking pressure group", ASH, one of whose spokesmen was reported to have said, with reference to this action, "we just need one breakthrough, we just need one victory. [...] We just have to win one case to win everything". Lord Gill said, at pp.20-21:
"From the many published comments on this case I can see why the defenders should have been concerned by the possibility that this action may have been brought primarily for the benefit of third parties. However, I have an assurance from senior counsel for the pursuer [Mr McEachran] that this concern is unfounded and that, whatever implications the action may have for third party onlookers, the pursuer is genuinely suing it on her own behalf and in her own interests, as executrix and widow, with the serious purpose of recovering damages in both of these capacities.
I also inferred from senior counsel's comments that, whatever impression may have been given in the media as to the extent of their involvement, ASH are contributing to the action no more than their enthusiastic moral support.
It may well be that third parties will benefit in various ways if this action succeeds; but that will always be the case where a cause of action is common to numerous claimants, for example relatives of disaster victims, or where an action raises the question of general public importance, for example the safety of a medicine or of a consumer product.
On the basis of the assurance given to me, I am not willing to grant the motion on this ground."
[1.21]On 19 July 1996 an Extra Division refused a reclaiming motion against Lord Gill's decision. It was held that he had not misdirected himself and was not plainly wrong. Notwithstanding this, the information provided to Lord Gill and on the basis of which he refused the motion may bear re-examination in light of subsequent events.
[1.22]The case thereafter called in the procedure roll before Lord McCluskey. The purpose of the debate was to determine which of the pursuer's averments should be allowed to go to proof. On 23 October 2001 Lord McCluskey allowed a proof under deletion of certain averments. Subject to this, he reserved all pleas and allowed the parties a proof before answer in respect of the averments that remained. It was on the basis of these averments that the parties made, or should have made, their preparations for the conduct of the case at the proof.
[1.23]After being nominated in 2003 as the judge before whom the proof was to take place, I held a number of By Order hearings to discuss the state of the parties' preparations for the conduct of the proof and to decide any incidental motions.
[1.24]One such motion was at the instance of ITL on a commission and diligence for recovery of documents called for in a specification of documents. After hearing counsel, I granted diligence against havers so far as related to call 1, which was amended at the bar. In brief, this call related to documents showing or tending to show (under deletion of any entry naming or enabling any third party to identify any subject or subjects of the studies)
(a)the data sets (including the baseline data for the subjects, all follow-up points and all outcome points thereof and the full descriptions of data files and all variables (including generated variables) within the data sets) for the British Doctors' Study or studies reported in six papers published between 1954 and 1977, of which Professor Sir Richard Doll, one of the expert witnesses for Mrs McTear, was a joint author;
(b)the age distribution and any other characteristics of the general population used for the purposes of the analysis reported in said papers;
(c)the statistical methods employed in the analysis of the data presented in said papers; and
(d)the statistical programmes used to perform the said analysis or analyses.
I am not aware that any documents falling within the terms of this call were among the productions for either party. I am not aware of the reason or reasons for this outcome.
[1.25]As has been apparent throughout, ITL have been prepared to devote considerable resources to the defence of this action. Its outcome is no less important for them than it is for the pursuer and the "third party onlookers". While the respective positions of the parties have thus been very unequal, I see no reason at all to treat this as a criticism of ITL. They are fully entitled to defend their interests as they have done, and, despite occasional complaints by Mr McEachran, there has been no point at which in my view they have unnecessarily protracted the proceedings or have otherwise resorted to tactics designed to exploit Mrs McTear's lack of funds. The inequality is an unavoidable consequence of the decision to continue with the conduct of the action without the benefit of legal aid or any other source of financial support.
[1.26]At one hearing before the proof, Mr McEachran advanced a motion, in terms similar to those of one which had previously been heard and refused by Lord Carloway, that I should restrict the number of days during which evidence would be led at the proof, and restrict the number of expert witnesses to be called on behalf of ITL. I refused this motion on the basis that I had no power to grant it and in any event because I could see no justification for it on the information then available to me. I indicated, however, that there would be scope for intervention during the course of the proof if it appeared that ITL were unnecessarily duplicating evidence or otherwise protracting the proceedings. In the event, as I have said, this did not happen.
[1.27]While there can be little doubt that the case for Mrs McTear would have been conducted differently had more resources been available, Mr McEachran accepted in his closing submissions that it was not open to me to take any account of this in reaching my decision.
[1.28]I emphasise, therefore, that my decision must, in accordance with our usual rules, be based solely on the parties' written pleadings, on the evidence led before me and on the submissions of counsel thereon, subject to the application of the law as I find it to be.
[1.29]The proof itself was conducted in accordance with our usual procedure. What was of great assistance was the use of modern systems. The documentary productions, on an estimate I have been given, extended to about 85,000 pages. At least four sets of paper copies would have been required for use in court; and experience shows how difficult this would have been to manage, and how much time would have been lost, had paper been used. Instead, all the documents were scanned into an electronic database, and the system was operated in court by an operator who was able on request to cause any page to be displayed on screens for all the participants to see. The evidence of witnesses and the submissions of counsel were transcribed by two operators using the LiveNote system, which produced an almost instantaneous transcript on separate screens with a high initial degree of accuracy. The transcript was thereafter edited, so that by the start of the next day's business there were very few remaining errors. Though there were occasions when paper was used for various reasons, the proof was in general conducted on a paperless basis. All of this was provided at the expense of ITL. I regard it as money well spent. I am confident that much time was saved, compared with the use of paper. The evidence of witnesses took thirty days, and counsel's submissions took twelve days. On reviewing the transcript, and the documents which were referred to by witnesses and counsel, I am struck by how much was covered in that time. The use of paper, traditional methods of note-taking, and so on, would have significantly added to the length of the proceedings, and the difficulties of my subsequent task in preparing this Opinion.
Published materials
(1)Legal authorities
[1.30]The following cases and legal textbooks are referred to in this Opinion. Some cases not listed here were mentioned in counsel's written submissions, but not at the hearing on evidence, and I see no need to include them. Since there will be readers of this Opinion who are not lawyers, do not have access to law libraries and are not familiar with the case law, I have decided, where reference is first made to a case, to set out the summary of it from the rubric or headnote in the report, so as to provide some context for the quotations of passages from the opinions or judgments which follow. The quotations are assemblies of all the passages referred to by counsel, albeit at different times.
List of cases
[1.31]Bogle v McDonald's Restaurants Ltd [2002] E.W.H.C. 490 (Q.B.)
Bow Valley Husky (Bermuda) Ltd v Saint John Shipbuilding Ltd [1997] 3 S.C.R. 1210
Cruz-Vargas v R.J. Reynolds Tobacco Company 348 F.3d 271 (1st Cir.2003)
Davie v Magistrates of Edinburgh 1953 S.C. 34
Dingley v The Chief Constable, Strathclyde Police 1998 S.C. 548, 2000 S.C. (H.L.) 77
Donoghue v Stevenson 1932 S.C. (H.L.) 31
Elf Caledonia Ltd v London Bridge Engineering Ltd, 2 September 1997
Fairchild v Glenhaven Funeral Services Ltd [2003] 1 A.C. 32
Fowler v Tierney 1974 S.L.T. (Notes) 23
Galbraith v HM Advocate (No.2) 2002 J.C. 1
Graham Barclay Oysters Pty Ltd v Ryan (2002) 211 C.L.R. 540
Grant v Australian Knitting Mills Ltd [1936] A.C. 85
Hamilton v Fife Health Board 1993 S.C. 369
Heine v Reemtsma Cigarettenfabriken GmbH 2 O 294/02
Hodge & Sons v Anglo-American Oil Co (1922) 12 Ll.L.R. 183
Holmes v Ashford [1950] 2 All.E.R. 76
Hotson v East Berkshire Area Health Authority [1987] A.C. 750
Imperial Chemical Industries Ltd v Shatwell [1965] A.C. 656
Law Hospital NHS Trust v Lord Advocate 1996 S.C. 301
Letang v Ottawa Electric Railway Co [1926] A.C. 725
Lewis v University of Bristol [1999] E.W.C.A. Civ. 1569
Létourneau v Imperial Tobacco Ltd (1998) 162 D.L.R. (4th) 734
London Graving Dock Co Ltd v Horton [1951] A.C. 737
Lund v J.L. Tiedemanns Tobaksfabrik A.S., H.R. - 2002 - 00753a, 31 October 2003
McCaig v Langan 1964 S.L.T. 121
McGhee v National Coal Board 1973 S.C. (H.L.) 37
McKillen v Barclay Curle & Co Ltd 1967 S.L.T. 41
McLean v William Denny & Bros Ltd 2004 S.L.T. 422, 2004 S.C. 656
McManus's Executrix v Babcock Energy Ltd 1999 S.C. 569
McTear v Scottish Legal Aid Board 1995 S.C.L.R. 611
McWilliams v Sir William Arrol & Co 1962 S.C. (H.L.) 70
Main v Andrew Wormald Ltd 1988 S.L.T. 141
Morris v Murray [1991] 2 Q.B. 6
Murphy v Brentwood District Council [1991] 1 A.C. 398
Murray's Executrix v Greenock Dockyard Co Ltd 2004 S.L.T. 346, 2004 S.L.T. 1104
Nettleship v Weston [1971] 2 Q.B. 691
National Justice Compania Naviera S.A. v Prudential Assurance Co. Ltd ("The Ikarian Reefer") [1993] 2 Lloyd's Rep.68
Overseas Tankship (UK) Ltd v Morts Dock & Engineering Co Ltd (The Wagon Mound) [1961] 1 A.C. 388
Paugh v R.J. Reynolds Tobacco Company 834 F.Supp. 228 (N.D.Ohio 1993)
Pelman v McDonald's Corporation 237 F.Supp.2d 512 (S.D.N.Y.2003)
John Pierce v Her Majesty's Advocate 1981 S.C.L.R. 783
R. v Abadom [1983] 1 W.L.R. 126
Reeves v Commissioner of Police of the Metropolis [2000] 1 A.C. 360
Rhesa Shipping Co S.A. v Edmunds [1985] 1 W.L.R. 948
Roysdon v R.J. Reynolds; Roysdon v R.J. Reynolds Tobacco Company 849 F.2d 230 (6th Cir. 1988)
Shaher v British Aerospace Flying College Ltd 2003 S.C. 540
Thompson v Johnson and Johnson Pty Ltd [1991] 2 V.R. 449
Thompson v Smith's Shiprepairers (North Shields) Ltd [1984] 1 Q.B. 405
Titchener v British Railways Board 1984 S.C. (H.L.) 34
Tompkin v American Brands 219 F.3d 566 (6th Cir. 2000)
Tomlinson v Congleton Borough Council [2004] 1 A.C. 46
Wardlaw v Bonnington Castings Ltd 1956 S.C. (H.L.) 26
Watson v Fram Reinforced Concrete Co (Scotland) Ltd 1960 S.C. (H.L.) 92
White v Blackmore [1972] 3 All.E.R. 158
Winnik v Dick 1984 S.L.T. 185
Wilsher v Essex Area Health Authority [1988] A.C. 1074
Wright v Dunlop Rubber Co Ltd (1972) 13 K.I.R. 255
Woods v Multi-Sport Holdings Pty Ltd (2002) 208 C.L.R. 460
List of textbooks
[1.32]Lewis, Manual of the Law of Evidence in Scotland (1925)
Salmond & Heuston, The Law of Torts, 21st ed. (1996), p.296
Walkers on Evidence (2nd edn., 2000)
Wilkinson, The Scottish Law of Evidence (1986)
(2)Non-legal publications
[1.33]I have decided to incorporate in this Opinion a list of references to all the publications, other than cases reported in law reports, which were discussed in the course of evidence and counsel's submissions. Following the general practice adopted by the expert witnesses in their written reports, I shall use the author-date (Harvard) system of reference. Where authorship is attributed to an organisation, rather than to an individual or individuals, I have used an acronym. In most instances, where evidence was given under reference to a passage in a publication, the passage in question was displayed on screens in court. My quotations of such passages have been checked against the original texts as then on view. In a very few instances witnesses in reading from their written reports gave quotations from publications without direct reference being made to the original texts. In these instances I have thought it best to give the author-date references and to check the quotations against the original texts. In general, however, it may be taken that where an author-date reference is given and a text is quoted, the original text was under discussion in the course of evidence. On occasions, witnesses gave evidence about publications without being asked to refer to the original texts. Such publications are in most cases not included in this list of references, and I have attempted to distinguish them from those which are by separating the authors' names from dates by one or more words; i.e. author-date references in the text are to publications included in the list and, except in a few cases where convenience dictated otherwise, no publication is included in the list unless reference was made to the original text at the proof.
[1.34]The citations in the list of references which follows are as complete and accurate as I can make them and are in a style which I believe to be generally acceptable.
List of references
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(3)Passages in documents not put to witnesses
[1.35]The documentary productions, as I have said, extend to many thousands of pages. Most of them are non-legal publications, of which there are many hundreds, including those in the list of references. At the proof, passages from only some of these publications were put to witnesses. It is open to question whether all of these passages were adopted by the witnesses to whom they were put, and thus became part of their evidence. Leaving that aside for later discussion, I feel obliged to say something at this stage about the question whether it is open to me to take into account any passage in any publication which was not put to any witness.
[1.36]The matter arose in this way. As will be seen, the presentation of the pursuer's case depended to a large extent on reliance on published reports. As Mr McEachran made a point of bringing out, some of these reports extended to hundreds of pages. At the hearing on evidence, he sought to draw to my attention various passages in these reports, some of which had been put to witnesses, and some of which had not. Mr Jones submitted that I should not take notice of any passage which had not been put to a witness. When I took this up with Mr McEachran, he said that he did not agree with the submission that I could only have regard to those passages which were expressly referred to in the evidence. This might be so, he said, where a matter was in dispute between the parties, but not where, as here, ITL's position was that they "just do not know", in particular that cigarette smoking can cause lung cancer. I asked Mr McEachran whether he was saying that it was open to me to pick up any of the reports that he had referred to and rely on any passage that happened to catch my attention. Mr McEachran said that I was entitled to read it, because otherwise I could not make sense of the whole thing. In a situation where ITL were not seeking to set up another case, that lung cancer was not caused by smoking but by something else, I was entitled, he submitted, to look at these documents more widely: "Otherwise, we would be here forever, if we have to go through 600 pages of every document. There has to be some realism about this." There was not an absolute bar to doing this in a situation where the parties had not led evidence which was totally contradictory. In a situation where the other side were not trying to prove the opposite, a witness was entitled to say that he adopted the terms of the full publication.
[1.37]I reject this approach. With a few well-recognised exceptions, the terms of a document which has been lodged as a production are not evidence. There are procedures, such as the joint minutes and notices to admit which have been used in this case, under which the terms of a document may be agreed to be accurate, and in such an event is not necessary for it to be put to any witness. Otherwise, evidence is required to establish its terms. I do not regard it as being open to me to take account of any passage in any document, the terms of which were not agreed, and to which reference was not made in the course of the evidence of any witness. This is because of the fundamental rule that I must decide the case on the basis of the evidence led before me, leaving aside any other considerations. It would risk doing a serious injustice if I were to allow myself to be influenced by, for example, my reading of further chapters in a textbook, other than those to which reference had been made in the course of evidence, just as it would be if I were to read letters in a correspondence file which had not been put to any witness. I refer also to the second passage from the opinion of the Lord President in Davie v Magistrates of Edinburgh, quoted at para.[5.5]. Accordingly, when I come to discuss the evidence, I propose to confine my consideration to those passages in the literature to which express reference was made.
[1.38]The views expressed in the preceding paragraph do not depend on the position of ITL, which I discuss in Part III, in particular on the question whether cigarette smoking can cause lung cancer. For reasons given there, the burden of proof of this averment is on the pursuer, regardless of what may or may not have been said by or on behalf of ITL on other occasions and must be discharged in accordance with the normal rules of evidence.
PART II: THE PARTIES' POSITIONS ON THE MAIN FACTUAL ISSUES
(1)The position of the pursuer
[2.1]Mr McEachran introduced his submissions on the positions of the parties by saying that it was a tribute to the steadfastness and resolution of Mrs McTear that she had persevered over all these years to get this case into court and to await my judgment. This was in spite of all the "pressure" ITL had "thrown at her", their constant objections to her application for legal aid and, in particular, the way they tried to make her put up "security for costs" (i.e. caution for expenses) in the figure of £2 million. Mr McTear said in evidence "cigarette companies are simply selling poison to make money". This gave one of the reasons as least why he felt strongly enough to bring an action. Mrs McTear gave evidence that this became his purpose and she hoped that it would become his great achievement. It was clear that Mrs McTear was fond of her husband, errant though he was, and was proud that at the end he was "prepared to challenge the big battalions".
[2.2]It is averred by the pursuer that:
1.Cigarette smoking can cause lung cancer, and the World Health Organization, the United Kingdom Government and the United States Government have accepted for many years that cigarette smoking can cause lung cancer.
2.Mr McTear's lung cancer was caused by his smoking.
3.When Mr McTear commenced smoking in 1964 he was unaware that smoking could cause fatal diseases.
4.Tobacco is addictive, "in the sense that once individuals such as [Mr McTear] have started smoking it is difficult for them to wean themselves off the habit".
5.After commencing smoking Mr McTear quickly became addicted to cigarettes, so that when in about 1971, following the appearance of Government health warnings on cigarette packets, he became aware of the risks to health caused by smoking, he was unable to give up smoking, despite attempts to do so, because of his addiction.
The pursuer relies in particular, in support of points 1 and 4, on a series of reports and similar publications which, in chronological order, are MRC 1957, RCP 1962, USSG 1964, RCP 1971, USSG 1971, RCP 1977, IARC 1986, USSG 1988, UKWP 1998, RCP 2000, UKHC 2000 and IARC 2004.
[2.3]Counsel submitted that this was a straightforward product liability case. In Donoghue v Stevenson 1932 S.C. (H.L.) 31 it was decided that a manufacturer was under a duty to take reasonable care for the consumers of his products. If he knew of a health risk involving death, it was his duty to cease production until the problem was dealt with. From the 1950s, there had been reports in the media that doctors had claimed that there were health risks associated with tobacco smoking. By 1957 at least, the tobacco industry and ITL were aware of the health risks from tobacco smoking and accordingly the duty arose then to cease manufacture. If they had done this Mr McTear would not have developed lung cancer because of ITL's products. There would have been none of ITL's products for him to have smoked.
[2.4]On a broad overview of the case, "standing back and trying to see the wood from the trees" and separating the essentials from the days of detailed evidence, counsel submitted:
"It respectfully seems to me that this case is relatively straightforward, although I think it is the first case of its type against the tobacco industry in the UK. There should not be much need for the court to go into much of the detailed evidence in the way of articles and things."
As will be seen, this approach has not found favour with me; though no doubt, if it had, I might have spared myself, and the reader, many hundreds of the pages which follow.
[2.5]When I asked Mr McEachran why, if all the facts necessary to establish liability were present from the late 1950s and at all material times thereafter, there had been no instance in the United Kingdom of a successful action against a tobacco manufacturer based on grounds similar to those in the present case, Mr McEachran submitted that this was attributable to the power of the tobacco industry. "It is the little man against the big battalions." They were a very well-funded industry who were able to fight off attacks. This was how they had obtained the exemption for tobacco under section 10 of the Consumer Protection Act 1987.
[2.6]In response to this, Mr Jones told me about the position in England. He said that in the summer of 1992 solicitors acting for plaintiffs placed advertisements in two newspapers inviting any persons who believed themselves to be suffering from illnesses caused by smoking to get in touch with them with a view to investigating the possibility of pursuing claims against various tobacco companies on their behalf. As a result, over the course of the next three months or so, some 300 people approached one or other of two firms of solicitors, and applications for legal aid were made on their behalf. In January 1995 the Legal Aid Board made a limited grant of legal aid for a full review of merits, quantum and the total likely costs involved in pursuing an action against the tobacco companies. This was undertaken by the applying solicitors, and the Board then took independent advice from leading counsel. In July 1996 all the applications were refused, the refusal being expressed to be on the merits. In the late summer of 1996 two firms of solicitors offered to fund claims against tobacco companies on behalf of a number of lung cancer sufferers under conditional fee arrangements. Following this, a cohort of about fifty-two plaintiffs who had all suffered lung cancer issued writs in England. Ten of these were selected to act as lead plaintiffs. Of these, it was accepted that eight had not commenced proceedings timeously, having regard to the English law of limitations. They were required to apply to the court to exercise discretionary powers to dispense with the limitation period. Trial of limitation issues was heard before Wright J in 1998, and in February 1999 he refused the applications. Of the fifty-two cases, all but seven dismissed of consent in March 1999. In April 1999 four of the remaining seven cases were also dismissed of consent. The court refused to exercise discretionary powers to dispense with the limitation period in the remaining three cases.
(2)The position of ITL
[2.7]ITL admit that the World Health Organization, the United Kingdom Government and the United States Government have accepted for many years that cigarette smoking can cause lung cancer, that Government health warnings first appeared on cigarette packets in 1971, and that they were aware of the publications relied upon by the pursuer. Otherwise they deny the foregoing averments. They aver that:
1.Cigarette smoking has not been scientifically established as a cause of lung cancer and, although various theories have been advanced, the cause or causes of lung cancer are unknown and the mechanism or mechanisms whereby lung cancer develops are unknown.
2.Smoking is correctly described as a habit and not an addiction, and while some smokers may find it difficult to stop smoking, smokers who choose to stop smoking are able to do so.
3.Assuming that Mr McTear commenced smoking in 1964, he did so against the background of general public awareness that there were health risks associated with smoking, and in particular general public awareness of the view that smoking could cause lung cancer.
4.At all relevant times the public at large understood that some smokers might find it difficult to stop smoking, and Mr McTear shared this understanding.
[2.8]Mr McEachran submitted that, having regard to the pleadings for ITL and to the position adopted by them over the years, to the effect that that it was not known whether cigarette smoking caused lung cancer, my approach to this factual issue should be different from what it would be if they not only denied that cigarette smoking could cause lung cancer but offered to prove a contrary case.
[2.9]This requires consideration of matters raised principally in the evidence of Mr Gareth Davis, Chief Executive Officer (CEO) of Imperial Tobacco Group plc. Before he was called as a witness, however, the scene was set in the evidence of three of the expert witnesses for the pursuer, Professor Sir Richard Doll, Professor Friend and Professor Hastings. An account of the first of these appears before that of Mr Davis, of the other two after it.
ITL's position before the House of Commons Health Committee
[2.10]Discussion of the position of ITL, as explained by Mr Davis, is more readily understood if I give a brief outline now of proceedings before the Health Committee of the House of Commons in 2000, as set out in UKHC 2000, Vol.II. This was brought out in somewhat fragmentary form in the examination-in-chief of Mr Davis. Prior to a hearing before the Committee on 13 January 2000 written memoranda of evidence were submitted by British American Tobacco, Gallaher Group plc, Imperial Tobacco Group plc, Philip Morris Europe SA and RG Reynolds Tobacco (UK) Ltd. Oral Evidence was given at the hearing by representatives of each of these companies. Mr Davis gave evidence as CEO of Imperial Tobacco Group plc.
[2.11]On 14 January 2000 the Clerk of the Committee wrote to each of these five companies asking for supplementary written evidence in response to five questions. One question was:
"Does smoking cause lung cancer, heart and circulation disease and respiratory illnesses, such as emphysema - 'cause' meaning that smoking is an activity that results in there being more lung cancer, heart and circulation disease and respiratory illness related deaths than there would otherwise be - other things being equal?"
In a letter dated 20 January 2000 the Corporate Affairs Director of Imperial Tobacco Group plc replied to this question:
"Imperial accepts that cigarette smoking may be a cause of lung cancer, cardiovascular disease and respiratory diseases, such as emphysema, and that cigarette smokers are more likely to develop these diseases than non-smokers. However, Imperial does not know whether or not there would be fewer deaths from these diseases in the absence of cigarette smoking."
The other four tobacco companies answered this question more or less in the affirmative. Another question was "Does your company believe that nicotine is addictive by reference to each of these criteria: (a)DSM-IV; (b)ICD-10?"
The reply to this question in the same letter was:
"We agree that nicotine could be regarded as addictive by reference to DSM-IV and ICD-10 but this does not mean that smokers are unable to stop smoking if they choose to do so."
[2.12]Under the heading "Research materials" the Corporate Affairs Director referred to a request by the Committee to Mr Davis to send them the documents from scientists and doctors employed by Imperial which had led Imperial to the conclusions which he communicated to the Committee. The letter continued:
"Our views on smoking and health are based on monitoring of the scientific literature, attending scientific conferences and meetings with and advice from external scientists. We maintain a substantial collection of smoking and health documents, consisting of articles from the scientific literature and other published material, and we are willing to furnish you with copies of these documents. However, we imagine that that may not assist the Committee both because they are readily available from other sources and because of their volume. The advice given by external scientists was not given in writing. If the Committee would find it helpful in its deliberations, we would be willing to ask the external scientists, who have advised us, to summarise their views and conclusions regarding smoking and health issues in writing."
[2.13]The letter concluded:
"The scientific issues which lie behind your questions are complex and answers can only be given on the basis of an exercise of judgment. Imperial's views on these issues reflect the judgment of the scientists whose advice it has received.
We agree that smoking may be a cause of disease. We recognise that other scientists and public health authorities have formed the judgment that smoking is a cause of certain diseases. This has been the consistent public health message for decades. We agree that there should be one consistent public health message. This is why, whatever our views on these complex issues, Imperial does not challenge the public health message. It has not done so for almost forty years and intends, in the future, to continue its policy of not challenging the public health message that smoking causes these diseases."
[2.14]Further oral evidence was given by the same five witnesses at a hearing of the Health Committee on 27 January 2000. In his evidence before the Committee, and again in his evidence before me, Mr Davis confirmed that the position of ITL was as set out in the passages from the letter dated 20 January 2000 quoted above.
Professor Sir Richard Doll
[2.15]The first substantive matter about which Sir Richard Doll (whose CV is set out at para.[5.189]) was asked was set out in a letter by him dated 8 September 1997 to Mrs McTear's Glasgow solicitor, Mr Cameron Fyfe. It related to a meeting which took place in London sometime between 1962, when RCP 1962 was published, and 1966, when Sir Richard started an investigation based on something that was said at the meeting. At the meeting there were the members of the Royal College of Physicians Committee on Smoking and Atmospheric Pollution, who had produced RCP 1962, and a couple of representatives of the tobacco industry. At that time ITL were the major tobacco company in the United Kingdom. They were represented at the meeting. There was a discussion about how the tobacco industry would react to the conclusions of RCP 1962. The tobacco industry representatives agreed that they would not contest the idea that cigarette smoking caused cancer of the lung, but said that they would continue selling their product because, in their view, it gave people pleasure. In the letter he wrote:
"You have only my word for it that the representative of the industry at the above meeting (I am not sure how many representatives were present, but there was certainly one) accepted the causal link between smoking and lung cancer and stated that the industry had agreed not to attempt to deny the causal link publicly."
He had, however, he said, other evidence that this was the case.
[2.16]First, Geoffrey Todd, the statistician to the tobacco industry, had from 1950 onwards tried to disprove the link. He came and discussed the evidence with Professor Bradford Hill and Sir Richard early in the 1950s. He produced several papers trying to disprove the relationship, but he finally came to the conclusion that they were correct, that cigarette smoking did cause cancer of the lung. He told the industry and, as a result, they concluded his contract. Sir Richard remembered this very well because Geoffrey Todd took Sir Richard and his wife out for dinner at a hotel in London and said that this was the last time he would have an expense account, as he was losing his job. A few days later he rang up and said that the tobacco industry had agreed to take him back on his own terms: namely, that they would accept that cigarette smoking caused lung cancer. So he went back to work for them for several more years. He would not work for them unless they accepted that cigarette smoking could cause lung cancer; he said that the evidence was so clear that he could not go on working for them unless they accepted that as the basis. This was in the early 1960s, Sir Richard could not say precisely when. Geoffrey Todd was, he thought, Secretary of the Tobacco Research Council, which had been formed by the members of the tobacco industry, including ITL.
[2.17]Secondly, this was confirmed by Professor Charles Fletcher in Fletcher 1992. He was a physician who worked at the Hammersmith Postgraduate Medical School and had done a lot of research initially into pneumoconiosis but became increasingly interested in smoking. He was a member of and Honorary Secretary to the committee which produced RCP 1962, which he edited. According to Fletcher 1992 he was instrumental, with others, in setting up the campaigning body ASH in 1971. During the interview Fletcher referred to Sir Richard's work on smoking and lung cancer. Sir Richard said that he started doing this work in 1947, and was paid to do it from 1948. This led in the first place to the publication of Doll and Hill 1950. Not so many people were interested in smoking, but there were a number of people interested in epidemiology. English epidemiologists were setting the international scene, and a lot of them were invited to go out and set up departments in America. Sir Richard did not agree with Fletcher's statement that epidemiology was really not regarded as part of medicine, but he said that it was not understood by physicians. Some of the leading physicians at the time embraced epidemiology, but it had not been understood by 90% of working doctors. Sir Richard agreed with Fletcher's remarks that the initial reaction to Doll and Hill 1950 was disbelief, in general, apart from some of the leading people like Sir Harold Himsworth of the MRC. The Medical Research Council's response to requests from the Government to advise them as to what were the causes of the increased mortality from lung cancer was MRC 1957.
[2.18]Fletcher 1992 mentioned the background to the formation of the Royal College of Physicians Committee. Fletcher had approached Sir Robert Platt, the President of the College, who agreed that it should produce a report on smoking and Fletcher suggested that he should invite Avery Jones, Guy Scadding and Bodley Scott to join it. Sir Richard said that Avery Jones was the leading gastroenterologist in the UK and a man with whom he had begun epidemiological research on the causes of gastric and duodenal ulcer in 1947. Guy Scadding was a respiratory physician and was the best doctor Sir Richard had ever known. Bodley Scott was a very well known haematological physician with a special interest in blood disease.
[2.19]According to Fletcher 1992 he was largely responsible for drafting RCP 1962. He had in mind the average Member of Parliament as the audience for this report. The response of the politicians was one of neglect. Enoch Powell was Minister of Health and he accepted the conclusions of the report. Asked what was the response of the tobacco industry, Fletcher said:
"That brings in Geoffrey Todd, who had been dismissed from his post as public relations officer with the tobacco manufacturers when he told them he accepted that smoking caused lung cancer. But they missed his administrative skills so much that they re-appointed him. He wrote to me before the report was published and said that he would like 20 copies to distribute to the main manufacturers because he wanted to insist that they took the issue seriously. Later the manufacturers set up a research division directed by Todd, which financed some of my work at Hammersmith. John Partridge, Chairman of Imperial Tobacco, accepted the evidence but was sure their scientists would be able to find a way of removing the cancer producing substance from the smoke."
Fletcher agreed that the tobacco industry's initial response was that they accepted the evidence but hoped they could change the product, take out the toxins. Sir Richard said that this passage in Fletcher 1992 confirmed his recollection of what Geoffrey Todd had said to him at dinner.
[2.20]Sir Richard was asked to comment the terms of the letter from the Corporate Affairs Director of Imperial Tobacco Group plc to the Clerk of the House of Commons Health Committee dated 20 January 2000. The letter concluded with the statement:
"[Imperial] intends, in the future, to continue its policy of not challenging the public health message that smoking causes these diseases."
Sir Richard said that this went back to the time of the meeting he was referring to in the early 1960s, which had been the catalyst for ITL's not denying the public health message.
[2.21]Sir Richard was asked in cross-examination about the position of Geoffrey Todd, who became Director of the Tobacco Research Council. Sir Richard said that his meeting with Todd was when he had been dismissed, and before he became Director of the Tobacco Research Council, probably around 1962. Reference to TRC 1967 did not assist his recollection.
[2.22]In Doll 1997 at p.25, Sir Richard said that following RCP 1962 and USSG 1964 "the tobacco industry in the UK agreed not to deny the causal relationship [between smoking and lung cancer] on the advice of Geoffrey Todd". Asked about this, Sir Richard said that Todd had told him that he had formed the judgment that the association was causal, and that the industry had accepted that they would not deny the causal relationship. To his knowledge, however, the tobacco industry did not say to the RCP or anybody else that they admitted that smoking caused lung cancer.
Mr Gareth Davis
[2.23]Gareth Davis, aged 53, CEO of Imperial Tobacco Group plc since 1996, was called as the last witness for the pursuer. It was brought out during his cross-examination by Mr Jones that, when it was suggested that Mr Davis should be called as a witness for Mrs McTear, an offer was made to her solicitors that the company's Corporate Affairs Director be made available instead of Mr Davis, as he had greater knowledge of some of the matters about which it was understood that Mr Davis would be asked, but the offer had been declined. I should also note that, throughout Mr Davis's examination-in-chief, no attempt was made to distinguish between Imperial Tobacco Group plc and its wholly-owned United Kingdom subsidiary ITL. I propose therefore to refer simply to "Imperial Tobacco", unless the context permits otherwise. For most of his examination-in-chief Mr McEachran treated Mr Davis as a hostile witness and subjected him to a form of cross-examination. The following summary of Mr Davis's evidence needs to be read in that light.
[2.24]Mr Davis said that prior to holding his present post he had been managing director of Imperial Tobacco Group plc and of their international subsidiary Imperial Tobacco International Limited. He had worked for Imperial Tobacco since 1972. He did not hold any professional qualification apart from a university degree. Imperial Tobacco Group plc were about thirtieth of the top 100 companies in the FTSE Index and were one of the largest companies in the United Kingdom. His salary and incentives were more than £1 million a year.
[2.25]Before coming to give evidence Mr Davis had spoken with Imperial Tobacco's advisers and was able to speak on behalf of the company. He was asked about an interview with him which had been published in the Daily Telegraph on 9 August 2003, under the headline "Just a good bloke who likes a good smoke". He told the interviewer that he was a smoker. About the age of 15 he started to smoke fairly regularly. His mother stopped smoking shortly after he started, but at the time he started both his parents were smokers. He told the interviewer how he "nicked" cigarettes from his parents. In those days, smoking was almost a rite of passage. He remembered "meeting that milestone" at the age of 14 on holiday in South Wales. He was still a smoker.
[2.26]Mr Davis was asked about an article by Ron Ferguson in The Herald of 9 October 2003. (At an earlier stage, during the evidence of Professor Hastings, Mr McEachran sought leave to add Mr Ferguson's name to the list of witnesses for the pursuer. After discussion I continued this motion, but it was subsequently dropped by Mr McEachran). In the article, Mr Ferguson stated:
"Attitudes to smoking have changed dramatically within the past three decades. I grew up at a time when nearly everybody smoked. Both my parents smoked, as did most of the adults I knew. [...] We were all influenced by the movies. All the glamorous American film stars smoked. [...] Every public place was a smoke-filled zone, and every jacket was a smoking jacket. Restaurants were filled with swirling clouds, as people smoked right through meals. To be a non-smoker was to be a freak with a headache."
Mr Davis said that it was fair to say that in his experience, as a teenager, when his parents and a great number of their friends smoked, smoking was fairly common. He thought that smoking was something that a lot of teenagers did. He regarded the latter part of the passage quoted as a slightly extreme representation of his recollection of society at the time, though he thought it was fair to say that there was a lot more smoking then than there was now.
[2.27]Mr McEachran asked Mr Davis whether he accepted that Imperial Tobacco, as manufacturers of cigarettes, had a duty to take reasonable care for the safety of the consumers of those cigarettes. Mr Davis said that he thought that Imperial Tobacco, as manufacturers, had a duty to provide products to their customers that were fit for their intended purpose. The responsibility was on them to produce cigarettes to their correct specification, that were fit for their purpose. Obviously, he said, other circumstances came into play about awareness etc. Asked whether his answer to the question was "Yes" or "No", he said that he supposed "I do not know" was the strict answer, in the sense that it depended on a lot of other circumstances, like the level of awareness in society of the various issues associated with the product.
[2.28]In UKHC 2000, Vol.I, p.xvii, para.14, figures were given for cigarette smoking levels in the United Kingdom. It was stated that by the end of World War II 65% of adult men and 41% of adult women smoked cigarettes. In 1974 cigarette smoking levels of 51% of men and 41% of women were recorded. In 1998 the figures indicated that in the United Kingdom 28% of men and 26% of women smoked. Mr Davis said that he had no reason to doubt these figures. He agreed that they confirmed that there was more smoking in 1974 than in 1998. In para.15, the committee stated that in Britain the market was dominated by two companies, Gallaher Group plc and Imperial Tobacco. Their manufactured cigarette brand shares were respectively 40.3% and 28.3% in 1996. The committee noted that Imperial Tobacco's market share was now nearer that of Gallaher, and Mr Davis's evidence was that Imperial Tobacco had overtaken Gallaher. In the 1960s, Imperial Tobacco's share of the UK market was in the order of 60% to 65%.
[2.29]On p.xviii, in para.16, the committee stated:
"Reductions in smoking rates have thus been substantial but they have not been evenly distributed among social classes with the result that smoking is a prime cause of health inequalities. The Royal College of Physicians report [RCP 2000] noted that, over the period in which the GHS [General Household Survey] has been conducted, smoking prevalence fell by more than 50% in the most advantaged sector of British society, but remained static amongst the least advantaged. [...] Men who lived in the unskilled manual groups were nearly three times as likely to smoke as those who lived in professional households (44% compared to 15%)."
Mr Davis said that he had no reason to doubt these figures. He would say that someone in Imperial Tobacco would be aware of them. He personally could not say that he was and he could not quote them accurately. There were people in Imperial Tobacco who looked at the marketing and saw where the sales took place and who would make reports to him. Imperial Tobacco also had scientists who worked for them and advised them on scientific matters, throughout the corporate affairs division. It was his understanding that Imperial Tobacco had had scientists since the 1960s. At p.xix, para.17, the committee stated:
"The papers we obtained from advertising agents handling tobacco accounts [...] showed that the agencies and their clients specifically targeted less well-off consumers."
Mr Davis said that this was not correct, so far as he was aware.
[2.30]In UKHC 2000, Vol.I, para.3 at p.xv it was stated that a more detailed analysis of the extent to which smoking contributed to death came from RCP 2000. This was followed by a table in the same terms as Table 1.2 on p.17 of RCP 2000. The table was headed "Estimated number and percentage of deaths attributable to smoking by cause, UK 1997". Under a sub-heading "Diseases caused in part by [smoking]" and "[cancer]" (the words "smoking" and "cancer", which appeared in RCP 2000, were inadvertently omitted in UKHC 2000), it was stated that 19,600 men died of cancer of the lung, caused in part by smoking, representing 89% of all deaths from this disease in men. It was also stated that a total of 118,800 men and women had died from diseases caused in part by smoking. Asked whether he accepted these figures, Mr Davis said that he had absolutely no reason to question them, but he did not know them. The figures had been provided to the committee and he had no reason to doubt them. He agreed that they were derived from RCP 2000. He did not know whether this would be a document which would be read by people in Imperial Tobacco; it was not a document he had read. There might be people in Imperial Tobacco who would read a document like this, but he could not say that he knew this. No one had complained to him, or to the board of directors, that the Royal College of Physicians was putting out incorrect information about deaths arising from smoking.
[2.31]Mr Davis was next asked about UKWP 1998. In the preface, the Prime Minister (the Rt. Hon. Tony Blair, M.P.), stated:
"In Britain today, more than 120,000 people are going to die over the next year from illnesses directly related to smoking."
Mr Davis said that he did not know this, it was something that the Prime Minister was saying. No one in Imperial Tobacco had suggested that these figures were wrong. The title of the White Paper was "Smoking Kills". Mr Davis said that, as he had already explained, Imperial Tobacco did not know this: smoking might or might not kill, but they did not know. This was the position of the company and endorsed by himself.
[2.32]Imperial Tobacco had decided some time before 1996, when he became CEO, that they did not know whether smoking killed. This was a position arrived at over several decades, probably thirty years or so, since the debate about smoking and health began in the early 1950s. He did not know whether the company had advice as to whether what was being said in the debate was correct or not. It was long before his time, but he was aware of the company's submission to the Health Committee that enumerated a lot of the advice and research that the company and the rest of the tobacco industry undertook. The position of the company had been arrived at over a number of decades, with a great deal of resources and a great deal of effort. As he said, it was a position he would endorse. He did not know the details of their archive, it was very substantial. But over the decades there was a great deal of research and contact involving not only their internal scientists but external scientists whose advice and opinions were sought. He did not know whether these would be provided in written form. He was not aware that among the productions in this case there was no written documentation of any type from Imperial Tobacco to back up what he was saying. He would expect there to have been presentations, but he would not like to speculate whether there would be hard copies of discussions and presentations.
[2.33]When UKWP 1998 came out, there was no comment to the board from the scientists as to whether they accepted what was stated in it, so far as he could recall. He had seen the figure of 120,000 deaths in various statements on television, in the press, from the Government, on many occasions. So he would not say it was ground-breaking news when the preface was written by the Prime Minister. If the statement was correct, then one would have to accept that cigarettes were dangerous. In the foreword to the White Paper, the Secretaries of State for Health, for Scotland, for Northern Ireland and for Wales stated: "Smoking kills. That has been known for years." Mr Davis said that he did not think it was the case that Imperial Tobacco knew this when the White Paper was published. In para.1.14 the White Paper stated:
"[F]or every 1,000 20-year-old smokers it is estimated that while one will be murdered and six will die in motor accidents, 250 will die in middle age from smoking, and 250 will die in older age from smoking."
Mr Davis said he had no idea whether this was correct. In para.1.25 it was stated:
"Tobacco is a uniquely dangerous product. If introduced today, it would not stand the remotest chance of being legal."
Mr Davis said he did not know, this was a very hypothetical point. He could not say he agreed or disagreed, it was a totally hypothetical situation. New products were tested, but he really could not say whether this statement was correct. He did not know whether the authors of the White Paper were correct. He did not think it was obvious, it was hypothetical.
[2.34]Mr Davis said he did not know that the other British tobacco manufacturing companies accepted that smoking caused lung cancer, but he believed they had slightly different positions to that of Imperial Tobacco. He was asked about a statement on the website of Philip Morris USA, dated 14 October 2003:
"We agree with the overwhelming medical and scientific consensus that cigarette smoking causes lung cancer, heart disease, emphysema and other serious diseases in smokers. Smokers are far more likely to develop serious diseases, like lung cancer, than non-smokers. There is no 'safe' cigarette."
Mr Davis said that there were parts of this that he would agree with, but not in its entirety. He thought it was fair to say that Imperial Tobacco believed smokers were far more likely to develop serious diseases, like lung cancer, than non-smokers, and they agreed that there was no safe cigarette. This did not mean that he agreed that smoking caused lung cancer. Over the years there had been a significant amount of statistical association between smoking and certain diseases, including lung cancer, but he thought most scientists would agree that statistical association did not equal causation. This was a "judgmental call" that Philip Morris had made in the light of their work. He did not know the circumstances or the thoughts behind their position, but Imperial Tobacco had a different position, they had come to a different judgment some years ago. Since he became CEO, the board of Imperial Tobacco had discussed the question whether smoking caused lung cancer. They had had a presentation on the position of the company and this had been raised at their board meeting. He was not sure that there were written papers prepared, but they had had a presentation on it within the last seven or eight years. He could not recall who had made the presentation.
[2.35]Philip Morris USA also stated on their website:
"We agree with the overwhelming medical and scientific consensus that cigarette smoking is addictive. It can be very difficult to quit smoking, but this should not deter smokers who want to quit from trying to do so."
Mr Davis said he thought that Imperial Tobacco's position was that they agreed that smoking would be categorised as addictive under certain definitions of the term, but if it meant that smokers were unable to give up smoking, then that was quite clearly not the case. People were able to give up smoking if they wished to. He accepted that some people had difficulty. Asked by me what definition of "addiction" he would agree with, he said that he thought that under certain of the public health body definitions, smoking could be regarded as addictive. But he reiterated that if "addiction" meant that people were unable to give up smoking, then quite clearly that was not the case.
[2.36]In the letter from the Corporate Affairs Director of Imperial Tobacco Group plc to the Clerk of the Health Committee dated 20 January 2000 reference was made to advice received by the company from scientists. Mr Davis said that he had been at one board meeting at which internal scientists had made presentations on the question whether smoking caused lung cancer, and he had attended presentations by outside scientists on occasions other than board meetings.
[2.37]Mr McEachran asked Mr Davis about statements printed on packs of cigarettes manufactured by ITL. On three of them was the statement "Smoking kills". Asked whether ITL accepted that this was so, he said that the answer was that they did not know; it might do, but they did not know. There was quite a long history of health warnings back to 1971, when Government health warnings first appeared on cigarette packets, and more recently EC Directives had come in to play. Reference was made to Directive 2001/37/EC of 5 June 2001 on the approximation of the laws, regulations and administrative provisions of the Member States concerning the manufacture, presentation and sale of tobacco products. (Although no express reference was made to earlier directives, I observe from the text of this one that Directive 89/622/EEC of 13 November 1989 established a general warning to be carried on the unit packaging of all tobacco products, together with additional warnings exclusively for cigarettes and, after amendment by Directive 92/41/EEC, from 1992 extended the requirement for additional warnings to other tobacco products.) One of the effects of the 2001 directive was that each unit packet of tobacco products must carry, in a prescribed manner, a general warning "Smoking kills/Smoking can kill" or "Smoking seriously harms you and others around you", and an additional warning taken from a list, among them "Smoking causes fatal lung cancer", "Smoking is highly addictive, don't start" and "Smoking can cause a slow and painful death".
[2.38]Asked whether his company accepted that these statements were accurate, Mr Davis said that they put the warnings on their packs. They did not challenge the public health message at all. So they fully complied with the requirements as to labelling. These warnings were giving a health message, but he had to say that they did not know whether some of them were correct. They did not know whether smoking caused fatal lung cancer. Under certain definitions they accepted that smoking could be categorised as addictive, but if this meant that smokers were unable to stop smoking, that was clearly not the case: if they wished to stop, they could. For some people it was difficult. These warnings were an integral part of the public health message which they did not challenge. Government health warnings were first put on cigarette packets in 1971. There were no warnings prior to that. In the United Kingdom, ITL had not, separately from these warnings, printed a manufacturer's health warning. For many years the contents, in terms of tar and nicotine yields, had been printed on packs.
[2.39]Mr McEachran asked Mr Davis whether the position adopted by his company was to avoid litigation. Mr Davis said it was not for this reason, their position was that they did not know whether smoking caused lung cancer. Epidemiological studies over the years had shown a statistical association between smoking and certain diseases, including lung cancer. Scientists generally would agree that a statistical association did not in itself establish a cause and effect relationship. After decades of research there were many questions that remained unanswered, and the biological mechanisms by which these diseases occurred and the part that smoking played in them were still unknown. Counsel asked: "Is it the position that you have been so long with this position that you do not know, you just dare not change from it because it will make you look ridiculous?", to which Mr Davis replied "No, not at all."
[2.40]It is admitted on record that ITL were aware at the time of their publication of various studies and reports in which, to put it briefly, it was concluded that the statistical association between cigarette smoking and lung cancer was one of cause and effect. Mr Davis said that he really did not know what the attitude of ITL was to these publications, it was long before his time. Mr McEachran drew attention to passages in newspaper reports which indicated that the tobacco manufacturers did not accept that this had been proved, and that they had agreed to make a grant of £25,000 available to the Medical Research Council for research. Reference was made to the ministerial statement of 12 February 1954, set out at para.[3.2]. Asked whether ITL, having paid towards the research, accepted what the researchers found, Mr Davis said that he did not know. He presumed that the position of the tobacco manufacturers was as stated in a newspaper report, that there was still no proof from any scientific field that smoking was a cause of lung cancer. The statistical evidence certainly did not prove a causal connection, and the pressing need was for a comprehensive attempt to close the gap between fact and speculation. They would continue to assist in research.
[2.41]It is admitted in the pleadings that in 1958 a Dr Herbert Bentley, a research scientist employed by ITL, accompanied two employees of other British tobacco companies on a trip to meet a number of scientists from the United States tobacco industry and other experts. An excerpt from their report, under the heading "'Causation' of lung cancer" was produced pursuant to an order of this court, but there was no evidence as to its origins. Mr Jones stated, during the course of discussion about the nature of this document, that it had come, not from ITL's archives, but from an entirely different source (see also para.[2.54]). The excerpt stated:
"With one exception [...] the individuals whom we met believed that smoking causes lung cancer if by 'causation' we mean any chain of events which leads finally to lung cancer and which involves smoking as an indispensable link. [...] We found disagreement however as to the likely mechanism by which smoking may cause lung cancer. [...] Otherwise we found general acceptance of the view that the most likely means of causation is that tobacco smoke contains carcinogenic substances present in sufficient quantity to provide lung cancer when acting for a long time in a sensitive individual. It was argued that the only positive experimental evidence to date, using animal tissues sensitive to carcinogens, is at the very least entirely consistent with this view as is the fact that several known carcinogens have already been found to be present in smoke condensates. It is generally accepted that tobacco smoke is only feebly carcinogenic. The main effort [...] therefore has switched from trying to confirm the direct causal hypothesis to trying to find biological test systems which will allow active substances in smoke to be identified."
Mr Davis agreed that these were important matters and it was possible that they had been reported to the board of ITL. Asked whether it was the situation that from that date the scientists in ITL did accept the causal link, Mr Davis said that so far as he was aware they did not.
[2.42]RCP 1962 contained the statement: "Cigarette smoking is a cause of lung cancer." Mr Davis said that he did not know what his company's reaction was to this report. He was aware that in about 1962 the Tobacco Manufacturers' Standing Committee opened a research laboratory at Harrogate. From a newspaper report in 1962, it appeared that the Committee were saying that more research needed to be done. Mr Davis agreed that, as was stated in this report, in that year an agreement was reached between the Independent Television Authority and the representatives of tobacco manufacturers to exclude certain kinds of cigarette advertisements from commercial television broadcasts. Under an agreed code, advertisements would be excluded which suggested that cigarette smoking was inseparable from masculinity, that it was a desirable recreation for young people, that it was a socially acceptable habit, that smoking produced ecstatic pleasure, and that smoking was enjoyed by popular heroes or heroines. Mr Davis agreed that prior to this agreement tobacco advertisements had contained such elements.
[2.43]Mr Davis was asked about expenditure on advertising, under reference to passages in RCP 1977. He was asked whether he accepted that there was much more tobacco advertising in the mid-1970s than there was Government anti-smoking publicity material. He said that this was not the right comparison, because there was also coverage in news stories and documentaries in the press and on television. He did not agree with a statement that brand advertising must inevitably increase the total market for tobacco products.
[2.44]Asked about the denial in the pleadings for ITL of the averment for Mrs McTear that "cigarette smoking can cause lung cancer", Mr Davis said that he thought the situation was that they did not know whether cigarette smoking caused lung cancer or not. They did not deny it, they did not know. He thought that it was reasonable to assume that Imperial Tobacco were aware of IARC 1986, the conclusions to which contained the statement that lung cancer was believed to be the most important cause of death from cancer in the world, with estimated total deaths in excess of 1 million annually, and that the major cause of the disease was tobacco smoking, primarily of cigarettes. Mr Davis said that he had no cause to doubt these numbers. He did not know whether the scientists drew the report to the attention of Imperial Tobacco's board. IARC 2004 contained, in the summary published in 2002, the statement that lung cancer was the most common cause of death from cancer in the world, the total number of cases was now estimated to be 1.2 million annually and was still increasing, and that the major cause of lung cancer was tobacco smoking, primarily of cigarettes. So far as he was aware, this had not been drawn to the attention of his company's board. Reports such as these would be considered by the company's corporate affairs department, which had the relevant specialists. It was fair to say that from the 1950s the whole smoking and health issue started to gather momentum and certainly there were considerations of health risk associated with smoking. The position of Imperial Tobacco had been and remained as was stated by the Corporate Affairs Director in his letter to the Health Committee.
[2.45]Mr Davis said he was not aware that the majority of people who smoked cigarettes manufactured by ITL came from the lowest social class. He was asked about statements in MacAskill et al. 2002. Mr Davis said that he was aware that there was a higher incidence of smoking among the lower socio-economic groups, but he was unaware of the detailed statistics. He thought that irrespective of socio-economic groups, certain smokers had experienced difficulty when trying to give up smoking. He was not aware that it was more difficult for members of one section of the community than others to give up smoking. Certain individuals would find it difficult to give up and he would not like to differentiate between them on any basis of social engineering. He did not agree with the statement that tobacco marketing ensured high levels of tobacco purchase and consumption in low-income communities.
[2.46]ITL's products were distributed to as many outlets as possible. Their marketing was intended to promote their brands at the expense of their competitors' brands and to get adults who had chosen to smoke to switch from other manufacturers' brands to their brand. This was the purpose of the advertising part of their marketing mix. Over the years of advertising, the United Kingdom market had declined by nearly one-half, which did not support the suggestion that marketing resulted in increased overall volume. As a company their objective was to maximise their sales on a world-wide basis, this was part of their mission, and tobacco marketing and advertising was one of the techniques that they used for this. ITL's advertising, as was general in the tobacco industry before the prohibition on advertising, was basically to create and develop awareness of ITL's brands and to attract smokers of other manufacturers' brands. It was admitted in the pleadings for ITL that they had spent millions of pounds since 1960 in the promotion of the smoking of their cigarettes and tobacco. This was primarily aimed at the smokers of other manufacturers' cigarettes. ITL were attempting to get conversion. If the advertising reinforced loyalty from their existing smokers, then so much the better. It was not the purpose of their advertising to bring in non-smokers.
[2.47]Mr Davis was asked further questions about the research at the Harrogate Laboratory. The Tobacco Manufacturers' Standing Committee changed its name to the Tobacco Research Council in 1963. The core activity at Harrogate was to obtain as much information as possible about the chemical nature of smoke by means of a mouse skin-painting programme to measure biological activity. By 1969 the major part of the research effort was concerned with the search for compounds in cigarette smoke with potential biological activity by breaking the smoke down into its constituent parts. The research was abandoned in 1970, with the statement that it had been taken as far as it profitably could. Mr Davis said that this was in accordance with his understanding. He did not agree with Mr McEachran's suggestion that the correct conclusion was that "the scientists got to a stage where the only way of keeping carcinogens from tobacco smoke was really to abolish the cigarette". He had not heard that story.
[2.48]Mr Davis was asked about oral evidence he had given to the Health Committee on 13 and 27 January 2000, as reported in UKHC 2000 Vol.II, pp.238-264 and 361-387. At p.240 Mr Davis said that ITL did not know whether a cigarette was safe or unsafe. They were aware of the public health debate. At p.241 he said:
"I think the situation is that the public health authorities have concluded that cigarette smoking causes certain diseases. That has been the situation for over four decades whilst the smoking issue and smoking and health debate has been in play. I think throughout that time I would say that certainly we have never sought to challenge the public health message that has been issued by the public health authorities, nor would I presume to challenge the figures put out by the public health authorities."
He personally was not qualified to challenge the figures and had no basis therefore on which to challenge them. At p.242 Mr Davis said in answer to a question of Dr Peter Brand, M.P.:
"We accept that smokers are more likely to develop lung cancer and certain other diseases than non-smokers. We do not deny that smoking is a cause of those diseases but we do not agree that smoking has been shown to be the cause of lung cancer and those other diseases."
Imperial Tobacco had never sought to challenge the public health message embedded in the conclusions the public authorities had come to that smoking did cause diseases, including lung cancer. At p.243 he said:
"Our people within the company have obviously reviewed the vast body of literature and studies that have taken place. They have sought expert advice from outside the company also. The judgment - and it is a judgment - that they have come to, and that I endorse, is that we do not agree that smoking has been shown [to cause disease]. We accept that smokers are more likely to develop diseases but we do not believe that it has been shown."
[2.49]Mr Davis explained that what he was saying to the Health Committee was that it was accepted that there was a significant statistical association between smoking and the diseases they were talking about, that scientists would agree that a statistical association did not equal the establishment of a causal effect, and that the biological mechanisms were unknown. He agreed that ITL had access to some very eminent scientists. The assistance and advice they had from outside scientific advisers had led them to the judgment that smoking had not been shown to be a cause of cancer. His position in giving evidence at the proof had been the same as when he gave evidence to the Health Committee. The positions they had arrived at were based on their internal experts reviewing the literature and taking expert advice from scientists outside the company. Over the previous ten years or so these positions had become more clear. Imperial Tobacco's position was that they did not know whether cigarette smoking was causally linked with lung cancer. He would expect an unemployed Class 5 Ayrshire man in 1964 (such as Mr McTear) to know that there were risks associated with smoking. He would not expect him to know that there was causality.
[2.50]In a brief cross-examination Mr Davis said that Imperial Tobacco had just under 17,000 employees world-wide. They sold to 150 countries and had factories or sales operations in ninety-eight countries. He had overall responsibility for the group's activities and ultimately the employees of the group were his responsibility at all of the locations world-wide. There was a management structure in which there was downwards delegation. The corporate affairs division was responsible for scientific affairs, research activity, economic affairs, legal affairs and corporate communications. There were other divisions concerned with manufacturing, sales and marketing. The members of the corporate affairs division reported ultimately to the Corporate Affairs Director, who was a member of the main board.
[2.51]Mr Davis did not have information that would allow him to understand what was meant by the phrase "highly addictive". In UKHC 2000 a table, derived from RCP 2000, gave "estimated number and percentage of deaths attributable to smoking by cause". Mr Davis did not have information that would allow him to know who carried out this estimate or by what method, or what was meant by use of the word "attributable". Equally, he had no information as to how the estimates of numbers of deaths from lung cancer caused by cigarette smoking in IARC 1986 and IARC 2004 had been arrived at.
Professor James Friend
[2.52]Professor Friend (whose CV is set out at para.[5.27]) offered a commentary on the position of ITL. I propose to summarise this quite briefly. He referred to the evidence given by Mr Davis to the Health Committee and to the letter by the Director of Corporate Affairs for Imperial Tobacco Group plc referred to in UKHC 2000, in particular statements that the company did not challenge the public health message that smoking caused disease. He said that in view of this he could not understand why ITL was denying what was stated on behalf of Mrs McTear. Of the five tobacco companies who gave evidence to the Health Committee, Imperial Tobacco Group plc were the only one who denied that smoking could cause lung cancer. He found the position adopted by ITL very difficult to understand and indeed illogical. The public health message was based on ongoing research which had continued for almost fifty years. The position of ITL was contradicted by statements in the Department of Health Memorandum which was before the Health Committee and in UKWP 1998. In Doll 1997 Sir Richard Doll stated at p.25 that following the publication of RCP 1962 and USSG 1964 "the idea that smoking was a major cause of lung cancer ceased to be seriously challenged." Professor Friend said that he agreed with this. That smoking caused lung cancer was not just a hypothesis, but a statement which was now well accepted in the whole medical and scientific community.
[2.53]Professor Friend said that he was told that ITL appeared to deny that they knew prior to 1964 that smoking could cause lung cancer, but they did accept that they were aware of the studies of Doll and Hill in 1952 and Hammond and Horn in 1954, and of the report RCP 1962. Furthermore, they agreed that in 1958, Dr Bentley, a research scientist employed by them, went to the United States. Having met a number of United Stated tobacco industry scientists and experts he reported that "with one exception the individuals whom we met believed that smoking causes lung cancer". Professor Friend said:
"Although in public the tobacco industry did not accept that smoking caused lung cancer, it seems clear that Imperial would have been aware that cigarette smoking can cause lung cancer prior to 1964."
Professor Gerard Hastings
[2.54]Professor Hastings (whose CV is set out at paras.[5.305] to [5.307]) had prepared a report for the purposes of a proof. In the introduction he wrote:
"I note that Imperial Tobacco are arguing that Alf McTear knew or ought to have known, about the risks of smoking in the 1960's. It is certainly true that the health consequences of smoking were becoming well known by this time. The first UK research had been published by Richard Doll and colleagues in the early 1950's. This was endorsed by the Royal College of Physicians in the UK (1962) and the Surgeon General in the US (1964). The issue would, as Imperial Tobacco state, have received a lot of media attention.
It is also clear that Imperial Tobacco was well aware of these developments, not only from the published medical evidence, but also from internal industry sources. Martyn Day, a solicitor in the firm of Leigh, Day and Co, which represented hundreds of claimants in unsuccessful actions against the tobacco companies between 1992-98 and had access to 'hundreds of thousands of pages' of internal tobacco company documents under the discovery process, stated to the Westminster [House of Commons] Health Select Committee (2000, para.34):
'in 1958 Dr Bentley, a leading research scientist for Imperial, accompanied two other British tobacco experts on a trip to meet a number of scientists from the US tobacco industry and other independent experts. In their report of the meeting to Imperial they said: 'with one exception... the individuals whom we met believed that smoking causes lung cancer'."
Submissions for Mrs McTear
[2.55]Mr McEachran submitted that the Corporate Affairs Director of Imperial Tobacco Group plc had written to the House of Commons Health Committee: "Imperial does not challenge the public health message and intends, in the future, to continue its policy of not challenging the public health message that smoking causes these diseases." Mr Davis said to the Committee that he would not presume to challenge the figures put out by the public health authorities. Therefore the evidence before the court was really unchallenged; the position of ITL was that they did not challenge the public health message and, in this case, the public health figures about the number of lung cancer deaths caused by cigarette smoking. In his evidence Mr Davis said that he thought it was fair to say that Imperial Tobacco believed smokers were far more likely to develop serious diseases like lung cancer than non-smokers, and they agreed that there was no safe cigarette. In counsel's submission, this was almost tantamount to admitting that cigarette smoking could cause lung cancer. This fell to be contrasted with ITL's pleadings, in which the averment for Mrs McTear that cigarette smoking could cause lung cancer was denied. In counsel's submission, properly viewed, the position of ITL was "not known but not challenged". This reflected the realities of the matter. The health message, embedded in the conclusion that the public health authorities had come to, that smoking did cause diseases, was not challenged. So ITL did not challenge the public health figures which showed the very large number of cases attributable to smoking.
[2.56]Counsel submitted that there seemed to have been occasions in the past when ITL accepted that cigarette smoking could cause lung cancer. Dr Bentley of ITL was recorded as accepting in 1958 that there was a causal relationship between cigarette smoking and cancer. By the 1950s the tobacco industry, including ITL, knew that cigarette smoking involved health risks, including an increased risk of death. This was the effect of the evidence given by representatives of the tobacco industry to the Health Committee. Mr Davis said that the Harrogate Laboratory was established in 1962 on the basis of that working hypothesis. So, counsel submitted, the response of the industry, including ITL, to the knowledge that cigarette smoking involved health risks was to start to do some research to try to remove the carcinogen from tobacco smoke which caused the lung cancer. This research caused problems for the industry and ITL, and they stopped the research.
[2.57]Whatever their public position, ITL's internal position seemed to be that they accepted causation. In addition to the evidence about Dr Bentley, counsel referred to Sir Richard Doll's evidence about the meeting in 1962 at which ITL were represented. The tobacco representatives, according to Sir Richard, agreed that they would not contest the idea that cigarette smoking caused cancer of the lung, but they would continue selling their product because, in their view, it gave people pleasure. He also referred to Sir Richard's evidence about Geoffrey Todd, who finally came to the conclusion that cigarette smoking did cause lung cancer. He told the tobacco industry and they concluded his contract. Later he told Sir Richard that the tobacco industry had agreed to take him back on his own terms, namely that they would not deny that - they would accept that cigarette smoking caused lung cancer. In Fletcher 1992 it was stated that John Partridge, the Chairman of ITL, accepted the evidence but was sure than scientists would be able to find a way of removing the cancer-producing substance from the smoke. All of these pieces of evidence, counsel submitted, indicated that ITL actually were accepting that cigarette smoking caused lung cancer: whatever their public position their internal position was that they did accept causation.
[2.58]Counsel submitted that the evidence on this matter was both overwhelming and not disputed. ITL admitted in their pleadings that they were aware on publication of articles by Doll and Hill in 1952 and Hammond and Horn in 1954, and the reports RCP 1962 and USSG 1964. It was not disputed by ITL that the United States Government, the United Kingdom Government and the World Health Organization had all accepted for many years that smoking could cause lung cancer. It also came out in the evidence, including that of Professor Platz, and was not challenged, that all the United States cigarette companies, and all the United Kingdom cigarette companies except ITL, accepted that cigarette smoking could cause lung cancer. The position of the United Kingdom companies was to be found in UKHC 2000.
[2.59]The position of ITL in their evidence to the Committee and through their CEO at the proof was that they did not know whether cigarette smoking caused lung cancer. They said it was not scientifically proved. They accepted that smokers were more likely to develop lung cancer than non-smokers. They did not deny that smoking was a cause of these diseases. They did not challenge the public health message that smoking could cause lung cancer or the public health figures. The clear inference was that this was done because the message was accepted. Mr Davis said that the position of ITL had been arrived at over a number of decades, with a great deal of resource and a great deal of effort. He, and ITL, said that they did not know whether or not smoking killed. He was not aware of any documentation of ITL relating to this. No documentation had been lodged by ITL to back up their position. The suspicion must be that this was entirely hocus pocus and just a position adopted by ITL to ward off litigation. When the Corporate Affairs Director wrote to the Committee stating that external scientists had not provided their advice in writing, counsel submitted that this was just a cover for explaining why there were not any documents available. The fact that Mr Davis could not point to written material, and none had been lodged as productions in the present case, demonstrated how incredible, unreliable and threadbare was the position of ITL on this issue.
[2.60]When Mr Davis said that it was fair to say that ITL believed that smokers were far more likely to develop serious diseases, like lung cancer, than non-smokers and that there was no safe cigarette, having taken advice before he gave evidence and speaking for the company, this was really tantamount to accepting that cigarette smoking caused or could cause lung cancer. Mr Davis had adopted the position before the Health Committee of the House of Commons that, after obtaining expert advice from outside the company, the judgment was that they agreed that smoking had not been shown to be a cause of lung cancer. He prevaricated before the Committee and again when giving evidence when he was unable to point to any written evidence in support of this position. He was initially unable to give the names of scientists who had advised ITL, but after a coffee break he was suddenly able to give the names of a number of them. Counsel submitted that this was an odd change of front and Mr Davis must have obtained the information during the coffee break.
[2.61]Counsel's general comment on Mr Davis was that his evidence was very unsatisfactory. He often refused to give a "Yes" or "No" answer. It was clear he prevaricated, in particular about documentation. He was very vague about the internal workings of ITL and how matters such as IARC 1986 would have been dealt with. He was very vague about presentations by internal or external scientists and whether they were to the board or not. Counsel suggested that he must have known about these things because he was briefed before giving evidence. He tried to say that he was not aware of IARC 1986 and then, when faced with the IARC 2004 conclusions (published in 2002), again he denied all knowledge. It was scarcely credible that he was not aware of IARC 1986. What was credible was that ITL in fact knew very well that cigarettes caused lung cancer and these matters were just filed as additional evidence supporting that. His evidence about the documentation, the "do not know" position, counsel submitted, was incredible and perhaps dishonest. He was asked in court, and by the House of Commons Health Committee, about it, and if there was any such documentation it would have been bound to be produced, considering the huge amount of material which had been produced by ITL. The real inference was that there was no documentary evidence here because the internal position of ITL, as counsel submitted had been shown by the evidence, was really far different from their public position. The position as put forward by Mr Davis was contrary to the position adopted by ITL in their pleadings. In the pleadings ITL denied that smoking caused lung cancer and that smoking was addictive. But when regard was had to Mr Davis's evidence in court, and to the Health Committee, ITL's position was that they did not know about smoking causing lung cancer and their evidence was that they accepted that smoking was addictive on the criteria put forward in the Surgeon General's report. This was extremely unsatisfactory in a case involving one of the largest companies in the United Kingdom.
Submissions for ITL
[2.62]Mr Jones referred to the historical background, as established at the proof. In 1950, epidemiologists in the United States and the United Kingdom reported a statistical association between lung cancer in males and heavy cigarette smoking. The research had been prompted by an apparent increase in the incidence of lung cancer. These epidemiological reports encouraged several researchers to conduct laboratory studies in animals, particularly mice, using tobacco derivatives and applying methods that had been developed and employed in the study of chemical carcinogens in the early part of the twentieth century. They believed that, if smoking caused lung cancer, they should be able to identify the constituent or constituents in tobacco smoke that was or were responsible with a view to its or their removal. By the 1970s, that research, having proved unavailing, came to a close.
[2.63]Running in parallel with the animal skin-painting experiments, researchers have begun to conduct studies in which laboratory animals were exposed to whole cigarette smoke by inhalation. The objectives of that research were to determine whether or not evidence could be produced that cigarette smoking could cause lung cancer in animals, and thereby investigate a possible relationship between human lung cancer and cigarette smoking. The research was unsuccessful. The evidence was that laboratory animals exposed to whole cigarette smoke by inhalation did not develop squamous cell carcinoma of the lung. Other laboratory work designed to discover a causal link between smoking and lung cancer failed to do so. Today the belief that cigarette smoking could cause lung cancer rested primarily on the statistical association.
[2.64]Furthermore, the determination of the question whether or not the statistical association was causal itself required an exercise of judgment to be formed in the light of all the available, relevant evidence. Both Professor Friend and Sir Richard Doll agreed with a passage in USSG 1964, p.20, to this effect. The distinction between association and causation had caused difficulty in various contexts in the course of the proof and Mr McEachran's submissions. It was clear from his brief review of the historical background that association and causation were not synonymous. ITL's view on causation, as expressed both at the House of Commons Health Committee hearings and during the proof, was that they accepted that there was a statistical association between cigarette smoking and lung cancer. They had been advised by appropriately qualified scientists that cigarette smoking had not been shown to be a cause of lung cancer. The statistical association therefore might or might not be causal, and ITL had accepted that advice. In view of this, they did not deny the public health message that cigarette smoking could cause lung cancer. On the same logic, however, they did not accept that cigarette smoking was a cause of lung cancer. Furthermore, it was ITL's general policy not to challenge the public health message by announcing in public that, in the view of the scientists who had advised them, smoking had not been shown to be a cause of lung cancer. There were of course exceptions to that generality, where the context required it, as for example at the Health Committee hearings or in litigation such as the present.
[2.65]Counsel turned to instances of the confusion of acceptance of association with acceptance of causation. It could be seen from the documentation referred to in evidence, and indeed Mr McEachran's submission, that the distinction between association and causation was not always understood or remembered. During the Health Committee hearing, Dr Brand, M.P. put questions on causation to the witnesses representing each of the tobacco manufacturers. In answer to a question by him, Mr Davis said:
"We accept that smokers are more likely to develop lung cancer and certain other diseases than non-smokers. We do not deny that smoking is a cause of those diseases but we do not agree that smoking has been shown to be the cause of lung cancer and those other diseases."
Mr Jones submitted that this was a proper acceptance of the existence of the statistical association between the one and the other, together with the observation that ITL did not agree that smoking had been shown to be the cause.
[2.66]Dr Brand, however, was wrong when he said in the next paragraph:
"I do not understand that. If you accept that a certain action results in a certain outcome in a certain number of people, and if that action increases an adverse outcome in people, then surely there is a link and there is a causality between the two?"
In counsel's submission, Dr Brand fell into error by failing to understand that, by acknowledging that there was a statistical association between cigarette smoking and lung cancer, ITL were not, as he put it, accepting that a certain action, i.e. smoking, resulted in a certain outcome, i.e. the disease, in a certain number of people. By acknowledging the statistical association all that one acknowledged was that it might do. Dr Brand was also incorrect when he said in the next paragraph:
"As far as the epidemiology and the science is concerned, you should be able to prove that the public health people are wrong if you believe that they are not right and vice versa."
Counsel said that ITL did not believe that the public health people were wrong. What they believed and had consistently said was that the public health authorities had formed their own judgment which might or might not be correct. To say that ITL did not challenge the public health message was not to say that they accepted that the judgment on which it was based was correct. ITL's views had been communicated by their Corporate Affairs Director to the Health Committee before Mr Davis gave evidence. This, counsel said, was a concise statement of what was and remained ITL's approach to the public health message. It was helpful to clarify this, in order to understand what use, if any, could be made in this litigation of the public health figures.
[2.67]On many occasions Mr McEachran reiterated that ITL did not challenge the public health figures. That came from another passage in the Health Committee report. At p.200 the Chairman (Mr David Hinchcliffe, M.P.) asked:
"Can I be more specific on the safety issue, and I will leave it to my colleagues to press you on that. The Government's White Paper 'Smoking Kills' [UKWP 1998] states that smoking causes - and I underline 'causes' - 84% of deaths from lung cancer, 46,500 deaths from cancer each year in the UK and 40,300 deaths from all circulatory diseases. Do you believe that the Government is wrong to say that these deaths are caused by smoking or are they correct or are you not sure?"
The evidence established that the figures quoted by the Chairman, and the same figures which were given in RCP 2000, were based on the estimates to be found in Callum 1998. The author gave "estimates" of the deaths "attributable" to cigarette smoking. Counsel submitted that the estimates proceeded on an assumption that smoking caused lung cancer, so that the estimates of mortality were of no assistance in determining the issue of causation in a population. If it was assumed that smoking caused disease, the figures could not be anything other than estimates. Mr Davis was accordingly right to say that he had no basis on which to challenge the figures. What was clear was that in declining to challenge these estimates, ITL were not thereby accepting them.
[2.68]When the Philip Morris statement was put to Mr Davis, he agreed that ITL believed that smokers were far more likely to develop serious diseases, like lung cancer, than non-smokers, and that there was no "safe" cigarette. This was not tantamount to accepting that cigarette smoking caused or could cause lung cancer. When the distinction between association and causation was understood, it was clear that the fact that smokers were far more likely to develop serious diseases like lung cancer was no more than appropriate recognition of the existence of the statistical association. Since ITL did not deny that the association might be causal, they could not responsibly describe any cigarette as "safe". They did not challenge the public health community's use of estimates of attributable fraction to help them get their message across. The use of creative epidemiology in order to get the message home in an effective way was perfectly proper. But by not challenging the use of estimates ITL were not inhibited from questioning the use to which figures might legitimately be put in the determination of the issues arising in this case.
[2.69]Mr McEachran had criticised ITL's denial in their pleadings of the averment for Mrs McTear that cigarette smoking could cause lung cancer, and under reference to the position adopted by Mr Davis before the Health Committee, submitted that, properly viewed, the position of ITL was not a denial but "not known and not challenged". Mr Jones referred, however, to Lees, A Handbook of Written and Oral Pleading (2nd edn., 1920, reprinted 1988), p.48:
"The defender is entitled to have every part of his answers taken into consideration. Each admission or denial must be taken with its qualifications and be fairly construed [...]."
Mr Jones submitted that, fairly construed, there was no contrast between the pleadings and what Mr Davis said in his evidence to the Committee and in court.
[2.70]Mr Jones addressed me on Mr McEachran's submissions alleging dishonesty of the part of Mr Davis and lack of candour in the presentation of the defence. Mr McEachran had relied on the evidence of Sir Richard Doll about the meeting in 1962 and about the position of Geoffrey Todd, under reference to Fletcher 1992. He suggested that these pieces of evidence indicated that ITL were accepting that cigarette smoking caused lung cancer. Then there was the evidence about Dr Bentley, and the Philip Morris letter. Mr Jones submitted that, to start in 1958, there might well have been scientists and other experts in the United States who believed that smoking caused lung cancer. The evidence established that in the 1950s and the 1960s, and until the present day, there were, and remained, serious scientists and other experts who believed that smoking had not been established as a cause of lung cancer. A report about what a number of scientists in the United States might have believed was no evidence that ITL themselves accepted in 1958, or at any time, that smoking could cause lung cancer. Moving to the early 1960s, and the meeting at the Royal College of Physicians, Sir Richard Doll in Doll 1997 set the matter out clearly when he spoke not of acceptance of causation but of not denying causation; in counsel's submission these were entirely different matters. The tobacco industry had agreed not to deny the causal relationship, and this could be clearly distinguished from their saying that they accepted the causal relationship. This was not evidence that in 1962 representatives of the tobacco industry accepted a causal relationship.
[2.71]If representatives of the tobacco industry, including ITL, had said to the Royal College of Physicians in 1962 that they accepted that there was a causal relationship between smoking and lung cancer, then this would have been one of the most sensational news stories and would have been publicized in every newspaper, magazine, radio broadcast and television news item throughout the United Kingdom. Sir Richard Doll had however accepted in cross-examination that he gave an accurate account of the position in Doll 1997, when he said that "even the tobacco industry in the UK agreed not to deny the causal relationship on the advice of Geoffrey Todd". He agreed that Todd himself had told him that he had formed the judgment that the association was causal and the industry had accepted that they were not going to deny it by contradicting what was regarded as the public health message. He said that the tobacco industry did not say to the Royal College of Physicians or to anybody else that they admitted that smoking caused lung cancer; not to his knowledge. It was therefore just not the case that ITL had accepted causation in the 1960s.
[2.72]In any event, the position of Geoffrey Todd in relation to ITL at the relevant time was not made clear in the evidence. If he had formed his own judgment that smoking could cause lung cancer, that told us no more than what he thought: there were bound to have been individuals in tobacco companies who formed their own views on many issues, but it could not be assumed that the company accepted the views of these individuals. Individuals would have views about all sorts of things, but these would not represent the company's position. This applied also to Dr Bentley. Accordingly, it was not open to me to form any view of what ITL's thinking or position or policy or anything else was at the time of this meeting. Counsel submitted that it was clear that what we were looking at was not evidence in the case. If it was evidence for anything, it was not evidence that ITL held the view that it had been established that cigarette smoking was a cause of lung cancer. When the evidence was properly considered, Mr McEachran was simply not entitled to advance the proposition that it established that ITL were saying one thing but in fact believed another.
[2.73]Mr McEachran had relied on passages in Mr Davis's evidence to the Health Committee, set out in UKHC 2000, and his evidence in this court in support of a submission that documentation had not been lodged to back up his statement that ITL had reviewed the literature and taken advice from outside. This, Mr Jones submitted, was utterly misconceived. The position about documentation was set out in the letter from the Corporate Affairs Director. This stated that the advice given by external scientists was not in writing and offered to ask them to summarise their views and conclusions regarding smoking and health issues in writing. There was nothing to show that the Health Committee took up this offer. There was in fact lodged in the present case a large body of articles from the scientific literature and other published material on which ITL's experts had relied, having carried out a review of the material. ITL had responded to a request to provide the Health Committee with documents by supplying details of the indices of the documents in an organised form.
[2.74]Mr McEachran had described Mr Davis's evidence as very unsatisfactory and said that he often refused to give a "Yes" or "No" answer. He said that he prevaricated, in particular about documentation and was very vague about the internal workings of ITL and how matters such as the IARC report would have dealt with. He suggested that his evidence about the documentation was incredible and perhaps dishonest: he was asked both by the Health Committee and in court about it, and if there was any such documentation, it would have been bound to have been produced. Mr McEachran suggested that the real inference was that there was no documentary evidence because the internal position of ITL was really far different from their public position. Mr Jones pointed out that what Mr Davis had been asked about was whether he had been briefed about the case and the issues which had been raised in it, and said he had spoken with ITL's advisers. This did not mean that he was given information or reminded about presentations, or that he should recall the details of the material that others in the company had considered in forming their views. Mr McEachran was told before Mr Davis gave evidence that he did not have day-to-day responsibility for or dealings with the issues in this litigation. An alternative witness was offered, the Corporate Affairs Director, who did have direct responsibility for and who did deal with these issues, and that offer was declined. Mr Davis was the CEO of a large multinational company, and responsibility was delegated by the main board of directors to other individuals and groups of individuals throughout the company, and therefore throughout the world. No chief executive of such a company could possess knowledge of everything that was known by everybody within the company. There was no example of Mr Davis having refused to answer a question. Any vagueness was expressed when the meaning of questions was unclear. Mr McEachran was confused about the issue of presentations by internal and external scientists respectively. Mr Davis was speaking of one presentation to the board by an employee of ITL about seven or eight years previously. When Mr Davis mentioned the names of some scientists, this was in the discussion of external scientists, who had made a different type of presentation. One of these was Professor MacRae, an epidemiologist, who died in 2003. Mr Davis's evidence after the break was accordingly in response to a quite different question from the one he had been asked before the break.
Discussion
[2.75]Mr McEachran's approach to his examination-in-chief of Mr Davis appeared to me to go beyond the immediate purposes of the proof. As is apparent from the evidence, of the tobacco manufacturers in the United Kingdom ITL (or, more broadly, Imperial Tobacco) have been the most unwilling to admit a causal connection between smoking and disease, especially lung cancer. For this reason they are no doubt viewed with particular dislike by organisations such as ASH. I had the impression that the opportunity was being taken to pillory Mr Davis, and through him his company, as well as to obtain his evidence. This did not have the desired effect, on me at least. Mr Davis appeared to me to give his evidence in a straightforward manner. He spoke only to matters which could reasonably be expected to be within his knowledge as CEO, and, when he did not know something, he was careful to say so. I can see no reason why he should have been expected to inform himself in advance of the proof about matters that did not lie within his province. Much of what he was asked about could more readily have been answered by the Corporate Affairs Director; and if those acting for Mrs McTear chose not to take advantage of the offer to make him available as a witness, they can hardly complain about the limits of Mr Davis's knowledge. At no time did I form the impression that Mr Davis was dishonest or evasive. I agree with Mr Jones's submissions about his evidence. I accept his evidence and, to the extent that he was able to give an account of ITL's policy, I accept that this was their policy. While ITL's current policy may differ from that of other tobacco companies in the United Kingdom, I draw no conclusions from this in the absence of any evidence about the basis on which any other tobacco company has decided on its current policy.
[2.76]I see no reason to doubt Sir Richard Doll's evidence, summarised above, and particularly his evidence about Geoffrey Todd, or the evidence about Dr Bentley's report. But it is one thing to establish that a number of individuals have formed views, it is quite another to say that their views have been accepted by the tobacco manufacturers, and in particular by ITL. In my opinion, there is no direct evidence that ITL, as a company, have ever accepted that there was a causal connection between smoking and disease, especially lung cancer, and the evidence before me does not satisfy me that this is the inference which should be drawn. I agree with Mr Jones that confusion has arisen through a failure to distinguish acceptance of the existence of a statistical association and acceptance of a judgment that the association is causal. This topic is explored at length in Part V. Participation by ITL in the work of the Harrogate Laboratories does not yield the inference contended for by Mr McEachran. As will be seen, again in Part V, work was done in a number of laboratories, not because it was accepted that tobacco smoke was carcinogenic, or contained carcinogenic substances, but to test experimentally under controlled conditions the causal hypothesis yielded by the epidemiological studies. This was consistent with the approach outlined in, for example, USSG 1964, quoted at para.[5.488]. The position about documentation appears to me to be entirely neutral, and I draw no inferences adverse to ITL from the fact that documentation has not been produced to vouch their position over the years. The only conclusion I draw is that such documents, if they ever existed, are no longer extant. I accept Mr Jones's submissions about this matter.
[2.77]Sir Richard Doll's final position was that, though the tobacco industry had, on Geoffrey Todd's advice, agreed not to deny the causal relationship between smoking and lung cancer, they did not admit it. There appears to me to be a clear difference between not denying a statement, especially one which depends on the exercise of judgment, and admitting it.
[2.78]I conclude that while ITL have at all material times been aware of statements in the published literature to the effect that cigarette smoking was associated with lung cancer and that views had been expressed, which had been accepted by inter alios the United Kingdom Government, that this association was causal, they have never, as a company, admitted this. A matter of such importance to their interests would, in my opinion, have required a decision of the board of directors, and there is no evidence that the board have ever decided to make such an admission. The fact that they have never sought to challenge the public health message does not in my opinion constitute such an admission. No doubt a judgment was made for commercial reasons to adopt this position, which is quite different from the judgment which requires to be exercised for the protection of ITL's interests as a party to litigation such as the present.
[2.79]I was not addressed on what the position in law would have been had ITL publicly admitted that cigarette smoking could cause lung cancer, and whether this would have barred them from denying the pursuer's averment to that effect, so I express no opinion on this.
[2.80]Accordingly, in my opinion, ITL are entitled to put the pursuer to proof of her averment that cigarette smoking can cause lung cancer, and the position adopted by them does not alter in any way the normal requirements of proof.
PART III:Public awareness
[3.1]Copies of numerous newspaper reports have been lodged on behalf of ITL. Some of these were referred to during the course of evidence. During the hearing on evidence Mr Jones provided me with a list of reports on which he sought to found in support of the averment (which, as will be seen, I find to be proved) that at all material times and in particular by 1964 the general public in the United Kingdom were well aware of the risks to health associated with smoking, above all the view that cigarette smoking could cause lung cancer. In response to a request by me at a subsequent By Order hearing a fresh document was prepared setting out more details of these, accompanied by copies of the reports themselves. The Edinburgh solicitors for Mrs McTear wrote that they had "no revisals to make" to this: they had not been able to check the accuracy of the list, due to lack of resources, but stressed that they had no reason to doubt it. The following passages are derived from this document. In the interests of brevity I propose only to quote the headlines which appeared over the reports. I have added the texts of three ministerial statements, which are not to be found elsewhere in this Opinion. Passages from three reports, MRC 1957, RCP 1962 and USSG 1964, are to be found in Part V, and I do not repeat them here. Further discussion of public awareness of these matters, and its implications, is also in Part V.
(1)Ministerial statement in 1954
[3.2]On 12 February 1954 the Minister of Health, Mr Iain Macleod, made a statement in a written reply to a Parliamentary Question on the advice he had received on the question of the relationship between smoking and lung cancer. He said:
"The Standing Advisory Committee on Cancer and Radiotherapy have had this matter under consideration for three years. As a result of preliminary investigations, a panel under the chairmanship of the Government Actuary was set up in 1953 to enquire and report. I have now been advised by the Committee in the following terms:
Having considered the report of the panel under the chairmanship of the Government Actuary on the statistical evidence of an association between smoking and cancer of the lung, and having reviewed the other evidence available to them, the Committee are of opinion:-
(1)It must be regarded as established that there is a relationship between smoking and cancer of the lung.
(2)Though there is a strong presumption that the relationship is causal, there is evidence that the relationship is not a simple one, since:-
(a)the evidence in support of the presence in tobacco smoke of a carcinogenic agent causing cancer of the lung is not yet certain;
(b)the statistical evidence indicates that it is unlikely that the increase in the incidence of cancer of the lung is due entirely to increases in smoking;
(c)the difference in incidence between urban and rural areas and between different towns, suggests that other factors may be operating, e.g., atmospheric pollution, occupational risks.
(3)Although no immediate dramatic fall in death-rates could be expected if smoking ceased, since the development of lung cancer may be the result of factors operating over many years, and although no reliable quantitative estimates can be made of the effect of smoking on the incidence of cancer of the lung, it is desirable that young people should be warned of the risks apparently attendant on excessive smoking. It would appear that the risk increases with the amount smoked, particularly of cigarettes.
I accept the Committee's view that the statistical evidence points to smoking as a factor in lung cancer, but I would draw attention to the fact that there is so far no firm evidence of the way in which smoking may cause lung cancer or of the extent to which it does so. Research into the causes of lung cancer has been pressed forward by the Government and by other agencies in view of the increase in the incidence of this disease and we must look to the results of its vigorous pursuit to determine future action.
I should also tell the House that before these recommendations were considered by Her Majesty's Government the tobacco companies had offered to give £250,000 for research. They have, on my advice, agreed to offer this money to the Medical Research Council."
This was reported in various newspapers.
[3.3]The Evening Citizen of 12 February 1954 reported it on the front page under the headline "Smoking link with cancer". The Evening Times of the same date reported it on p.7 under the headline "Smoking: Research to be speeded". The Daily Record of 13 February 1954 reported it on the front page under the headline "A gasper" and on p.9 under the headlines "Smoking is cancer risk" and "But there's no proof, say tobacco firms: They offer £250,000 for research"; and on p.4 an editorial appeared with the headline "They'll chance it". The Daily Mirror of 13 February 1954 reported it on the front page under the headline "Smoking and health: 4 new moves are forecast" and on the back page under the headlines "Smoking: 'vigorous probe'" and "They switch to filter-tips". A cartoon on p.3 showed one man offering to another a cigarette from a packet with a skull-and-crossbones symbol. The Daily Mail of 13 February 1954 reported it on the front page under the headline "Smoking and cancer: Millions off tobacco shares after Minister's statement" and on p.5 under the headline "Minister gives a cigarette warning: Young people should know about 'apparent risk of excessive smoking': Speedy research promised: £250,000 gift". The Daily Express of the same date carried a report on the front page under the headline "Smoking and cancer - shares hit" and on p.5 under the headline "The 25-a-day Minister warns of danger link above five". The Daily Sketch of the same date carried reports on the front page under the headline "The startling facts: Cigarettes and you: Are 5 a day a safe limit?" and on p.5 under the headlines "The big debate: Is it safe to smoke?", "'Risk in too many cigarettes'", "10-a-day chairman won't stop", "A pipe may be safer, hints Macleod", "No proof, say trade", "Warning by the man who started it all" and "What about Sir Winston?". A cartoon on the same page called "Laugh with the news" showed a man sitting on a train, reading a newspaper and smoking a pipe under a "No smoking" sign. Another report on p.4 appeared under the headline "Britain to-day spends more on tobacco than on rent: And it all goes up in smoke and taxes".
[3.4]The Times of 13 February 1954 carried a report on p.6 under the headline "Heavy smoking and cancer: Some relationship established: Results of three years' study" and on p.7 an editorial appeared under the headline "Smoking and cancer". The Manchester Guardian carried a report on the same date on the front page under the headline "Link between smoking and cancer: Government acts: Tobacco firms' research offer" and a further headline "Rejoinder by companies: 'No proof'". An editorial appeared on p.4 under the headline "Tobacco and cancer". The Daily Telegraph of 13 February 1954 carried reports on the front page under the headline "Link between smoking and cancer: Committee's view" and on p.5 under the headlines "Committee says smoking increases cancer risk: Ministry warning against 'alarmist conclusions'" and "'No proof' say tobacco firms: £250,000 research", and an editorial appeared on p.4 under the headline "News about cancer".
[3.5]The Scotsman of the same date carried a report on p.7 under the headlines "Smoking-cancer link shown: Warning against public alarm: Statistical proof" and "Conclusive proof claimed in US: Cigarette sales fall". On p.6 an editorial appeared under the headline "Smoking and cancer". On p.8 a further report appeared under the headlines "Cancer research pledge by Health Minister: Relationship with smoking" and "No proof, say makers: £250,000 grant for research". The Glasgow Herald of the same date carried a report on p.5 under the headline "Smoking and cancer related: Government pledge to investigate implications of statistics: Other factors probable", and on p.4 an editorial appeared under the headline "Cancer, smoking and smoke". The Sunday Pictorial of 14 February 1954 reported the statement on p.7 under the headline "The odds... and the perils we must weigh against pleasure".
(2)Ministerial statement in 1956
[3.6]On 7 May 1956 the Minister of Health, Mr R.H. Turton, MP, made a statement to the House of Commons in relation to smoking and health. He said:
"Since my predecessor made a statement in February, 1954, investigations into the possible connection of smoking and cancer of the lung have been proceeding in this and other countries. Two known cancer-producing agents have been identified in tobacco smoke, but whether they have a direct rôle in producing lung cancer, and if so what, has not been proved.
The extent of the problem should be neither minimised nor exaggerated. The number of deaths from cancer of the lung has risen from 2,286 in 1931 to 17,271 last year. To place the figures in perspective - in 1954, out of every thousand deaths of men aged between 45 and 74, 77 were from bronchitis, 112 were from strokes and apoplexies and 234 were from cancer, of which 85 were cancer of the lung. Deaths of women from cancer of the lung are still not very significant and represent a small fraction of the total.
The chairman of a committee of the Medical Research Council which has been investigating the subject considers that the fact that a causal agent has not yet been recognised should not be allowed to obscure the fact that there is, statistically, an incontrovertible association between cigarette smoking and the incidence of lung cancer. The statistical evidence from this and other countries to which he refers tends to show that mortality from cancer of the lung is twenty times greater amongst heavy smokers than amongst non-smokers.
The Government will take such steps as are necessary to ensure that the public are kept informed of all the relevant information as and when it becomes available."
This was reported in various newspapers.
[3.7]In the Daily Record of 7 May 1956 it was reported on p.9 under the headline "Govt. report on smoking is complete". In the same newspaper of 8 May 1956 it was reported under the headline "You and smoking: What the risk is in that fag...". In the Evening Times of the same date there were reports on an inside page under the headlines "Cancer: Tobacco men urge more research" and "Tobacco leaders dull after lung cancer statement", and on p.2 a leader appeared under the headline "Think before you smoke".
[3.8]In the Daily Mirror of 8 May 1956 there were reports on p.4 under the headlines "Smoking and cancer: 'Tell all' pledge" and "The two sets of figures". In the Daily Mail of the same date there was a report on the front page under the headline "Smoking report hustled: Cabinet asks doctors for cancer views in twelve months: The twenty-to-one chance: Cut-it-down campaign refused". In the Daily Express of the same date there was a report on the front page under the headline "Smoking - the 20-1 chance: But no action says Minister". In the Daily Sketch of 8 May 1956 there was a report on the front page under the headline "Do cigarettes kill? Health Minister says it has still to be proved, but - 20-1 is heavy smokers' risk!". The report was continued on p.16 under the headline "Heavy smokers take risk". An editorial appeared on p.2 under the headline "End this panic!".
[3.9]In the Daily Herald of 8 May 1956 a report on the front page appeared under the headline "There is no positive proof, but... heavy smokers are warned". In the News Chronicle of 8 May 1956 a report appeared on the front page under the headlines "Chances of lung cancer 20 times higher for heavy smokers: Two suspects in tobacco: Figures yield a clue - but no proof yet", "The secret may lie in two words" and "Not enough evidence yet, say firms", and an editorial on an inside page carried the headline "The verdict postponed". The Times of the same date carried reports on p.7 under the headline "Effect of smoking on health: Tobacco firms call for more evidence" and on p.12 under the headline "Smoking and cancer: Minister rejects plea for campaign", and an editorial appeared on p.13 under the headline "Little by little". The Daily Telegraph of the same date carried reports on the front page under the headline "2 cancer agents in tobacco smoke: No proved effect on lungs, says Minister", on p.14 under the headlines "Tobacco smoke" and "20 pc of victims never smoked", on p.13 under the headline "No campaign on smoking: Lung cancer association", and a leader appeared on p.8 under the headline "Smoking and our health".
[3.10]The Scotsman of 8 May 1956 carried reports on p.7 under the headlines "Cancer of lung and smoking: No public campaign, says Minister" and "Benefits of smoking: Not yet understood, say tobacco firms", and an editorial on p.6 carried the headline "Smoking and cancer". The Glasgow Herald of 8 May 1956 reported the statement on p.7 under the headline "Minister's statement on lung cancer: Mortality 20 times greater among heavy smokers: Medical research opinion", and an editorial appeared on p.6 under the headline "Smoking and cancer".
(3)Publication of MRC 1957 and ministerial statement
[3.11]On 27 June 1957 the Medical Research Council published a report on tobacco smoking and cancer of the lung: MRC 1957. The Parliamentary Secretary to the Ministry of Health, Mr J.K. Vaughan-Morgan, made a statement about smoking and lung cancer in the House of Commons. He said:
"In its Annual Report, and more particularly in its special report on tobacco smoking and cancer of the lung [...] the Medical Research Council has advised the Government that the most reasonable interpretation of the very great increase in deaths from lung cancer in males during the past twenty-five years is that a major part of it is caused by smoking tobacco, particularly heavy cigarette smoking. The Council points to the evidence derived from investigations in many countries in support of this conclusion, in particular of identification of several carcinogenic substances in tobacco smoke.
The Government feel that it is right to ensure that this latest authoritative opinion is brought effectively to public notice, so that everyone may know the risks involved in smoking. The Government consider that these facts should be made known to all those with responsibility for health education. The Minister of Education included in his recently published Handbook for Teachers on Health Education advice about the dangers of smoking and he is circulating copies of this statement to local education authorities and education authorities generally. Corresponding action will be taken by the Scottish Education Department in Scotland.
The Government now propose to bring these views to the notice of the local health authorities who are concerned under Statute in the prevention of illness and who are responsible for health education as a means of prevention. Local health authorities will be asked to take appropriate steps to inform the general public and in this task they will have the assistance of the Central and Scottish Councils for Health Education.
Once the risks are known everyone who smokes will have to measure them and made up his or her own mind, and must be relied upon, as a responsible person, to act as seems best.
The Medical Research Council is at present supporting an extensive programme of work designed to discover the way in which tobacco smoke exerts its effect and the relative importance of other factors, such as atmospheric pollution, which may also play a part in the causation of lung cancer. The recent expansion of this programme has been greatly assisted by a substantial grant made in 1954 by a leading group of tobacco manufacturers; on the advice of my right hon. Friend's predecessor, the present Minister of Labour, this sum was given to the Medical Research Council with complete discretion as to the choice of research projects to be supported and to the publication of results.
The work at present in progress consists largely of chemical and biological studies of the many different constituents of tobacco smoke and atmospheric pollution. In addition, surveys of the role of atmospheric pollution and of specific industrial hazards in the causation of the disease are being undertaken. Work along these lines is being supported in many centres in different parts of the country and the Council has also established, as part of its own organisation, three new research groups in Exeter, London and Sheffield, where long-term studies of different aspects of the problem are being carried out. Every opportunity will be taken by the Medical Research Council to pursue any promising new lines of research which may become apparent."
Newspaper reports on the issue of smoking and health were published both before and after publication of MRC 1957 and the Government statement.
[3.12]The Daily Record of 25 June 1957 carried a report on p.16 under the headline "Smoke signal to youth". The Evening Citizen of 27 June 1957 carried reports on the front page under the headline "Smoking: Shock report: One in 18 may die from lung disease", "'It's up to you' says Minister" and "Cause: a careful choice of words". A report on p.4 appeared under the headline "Because of the great importance of this document, released at 5 o'clock tonight, the Citizen prints it in full: The risk is one in 18: The doctors give their verdict on the dangers of smoking". The Daily Record of 28 June 1957 carried a report on the front page under the headline "Smoking and you: All Britain warned of the dangers". On pp.12 and 13 a report appeared under the headline "Smoking: 40,000 doctors aided probe: They say that cigs can kill..." and "'Stop youngsters' doctors are told". On p.2 an editorial appeared under the headline "A smoke warning" and on the same page the Onlooker column stated: "If you haven't decided to give up smoking yet, the new Medical Research Council report may remove your last dowts [sic]." On p.8 a report appeared under the headline "I'm frightened" and on p.24 under the headline "Smoking: Firms reply to the report".
[3.13]The Paisley Daily Express of 28 June 1957 carried a report on p.4 under the headline "The danger of smoking: Government launch public campaign: Research Council's findings" and "'Little change' in cigarette sales: Paisley reaction to Medical Council's report". The Evening Times of the same date carried a report on p.20 under the headline "Glasgow keeps puffing away". The Sunday Times of 26 May 1957 carried a report on the front page under the headline "Warning on smoking likely soon". The same paper of 2 June 1957 carried a report on p.20 under the headline "Family clinic: Smoking - lady beware!" The Sunday Express of 28 May 1956 carried a report on the front page under the headline "A health shock for smokers".
[3.14]The Daily Mirror carried numerous reports. On 28 May 1957 a report appeared on p.10 under the headline "Smoking: 'Time for action'". On 2 June 1957 a report appeared on p.3 under the headline "Smoking - the hour of decision". On 25 June 1957 a report appeared on p.3 under the headline "Smoking - a new warning from the Government". On 27 June 1957 a report appeared on p.13 under the headline "Smoking: Report today". On 28 June 1957 a report appeared on the front page under the headline "Smoking and cancer and you: It's every man for himself!" Further reports appeared on pp.10 and 11 under the headlines "Smoking: Grim facts - deaths are going up", "What the firms say", "Gasper!", "We'll 'carry on smoking'", "'How to stop", "'Ban smokes in tube and cinemas'" and "'Change to a pipe or cigar'". On p.2 a report appeared under the headline "Call in Dr Hill [the Government's 'propaganda chief']".
[3.15]The Daily Mail also carried several reports. On 27 May 1957 a report appeared on p.5 under the headline "Smoking IS to blame". On 27 June 1957 a report appeared on the front page under the headline "Shock for smokers today: Report will confirm peril". On 28 June 1957 a report appeared under the headline "Smoker's risk is 40 to 1: That is the extra danger he runs" and a comment on the same page appeared under the headline "The last gasper". A further report appeared on 28 June 1957 on an inside page under the headline "Heavy smokers warned: Cigarettes will kill 1 in 8; Research still on; Acid may be the clue".
[3.16]The Daily Express carried a report on 28 May 1957 on p.3 under the headline "Facts soon on smoking". On 25 June 1957 a report appeared on the front page under the headline "Cancer: Minister to speak". On 27 June 1957 a report appeared on the front page under the headline "Smokers face a shock today". On 28 June 1957 a report appeared on the front page under the headline "Smoking: It's up to you: Go gently - but very quietly" and on p.6 an editorial appeared under the headline "Personal choice". In the Daily Sketch of 17 June 1957 a report appeared on p.6 under the headline "Smokus pocus! Gimmick men cash in on the scare over lung cancer". The report reproduced part of the front page of the same paper of 7 June 1957 with the headline "Lung cancer: Cabinet to warn heavy smokers". On p.2 a report appeared under the headline "Verdict on smoking to-day". On 28 June 1957 a report appeared on the front page under the headline "Smoking: Safe limit may be 15 a day". There were further reports on p.2 under the headlines "Cheer up! It's not all gloomy" and "The truth about smoking". The Daily Herald carried a report on the front page on 7 June 1957 under the headline "'Ban smoking in cinemas'". On 28 June 1957 a report appeared on the front page under the headline "Smoking: You must decide: Report stresses the 25-a-day risk, but no Cabinet action" and a further report on p.4 appeared under the headline "Smoking and the Nation: Are cigarettes to blame for this [a graph showing an increase in deaths from cancer of the lung]?".
[3.17]The News Chronicle of 27 May 1957 carried a report on the front page under the headline "New facts about smoking". On 27 June 1957 a report appeared on the front page under the headline "Smoking report out today". On 28 June 1957 a report appeared on the front page under the headline "Leading doctors say '1 in 8 cancer risk for the 25-a-day folk': The Government says 'We are presenting the facts' and now... smokers - it's up to you: 'Cigarettes can kill' warning". A further report on the front page appeared under the headline "Call for ban in cinemas". On p.4 an editorial appeared under the headline "Smoking and cancer" and on the same page an article appeared under the headline "And now... how to stop".
[3.18]The Times of 28 May 1957 carried a report under the headline "Lung cancer and smoking" in a column about Parliament. On 27 June 1957 a report appeared on p.7 under the headline "Government view on cancer link: Commons statement to-day". On 28 June 1957 a report appeared on p.6, in the Parliament column, under the headline "Public warned on smoking: Major risk of lung cancer" and on p.10 reports appeared under the headlines "Lung cancer increase 'due to smoking': Medical findings accepted by Government: Local authorities asked to make facts known", "£698m. tobacco revenue: MP's question on alternative tax", "Reply on advertising", "'Not established with certainty': Manufacturers on 'a matter of opinion'" and "Discrepancies 'not surprising': 100 constituents of smoke identified". A leader appeared on p.11 under the headline "More than smoke".
[3.19]In the Manchester Guardian of 24 June 1957 a report appeared on p.6 under the headline "Smoking and lung cancer: Accumulating evidence". On 28 June 1957 a report appeared on the front page under the headline "One in eight of heavy smokers 'doomed': Government leaves it to the individual". Further reports on the front page appeared under the headlines "Lung cancer not yet at peak" and "Manufacturers say unproven: 'No new evidence'" and "Government's plans for bringing facts to the public's notice: Circulars to local authorities". On p.2 a report carried the headline "Ban on smoking in places of public assembly suggested: MP speaks of trains and buses" and on p.8 an editorial appeared under the headline "Smoking and cancer".
[3.20]In the Daily Telegraph of 27 May 1957 a report appeared on p.13 under the headline "New evidence on effects of smoking: Questions by MPs". On 28 May 1957 a report appeared on p.13 under the headline "Smoking & cancer: Report in a few weeks". On 7 June 1957 a report appeared on the front page under the headline "Statement on smoking soon: Cabinet discussion". On 25 June 1957 a report appeared on p.13 under the headline "Smoking risks: Government view this week". On 27 June 1957 a report appeared on the front page under the headline "Smoking risks". On 28 June 1957 a report appeared on the front page under the headline "Campaign on danger of smoking opens: Government acts after taking medical advice". Further reports on the front page appeared under the headlines "MPs approve decision: No compulsion" and "Little effect on shares: Earlier losses". On p.18 further reports appeared under the headlines "Smoking and cancer" and "No proof, say tobacco firms: 'Matter of opinion'". On p.11 reports appeared under the headlines "Smoking a cause of cancer, says report: Firm conclusion by Research Council: One-in-8 risk: Cigarettes worst", "Wide inquiries: Essential facts the same" and "Atmospheric pollution: Minor contribution". Further reports on the same page appeared under the headlines "Steps to warn public: Government call to local councils", "Tobacco trade redundancy: Socialist's fear" and "Checking habit: Medical journals' advice". An editorial appeared on p.8 under the headline "Smoking and cancer".
[3.21]In The Scotsman of 27 June 1957 a report appeared on the front page under the headline "Smoking-and-cancer report to-day". In the same newspaper on 28 June 1957 front page reports appeared under the headlines "Grave warning to heavy smokers: One in eight may die of lung cancer: Startling report by Research Council", "Public must decide: Government to put facts before them: Minister's statement", "Disease causes one in 18 of all male deaths: Incidence not yet at peak", "Manufacturers cautious: 'No new proof' of causal connection: Matter of opinion", "Report challenged by US body: 'Not confirmed by science'" and "Heavy smoker defined: Person who smokes 25 or more cigarettes a day". An editorial appeared on p.8 under the headline "Smoking and cancer".
[3.22]The Glasgow Herald of 4 June 1957 carried a report on p.8 under the headline "Lung cancer". On 25 June 1957 a report appeared on p.11 under the headline "Lung cancer report". On 28 June 1957 reports appeared on p.7 under the headlines "Smoking as cause of cancer of lung: Government to publicise medical report" and "Bringing the risks home to children: Request to local authorities" and on p.9 under the headline "Association of smoking and lung cancer: Medical Research Council's report on evidence". An editorial appeared on p.6 under the headline "Smoker's risk".
[3.23]The Daily Worker of 28 June 1957 carried a report on the front page under the headlines "Greatest single cause of lung cancer: Still hope if you give them up" and "Now it's up to the smokers". The Financial Times of the same date carried a report on the front page under the headline "Smoking: Govt. to tell of dangers: Publicity-drive to be launched: 'Case not proved' say manufacturers". A further report on the front page appeared under the headline "Tobacco makers' view". An editorial appeared on p.10 under the headline "Tobacco and health". The Evening News of 28 June 1957 carried news reports and an editorial on p.8 under the headline "Lung cancer and smoking".
[3.24]The Western Mail of 27 June 1957 carried a report on the front page under the headline "Shocks for smoker today". On 28 June 1957 a report appeared on the front page under the headline "25 or more cigarettes a day and you may be smoking yourself to death: Doctors link tobacco with lung cancer". An editorial on p.6 carried the headline "Smoking and its dangers". Other reports in the same issue appeared under the headlines "Smoking and you: Lung cancer may kill 1 in 8" and "Government will warn the people".
[3.25]The Press & Journal of 28 June 1957 carried reports on the front page under the headline "Medical experts warn pipe and 'fag' folk: It might mean 'no smoking' in the cinemas: Smoking - over to you: Report says one heavy smoker in eight risks death from lung cancer: Local campaigns planned" and on p.3 under the headline "Smoking, man in the street says...". An editorial appeared on p.4 under the headline "Cigarette danger".
[3.26]The Newcastle Journal of 28 June 1957 carried reports on the front page under the headlines "Smoking: 25-a-day men warned: One in eight likely to die of lung cancer: Call for cigarette ban in cinemas", "All must know the risks - Minister", "'No proof smoking is the cause'" and a commentary under the headline "Tobacco in the dock". Further reports on an inside page carried the headlines "'Cigarettes mainly to blame for cancer': 'Men who stop smoking cut the risk by half,' says report" and "Chain smoker says 'I am not giving up'".
[3.27]The Inverness Courier of 28 June 1957 carried a report under the headline "Increase in lung cancer: Smoking said to be chief cause". The Western Daily Press of 28 June 1957 carried a report on the front page under the headline "Smoking - decide for yourself: Govt. attitude to lung cancer report: One in eight may die: No proof tobacco men say". An editorial on p.4 appeared under the headline "'The weed'". The Bristol Evening Post of 28 June 1957 carried a report on an inside page under the headline "Smoking and cancer: Statement by MOH likely" and "No scientific proof, say the manufacturers".
(4)Publication of RCP 1962
[3.28]On 7 March 1962 the Royal College of Physicians published a report on smoking and health: RCP 1962. Following its publication the Government took action to publicise the conclusions of the report. Both before and after publication of the report numerous articles on the issue of smoking and health appeared in newspapers.
[3.29]The Daily Record of 16 February 1962 carried a report on the front page with the headline "If you must smoke (doctors' tax plan)". The Evening Times of 7 March 1962 carried a report on the front page under the headline "Doctors blame cigarettes and suggest higher tax: Stub-or-stop smokes shock". The Evening Citizen of 7 March 1962 carried a report on the front page under the headline "Smoking and your health: Nine top doctors give their views", continued on p.7 under the headline "'Stub out cigarette when half-smoked'". The Daily Record of 8 March 1962 carried a report on p.24 under the headline "Shock... shock... shock: Stop this [arrow pointing to burning cigarette]: Raise the price doctors plead". On p.18 a report appeared under the headlines "A shock report: A hidden menace in cigarettes" and "Tips for 'can't help it' smokers". The same newspaper of 9 March 1962 carried a report on p.13 under the headline "Should YOUR cash go up in smoke?" and on p.17 under the headline "Get some sense into smoking". The Sunday Post of 11 March 1962 carried a report on p.7 under the headline "Will you stop smoking now? Well-known people give their answer" and on pp.16 and 17 under the headline "Why does Scotland have such a shocking record?" The Sunday Pictorial of 21 January 1962 carried a report under the headline "Shocks in a new report on smoking".
[3.30]The Daily Record of 12 March 1962 carried a report on p.9 under the headline "Doctor seeks smoking ban". Further reports appeared on p.2 under the headline "Cigs warning won't scare this smoker" and on p.8 under the headline "Smoking danger has MPs worried". The same newspaper of 13 March 1962 carried a story on the front page under the headline "Smokes plea to teacher: Show 'em the light: But don't light up" and on p.2 under the headline "No smoking - after 50 years". The same newspaper of 14 March 1962 carried reports on p.7 under the headlines "The smokes war hots up" and "'Ban' man smokes... twenty-a-day!" A report appeared on p.2 under the headline "Why smoking is a sin: A selfish habit, says a woman". In the same newspaper, reports appeared on 15 March 1962, p.2, under the headline "Home-made", on 16 March 1962, p.2, under the headline "Easier?" and on 17 March 1962, p.2, under the headline "Old cure".
[3.31]The Sunday Post of 18 March 1962 carried reports on p.3 under the headline "Children who smoke", on p.10 under the headline "Smoking" and on p.17 under the headline "Chemists are sold out of anti-smoking pills". The Daily Record of 21 March 1962 carried a report on an inside page under the headline "No smoking in the cinema: City asked: Is ban possible?" In the same newspaper reports appeared on 22 March 1962 on p.3, under the headline "No smokes in hospital MP asks", and on 23 March 1962, p.32, under the headline "'Horror' for the smoker: 'X' films in schools". The Evening Citizen of 23 March 1962 carried a report on the front page under the headline "['Government Leader in the Lords'] Hailsham's £25m shocker for tobacco firms". In the Daily Record reports appeared on 24 March 1962 on the front page under the headline "£14m cig slump" and on 30 March 1962, p.19, under the headline "Clinics may help to cut smoking".
[3.32]Numerous reports appeared in the Daily Mail. On 22 January 1962 a report on p.8 carried the headline "Doctors want campaign to warn of disease dangers of smoking". On 16 February 1962 a report on the front page carried the headline "Hit the cigarette smokers, say doctors". On 6 March 1962 a report appeared on p.5 under the headline "Black book aimed at every smoker". On 7 March 1962 a report on p.15 carried the headline "Turmoil day for tobaccos: How will they fare on doctors' smoking report?" On 8 March 1962 a report appeared on the front page under the headline "Smoking: Ministers speak next week". A comment column on the front page bore the headline "Risk in a cigarette". A report appeared on p.13 under the headline "Cigarettes and cancer: Doctors warn 'smoking can cut life'". On 13 March 1962 a report appeared on the front page under the headline "Don't smoke: Schools drive".
[3.33]Numerous reports appeared in the Daily Telegraph. On 22 January 1962 a report on p.16 bore the headline "Doctors attack smoking: Call for controls". On 8 March 1962 a report on the front page appeared under the headline "Doctors urge more tax on cigarette smokers: Action to cut lung cancer" and further reports on p.21 appeared under the headlines "Official anti-smoking campaign urged: Convincing evidence of danger, say doctors", "Children to be warned", "Some effects 'of real value': Firms stress need for more research". An editorial appeared on p.12 under the headline "Smoking and health". A report on the same page bore the headline "Hidden cigarettes". A report on 13 March 1962 carried the headline "Government's drive against smoking: Special attention to schoolchildren: Discouraging young smokers: Minister's advice".
[3.34]The Times of 23 January 1962 carried a report on p.15 under the headline "Lung cancer report in March". On 16 February 1962 a report appeared on p.12 under the headline "Cancer danger in second half of cigarette". On 8 March 1962 a report appeared on p.4 under the headlines "Doctors urge Government to curb smoking: Proposed higher taxation and advertising restrictions", "Investigators took their own advice" and "Report called incomplete", and on p.13 an editorial appeared under the headline "Where there's smoke". The Sunday Times of 28 January 1962 carried a report on p.3 under the headline "Doctors to press for all-out anti-smoking drive".
[3.35]The Scotsman of 14 February 1962 carried a report on the front page under the headline "Cancer-report fears hit tobacco shares". On 8 March 1962 a report on the front page appeared under the headline "Doctors repeat cigarettes warning". A further report on p.10 bore the headline "Report suggests higher tax on cigarettes: 'Primarily educational problem'", and an editorial appeared under the headline "None so blind". On 13 March 1962 the same newspaper carried a story on the front page under the headline "Action on smoking: SYHA ban sales: [the Secretary of State for Scotland John] Maclay issues circular" and on p.5 under the headline "Government backing for report on smoking: 'Authoritative and crushing'".
[3.36]The Daily Express of 16 February 1962 carried a report on the front page under the headline "Doctors say pipes and cigars cause less ill-health: Cigarettes shocker: Put the cost up Government is advised". On 8 March 1962 a report appeared on p.6 under the headline "The danger: Doctors urge Government 'act against smoking': Nine-man inquiry (not a cigarette between them)" and on p.5 an editorial appeared under the headline "Good sense and good health". On 13 March 1962 a report on the front page bore the headline "Please teacher, smoke in private asks [the Minister of Education Sir David] Eccles". A report on p.6 carried the headline "[the Minister of Health] Enoch Powell orders new 'don't smoke' campaign".
[3.37]The Daily Mirror of 16 February 1962 carried a report on the front page under the headline "Doctors' shock plan: A 'lifesaver' tax on cigs?" On 8 March 1962 a report on the front page carried the headline "Government gets 25,000-word report: Cigarettes peril: Doctors say 'act now'", and reports appeared on pp.16 and 17 under the headlines "Out today - a startling report from nine doctors: The case against cigarettes", "More research planned by tobacco firms" and "And if you must smoke...". An editorial on p.2 appeared under the headline "Smoking and you". On 13 March 1962 a report appeared on the front page under the headline "Smoking - plea to schools".
[3.38]The Daily Herald of 7 March 1962 carried a report on p.8 under the headline "Doctors take their own advice". On 8 March 1962 reports appeared on various pages under the headlines "The cigarette", "Smoking and health: The medical evidence", "Smoking and you - what action?" and "Smoke of controversy". On 13 March 1962 a report appeared under the headline "Please don't smoke at school: Government plea to teachers".
[3.39]The Glasgow Herald of 8 March 1962 carried reports on the front page under the headlines "Doctors blame the cigarette: Physicians' report demands ban on advertising" and "Ministers put their smoking caps on" and on other pages under the headlines "Report on smoking and cancer: Doctors want action by Government: Convincing evidence on cigarette harm", "A warning in Denmark", "Dr Soper's advice to clergy", "Manufacturers reply to doctors: Need for more research" and "Demands for non-smoking public: Society call for warning films". An editorial appeared on p.8 under the headline "Smoking". On 13 March 1962 a report appeared on the front page under the headline "Government action on smoking: Emphasising dangers to children". A further report on the front page, continued on p.14, carried the headline "Advertising of tobacco: MP's questions".
[3.40]In the Daily Sketch of 8 March 1962 a cartoon directed attention to reports on p.6 under the headlines "'For the price of 23 cigarettes, you can see the risk you run': Nine top physicians give you a pocket full of advice" and "What the tobacco men say", and on p.7 under the headlines "Sketch smoking clinic: Action - at once: Girls, this is how to choose a pipe: How can I give it all up so easily?" An editorial appeared on p.2 accompanied by a cartoon comment. On 13 March 1962 a report appeared on the front page under the headline "A smoking 'war': Don't puff in front of children".
[3.41]In The Guardian of 8 March 1962 reports appeared on the front page under the headlines "Doctors ask for Government campaign against smoking: Lung cancer not the only danger", "Tobacco shares rise slightly" and "An unequivocal condemnation". On p.3 a report appeared under the headlines "Royal College of Physicians report: Overwhelming case against smoking: Doctors find relation to lung cancer proved", "Primary teachers to tell children of dangers", "Estimating size of risk", "Smoking has a 'real value': Makers' statement" and "Tobacco trade answers back: Four main points". An editorial appeared on p.8 under the headline "The verdict on cigarettes". On 13 March 1962 a report appeared on the front page under the headline "Government to launch anti-smoking drive: Leaflets will warn of dangers to health". A further report appeared on p.3 under the headlines "Antismoking campaign: Minister's call to schools" and "Advertising control being considered, Minister says".
[3.42]The Financial Times carried reports on 8 March 1962 on the front page under the headline "Ministers urged to cut smoking" and on p.10 under the headlines "Doctors report on smoking: Need for prompt preventive measures", "'Unpleasant facts must be faced'", "Manufacturers reply" and "Inconsistencies in report - US industry". The Daily Worker of the same date carried a story on the front page under the headline "Killer fags: Doctors tell Govt 'act'" and an editorial under the headline "Lives at stake". The Evening News of 7 March 1962 carried stories on various pages under the headlines "Doctors give heavy smokers a grim warning: '30 times more likely to die of cancer': Government action urged", and an editorial under the headline "Smoking and health". On the next day a report appeared under the headline "Cabinet discuss the report on smoking".
[3.43]The Evening Chronicle of 7 March 1962 carried a report on the front page under the headline "Top doctors urge Government to help cut 'harmful habit': Shock for smokers: Link with cancer 'is now so convincing'". The Bristol Evening Post of the same date carried a report on the front page under the headline "Seven steps to curb consumption: Doctors warn on cigarette smoke peril: 'Cigarette smoking is a cause of lung cancer'", and a further report bore the headline "Don't smoke doctors: These are the plain facts: To prevent smoking - £5,000: To encourage it - £38m.". An editorial comment bore the headline "Smoking: The time to act". The South Wales Echo of the same date carried a report under the headline "Smoking does kill, warn doctors". On 8 March 1962 a report appeared under the headline "Cabinet talk over report on smoking". On the same day the Press & Journal carried a report on the front page under the headline "Health of nation v. rake-off on taxation: Doctors' spotlight on danger to smokers puts Government in a spot" and on p.5 under the headline "Smoking does kill, say the doctors".
[3.44]The Newcastle Journal published reports on 8 March 1962 on various pages under the headlines "Solace or menace?", "Tobacco shares rise and defy medical experts", "Report on smoking: No joy for slaves to the cigarette: Doctors' warning on health dangers is grim and categorical" and "Just another scare say North's 30-a-day men: It's the cash that controls their smoking". On the same date the Western Daily Press carried reports under the headlines "Terrible tale of Ash Wednesday: Smoking is a killer, says Sir Robert [Platt, President of the Royal College of Physicians]", "Britain has highest death rate" and "West doctors back warning to smokers" and an editorial appeared under the headline "Argument is going up in smoke". The Western Mail of the same date carried reports under the headlines "Smokers are warned it could kill you: Doctors claim big death rate", "Old stuff, say the firms" and "We will go on smoking they say" and an editorial appeared under the headline "A cloud of suspicion".
(5)Publication of USSG 1964
[3.45]On 11 January 1964 a report by the United States Surgeon General on Smoking and Health was published: USSG 1964. There were numerous reports in British newspapers, both before and after publication of the report.
[3.46]The Sunday Post of 12 January 1964 carried a report on the front page under the headline "Linked with lung cancer and other diseases: Cigarette smoking - US scientists want action: 'Cigars and pipes have little significance'". The Sunday Mail of the same date carried a report on p.5 under the headline "Outlaw the fag menace say US". The Evening Times of 13 January 1964 carried a front page report with the headline "Glasgow goes on puffing". The Daily Record of 13 January 1964 carried reports on various pages under the headlines "Scots smoke on despite US report", "Don't blame smoking says new probe: Killer car fumes - by Germans", "First target hairy chests in adverts!" and "Emergency meeting - in Britain". The Sunday Mirror of 5 January 1964 carried reports on the front page under the headline "Smoking: Sensational report: The claim is that death from cancer is ten times higher among smokers: Cigarettes are blamed", and on p.3 under the headline "3,000,000 smokers help fight the great killer". A further report on 12 January 1964, on p.2, carried the headline "Heavy smokers in 20 times more peril".
[3.47]The Sunday Times of 5 January 1964 carried a report on p.3 under the headline "US warning to smokers". On 12 January 1964 a report appeared on the front page under the headline "American experts urge prompt action on smoking and cancer", and on p.14, under the headline "Dr Alfred Byrne sums up the situation: Saving smokers". Further reports appeared on p.3 under the headlines "Cancer report", "Doctors' death rate cut", "Smoke haze in W1" and "The ten years of warnings". The Daily Herald of 7 January 1964 carried a report on p.7 under the headline "Smokers' 14-minute warning" and a further report on p.8 under the headline "That report hits tobacco shares". The Daily Telegraph of 7 January 1964 carried a report on p.2 under the headline "Around America today: US smoking report is top secret". The Daily Mail reported on 7 January 1964 on p.2 under the headlines "The scientists' verdict on tobacco road" and "British firms say no". The same newspaper carried a report on 14 July 1964, p.10, under the headlines "Minister plans a new drive against smoking" and "Long hunt for a cure collapses". The Guardian of 8 January 1964 carried a report on p.11 under the headline "For the record: Top secret smoking report". The Daily Sketch of 10 January 1964 carried a report on p.6 under the headline "On the eve of a shock report from America the Sketch asks this question: Can 25,000 lives be saved?" The Financial Times of 10 January 1964 carried a report on p.12 under the headline "US tobacco faces its biggest test".
[3.48]The Glasgow Herald of 11 January 1964 carried a report on p.7 under the headline "American report on smoking awaited". The same newspaper carried a report on 14 January 1964 on p.9, under the headline "Gallant defence of tobacco". The Sunday Express of 12 January 1964 carried a report on the front page under the headline "Shock figures in the big American inquiry: US doctors denounce cigarettes as killers: But they find little risk in pipe smoking". This was continued on p.17 under the headline "Smoking". The News of the World of 12 January 1964 carried a report on the front page under the headline "Smoking: Shock report". The Sunday Telegraph of the same date carried a report on the front page under the headline "America gets a stern warning on smoking". This was continued on p.28 under the headline "Cancer warning". On the same page reports appeared under the headlines "'Choice for smokers'" and "No ITV advertisements". An editorial appeared on p.14 under the headline "Smoking risks". The People of the same date carried a report on the front page under the headline "Smokes that kill - now US says it". The Observer of the same date carried a report on the front page under the headline "America told to act against smoking". This was continued on p.2 under the headline "Smoking death rates", and a further report on that page carried the headline "'Stop or face the risks'". The Sunday Citizen of the same date carried a report on p.28 under the headline "US nails the big killer: Cigarettes".
[3.49]The Press & Journal of 13 January 1964 carried reports on an inside page under the headlines "Swift reaction to US shock report on smoking risks" and "Smokers confess to doubts, but refuse to panic". The Evening Express of 11 January 1964 carried a report under the headline "Fantastic key-code system to hush-hush files: Secrecy blanket on US smoking report". The same newspaper carried a report on 13 January 1964 under the headline "Aberdeen leads the way in campaign: Now it's 'smokers anonymous' in NE: Minister to start kirk clinic". On another page a report appeared under the headline "Warning, now what next?" The Daily Worker of 15 January 1964 carried a report on p.2 under the headline "Smoking - Government action needed". The Scotsman of 13 January 1964 carried reports on the front page under the headline "Tobacco firms study report: 'More research' call welcomed: US investigation" and on p.8 under the headlines "US report 'confirms Royal College's findings': Copies specially flown to Britain", "'A health hazard'", "Big debate on smoking starts in America: Senator to introduce two bills" and "German view differs: Polluted air main cancer risk".
[3.50]The Times of 13 January 1964 carried reports on p.7 under the headlines "US call for action against smoking meets opposition: Experts emphasise link with cancer", "Call for research welcomed" and "German team blames polluted air". On p.9 an editorial appeared under the headline "Smoking can cause lung cancer". The same newspaper carried reports on 14 January 1964 on p.6 under the headlines "Efficiency of cigarette filters doubted: Findings of American investigators", "'No serious doubt on conclusions'", "Danes to limit advertising", "Health Ministry study of report" and "International inquiry sought".
[3.51]The Daily Mirror of 13 January 1964 carried a report on the front page under the headline "British tobacco chiefs see shock report: Minister in talks on smoking: Action demanded in America". The same newspaper of 14 January 1964 carried a report on p.2 under the headline "Smokers carry on as usual". The Daily Herald of 13 January 1964 carried reports on the front page under the headlines "Tobacco chiefs not convinced" and "Free smoking cure from the boss". Further reports appeared on p.2 under the headlines "Tobacco men fear flood of claims" and "What the US report said", and an editorial appeared on p.6 under the headline "To smoke or not to smoke". The same newspaper of 14 January 1964 carried a report on p.18 under the headline "[Science Minister] Hogg to see report on smoking". The Guardian of 13 January 1964 carried reports on p.9 under the headlines "US tobacco industry's fears confirmed: Report links smoking and cancer" and "Germans blame pollution". On p.8 an editorial appeared under the headline "No smoking without cancer risk". On p.16 a further report carried the headline "If you enjoy smoking...". On 14 January 1964 the same newspaper carried a report on p.4 under the headline "Calming the new non-smokers: Simple breathing exercises to ease the pangs of abstinence".
[3.52]The Glasgow Herald of 13 January 1964 carried a report on the front page under the headline "Tobacco firms want still more research: 'Great deal yet to be known'". In the same issue an editorial appeared on p.6 under the headline "Addiction", and further reports appeared on p.7 under the headlines "American report on smoking: Worst fears confirmed" and "German study". The same newspaper carried reports on 14 January 1964 under the headlines "Minister opens clinic against smoking: Lead to congregation with example and prayer" and "Government duty to smokers: 'Young must absorb facts'". The Financial Times of 13 January 1964 carried reports on the front page under the headline "Report on smoking: Tobacco industry in US awaits 'remedial action': Filter tip research to be intensified" and on p.9 under the headline "UK tobacco industry considers US report". The Daily Mail of the same date carried a report on the front page under the headline "Health Minister calls smoking talks", continued on p.2 with a further report under the headline "Stop smoking! (and all on the firm)". In the same issue an article appeared on p.6 under the headline "How can you give up smoking?"
[3.53]The Daily Sketch of 13 February 1964 carried a comment on p.4 headed "This to-do about smoking". On another page a report appeared under the headline "US tobacco men are not worried". The Daily Telegraph of the same date carried a report on p.19 under the headline "Anti-smoking campaign demanded in US: Senator to introduce bill" and an editorial on p.12 under the headline "Cigarette warning". The Daily Express of the same date carried reports on p.10 under the headlines "'Don't smoke' boss gives his men pills" and "Hunt is on for safer cigarette", and an article on p.6 under the headline "Why I am still smoking 25 a day: By a professor on the 'Stop smoking' Committee".
(6)Ban on television advertising of cigarettes in 1965
[3.54]On 8 February 1965 the Minister of Health, Mr Kenneth Robinson, announced in the House of Commons that the Government intended to ban the advertising of cigarettes on television. There were reports in the press both before and after the announcement.
[3.55]The Evening Citizen of 8 February 1965 carried a report on the front page under the headline "The end of the TV cigarette". The Daily Record of 9 February 1965 carried a report on the front page under the headline "Cigarette ads banned from TV", continued on p.20 under the headline "Cigarette ban on TV". The Evening Times of 9 February 1965 carried an editorial on p.4 under the headline "The TV puff". The Sunday Express of 7 February 1965 carried a report on the front page under the headline "Drastic action expected as the Cabinet prepares to tackle the problem of smoking and health: TV cigarette ban? Government may stop the 'commercials'". The News of the World of the same date carried a report on the front page under the headline "Cigarette ads may be banned: New smoking shock for TV". The Daily Mirror of 8 February 1965 carried a report on p.9 under the headline "Ban on smokes adverts ready". The same newspaper carried a report on the front page on 9 February 1965 under the headline "Cigarette TV ban - and it's just the first step". The Glasgow Herald of 8 February 1965 carried a report on the front page under the headline "Ban on cigarette ads on TV?"
[3.56]The Times of 8 February 1965 carried a report on p.10 under the headline "TV cigarette ban today, MP says". On the next day it carried reports on p.12 under the headline "Minister considering more anti-smoking measures: Cigarette advertising banned on TV" and on p.15 under the headline "Government ban on TV cigarette advertising". The Sun of 8 February 1965 carried a report on the front page under the headline "TV cigarette adverts will be banned". The same newspaper carried reports on the next day on the front page under the headlines "New blitz to hit smoking: TV adverts ban may be extended" and "Let people decide, say tobacco men". The Daily Mail of 8 February 1965 carried a report on p.3 under the headline "Cigarette adverts to be banned from TV". On the next day the same newspaper carried a report on the front page under the headline "Cigarette ban will cost TV firms £5m". In the same issue a feature appeared on p.8 under the headline "Behind the smoke screen". The Financial Times of 8 February 1965 carried a report on the front page under the headline "Ban on cigarette advertising on TV expected: Statement to-day by Mr Wedgwood Benn [the Postmaster-General]". The same newspaper of 9 February 1965 carried reports on the front page under the headline "Ban on TV cigarette advertising - other media being examined", on p.13 under the headlines "Where will tobacco's TV money go?" and "Reaction to TV cigarette ban", and an editorial on p.12 under the headline "A controversial half measure". The Guardian of 8 February 1965 carried a report on the front page under the headline "Cigarette advertising ban likely". The same newspaper on the next day carried reports on the front page under the headlines "Sharp reactions to cigarette TV ban: Doctors support move" and "Fall in tobacco and TV shares" and on p.3 under the headline "Minister explains TV cigarette advertising ban", and an editorial on p.10 appeared under the headline "The Minister of Health on smoking".
[3.57]The Daily Express of 8 February 1965 carried a report on p.8 under the headline "ITV won't charge for 'don't smoke' plugs". The same newspaper on 9 February 1965 carried a report on the front page under the headline "Manufacturers protest after ban on ads: TV cigarettes row" and "Review promise" and on p.8 an editorial appeared under the headline "Blow to freedom". The Daily Telegraph of 8 February 1965 carried a report on the front page under the headline "Cigarette advertising on TV to end: Present contracts stay". The same newspaper carried reports on 9 February 1965 on the front page under the headline "Cigarette ban will cost TV firms £5m", "Commons give ban mixed reception" and "TV shares fall" and on p.26 under the headline "TV advertising ban attacked", and an editorial on p.16 under the headline "No smoke on the screen". The Scotsman of 9 February 1965 carried a report on the front page under the headline "'Singled out' for cigarettes ban, say ITV" and "Dangerous principle, say [tobacco manufacturers] Carreras" and on p.5 under the headline "Labour welcome ban on advertisements: Step in health campaign". The Glasgow Herald of 9 February 1965 carried reports on the front page under the headlines "The fag end for television: Cigarette advertising stops to aid health campaign", continued on p.16 under the headline "Cigarette advertising ban on television", and "Extension of ban being considered". An editorial appeared on p.8 under the headline "Cigarettes and cigars".
(7)Coverage of science
[3.58]A selection of newspaper reports about scientific research into the issue of smoking and health was referred to. In the Daily Mirror of 29 September 1950 a report appeared under the headline "Smokers take this risk". In the Manchester Guardian of 19 September 1950 a report appeared under the headline "Smoking and cancer of the lung". In the Daily Mirror of 29 June 1951 a report appeared on p.3 under the headline "Cigarettes ARE risky says a doctor". In the Daily Mail of 29 June 1951 a report appeared on p.5 under the headline "Doctors blame smoking for rise in lung cancer deaths: 'Alarming'". In the Daily Graphic of 29 June 1951 a report appeared on p.5 under the headline "Less risk in pipe - doctor". In the Daily Mail of 12 December 1952 a report appeared on p.2 under the headline "The doctors' case against smoking". In the Manchester Guardian of the same date a report appeared on p.5 under the headline "Lung cancer death rate rising: Cigarettes a cause?" In the Daily Express of 13 January 1953 a report appeared on p.5 under the headline "Smokers' terror...". In the News Chronicle of 24 June 1954 a report appeared on p.3 under the headline "Shares hit by smoke reports".
[3.59]In the Manchester Guardian of 25 June 1954 a report appeared under the headline "Smoking and lung cancer: Inquiry among the doctors brings corroboratory evidence". In the Daily Herald of 25 June 1954 a report appeared on the front page under the headline "Smoking and cancer: 40,000 doctors in new tests". The Daily Express of 18 May 1956 carried reports on the front page under the headline "Doctors: Fight smoking: Start a campaign, 40,000 are told" and on p.7 under the headline "A report to the 25-a-day man: It's double danger for Londoners". The Daily Mail of the same date carried a report on the front page under the headline "Smoking: Doctors answer: Evidence of a possible cause-and-effect relationship: Pipe habit is said to be safer", continued on p.2 under the headline "Smoking".
[3.60]The Daily Record of 18 May 1956 carried a report on p.11 under the headline "All you want to know about smoking risk". The Manchester Guardian of the same date carried a report on the front page under the headline "Replies to a smoker: Lung cancer analysis", continued on p.6 under the headline "Replies to a smoker". The Times of the same date carried a report on p.7 under the headline "Smoking and lung cancer: Questions put to research head". The News Chronicle of 9 November 1956 carried a report on the front page under the headline "New health warning on cigarettes". The Daily Record of the same date carried a report on p.9 under the headline "The doctors who kept on smoking...". The Manchester Guardian of the same date carried a report on p.5 under the headline "Gloomy results from survey into lung cancer and smoking: But hope for the smoker who can stop". The Daily Record of 6 February 1959 carried a report on p.11 under the headline "Fag-ends prove it!" The Daily Mirror of the same date carried a report on p.17 under the headline "Fag-end clues in cancer probe". The Daily Express of 13 January 1953 carried a report on p.5 under the headline "Smokers' terror...".
(8)Coverage of views of the medical profession
[3.61]A selection of newspaper articles was produced which covered the views of the medical profession on the issue of smoking and health. In the Sunday Pictorial of 24 February 1952 a report appeared on the front page under the headline "Smoking - doctors alarmed: Majority of the doctors in Britain now believe that heavy smoking increases the risk of cancer of the lung". In the Sunday Dispatch of 25 April 1954 a report appeared on the front page under the headline "Doctors' journal launches a startling campaign: Smoking sensation: MP urges ban on manufacture of cigarettes as move against cancer peril". Reynolds News of 25 April 1954 carried a report on the front page under the headline "Smoking and cancer: New warning: Stop your young patients from learning to smoke, you will reduce their risk of dying from lung cancer". The Sunday Post of 25 April 1954 carried a report on p.3 under the headline "'Doctors should warn young folk about smoking'". The Sunday Express of the same date carried a report on p.7 under the headline "Cancer, smoking and the doctors". The News of the World of the same date carried a report on the front page under the headline "Doctors and smoking".
[3.62]The Sunday Graphic of 25 January 1958 carried a report on p.3 under the headline "Cigarettes are to blame says BMA". The Scotsman of 27 January 1958 carried a report on p.7 under the headline "BMA book on lung cancer: Cigarette smoking 'principal factor'". The Glasgow Herald of the same date carried a report on p.10 under the headline "Cigarette smoking and lung cancer: 'A definite cause' claims BMA pamphlet". The Manchester Guardian of the same date carried a report on p.18 under the headline "Cigarettes the 'main cause': Smoking and cancer". The Daily Mail of 29 January 1958 carried a report on p.5 under the headline "Cigarettes kill, say BMA". The Daily Telegraph of the same date carried a report on p.11 under the headline "BMA endorse warning on cigarettes: Cancer danger". The Daily Record of 3 February 1958 carried an advertisement on p.8 for the BMA publication "Smoking - the facts" under the headline "Every responsible parent should get this important booklet". The Daily Mirror of 15 December 1961 carried a report on p.21 under the headline "'Make it no smoking by order' plea".
(9)Giving up smoking
[3.63]A selection of articles relating to giving up smoking were produced. In the Daily Graphic of 24 November 1950 an article appeared under the headline "Cigarette in case is the cure". In the Daily Mirror of the same date a report appeared under the headline "Their way to cut out smoking - carry a packet of cigarettes". The Sunday Express of 1 April 1951 carried an article under the headline "If you want to give up cigarettes and beer... try chewing gum and 'beacon pills'".
[3.64]The Daily Record carried various reports in its "News in medicine" column. On 14 January 1952 a report appeared under the headline "What's in those pills for bankrupt smokers". On 28 January 1952 a report carried the headline "Those pills". On 4 February 1952 a report carried the headline "Heavy smoking". The Paisley Daily Express of 4 March 1952 carried a report under the headline "'Joys' of tobacco stage by stage: From pleasure to poison". The Daily Record of 5 September 1952 carried a report under the headline "How to stop smoking". The same newspaper carried reports in its "News in medicine" column on 29 September 1952 under the headline "The Professor agrees it's a smoking cure" and on 11 May 1953 under the headline "There's a'thing intilt". The Sunday Post of 19 September 1954 carried a report on p.13 under the headline "These pills are all the rage with men". The Daily Record of 18 January 1955 carried a report under the headline "Want to stop smoking? Here's a man who can help".
[3.65]The Daily Herald of 12 May 1956 contained a cartoon with the caption "Aren't you glad you've given up smoking when you see a miserable addict like that?". The Sunday Post of 19 August 1956 carried a report under the headline "Hundreds are going to hypnotists to see if they can stop smoking". The Sunday Graphic of 20 January 1957 carried a report on the front page under the headline "Smokers on trial: It was all done by tape-recorder!", continued on p.20 under the headline "The smoking test". The Daily Herald of 29 June 1953 carried a report on p.3 under the headline "Treatment for those who try to give it up, but can't...: MP pleads for smoke addicts". The Sunday Post of 30 June 1957 carried a report under the headline "Doctors tell how to stop smoking". The Daily Record of 1 July 1957 carried a report on p.6 under the headline "I'm taking the truth drug to stop smoking". The same newspaper of 3 July 1957 carried a report on p.6 "Jean MacAulay's focus on smoking: I am under the influence! One 'truth drug' jag and I call for my teddy bear!" The Daily Record of 12 July 1957 carried a report on p.11 under the headline "Here's how you stop smoking - it's easy!" The Sunday Post of 14 July 1957 carried a report on p.7 under the headline "Wins £10 because he's given up smoking". The Daily Record of 27 March 1958 carried a report on p.13 under the headline "Stop smoking by using your eyes: A doctor tells how". Reynolds News of 6 April 1958 carried an article on "Sheila Duncan's page" under the headline "Weak, insecure drug addict... is that me?" The Times of 4 August 1958 carried a story on p.4 under the headline "'Lost' weekend for smokers: Helping addicts to go straight".
(10)Newspaper reports of campaigns
[3.66]Reference was made to a selection of newspaper reports relating to campaigns, proposals and initiatives on the issue of smoking and health. The Daily Mirror of 29 June 1957 carried a report under the headline "Smoking: Now the poster campaign is on". The Daily Sketch of 6 July 1957 carried a report on p.5 under the headline "School smoking talk starts row". The Evening Citizen of 25 July 1957 carried a report on the front page under the headline "No smoking at meetings". The Daily Record of 18 September 1957 carried a report on p.9 under the headline "Smoke in the air of two councils". The Paisley Daily Express of 11 September 1957 carried a report on p.42 under the headline "Smoking ban in Paisley cinemas: Ex-Provost's suggestion" and a further report under the headline "Greenock ex-cricketer condemns smoking". The Daily Record of 11 September 1957 carried a report on p.3 under the headline "Ban smoking here [on church premises], says a minister". A report in the Sunday Post of 26 July 1959 appeared on p.22 under the headline "'No-one should smoke on TV'". The Daily Mirror of 21 March 1962 carried a report on the front page under the headline "'Ban the smokers' bid in four cities". The Daily Express of 4 April 1962 carried a report on p.15 under the headline "400,000 posters go up to scare smokers".
[3.67]The Daily Mail of 6 April 1962 carried reports on the front page under the headlines "Rothmans [tobacco manufacturers] bars 6,000 cigarette machines" and "Smoking addicts may get help". The Glasgow Herald of 6 April 1962 carried a report on the front page under the headline "Curb on cigarette TV advertising: Industry's plans to protect children". The Daily Record of 21 June 1962 carried a report on p.13 under the headline "Cig. chiefs shun teens...". The Daily Record of 22 June 1962 carried a report on the front page under the headline "City slaps a ban on smoking on buses". On the same date it carried a report on p.9 under the headline "Choice is girls or smoking". The Glasgow Herald of 17 August 1962 carried a report on p.7 under the headline "Transport smoking ban rejected: Tobacco advertising to continue". The Daily Mirror of 18 September 1962 carried a report on p.6 under the headline "TV class on smoke risks". The Times of 9 October 1962 carried a report under the headline "Anti-smoking vans begin tour: Two-year campaign". The same newspaper carried a report on 18 October 1962 on p.7 under the headline "No prohibition of smoking". The Daily Record of 3 December 1962 carried a report on p.20 under the headline "Smokers' clinic for city soon". The same newspaper carried a report on 3 April 1965, p.5, under the headline "Hospitals are asked: Ban cigs".
[3.68]The Daily Mirror of 11 April 1963 carried a report under the headline "1,000 more die - and smoking is blamed". The Times of 22 April 1963 carried a report on p.19 under the headline "Industrial films: Lung cancer and smoking: Ministry of Health production". The Daily Mirror of 25 April 1963 carried a report on p.25 under the headline "Will posters like this work?" beside a picture of a coffin captioned "The big flip-top box for the smoker". The News of the World of 12 May 1963 carried a report on the front page under the headline "Hospitals to put a curb on smoking". The Daily Record of 21 June 1963 carried a report on p.6 under the headline "Clinic finds the 'cure' for smokers". The Daily Telegraph of 25 July 1963 carried a report on the front page under the headline "TV warnings on smoking considered". The Daily Herald of 25 July 1963 carried a report on p.9 under the headline "TV warnings on smoking: Ministry may advertise". The Daily Record of 9 October 1963 carried a report on p.19 under the headline "Smoking under fire". The Sunday Post of 13 October 1963 carried a report on p.5 under the headline "The anti-smoking show with an 'X' certificate". The Daily Mirror of 13 November 1963 carried a report on p.3 under the headline "65 MPs say: Ban TV smoking ads".
PART IV: MR AND MRS McTEAR: QUESTIONS OF FACT
[4.1]The personal history of Mr McTear, and consequently also that of Mrs McTear, was brought out in remarkable, but by no means unnecessary, detail. This was done for three principal reasons: first, because it is relevant to my assessment of his credibility and reliability as a witness when he gave evidence on commission, especially about his smoking history; secondly, because some of his personal characteristics and family history are relevant to scientific issues bearing on the question whether cigarette smoking caused his lung cancer; and, thirdly, because it is relevant to the assessment of the damages which I would award if I were to find ITL liable.
[4.2]The history that follows is derived from admissions in the pleadings, from the evidence taken from Mr McTear on commission, from joint minutes of admissions and notices to admit and from the evidence of Mrs McTear and other witnesses of fact. If this history tends to dwell on the more negative aspects of Mr McTear's personality and life, this is because most of it was brought out in the cross-examination of Mrs McTear and in the evidence of witnesses called for ITL.
Family, education, employment and criminal history
[4.3]None of the information in this section is controversial. It is derived from agreed documents and the evidence of witnesses whose credibility and reliability were not in issue.
[4.4]Mr McTear was born in Paisley on 25 September 1944. His parents then lived at 8 Shortroods Crescent, Paisley. He lived with them at that address until he was 16 years old, when he left to serve with the Junior Leaders. He attended Mossvale Primary and Junior Secondary School until he reached the compulsory leaving age of 15. It was not possible to sit O Grade or O Level examinations at a junior secondary school. He joined the Infantry Junior Leaders Battalion on 22 February 1960. He was discharged on compassionate grounds on 30 January 1962. While in the Junior Leaders he gained the Army Certificate of Education Class 3 in mathematics, English and history and the Army Certificate of Education Class 2. He did not gain the Army Certificate of Education Class 1.
[4.5]Charles McGrogan, aged 59, a retired company director, gave evidence about his life in the Army, which was similar to that of Mr McTear. He left school at the age of 15 in 1959 and signed up with the Army on a twelve-year engagement. He joined the Infantry Junior Leaders Battalion for two and a half years, being based at Plymouth and thereafter at Oswestry. The function of the Junior Leaders was to train the future non-commissioned officers and warrant officers of the Army. The normal period spent in the Junior Leaders was two and a half years. The time was divided between military training, education and sports. The standard of teaching carried out by the Royal Army Education Corps was very high. The Army Certificate of Education Class 1 was not much more advanced than the civilian 11+ examination. It was followed by Class 2, which was intermediate, and Class 3, which was the equivalent of O level. Mr McGrogan left boy service with five passes in Class 1.
[4.6]The military training was the same for boy soldiers as for older soldiers. The discipline was very strict. Instruction was given in rules and regulations both through normal squad training and by instruction by the Royal Army Education Corps. All Junior Leaders would know that being absent from barracks or from a place of duty without permission was an offence which would lead to a charge and an appearance before a company commander, who would decide on the form of punishment. One punishment was restriction of privileges, recorded as "RP". This varied. Normally it meant confinement to barracks for a week, and parading at the guardroom four times a day in full kit. Another punishment was confinement to barracks, recorded as "CTB", and deduction of pay, under reference to the relevant Royal Warrant ("RW") number.
[4.7]Mr McGrogan said that Junior Leaders had access to daily and Sunday newspapers, which were provided free, and to both BBC and ITV television channels. The newspapers would include Scottish as well as English newspapers, such as the Sunday Mail and the Sunday Post. After Mr McGrogan was posted to Germany in 1964, it was necessary for soldiers to buy their newspapers from newsagents or the NAAFI. A full range of BBC television and radio news programmes was available through the British Forces Broadcasting Service.
[4.8]In cross-examination Mr McGrogan said that he left the Army as a sergeant after twelve years. He then joined the Territorial Army and finished as warrant officer. He had come to be a witness because he was the Secretary/Treasurer of a regimental association that represented Army boys and Infantry Junior Leaders. Bullying was no more rife in the Army in the 1950s and 1960s than it was at any time. There was some bullying, which was mostly dealt with by the lads themselves. The Army were very sympathetic to problems that the junior soldiers had at home, and readily granted compassionate leave. Leave would be authorised by the commanding officer or the unit welfare officer, and the Ministry of Defence would pay for a travel warrant. It was normal for compassionate leave to be granted where a close family member had died or was seriously ill.
[4.9]On 31 January 1962, the day after leaving the Infantry Junior Leaders Battalion, Mr McTear registered for unemployment benefit. On 19 March 1962 he claimed sickness benefit for urticaria or nettle rash. On 6 July 1962 he underwent a military medical examination before joining the Army. On the form relative thereto he stated that his mother was 50 years old and in good health. On 21 July 1962 he signed on to serve for twenty-two years with the Royal Scots Greys, and was posted to the Royal Armoured Corps Depot in England. During his time in the Army Mr McTear was stationed in Britain from July 1962 to January 1963, in Aden from January to May 1963, in Britain from 1 June 1963 to 23 January 1964, and in Germany thereafter until being sent home in June 1964. He started going out with Mrs McTear while he was in the Army. On 7 August 1962, at Paisley Sheriff Court, he was convicted of an offence under the Criminal Law Amendment Act 1885, section 5 (1). He was admonished. He should have notified the Army of this conviction, which would then have been written into his army record, but did not do so.
[4.10]Lieutenant Colonel Michael Blacklock, aged 75, said that he joined the Royal Scots Greys in 1948 and remained with that regiment, latterly as a Lieutenant Colonel commanding it, until he retired from the Army in 1971. He gave evidence about Mr McTear's time in the Army, under reference to the relevant Army records. Colonel Blacklock explained that any new recruit would be told that he was joining a disciplined organisation and that there would be consequences for breaches of military discipline, for which he might be punished. Absence without leave was a serious offence, which would be dealt with by the commanding officer. During his time in the Junior Leaders Mr McTear was awarded fourteen days' detention on 4 October 1961 by his commanding officer for being absent without leave for five days, 101/2 hours. He joined the Royal Scots Greys on 12 July 1962. On 1 October 1962 he was punished with ten days' restriction of privileges and forfeited £1 for being absent without leave for two hours. Colonel Blacklock said that the commanding officer would have made a soldier who was absent without leave aware that he was letting down his fellow soldiers and given him every encouragement not to do it again. If he was absent for more than a short time, such as two hours, he would be told quite firmly that if he persisted in this line of stupidity he would incur a much more serious punishment.
[4.11]During 1963 Mr McTear was transferred for a time to the Ayrshire Yeomanry. Colonel Blacklock interpreted this posting as being for compassionate reasons, because the Ayrshire Yeomanry was the nearest regiment to his home address. On 24 August 1963 Mr McTear's mother died at Paisley Royal infirmary and on 26 August he registered the death with the Paisley registrar. On 19 September 1963 he was punished by forfeiture of pay for being absent without leave from 8.00am on 13 September to 7.40am on 19 September. Colonel Blacklock said that the Ayrshire Yeomanry, being a Territorial Unit, did not have a guardroom, so it appeared that Mr McTear was punished by forfeiture of pay rather than detention, especially as he was about to be sent to his own regimental depot. On 4 November 1963, at a time when he was attached to the Blues & Royals in England, Mr McTear was convicted at Andover Magistrates Court of getting into and tampering with a motor vehicle. He should have notified the Army of this conviction, which would then have been written into his Army record, but did not do so.
[4.12]On 9 March 1964, while the Royal Scots Greys were stationed in Germany, Mr McTear was punished with twenty-eight days' detention and one day's forfeiture of pay for being absent without leave for nearly fifteen hours on 26 February and for taking and driving away a motor car without the owner's consent. Colonel Blacklock explained that the purpose of detention was to try to sharpen up a soldier, to encourage him and make him realise that there was a better life outside the guardroom. He would have to parade in the morning, and then perform useful jobs, of the kind which the average soldier did not want to get involved in, such as clearing blocked drains. It would be made clear to him by the commanding officer in imposing this punishment that if he re-offended the consequences inevitably would be more severe. On 9 March 1964 Mr McTear was warned by his commanding officer, Lieutenant Colonel Wheeler, that, unless his behaviour improved within three calendar months from that date, application would be made for his discharge from the Army.
[4.13]Mr McTear was released from detention on 6 April 1964, with no remission for good conduct. On 4 April 1964, shortly after returning to duty, Mr McTear was found drunk and disorderly by the town patrol. He was suffering from a laceration to the right wrist. He persistently refused penicillin and tetanus toxoid injections, contrary to advice by the medical officer. On 27 April 1964 he was awarded twenty-eight days' detention for having been in bed when he should not have been, for insubordination, for improper possession and for disobeying an order. Colonel Blacklock interpreted this as having related to Mr McTear's failure to get up in the morning when reveille was sounded, having disobeyed an order instructing him directly to get up and go to his parade, and having had a piece of equipment which he should not have had or should have handed in. On 9 May 1964 Mr McTear was punished with the loss of four days' remission for escaping from custody. He was released from detention on 23 May 1964 with no remission.
[4.14]Meanwhile, on 11 May 1964 Lieutenant Colonel Wheeler applied for Mr McTear's discharge on the ground that his retention was undesirable in the interest of the service. He wrote:
"This man is utterly selfish and bone idle. He has no interest other than in his own personal appearance. He is useless and a nuisance in the Army. I do not consider he has misconducted himself with a view to obtaining a discharge."
On 29 May 1964 the brigade commander authorised the discharge. Mr McTear was posted back to the United Kingdom and was discharged on 9 June 1964. He was given a military conduct rating of "unsatisfactory", which was the lowest possible rating.
[4.15]In cross-examination, Colonel Blacklock said that he did not remember Mr McTear as a person at all, but he did remember the fact of his discharge because it was such an unusual occurrence. In Mr McTear's certificate of service, dated 29 May 1964, it was stated by way of testimonial with a view to civilian employment:
"McTear is a person who appears not to know where he is going in life. He has not made a serious attempt to become a soldier in this Regiment. He is not entirely unintelligent and, if he found a job in which he was interested, he might do good work."
[4.16]Asked about Mr McTear's discharge from the Junior Leaders in January 1962, which was stated to have been on compassionate grounds, Colonel Blacklock said that he had become aware from other documents that Mr McTear's mother had problems at home, which made it difficult for him, and he was discharged for that reason. If further compassionate leave was needed after Mr McTear's mother's death on 24 August 1963, he would have been given it, and there would have been no need for him to go absent without leave in September 1963. The Army was not an unsympathetic organisation.
[4.17]After he left the Army, Mr McTear moved in with Mrs McTear's parents, Mr and Mrs McBarron, at 1 Walkinshaw Road, Paisley. Mr and Mrs McTear were married in St James' Roman Catholic Church, Paisley, on 25 September 1964, his twentieth birthday. On 24 September 1964, the day before the wedding, Mr McTear attended his general practitioner (GP) and reported that he had "strained back while lifting machine". He was certified as unfit for work with a diagnosis of "back strain". From 25 to 30 September 1964 he claimed sickness benefit for the "back strain".
[4.18]On 31 May 1965 Mr McTear started work at Brown & Polson on a production line in the Gerber babyfood section. On Monday 10 July 1965 he appeared at St Andrews police court and admitted committing a breach of the peace at St Andrews, having argued and fought with colleagues from Paisley when their bus did not turn up. He had spent the previous two nights in the police cells. He was convicted of a breach of the peace and was fined £20. On 29 October 1965 he resigned from work at Brown & Polson giving the reason "Improved position". He never worked for Brown & Polson again. On 3 December 1965 Mr McTear behaved indecently and attempted to head-butt a police constable in the face in Paisley Road West, Glasgow. On 4 December 1965 he pled guilty to these offences and was fined a total of £15. The incident was reported in the Paisley Daily Express on 7 December 1965. On 5 March 1966 he was convicted of theft at Paisley Sheriff Court and was fined £10. On 8 March 1966 he started work at Cadbury's in Paisley. Ten days later, on 12 August 1966, he stopped working there. From 23 to 30 November 1966 he claimed sickness benefit for "pharyngitis". From 30 January to 4 February 1967 he claimed sickness benefit for "strained back". From 20 to 26 July 1967 he claimed sickness benefit for "enteritis". From 25 to 28 October 1967 Mr McTear claimed sickness benefit for "strain[ed] shoulder". On 4 November 1967 he was convicted of assault at Paisley Sheriff Court and was fined £5, with an alternative of 30 days' imprisonment.
[4.19]On 28 July 1966 Mr and Mrs McTear's first child, Sandra, and on 8 August 1967 their second child, Alan, were born. Mr and Mrs McTear lived at 13 Schaw Road, Paisley from 1968 to 1980. On 6 February 1968 his appeal through his MP to be accepted for re-enlistment in the Army was turned down. From 27 February to 2 March 1968 he claimed sickness benefit for "gastritis". Between 27 February and 18 November 1968 there was no continuous period lasting in excess of eight weeks in which he did not claim either unemployment benefit or sickness benefit. On 3 April 1968 Mr McTear was convicted at Paisley Sheriff Court of an offence under section 30 of the Ministry of Social Security Act 1966 (the offence of persistently refusing or neglecting to maintain himself or any person whom he was liable to maintain and benefit was paid), and sentence was deferred to 6 January 1969, when he was fined £30 with an alternative of sixty days' imprisonment. On 1 May 1968 he started work at Cadbury's in Paisley as a warehouseman working nightshifts. From 18 to 22 May 1968 he claimed sickness benefit for "backache". On 31 May 1968 he was "Discharged" from work at Cadbury's as he was "unsuitable". On 6 November 1968 he attended the Royal Alexandra Infirmary, Paisley and had a cast applied for tenosynovitis of right wrist extensors. From 12 to 18 November 1968 he claimed sickness benefit for "Injury to right arm". On 28 November 1968 Mr and Mrs McTear's third child, Lesley, was born.
[4.20]On 13 June 1969 he was working at BOCM in Renfrew as a process operator. He was palletising in the morning. He asked for assistance to help pull a pallet from the top of a six-foot high stow. Before help could be provided, he pulled the pallet and injured himself, suffering abrasions and contusion on his right chest. He carried on working until 17 June 1969 and claimed sickness benefit for the injury from 18 to 28 June 1969. On 16 July 1969 he started work as a labourer in the Mechanical Engineer's Department of Clyde Port Authority. From 5 to 8 August 1969 he claimed sickness benefit for "enteritis". On 10 October 1969 he resigned from his job at the Clyde Port Authority. From 5 to 10 January 1970 he claimed sickness benefit for "influenza". From 14 to 18 July 1970 he claimed sickness benefit for "gastroenteritis". Between 14 July 1970 and 6 March 1971 there was no continuous period lasting in excess of eight weeks in which he did not claim either unemployment benefit or sickness benefit. On 30 September 1970, at Paisley Sheriff Court, he was convicted of theft and was fined £20 with the alternative of sixty days' imprisonment. From 10 to 28 October 1970 he claimed sickness benefit for "infection to foot".
[4.21]Ronald Green, aged 60, was a social worker employed by Glasgow City Council. He knew Mr and Mrs McTear in the period between 1970 and 1976, when he lived in the flat opposite them at 12 Schaw Road, Gallowhill, Paisley. Both flats were on the ground floor. He said that Mr McTear was fond of a drink and sometimes overdid it a bit, so that he (Mr Green) had to go and knock on his door and remonstrate with him if he had said something to Mrs Green or something like that. This happened a few times rather than frequently. He would say that Mr McTear was drinking away from the house. He did not know whether he was drinking in the house. He used to come in on Friday and Saturday nights, usually with a drink in him, by which he meant that he was drunk.
[4.22]On 8 February 1971 Mr McTear started work at Chrysler Motors as an operator. From 1 to 6 March 1971 he claimed sickness benefit for "enteritis". On 14 May 1971 he resigned from Chrysler Motors for his own reasons which were noted as "going to England for work". The employment record for him originally stated that he was suitable for re-employment. This record was revised in 1973 to "re-engage? -- no" following an interview on 15 November 1973 at which he falsely "stated he was never employed by the company". Employment was refused. On 13 December 1971, at Newcastle-upon-Tyne Magistrates Court, Mr McTear was convicted of wounding and sentenced to three months' imprisonment, suspended for two years.
[4.23]On 6 March 1974, at Paisley Sheriff Court, he was convicted of a breach of the peace and was fined £30, with an alternative of thirty days' imprisonment. Between 15 March 1974 and 20 July 1974 there was no continuous period lasting in excess of eight weeks in which he did not claim either unemployment benefit or sickness benefit. On 15 May 1974 Mr McTear was re-employed at Chrysler Motors as an operator. On 15 June 1974 he was seen by the duty casualty officer at the Royal Alexandra Infirmary, Paisley, having fallen on the previous night, injuring his right knee. He was suspected to have fractured his patella. He was given an anti-tetanus toxoid and penidural. No fracture was found but he was admitted to the casualty ward and a padded guard plaster was applied. From 15 June to 20 July 1974 he claimed sickness benefit for "injury to right knee". During this period, he claimed dependant's benefit for his wife when he was not entitled to do so. From 28 to 30 November 1974 he claimed sickness benefit for "influenza". Between 28 November 1974 and 13 July 1976 there was no continuous period lasting in excess of eight weeks in which he did not claim either unemployment benefit or sickness benefit.
[4.24]On 4 December 1974, at Paisley Sheriff Court, Mr McTear was convicted of a breach of the peace and was fined £10, with an alternative of seven days' imprisonment. From 13 to 17 February 1975 he claimed sickness benefit for "coryza", and from 15 to 24 March 1975 for "lumbar strain". During both these periods he claimed dependant's benefit for his wife when he was not entitled to do so. On 28 March 1975 he resigned from his job at Chrysler Motors for his own reasons. His employment record was marked "no" to re-engagement. The reason for this was given as "bad timekeeping". From 31 March 1975 until 15 August 1975 he claimed sickness benefit for "lumbar pain". During this period also he claimed dependant's benefit for his wife when he was not entitled to do so.
[4.25]On 29 October 1975, a National Insurance Officer reviewed Mr McTear's awards of dependant's benefit for his wife during the periods 15 June 1974 to 20 July 1974, 13 February 1975 to 17 February 1975, 15 March 1975 to 24 March 1975 and 31 March 1975 to 2 August 1975. On 19 November 1975 it was determined that benefit had been overpaid for Mr McTear's wife to the amount of £126.09 and the relevant Government department wrote to him demanding repayment of this amount. On 16 January 1976 the department wrote to him noting that there had been no adequate response to intimation of overpayment of benefit and requesting a satisfactory offer of payment within seven days. On 20 January 1976 Mr McTear replied to the second letter stating that he was unemployed and was receiving unemployment benefit from which £2 was being deducted in respect of an overpayment. He wrote: "It seems ridiculous that I should pay this as it was my wife's fault that I got into this mess." From 29 June to 13 July 1976 he claimed sickness benefit for "multiple bruises". On 9 July 1976 the relevant Government department wrote to him again seeking proposals for repayment of the overpaid benefit, which remained unpaid.
[4.26]On 18 August 1976, at Renfrew District Court, Mr McTear was convicted of the offence of being "drunk and incapable" and was fined £5. On 19 November 1976, at Paisley Sheriff Court, he was convicted of contraventions of section 93(1)(c)(i) of the National Insurance Act 1965 and the Ministry of Social Security Act 1966 in respect of the awards of dependant's benefit referred to above, and was sentenced to thirty days' imprisonment. From 16 to 20 August 1977 he claimed sickness benefit for "influenza/chill", and from 5 to 10 September 1977 for "enteritis". On 29 September 1977 the relevant Government department wrote to him again, seeking proposals for repayment of the overpaid benefit referred to above. Deductions of £4.30 a week had been made but the balance outstanding was still £112.54. From 7 to 10 December 1977 Mr McTear claimed sickness benefit for influenza.
[4.27]On 17 July 1978 he started work for Plessey Telecommunications (Plessey) as a wireman. After some initial training he worked at a telephone exchange in Renfrew as a grade 4 wireman. No educational qualifications were marked on his Plessey employment record. From 15 to 23 September 1978 he claimed sickness benefit for "influenza/chill". On 3 October 1978, the relevant Government department sent a letter to him noting that £63.51 was still outstanding from the overpayment of benefit and seeking proposals for repayment. On 30 October 1978 he attended the Royal Alexandra Infirmary having fractured the lower end of his left radius. A cast was applied. He claimed that the injury was a result of an accident at work at Plessey. From 31 October until 9 December 1978 he remained off work and claimed sickness benefit for "fractured wrist". On 3 November 1978 Mrs McTear signed a DHSS form on behalf of Mr McTear stating that he was agreeable to have £2 per week deducted from his benefit.
[4.28]From 9 to 13 January 1979 he claimed sickness benefit for "injury to knee". In March 1979 he applied to Gartloch Hospital to train as a psychiatric nurse. On 25 April 1979 he resigned from his job as a wireman with Plessey. His employment record was marked "unsuitable for re-employment". He had written to say he could not comply with the essential requirement of the job to be mobile. He was never employed by Plessey again. On 4 June 1979 he repaid in full the overpayment for which he was imprisoned for thirty days in 1976 and which had been due since 19 November 1975. From 30 July to 4 August 1979 he claimed sickness benefit for "facial injuries", having been attacked by his brother-in-law. From 22 to 27 October 1979 he claimed sickness benefit for "viral illness". Between 30 July 1979 and 17 April 1984 there was no continuous period lasting in excess of eight weeks in which he did not claim either unemployment benefit or sickness benefit. Between 26 February and 1 March 1980 he was in receipt of sickness benefit for "chest pain".
[4.29]From 1980 to 1983 Mr and Mrs McTear lived at 3 Albion Street, Paisley. On 2 May 1981 Mr McTear wilfully set fire to his house, to the danger of his family and neighbouring houses. He was admitted to the Royal Alexandra Infirmary overnight, after burning his right leg and hand. He was very aggressive to medical staff and was in police custody at the hospital. Between 7 May and 31 July 1981 he was in receipt or sickness benefit for "bursitis of leg". On 14 May 1981 he received supplementary benefit, pending the result of a claim for sickness benefit. On 5 November 1981, he was convicted at Paisley Sheriff Court of wilfully setting fire to his house at 3 Albion Street to the danger of his family and neighbouring houses. Sentence was deferred to 25 November for a social inquiry report. On 20 November 1981 he told the social worker who interviewed him for the purposes of the report that he was a "radial arm driller", his last job was in Germany eighteen months previously, since then he had been unable to obtain any further employment, his unemployment had caused emotional and financial stresses and imposed strains on his marriage, he was very depressed when he committed the offence on 2 May 1981 and since then matters had been quieter within the family and relationships were good. On 25 November 1981 at Paisley Sheriff Court he was made the subject of a probation order for two years, for the offence committed on 2 May 1981. The sheriff explained to him that, if he failed to comply with the order, he could be brought before the court by his supervising officer for a breach of probation and could be dealt with for the original offence, and that, if he committed another offence during the period of the probation order, he could be dealt with likewise. He expressed his willingness to comply with the requirements of the order and the court ordered that he should inter alia be of good behaviour. On Friday 18 December 1981, however, he wrecked furniture at his home at 3 Albion Street, tried to rip a lit gas fire from a wall and threatened his son Alan McTear. On 21 December 1981 he was convicted at Paisley Sheriff Court of a breach of the peace and was fined £30. On 6 January 1982 he was referred to Renfrew District Council on Alcoholism by his GP.
[4.30]Colin McLatchie, aged 55, a retired police constable, gave evidence about occasions when the police had to deal with Mr McTear. On a number of occasions during a period of about one year in 1982 or 1983 Mr McLatchie and a colleague would be called to Mr McTear's house. They would find him drunk and Mrs McTear upset. Mrs McTear would be warned about his conduct. On one occasion he was arrested and charged with breach of the peace. Mr McLatchie never saw Mr McTear sober. He saw him on about four or five occasions and it was obvious that he had a problem with drink, this was well known. In January 1983 Mr McTear committed a breach of the peace within the jurisdiction of Paisley Sheriff Court. On 15 April 1983 he was convicted of this offence and was fined £50. In August 1983 he again committed a breach of the peace within the jurisdiction of Paisley Sheriff Court. On 24 November 1983 his probation order came to an end. On 14 December 1983 he was convicted of the breach of the peace committed in August 1983 and was fined £60.
[4.31]Mr and Mrs McTear lived in Beith, initially at 60 Main Street, and thereafter at 20 Cherrywood Drive, from 1983 until his death. Police Constable Henry Graham gave evidence that during the course of his duties as a police officer he had come across Mr McTear in 1984 or 1985 in Main Street in Beith. He had been on foot patrol and attended Mr McTear's flat until a vehicle came from Kilbirnie to assist. He could hear banging and shouting coming from the landing upstairs. When he went up, he found that Mr McTear had broken part of a cast iron grate used as a foot scraper and was using it to try and break the door. When the police approached he turned and a struggle started. He was about to swing at the police with the bit of grate. They arrested him and then there was a struggle. There was another occasion that PC Graham remembered, when Mr McTear lived in Cherrywood Drive, Beith. Mrs McTear had called. When the police arrived Mr McTear was lying, apparently asleep, on the couch in the livingroom. The stereo system was playing loud music, so PC Graham turned it off. At that point Mr McTear jumped from the couch and immediately started cursing and swearing. PC Graham told him to calm down, but Mr McTear swore and said he would do exactly what he wanted in his house. He was then arrested. PC Graham recalled two other occasions when he spoke to Mr McTear at Cherrywood Drive, once to give him a warning and on another occasion to arrest him. He described him as "not quite the man to take a telling". Whenever he spoke to PC Graham, he tended to come very close and act aggressively, cursing and swearing. He had been drinking on each occasion that PC Graham saw him.
[4.32]On 27 February 1984 Mr McTear was convicted at Kilmarnock Sheriff Court on charges of breach of the peace and assault. Sentence was deferred to 6 August 1984 and he was ordained to be of good behaviour. In March 1984 he committed a breach of the peace and resisted arrest. On 7 March 1984 he was convicted of these offences at Kilmarnock Sheriff Court and was fined £80. Between 26 March and 29 April 1984 Mr McTear attended a training course organised through the local job centre. On 29 March 1984 he was convicted at Kilmarnock Sheriff Court of a further assault committed that month and was fined £75. Between 10 and 17 April 1984 he received sickness benefit for "virus infection". On 18 April 1984 he registered as unemployed. In May 1984 he committed two assaults and two breaches of the peace. In July 1984 he committed two assaults, two breaches of the peace and two contraventions of the Police (Scotland) Act 1967. On 6 August 1984 he was sentenced to sixty days' imprisonment for the offences of which he had been convicted on 27 February 1984. On the same date he was convicted at Kilmarnock Sheriff Court of the offences committed in May 1984, for which he was sentenced to three months' imprisonment, and the offences committed in July 1984, for which he was sentenced to a total of fifteen months' imprisonment, to run consecutively. On 7 August 1984 he was admitted to Low Moss Prison. On 2 October 1984 he was transferred from there to Longriggend Prison. 5 December 1984 was noted as the earliest date on which he could be liberated from this sentence.
[4.33]On 12 July 1985 Mr McTear visited his GP, who noted that he was unemployed and suffering from depression. His GP counselled him and prescribed Prothiaden, a tricyclic anti-depressant. On 16 July 1985, at 60 Main Street, Beith, Mr McTear (1) assaulted his daughter Sandra McTear, grabbed her by the hair, pulled her to the floor, kicked her, dragged her along the floor, pushed her into a bath and banged her head on a bath; and (2) conducted himself in a disorderly manner, shouted and swore, and committed a breach of the peace. On 9 August 1985, at the same address, he: (1) conducted himself in a disorderly manner, continually rang the doorbell and banged on the door of the premises to the alarm of the occupants, shouted and swore, uttered threats, forced a piece of metal or similar instrument through the door and struck the door repeatedly therewith and committed a breach of the peace; and (2) resisted arrest by Henry Graham and Scott Laughlan, both police constables, then in uniform and engaged in the execution of their duty in arresting him on a charge of breach of the peace, contrary to the Police (Scotland) Act 1967, section 41(1)(a). On 23 October 1985 he was drunk and was involved in a domestic dispute. He suffered a one-inch laceration in the occipital area of his scalp. He was taken to the Beith health centre by the police. He was very uncooperative with his GP and refused advice to have one or two stitches inserted in his wound.
[4.34]On 18 December 1985 Mr McTear was living at 34 Festing Grove, Southsea, Hampshire. On 19 December 1985 at Kilmarnock Sheriff Court he pled guilty by letter to two charges in a complaint relating to the offences committed on 16 July 1985. Sentence was deferred until 6 January 1986, when he was required to appear in person. On 6 January 1986 he appeared in person. Sentence was deferred until 24 March 1986 and he was ordained to be of good behaviour in the meantime. On 16 January 1986 at Kilmarnock Sheriff Court he pled guilty by letter to the first charge in a complaint, relating to the offence of breach of the peace committed on 9 August 1985, but not guilty to the second charge, relating to the contravention of the Police (Scotland) Act 1967. Trial was fixed for 29 April 1986 in relation to the second charge, with an intermediate diet on 11 March 1986. Sentence was deferred in relation to the first charge. He was ordained to appear at the intermediate diet.
[4.35]On 29 January 1986, at 60 Main Street, Beith, Mr McTear: (1) assaulted Mrs McTear, spat on her and struck her on the face; (2) conducted himself in a disorderly manner, shouted and swore and committed a breach of the peace; and (3) resisted John Hanson and John McDonald, police constables, then in uniform and engaged in the lawful execution of their duty and struggled violently with them, contrary to the Police (Scotland) Act 1967, section 41(1)(a). On 12 February 1986 he was convicted at Cunninghame District Court of a breach of the peace and was fined £50. On 11 March 1986 he failed to appear at Kilmarnock Sheriff Court for the above-mentioned intermediate diet and warrant was granted for his apprehension. On 24 March 1986 he failed to appear at Kilmarnock Sheriff Court for the sentence which had been deferred on 6 January 1986, and warrant was granted for his apprehension. Also on 24 March 1986, Mr McTear started work for Britax Winguard Ltd (Britax) in Arundel, West Sussex, for a four-week probationary period as a hand-press operator. On 25 April he left this employment. The company considered that he was "unsuitable" and that he should not be re-employed.
[4.36]On 29 April 1986 Mr McTear failed to appear at Kilmarnock Sheriff Court for the diet of trial that had been fixed on 16 January 1986, and warrant was granted for his apprehension. On 12 May 1986, on the application of the Procurator Fiscal, the sheriff at Kilmarnock granted warrant to apprehend Mr McTear in respect of a complaint containing three charges relating to the offences committed on 29 January 1986. He was designed as "formerly of 60 Main Street, Beith [...] whose present whereabouts are meantime unknown". On 15 May 1986 he appeared at Kilmarnock Sheriff Court. He pled guilty to all outstanding charges against him in the three above-mentioned complaints and was sentenced to a total of 150 days' imprisonment, to run consecutively. On 16 May 1986 he was admitted to Low Moss Prison, and on 6 June 1986 he was transferred to Longriggend Prison. The earliest date on which he could have been liberated from this sentence was 22 August 1986. On 18 September 1986, at the house at 60 Main Street, Beith, Mr McTear conducted himself in a disorderly manner, shouted and swore, smashed and damaged furniture and fitments in the house and committed a breach of the peace. On the same date he appeared at Kilmarnock Sheriff Court in answer to a complaint relating to this offence. He pled guilty and was sentenced to forty days' imprisonment. On 19 September 1986 he was admitted to Low Moss Prison. The earliest date on which he could have been liberated from this sentence was 14 October 1986.
[4.37]On 20 October 1986, at 60 Main Street, Beith, Mr McTear: (1) assaulted Sandra McTear, pushed her to the ground and punched her about the head to her injury; and (2) conducted himself in a disorderly manner, shouted and swore, threatened violence, smashed furniture and fitments and committed a breach of the peace. On the same date he appeared at Kilmarnock Sheriff Court in answer to a complaint relating to these offences. He pled guilty to both charges. Sentence was deferred until 10 November 1986 and he was allowed bail on condition that he be of good behaviour. On 10 November 1986, at 60 Main Street, Beith, Mr McTear conducted himself in a disorderly manner, shouted and swore, threatened his wife and family with violence and committed a breach of the peace. On the same day he appeared at Kilmarnock Sheriff Court in answer to a complaint relating to this offence and a consequent contravention of the Bail etc (Scotland) Act 1980, section 3(1)(b). He pled guilty to both charges. He appeared also for the sentence which had been deferred from 20 October 1986. He was sentenced to a total of ninety days' imprisonment, to run consecutively. On 11 November 1986 he was admitted to Low Moss Prison. On 26 November 1986 he was granted interim liberation and was released from Low Moss Prison on bail while he appealed against the sentence. On 16 March 1987 his appeal was refused and he returned to Low Moss Prison. The earliest date for his liberation from this sentence was 24 April 1987.
[4.38]On 30 April 1987, at 60 Main Street, Beith, Mr McTear: (1) assaulted Mrs McTear, pushed her onto a bed, seized her round the neck and attempted to strike her with a wooden shaft; (2) assaulted Alan McTear by attempting to strike him with a wooden shaft; and (3) conducted himself in a disorderly manner, shouted and swore and committed a breach of the peace. On the same day he appeared at Kilmarnock Sheriff Court to answer a complaint containing three charges relating to these offences. He pled not guilty, and was remanded in custody until trial, which was fixed for 2 June 1987. On 11 May 1987, having changed his plea to one of guilty, he was convicted of his charges and was sentenced to three months' imprisonment, backdated to 30 April 1987. On 23 July 1987, at 20 Cherrywood Drive, Beith, Mr McTear: (1) assaulted Alan McTear, burnt him on the back with a lighted cigarette, grabbed hold of him and pushed his head through a window, all to his injury; and (2) conducted himself in a disorderly manner, shouted and swore and committed a breach of the peace. On the same day he appeared from custody at Kilmarnock Sheriff Court to answer a complaint containing two charges relating to these offences. The case was continued without plea until the following day and he was remanded in custody in the meantime. On 24 July 1987 he again appeared at Kilmarnock Sheriff Court and pled guilty to these charges. He was sentenced to six months' imprisonment on the first charge and to thirty days' imprisonment on the second charge, to run concurrently.
[4.39]Mr McTear did not work a sufficient amount in the tax year 1987/1988 to have enough contributions to qualify for sickness benefit. On 1 August 1988, he started work with Garnock Valley Arts and Crafts Group ("Valley Arc") as a temporary arts assistant, employed by Cunninghame District Council under a Manpower Services Commission scheme, on a contract due to expire on 3 March 1989. He was engaged to work twenty-two hours per week. He did not pay enough national insurance contributions in the tax year 1988/1989 to obtain contributions sufficient to qualify for sickness benefit. On 7 November 1988 he visited his GP, who diagnosed him as suffering from bronchitis. The GP recorded that he was to be referred to a psychiatrist for depression. On 8 December 1988 he was offered appointment as resident caretaker at 71/75 Robertson Street, Glasgow.
[4.40]On 25 December 1988, at 20 Cherrywood Drive, Beith, Mr McTear conducted himself in a disorderly manner, played music at excessive volume, shouted and swore and committed a breach of the peace. On 24 January 1989, at the same address, he: (1) assaulted Alan McTear and turned him out of bed; and (2) conducted himself in a disorderly manner and committed a breach of the peace. On 26 January 1989, at Kilmarnock Sheriff Court, he pled guilty by letter to a complaint containing a charge which related to the offence committed on 25 December 1988. He was fined £150, payable in instalments of £5 per week. On 21 February 1989 at The Cross, Dalry, he conducted himself in a disorderly manner, shouted and swore, caused vehicles to swerve to avoid striking him and committed a breach of the peace. On 3 March 1989 he failed to attend at Kilmarnock Sheriff Court to answer to a complaint containing two charges relating to the offences committed on 24 January 1989. Warrant for his apprehension was granted. On 24 April 1989 he appeared at Kilmarnock Sheriff Court to answer to this complaint. He pled guilty and was fined £150, payable in instalments of £10 per week, with the alternative of thirty days' imprisonment.
[4.41]Mrs Isobel McCutcheon, aged 61, gave evidence about the extension of Mr McTear's employment with Cunninghame District Council. She had been employed as a senior personnel assistant with Cunninghame District Council since 1978, and with North Ayrshire Council following local government reorganisation in April 1996, until she retired in 2002. On 17 February 1989 Mr McTear completed a Cunninghame District Council application form for re-employment as a temporary arts assistant at Valley Arc. He signed a certificate at the end of the form that to the best of his knowledge the information given in it was correct. It would have been a requirement that applicants had three O levels. He claimed to have attended Camphill Secondary School, Paisley, from 1956 to 1960. This was a school where it was possible to gain O grade and later O level qualifications. He told Mrs McCutcheon at interview on 3 March 1989 that he had O levels in mathematics, English and history. These claims were untrue. In the application form he also claimed untruthfully to have gained Army certificates of education Class 1, Class 2 and Class 3 in 1961. He also stated untruthfully that he had been employed by Plessey Telecom as a telecommunications installer from 1982 to November 1987. He told Mrs McCutcheon at interview that he had been made redundant. He gave no employment history for any period prior to 1982. When Mrs McCutcheon asked him what he did between 1960 and 1982 he told her, untruthfully, that he had spent eleven years in the Army, and had thereafter been employed in telecommunications in West Germany from 1973 to 1974, by Component Tools in the USA from 1974 to 1975, by Scottish Cables at Renfrew from 1978 to 1979 and at Portsmouth on a one-year contract.
[4.42]On 28 February, following his having been shortlisted for interview, Mr McTear completed a form headed "Medical examinations" in which he denied a history of spitting up blood, bronchitis, pleurisy, asthma or tuberculosis, stated that he had never been in hospital or had medical or surgical advice for any cause not already mentioned, stated that he had only three days off work due to sickness over the previous years, and signed a declaration that he had not withheld any material information and that to the best of his knowledge and belief the information given was true. At interview he told Mrs McCutcheon that the reason for this absence from work was "chest". In answer to direct questions by her, he said that he did not have a police record, that no previous employers had disciplined him for any reason, and that he had no problem with alcohol or drugs. Although Mrs McCutcheon did not regard Mr McTear as scoring sufficient marks according to her personal system to justify offering him employment, she was instructed by the district librarian to appoint him on a temporary basis until 26 May 1989. On 25 May 1989 he was offered an extension of his employment until 23 August 1989, but resigned from his employment with Cunninghame District Council on 23 June 1989.
[4.43]On 6 June 1989 Royal Mail Letters offered Mr McTear a job as a postman in Dorking, Surrey. On 8 June 1989, at Kilmarnock Sheriff Court, he pled not guilty by letter to a complaint containing a charge relating to the offence committed on 21 February 1989. An intermediate diet was fixed for 14 August 1989 and a trial diet for 8 September 1989. He was ordained to appear on 14 August 1989. Between 26 and 29 June 1989 he worked as a postman in Dorking. On 14 August 1989 he appeared at Kilmarnock Sheriff Court and adhered to his plea of not guilty in respect of the above-mentioned complaint. On 8 September 1989 he appeared for trial. He changed his plea to guilty and was fined £500, payable in instalments of £10 per week, with the alternative of sixty days' imprisonment.
[4.44]James Martin, aged 57, was a special account director for Initial Security. From 1984 to 1998 he was a director of Burns International Security Services UK Ltd (Burns International). He gave evidence about an application which Mr McTear made for employment with Burns International. Mr McTear completed an application form on 15 June 1989, and when he was interviewed by a personnel officer on 27 October 1989 he was asked to confirm that the statements made in the form were true. In the form Mr McTear stated inter alia that he attended school at Camphill, Paisley and obtained O level passes in mathematics, English and history. He stated that he had not undertaken military service, that he had never been interviewed as a suspect in a criminal case, that he had never been a defendant in a criminal action, that he had never been arrested or convicted of an offence other than parking and that he had no court charges pending against him. In giving his employment history he claimed inter alia that he had been employed by Plessey from January 1981 to November 1987, and that the reason he left that employment was redundancy. The form was signed by Mr McTear. Immediately above his signature was the statement that he certified that the information he had given on the application was true and that he realised that any misrepresentation of the facts on his part would be grounds for immediate dismissal.
[4.45]During the course of the interview his attention was drawn to the Burns International handbook. This set out inter alia a code of conduct and a disciplinary code. Under the heading "Intoxicating liquor" there was a prohibition on the drinking of alcohol during working hours and a requirement that all employees must attend for work sober. Gross misconduct, which might result in summary dismissal, was defined in terms which included being under the influence of intoxicating liquor. After being interviewed Mr McTear was regarded as suitable for training. The first day he worked was 1 November 1989. The last day he worked was 20 November 1989, and his employment was terminated on 21 November 1989. The reason for termination was that he was under the influence of alcohol at the premises where he was working as a security guard.
[4.46]On 23 November 1989, outside 20 Cherrywood Drive, Beith, Mr McTear conducted himself in a disorderly manner, shouted, swore, set fire to a quilt and committed a breach of the peace. Between 1 February 1990 and 28 April 1990 there was no continuous period of eight weeks or more in which Mr McTear did not claim either unemployment benefit or sickness benefit. In February 1990 he did not qualify for unemployment benefit because he had not made sufficient national insurance contributions in the tax year 1988/1989. He did not make enough national insurance contributions for the tax year 1989/1990 to meet the contributions threshold which would have entitled him to claim sickness benefit. He claimed unemployment benefit for nine weeks in that tax year.
[4.47]On 7 February 1990 he attended Renfrew Council on Alcohol. He told a member of the medical staff that he was due in court the following Wednesday, he and his wife were maintaining the status quo until the outcome of the court hearing, he was not drinking because he had no money, he was feeling depressed and negative despite his not drinking and he had applied unsuccessfully for about six jobs locally and in England.
[4.48]On 1 April 1990, at Kilmarnock Sheriff Court, Mr McTear pled guilty by letter to a complaint containing a charge which related to the offence committed on 23 November 1989. Sentence was deferred until 10 May 1990 for personal appearance. On 10 May 1990 sentence was further deferred until 3 September 1990, and he was ordained to be of good behaviour in the meantime. In July 1990 he committed a breach of the peace and a contravention of the Criminal Justice (Scotland) Act 1980. On 19 July 1990 Mr McTear attended Renfrew Council on Alcohol and told the interviewer that he felt his drinking was getting out of control, that he was a binge drinker and that when he started he really did not know when to stop drinking. At the same interview Mrs McTear stated that Mr McTear "had been becoming a man she really did not know and [she] really did not like what she was seeing". On 2 August 1990 Mr McTear cancelled an appointment at Renfrew Council on Alcohol.
[4.49]On 10 April 1990 Mr McTear successfully applied for a job as a temporary part-time attendant at the Hunterian Museum, University of Glasgow. In his application form, he again claimed to have attended Camphill School, Paisley and to have obtained O level passes in mathematics, English and history at B grade. He misrepresented his employment history, concealing his employment with Burns International, and stating that he had been employed by Plessey from 1980 to 1988 and was made redundant.
[4.50]Aileen Nisbet, aged 39, was conservation manager at the Hunterian Museum. She had worked there for sixteen years, as an archaeology technician and then as conservation manager. She remembered Mr McTear. He was an attendant at an exhibition called "Giants, Gems and Jewels", which was the museum's contribution to Glasgow's Year of Culture in 1990. She was the assistant for the exhibition, which was held in the Kelvin Gallery of the museum. She remembered that one day he came back after lunch "slightly the worse for wear" and was "rather friendly" with a female member of the public, getting close to her, touching her arm and being chatty and effusive. The member of the public was very embarrassed by this behaviour. Mr McTear was taken off duty. The policy of the gallery was to discourage drinking during duty hours, for reasons of security, health and safety. There had been a number of previous occasions when Mr McTear had come back late from lunch and asked to improve his timekeeping. Her impression was that he had been sacked after the last incident.
[4.51]Roger Gray, aged 46, was human resources manager at the University of Glasgow. He had held similar posts since April 1990. In August 1990 he was assistant personnel officer (non-academic). Following an incident on 11 August 1990 he became involved in the disciplinary proceedings against Mr McTear. Although Mr Gray had no personal recollection of the matter, the following narrative can be taken from documents written by him, the accuracy of which was not disputed. Mr McTear was appointed as a temporary part-time attendant for the Giants, Gems and Jewels exhibition within the Hunterian Museum. He was appointed on 20 April 1990 for the duration of the exhibition. His average pay package was £65 to £75 per week. Saturday 11 August was the first day on which Mr McTear was scheduled to work for the whole day. The exhibition was very busy that day, and he could not leave for his lunch-break until 2.20pm. He was due to return at 3.20pm, but instead returned at 3.55pm, smelling of drink. He did not pick up his radio, thereby neglecting his security duties, and made himself a nuisance to visitors in an embarrassing manner. He was considered to be incapable of continuing with his duties. He told the floor manager that while he was having a pub lunch he was approached by a stranger who had suffered a bereavement and accepted the stranger's offer of whisky. Thereafter the floor manager instructed him to go home, but he refused. He left when the museum was closed.
[4.52]Mr McTear did not report for work the next day, Sunday 12 August, and made no contact with the museum, so that he was considered to be on unauthorised absence. He telephoned at 8.00am on Monday 13 August to report that he was sick, offering no further explanation of the nature of his sickness or its expected duration. Later that day Mr Gray telephoned him, requesting him to attend an investigatory meeting on Tuesday 14 August at 11.00am. During this telephone call Mr McTear stated that he had attended his GP earlier that day and expected to return to work on Tuesday 14 August and to attend the investigatory hearing. On Tuesday 14 August Mr McTear telephone Mr Gray to tell him that he was unable to attend the investigatory hearing as he had chest pains and intended to consult his doctor. Mr Gray told him that in view of his failure to adhere to the University's notification procedure for reporting absence he now suspected an abuse of the sick pay scheme, since Mr McTear had said the previous day that he would be fit to return to work. Accordingly he was suspending payment of sick pay. On Friday 17 August Mr Gray telephoned Mr McTear requesting his attendance at an investigatory hearing, which he now intended to hold on Monday 20 August. Mr McTear said that he would attend the hearing and that he had consulted his GP, who had issued him with a medical certificate for two weeks. Mr McTear sent to the personnel office a medical certificate for two weeks dated Friday 17 August, indicating the nature of incapacity as "anxiety state". He also sent a self-certification of sickness form. Nothing was submitted from the GP dated 14 August.
[4.53]The investigatory hearing took place on 20 August. It was conducted by Mr Gray and was attended by Professor Willett, the head of the relevant department. It was followed by a disciplinary hearing, at which the same persons were present. Mr McTear claimed to have only consumed one alcoholic drink, and did not consider his behaviour to have been a nuisance to visitors to the exhibition. This was rejected by the disciplinary hearing, who decided that gross misconduct had been established and that Mr McTear should be dismissed. Further investigations carried out by Mr Gray established that Mr McTear had been in the habit of having a pub lunch before reporting for work at his normal shift starting time of 12.30pm. This was a matter taken into account by an appeal committee who considered an appeal by Mr McTear against the decision to dismiss him. The decision of the appeal committee was to reduce the dismissal to a final warning. One of the reasons given by the appeal committee for this decision was that it was felt that a firmer line should have been taken with Mr McTear on previous occasions when he had arrived at work after drinking.
[4.54]On 14 August 1990 Mr McTear had attended his GP, Dr McCarroll, for the first time since 7 May 1990. He explained to her that he had been drinking at lunchtime. On 16 August 1990 she referred him to Dr Lind, a psychiatrist at Ailsa Hospital, for help to cope with his alcohol problem. She noted that he had a long history of excessive alcohol intake, had never really tried to do anything serious about it, had held down a steady job which he appeared to have lost since he returned from lunch drunk one day, and was drinking every lunchtime, as well as every evening, large quantities of beer and spirits. On 17 August 1990 Mr McTear signed forms to claim statutory sick pay, stating that he was suffering from an "anxiety state". He represented that he had been unfit for work since 12 August 1990 and that he expected to be unfit for more than six days. Between 21 August and 13 September 1990 he received sickness benefit for "anxiety state". On 23 August 1990 Mr McTear attended an appointment at Renfrew Council on Alcohol, at which he was abusive to the interviewer. He told the interviewer that he was very depressed, that he had been dismissed from his job for being drunk and abusive to the public and that he had only had one pint of lager. He failed to attend a further appointment on 30 August 1990.
[4.55]On 30 August 1990 Glasgow University issued Mr McTear with a form SSP1 stating that he was no longer employed by them with effect from 20 August 1990 and accordingly was no longer eligible for statutory sick pay. On 31 August 1990 he and his GP completed medical certificates for him to claim statutory sick pay because he was suffering from "anxiety state". He complained to his GP that he was suffering from dizzy spells, a stiff neck and anxiety. On 3 September 1990 Mr McTear appeared at Kilmarnock Sheriff Court in respect of the complaint relating to the offence committed on 23 November 1989. Sentence was further deferred until 8 January 1991 and he was ordained to be of good behaviour in the meantime. On 25 October 1990 Mr McTear sent a sick line from his GP covering the period until the end of his contract on 28 October 1990.
[4.56]On 9 October 1990 Mr McTear attended an appointment with Dr Lind. He said that he spent £70 to £80 on whisky and beer on Friday and Saturday nights. He also told Dr Lind that his wife worked regularly, which kept her out of the way of most of his problems. He was lucky she had stayed with him. He had alienated his children because of his drinking. He had always drunk. He liked the pub atmosphere and enjoyed company. He enjoyed the taste and the initial effect of drinking alcohol, which was to increase his confidence when in company, which he felt was usually lacking. On 21 October 1990 he signed a medical claim form SC1 claiming benefit for suffering from anxiety, blackouts and dizziness, stating that he had been unfit for work from 19 October 1990 and that he did not know when he would be fit to return to work.
[4.57]On 23 October 1990 Dr Lind wrote to Dr McCarroll about Mr McTear in inter alia the following terms:
"[F]or many years he has been a 'bout drinker' by which he means that on virtually every week-end he will spend between £70-£80 on whisky and beer between a Friday and a Saturday night. He then drinks on most days for the rest of the week but limits himself to one pint of Guinness before or after his work [...]. When I saw him his last drink had been the previous night when he had had 5 vodkas and prior to that he had had a '12 hour binge' 10 days before. [...] He has been in prison he says upwards of 22 times for breach of the peace and he feels that he is harming his wife and his children.
He says also that his 'memory is away' when drinking by which he seems to mean that he has black-outs for periods when drunk [...]. After he has been drinking he describes himself as being aggressive and suspicious of other people, which leads on a number of occasions to violence."
[4.58]On 23 October 1990, after talking with Mr and Mrs McTear, Dr Lind decided that the most appropriate option was to admit him to the next programme at Loudoun House, which started on 29 October. On 25 October 1990 Mr McTear and his GP signed a form Med3 which certified that he was suffering from an anxiety state and would be unfit for work until 29 October 1990. On 31 October 1990, at Cunninghame District Court, Mr McTear answered to a complaint containing charges which related to the offences committed in July 1990. He was convicted and sentence was deferred to 12 February 1991.
[4.59]On 8 November 1990 Mr McTear attended an appointment at Renfrew Council on Alcohol. He was noted as being pale, lacking in energy and undernourished. He described his lifestyle over the previous few weeks as "abstinence v. social drinking". He said that over the previous week he spent £30 on alcohol on the Monday and that thereafter he had no more money and consequently did not drink. On the basis of what he said, the interviewer noted:
"binge drinking style, Paisley pubs, unemployed since 31/10/90 as university museum attendant, wife works and 'holds the purse strings'. Court case pending in Irvine, thought this time he would go to jail. Charges were breach of peace, and being drunk and disorderly."
[4.60]On 15 November 1990 Mr McTear failed to attend an appointment at Renfrew Council on Alcohol. On 22 November 1990, however, he and Mrs McTear attended an appointment there. The interviewer noted that both were pale and tired, that Mr McTear's court sentence had been deferred until February 1991, that he had abstained from alcohol for one week and that Mrs McTear handled the money. The interviewer also noted that Mr McTear was decorating five rooms, was job searching, had an interview as caretaker with "tied house" in Portsmouth and had an appointment at the alcohol unit in Ailsa Hospital, for which he was awaiting a date. The interviewer commented: "Alfred McTear is going along with the plans as above meantime. Time alone will tell how committed he is."
[4.61]Mr McTear arranged to attend an appointment at Loudoun House on 29 October 1990. He subsequently rearranged the appointment for 10 December 1990, but he failed to attend this appointment. On 13 December 1990 he attended an appointment at Renfrew Council on Alcohol. The interviewer noted:
"Alfred says that he is easy going --its [sic] as though he feels he has no control over change. Disease model perhaps. A 'what will be attitude'. Negative thinking and both need to be more motivated into being more assertive as individuals. Alfred lacks responsibility in some ways, opts out of decision making and then argues with Mgt. when she is in control."
[4.62]On 3 January 1991 Mr McTear failed to attend an appointment at Renfrew Council on Alcohol. On 8 January 1991, at Kilmarnock Sheriff Court, he appeared on deferred sentence in respect of the complaint relating to the offence committed on 23 November 1989. Sentence was further deferred until 15 January 1991, and he was ordained to be of good behaviour in the meantime. On 10 January 1991 he cancelled an appointment at Renfrew Council on Alcohol. On 15 January 1991, at Kilmarnock Sheriff Court, he again appeared for the above-mentioned deferred sentence. He was fined £150, payable in instalments of £5 per week, with an alternative of thirty days' imprisonment. On 17 January 1991 Mr and Mrs McTear were seen at Renfrew Council on Alcohol. Mr McTear indicated that he had coped "very well" over the festive season. Mrs McTear stated that "he was penniless and that was the reason". The interviewer noted: "No matter what you try to discuss with Alfred, he seems to have all the answers." On 31 January 1991 Mrs McTear cancelled an appointment for Mr McTear at Renfrew Council on Alcohol, but on 7 February 1991 he attended an appointment. The interviewer noted that he had an upcoming court case, that he was maintaining the "status quo" until the outcome; "no money -- no drinking"; "depressed, negative despite non-drinking, applied for 6 jobs locally and down south". On 12 February 1991 at Cunninghame District Court Mr McTear appeared on deferred sentence in respect of the offences committed in July 1990. He was admonished. On 21 February 1991 Mrs McTear attended Renfrew Council on Alcohol without Mr McTear.
[4.63]On 6 April 1991 Mr McTear commenced work with the Royal Scottish Automobile Club (RSAC) as a night porter. John Lyon, aged 55, was employed as clubhouse manager at the (RSAC), Blythswood Square, Glasgow, between August 1990 and September 1994. He dealt with personnel matters. He interviewed Mr McTear for the job and told him, as part of the induction system, about the rules which applied to him and the behaviour which was expected of staff at the club. Apart from ordinary everyday rules, two more specific rules were to do with drinking and smoking. Drinking at any time on duty was a dismissable offence. Smoking was not permitted except in designated areas. When he was told about the smoking rule, which existed for safety reasons, Mr McTear said he did not smoke. Mr McTear worked as a night porter from 10.30pm to 7.00am.
[4.64]Mr Lyon said that he arrived at the club one morning (4 July 1981) at about 8.30am. The housekeeper told him that when she had come in at 7.00am she had found Mr McTear drunk. She had gone through the formalities of suspending him until an enquiry could be made. Mr McTear had gone home. Mr Lyon telephoned his house, but Mrs McTear said that he was unavailable. He told her that Mr McTear had been sent home and suspended from work because he was drunk, and asked her to ask him to telephone Mr Lyon at the club. Mr McTear telephoned at about 1.00pm or 2.00pm and did not deny that he had been drunk. He had accepted a drink from a group of men who were resident in the club and "one led to another and led to another". He said he would not be coming in again, he knew what the outcome was going to be, he would be sacked. Mr McTear was summarily dismissed. On the same day Renfrew Council on Alcohol closed its case file on him as they had had no further contact with him.
[4.65]Between 23 August 1991 and 5 November 1991, there was no continuous period of eight weeks or more in which Mr McTear did not claim either unemployment benefit or sickness benefit. Between November 1991 and 16 January 1992 he was employed by John Churchill & Co. On 24 June 1992 Mr McTear told Dr Kirsty Muirhead of the Ayrshire Hospice that he had stopped smoking when he was diagnosed as suffering from lung cancer, that his mother had died of lung cancer when he was 18, that his half-brother had died of cancer, that he was unemployed and that he used to install telephones. On 1 July 1992 Mr McTear was awarded disability living allowance for life. On 14 July 1992 he completed and signed a claim a form for sickness benefit from 7 April 1992, and represented that he normally worked as an "installer". On 11 August 1992 he signed an application for severe disablement allowance claiming that the date when he last worked was 20 June 1991 and that his incapacity for work began on 23 December 1991. On 17 August 1992 the DSS wrote to Mr McTear to inform him that his claim for severe disablement allowance could not predate 5 November 1991 since he had signed fit for work at the unemployment benefit office up to and including that date, and asking him to produce a backdated medical certificate if he wished to claim benefit for any period between 5 November 1991 and 7 April 1992. On 20 August 1992 he sent a backdated sick line from 23 December 1991 to the DSS.
[4.66]On 12 August 1992 Mr McTear told Professor John Smyth at the Western General Hospital, Edinburgh, that he was a telephone engineer until the previous year when he suffered a collapsed lung and decided not to work after that because he did not feel well. On 13 August 1992 he completed an application for a bursary fund for attendance at Bristol Cancer Help Centre on which he represented that he had been unemployed for two years, he received no income support or any other source of income, he had smoked for twenty-seven years, and he had not suffered any stress, unhappiness or shocks in the last five years before the onset of cancer. On 22 October 1992, having visited the Bristol Cancer Help Centre for one day, Mr McTear told a nurse from the Ayrshire Hospice that he had not been very impressed, that he did not think it was suitable for himself, as most people there he thought were curable, and that he did not like the food there. On the same day he wrote to Bristol Cancer Help Centre and stated that he left on the introductory day at lunch because he felt unwell.
Medical history
(1)Dr Sheila McCarroll
[4.67]Dr Sheila McCarroll, aged 44, practised as a general practitioner (GP) at the Health Centre, Reform Street, Beith, Ayrshire. In a letter to Mrs McTear's Glasgow solicitors dated 20 November 2002 Dr McCarroll wrote:
"I was the General Practitioner involved in the majority of Mr McTear's care following his diagnosis with bronchial carcinoma in May 1992. My role was in controlling the symptoms associated with that and coordinating specialist opinion.
Mr McTear's treatment involved controlling his pain which [latterly] was substantial. He required very high doses of Morphine Sulphate. The pain was difficult to control and towards the end of his life he was in considerable distress as a result of both the pain and breathlessness.
I would be in no doubt that the cause of Mr McTear's death was from an inoperable moderately differentiated squamous carcinoma of his left lung."
Dr McCarroll said that she had received advice from consultants as to the cause of Mr McTear's death.
[4.68]On 30 May 1991 Mr McTear attended Dr McCarroll, who recorded that he was suffering from haemoptysis and chest pain. She prescribed an antibiotic and arranged for a chest x-ray. On 11 June 1991 a consultant radiologist at Ayrshire Central Hospital in Irvine reported that there was an area of linear subsegmental collapse in the left mid-zone with slight prominence of the lateral aspect of the left hilar shadow. Follow-up examination after a short interval was suggested to exclude an underlying central bronchial lesion. A further chest x-ray was carried out and on 3 July 1991 it was reported that there was an area of scarring in the left mid-zone, with no change since 11 June 1991. Dr McCarroll agreed that this report did not exclude an underlying central bronchial lesion. In retrospect further enquiry was called for, but perhaps not at the time. It might have been better if the matter had been followed up following the report, but it might not have made any long-term difference.
[4.69]Dr McCarroll was asked about a series of letters written to her after this. In a letter dated 27 May 1992 Dr Glynne Jones, Consultant Physician at the Chest Unit, Ayrshire Central Hospital, Irvine, wrote:
"He had a chest infection involving the left side last year since when there has been a persistent cough but currently no sputum. He did have wheeze localised to the left side which has now moved up to the throat region. There has also been some left anterior chest pain and he did have haemoptysis which has stopped. He is also somewhat anorexic and has lost half a stone in weight. [...] Chest x-ray shows collapse of the left upper lobe with a probable mass at the left hilum on the present film. [...]
It looks very much as though he has a bronchial carcinoma at left hilum causing collapse of the left upper lobe. There is a background of mild chronic bronchitis. He is aware that there might be an underlying carcinoma and has agreed to be admitted shortly for further investigation."
[4.70]In his next letter, dated 25 June 1992, Dr Jones wrote:
"[T]his unfortunate young man has been found to have an inoperable moderately differentiated squamous carcinoma at the left hilum which is extending up the left main bronchus towards the trachea. [...]
He has been told the diagnosis and treated with a single dose of Mustine covered by Prednisolone. Obviously the outlook here is not good. No regular review has been arranged but I would be pleased to hear from you whenever further symptoms arise requiring palliation."
The final diagnoses were epidermoid carcinoma of the left hilum and mild chronic obstructive airways disease. Dr McCarroll explained that Mustine was a cytotoxic drug which was used at that time. She referred Mr McTear to the Ayrshire Hospice in Ayr, in order to provide support for him and his family. Dr Jones next wrote about him on 8 July 1992, in a letter which stated:
"Currently he has some dyspnoea on the stairs and a little left sided chest discomfort controlled with a combination of MST [morphine sulphate], Distalgesic and Naprosyn."
Dr McCarroll said that these were all painkillers and that Mr McTear had been prescribed morphine from then until his death.
[4.71]Thereafter Mr McTear referred himself for a second opinion about the possibility of further therapy for his cancer. He was examined at the Western General Hospital, Edinburgh by Professor J F Smyth on 12 August 1992. Professor Smyth reported that his principal problem at that time was of breathlessness, and clinical examination confirmed that this was due to the tumour in his left upper lobe. He suggested that a course of radiation therapy in Glasgow should be considered. Thereafter Dr McCarroll arranged for Mr McTear to be seen by Dr F M McGurk, Consultant Oncologist at the Beatson Oncology Centre, Western Infirmary, Glasgow. Dr McGurk wrote on 2 September 1992 that he had seen Mr McTear that week. He said that he was systematically very well, complaining only of slowly progressive dyspnoea and substernal boring left upper anterior pains, which were aching rather than anything more severe and were well controlled with his current medication. Dr McGurk came to no definite decision as to whether Mr McTear might benefit from palliative radiotherapy. Mr McTear returned to Edinburgh to see Professor Smyth on 21 October 1992. Professor Smyth wrote that his chest pain had increased in severity. He tried to explain to Mr McTear why sometimes radiotherapists felt that it was not advantageous to give treatment, and he hoped that his conversation helped to reassure him.
[4.72]On 3 November 1992 Dr Jones wrote that in recent weeks Mr McTear had had several infective episodes which appeared to have been obstructive pneumonitis. These responded only partly to antibiotic at home and he had therefore admitted Mr McTear to Crosshouse Hospital on 27 October 1992 for a seven-day course of medication, which appeared to have suppressed the infection. Dr Jones was suspicious that Mr McTear now had significant obstructive disease at the distal end of the main bronchus. He hoped that the disease in this area was amenable to laser therapy which, in turn, might reduce the tendency to obstructive pneumonitis. He therefore arranged for Mr McTear to be admitted to Hairmyres Hospital, East Kilbride, with a view to being treated by a consultant thoracic surgeon, Mr D Prakash.
[4.73]This did not happen, however, because Mr McTear began to receive a course of palliative radiotherapy at the Radiation Oncology Unit at the Western General Hospital, Edinburgh. Dr A Gregor, Senior Lecturer in Radiation Oncology there, wrote on 25 November 1992 that, when he first met Mr McTear two days previously, his main problems were related to complete left lung collapse with increasing breathlessness, intermittent sweating, left sided chest pain and intermittent infective exacerbations. Palliative radiotherapy was aimed at reducing the bronchial obstruction in order to improve not only his breathlessness but to prevent further infective episodes and subsequent lung abscess. On 5 January 1993 Dr Gregor reported that Mr McTear had come for review that day. He had had some improvement in his breathlessness following radiotherapy, but clinically and on chest x-rays taken that day there had been a development of left sided pleural effusion with some encysted changes and the possibility of underlying lung abscess. This, he wrote, would certainly explain his weight loss and general feeling of malaise. He made an appointment for Mr McTear to return to the clinic in Edinburgh after six weeks.
[4.74]On 15 January 1993 Mr McTear was admitted to Crosshouse Hospital under the care of Dr Jones. He was discharged on 19 January. In a letter dictated on 21 January and dated 29 January 1993 Dr Jones reported that Mr McTear had been treated with antibiotics and his analgesia had been increased. He found a trans- cutaneous nerve stimulator useful. Mr McTear was reviewed at home on 26 January 1993 by Dr John C Bass, Medical Director of the Ayrshire Hospice. In a letter of that date Dr Bass wrote:
"The main problem now is that he has developed pain in his right chest and also his right hypochondrial area. He regards these as separate pains, the former a dull constant ache and the latter being sharp and exacerbated by inspiration, moving or coughing. Both can disturb his sleep and are quite severe at times. He has also become increasingly breathless over the last few weeks and has been losing weight, lacking in energy and sweating on his right side, particularly at night."
Dr McCarroll confirmed that this was the case.
[4.75]Mr McTear was again seen by Dr Gregor at the clinic in Edinburgh on 2 February 1993 and was subsequently admitted to hospital there. In a letter dated 17 February 1993 Dr H Phillips, Senior Lecturer in Radiation Oncology, reported that Mr McTear had been troubled by some right upper quadrant pain and right sided chest pain. On examination, he had a marked pleural rub. Further investigation raised the possibility that the changes in his right base were due to disease progression. Mr McTear was anxious to be discharged home as soon as possible and was due to go on holiday shortly, returning on 2 March. Dr Phillips wrote that if the right sided chest pain continued to be a problem, it might be appropriate for them to refer him to their pain clinic. Dr McCarroll said that pain was by then a big problem.
[4.76]On 25 March 1993 Dr Kirsty Muirhead, Deputy Medical Director at the Ayrshire Hospice, wrote:
"I am writing to confirm that Mr McTear died in the Hospice in the early hours of the 23rd March 1993. As you know his condition had markedly deteriorated during the previous week with increasing breathlessness, increasing production of purulent sputum and increasing drowsiness. Indeed I understand that when visited by one of the Macmillan Sisters on 19th March 1993, he had been comfortable and virtually bedfast with increasing doses of MST and an antibiotic.
However, he had appeared generally, [according] to his family, a little better over the week-end but on 22nd March 1993, had been confused, agitated, extremely breathless and had required constant reassurance from his wife with virtually constant requests for GP assistance.
Having discussed his care over the telephone it became clear in the late afternoon that he was not settling at home and he was therefore admitted to the Hospice in the early evening. His wife Margaret accompanied him.
When Mr McTear was admitted he was obviously extremely frail with severe dyspnoea, agitation, probable hypoxia and it was clear that he was going to die in the near future. In view of his extreme dyspnoea it was not possible to give him adequate intravenous doses of Diamorphine and Diazepam and the subcutaneous and intramuscular routes were employed and increasing doses of drugs were given.
He finally settled at approximately 1 a.m. the following morning and died very peacefully about an hour later. His wife was present when he died."
Dr Muirhead stated that Mrs McTear and her daughter had not given permission for a post mortem examination to be carried out because Mr McTear had not wanted this to be done.
[4.77]Dr McCarroll said that, in the months before his death, what was unusual about Mr McTear's case was the amount of pain he had, which was difficult to control. He required support and services from his wife, who was there all the time. She fed him and helped with general daily living activities. Eventually she needed to dress him when he became unable to dress himself and when he was bedridden she had to help with general hygiene. She helped with his medication. Over the weekend before Mr McTear's death, Dr McCarroll and her colleagues had been on call, responding to telephone calls from the family, and were in and out coping with pain control and agitation.
[4.78]In cross-examination Dr McCarroll was asked about a number of entries in the records held by her practice and records produced by the Department of Social Security (Benefits Agency) relating to Mr McTear. From 23 to 30 November 1966 Mr McTear was absent from work for a week suffering from pharyngitis. Dr McCarroll agreed that pharyngitis involved inflammation of the mucous membrane of the pharynx, which was part of the respiratory tract, and was commonly caused by a viral infection. It was sufficiently severe to justify Mr McTear's having been signed off from work for a week. Dr McCarroll was unable to read an entry which might have related to Mr McTear's smoking, but she said that it would not be surprising if a GP were interested in the question whether a patient suffering from pharyngitis was a smoker, and were to give the patient advice about the risks to health associated with smoking.
[4.79]From 5 to 10 January 1970 Mr McTear was signed off work with a diagnosis of influenza, which Dr McCarroll agreed was a viral infection affecting the respiratory system. He was also signed off work from 28 to 30 November 1974, with a diagnosis of influenza. From 13 to 17 February 1975 he was signed off work with a diagnosis of coryza (the common cold), having complained of a febrile catarrh, which Dr McCarroll interpreted as meaning that he probably had a temperature and a runny nose. She agreed that this suggested that he was suffering from a viral infection causing inflammation of the mucous membrane of the upper respiratory tract. On 17 August 1977 Mr McTear was diagnosed as suffering from "influenza/chill", having complained of feeling sick and suffering from diarrhoea. Dr McCarroll was unable to take from this entry that Mr McTear was suffering from a viral infection infecting the respiratory tract, although she agreed that the GP who saw Mr McTear had been prepared to use the word "influenza" in respect of the symptoms he observed. She agreed that an entry for 8 December 1977 also read "flu". She was unable to read the GP's notes for 18 September 1978. She interpreted the GP records for 24 October 1979 as reading "cold, glands". She agreed that it could be inferred from these words taken together that Mr McTear was suffering from a viral infection. She interpreted the entry in the GP records for 28 February 1980 as reading "backache and cough", with a reference to cigarettes. She agreed that it would be reasonable to infer that the GP had spoken to Mr McTear about his smoking and gave advice about the risks associated with it, including advice about giving up smoking.
[4.80]There was no entry in the GP records relating to Mr McTear's having been signed off during the period from 10 to 17 April 1984, though he received sickness benefit during this period for "virus infection". Dr McCarroll agreed that Mr McTear had presented with a clinical depression on 12 July 1985. On 7 November 1988 a GP recorded that Mr McTear had presented with bronchitis, and was to be referred to a psychiatrist for treatment for depression. The entry referred to alcohol. Dr McCarroll agreed that the symptoms exhibited by Mr McTear had been considered sufficiently severe to justify reference to a psychiatrist. There was no record of his attendance with a psychiatrist, and she suggested that maybe he had failed to attend.
[4.81]Dr McCarroll noted that he was sober when she saw him on 14 August 1990 and genuinely seemed to want help. He had a mild attack of delirium tremens for which she prescribed a short course of chlordiazepoxide. He also had a course of injections of parentrovite, a vitamin complex. Dr McCarroll agreed that one of the reasons for administering this to people who presented in circumstances such as these was that people who abused alcohol often suffered from a vitamin deficiency. On 23 December 1991 Mr McTear attended his GP, suffering from "flu and tracheitis", for which he was prescribed a painkiller and an antibiotic.
[4.82]Dr McCarroll agreed that in expressing the view that the cause of Mr McTear's death was from an inoperable moderately differentiated squamous carcinoma of his left lung, she was reporting advice she had received. She herself had not carried out the investigations required for such a diagnosis. On 2 October 1992 Mr McTear was recorded as experiencing pain only if he forgot his tablets.
In February 1993 he was well enough to go for a two-week holiday in Malta. On 11 February 1993 it was recorded that he was now pain-free on his medication, and that his breathlessness had increased and his weight had decreased. He was determined to go on holiday. On 8 March 1993, following his return from holiday, Mr McTear was recorded as having suffered a sudden collapse and severe dyspnoea after lifting a television set. Dr McCarroll agreed that he was not bedridden at that stage of his illness. He required admission to the hospice only on the day before he died.
[4.83]On 7 August 1992 Mr McTear's Glasgow solicitors, Ross Harper, wrote to Dr McCarroll asking for her participation in a documentary being made by the BBC about the effects of smoking on the health of individuals, and with which Mr McTear was said to be co-operating. Dr McCarroll declined this invitation for ethical reasons.
[4.84]In re-examination, Dr McCarroll said that the number of references to influenza in the medical records relating to Mr McTear was unusual, because most people only had it once or maybe twice in their life. A lot of what people thought was influenza was not, they had a cold. When it came to writing medical certificates "quite often euphemisms are used".
(2)Professor James Friend
[4.85]Professor Friend, whose CV is set out at para.[5.27], in addition to giving expert evidence had written a medical report on the case of Mr McTear. His sources of information were: GP notes with entries from 1950 until 9 March 1993; hospital notes from Crosshouse Hospital from 8 June 1992 to 19 January 1993 and the Western General Hospital, Edinburgh, from 12 August 1992 to 3 February 1993; chest radiographs (x-rays) from Crosshouse Hospital from 11 June 1991 to 15 January 1993 and the Western General Hospital, Edinburgh, from 15 August 1992 to 3 February 1993. Pathological material (biopsy slides, and cytology slides obtained at bronchoscopy on 10 June 1992) from the time of diagnosis in 1992 had been reviewed by Dr Keith Kerr, Consultant Pathologist, Aberdeen Royal Infirmary. As summarised by Professor Friend, from his reading of these documents, the relevant medical history was as follows.
[4.86]On 30 May 1991 Mr McTear was seen with a report of haemoptysis (coughing up blood) and chest pain. A chest x-ray was arranged and taken on 11 June 1991. This was reported as showing that there was an area of linear sub-segmental collapse in the left mid-zone with slight prominence of the lateral aspect of the left hilar shadow. Follow-up examination was suggested to exclude an underlying central bronchial lesion. A repeat x-ray was taken and on 3 July 1991 it was reported as showing an area of scarring in the left mid-zone, with no change since 11 June. He reported back to his GP on 17 April 1992, feeling awful, with chest tightness, breathlessness and anorexia. A chest x-ray taken on 30 April 1992 was reported as showing "consolidation of the left upper lobe [which raised] the possibility of a central broncho-occlusive lesion". Professor Friend agreed with this x-ray report.
[4.87]Mr McTear was referred to Ayrshire Central Hospital and seen by Dr Glynne Jones on 19 May 1992. Following this, Dr Jones wrote a letter in which he concluded that there was a strong clinical suspicion of bronchial carcinoma, and arranged to admit him to Crosshouse Hospital on 8 June 1992 for investigations. At this point, Mr McTear told the admitting doctor at Crosshouse Hospital that he had had recurrent chest infections over the last year, initially with white sputum, but more recently producing fresh blood. He had been smoking about sixty cigarettes daily, but had stopped a few weeks prior to his admission. Investigations which were arranged included an isotope bone scan and an ultrasound scan of the abdomen, done on 9 June 1992, both with normal results. A new chest x-ray on the same day was reported as showing that there was extensive collapse of the left upper lobe associated with a bulky left hilum. The appearances were highly suspicious of underlying bronchial carcinoma.
[4.88]On 10 June 1992 bronchoscopy (a telescopic examination of the bronchial tubes) was performed, and the report stated:
"Left upper lobe orifice occluded by tumour; tumour in the left main bronchus with submucosal infiltration definitely stretching up to within 1-1.5cm of the main carina (measured). Impression - not operable."
Professor Friend said that the tumour was clearly very centrally placed, very near to the division between the bronchi entering the right and left lungs, and it would have been technically impossible for a surgeon to remove it from that position. Subsequent pathology reports on the bronchial brushings reported "malignant epithelial cells of probable squamous origin", and a bronchial biopsy was reported as showing "infiltrating moderately differentiated squamous carcinoma".
[4.89]The diagnosis of inoperable lung cancer was communicated to Mr McTear, and he was offered and accepted a single dose of mustine intravenously on 15 September 1992, and started on corticosteroid therapy with prednisolone and discharged. Professor Friend explained that mustine was a rather crude and fairly toxic compound, which was used as a fairly basic initial form of chemotherapy treatment at that time, being the best that was then available.
[4.90]Mr McTear then decided to seek a second opinion about options for further treatment of his tumour, and he was seen by Professor J F Smyth at the Department of Clinical Oncology, Western General Hospital, Edinburgh on 12 August 1992. Professor Smyth considered that a course of radiotherapy treatment should be recommended, and suggested that he should be seen at a unit nearer Mr McTear's home for this to be undertaken. When Mr McTear was seen at the Beatson Institute in Glasgow by Dr F M McGurk on 2 September 1992, however, it was felt that his condition was reasonably stable and treatment was not needed at that point. Following this, Dr Glynne Jones at Crosshouse Hospital referred him to Mr D Prakash, Consultant Thoracic Surgeon at Hairmyres Hospital in East Kilbride, for possible laser therapy to the obstructed bronchus, but before this consultation took place Mr McTear had returned to the Western General Hospital in Edinburgh. At this point he was seen by Dr Anna Gregor, Consultant in Radiation Oncology, who arranged a course of ten fractions of radiotherapy which took place during November 1992. Following this treatment, there was some improvement in his breathlessness. Professor Friend explained that the idea would have been to shrink the tumour, so as to allow air to pass to the part of the lung which had previously been excluded from the breathing process.
[4.91]He was admitted to Crosshouse Hospital on 15 January 1993 with shortness of breath and collapse/consolidation of the left lung, treated with antibiotics and producing some relief. There was a further review by Dr Bass from the Ayrshire Hospice on 26 January 1993. On review at the Western General Hospital in Edinburgh on 2 February 1993 he was admitted there with right chest pain, and a right pleural effusion was thought possible. Chest x-rays taken on that date showed extensive opacification of the left lung field, with a high left diaphragm, suggesting collapse and consolidation of the left lung and possible associated pleural effusion. However, the presence of pleural fluid was not confirmed by ultrasound scan, so he was allowed home on strong analgesics (long acting morphine tablets). Professor Friend thought that Mr McTear was on a strikingly large dose to control his pain, which suggested that he had severe pain. Higher doses might, however, be required with the passage of time, not only because the condition was progressing, but because the patient was becoming more accustomed to the morphine.
[4.92]When he prepared his written report, Professor Friend had not seen records showing Mr McTear's clinical progress from 2 February 1993 until his death on 23 March 1993. While giving evidence, he was asked to note a number of passages in the records of the Ayrshire Hospice. According to these records, when Mr McTear was seen at the hospice on 10 February 1993, he had a cough with dirty sputum. Professor Friend said that where a tumour was causing obstruction, the lung beyond it was much more vulnerable to infection. Mr McTear's voice was recorded as being hoarse and husky. Professor Friend said that it was a common symptom of lung cancer that the recurrent laryngeal nerve, which passes down from the middle of the neck into the middle of the chest and back up again, and controls the vocal cords, was interrupted. On 5 February 1993 Mr McTear was reported as being anxious and very breathless on exertion. He had a bricanyl nebuliser; this was a broncho-dilator which could sometimes help breathlessness, but Professor Friend thought it would not greatly have helped him.
[4.93]Mr McTear went on holiday to Malta on 16 February 1993. On his return, Mrs McTear reported on 3 March 1993 that he had enjoyed the holiday but during the last few days of it he had had some pain. When he was seen on 12 March 1993, Mr McTear was complaining of breathlessness. His pain was being controlled with morphine sulphate, in a dose which Professor Friend described as "very large", and he was also being prescribed diazepam. On 19 March 1993 there was a marked deterioration. Mr McTear was in bed with a chest infection. He had been prescribed antibiotics and an increase in the dosage of morphine sulphate. His chest was moist and he was unable to expectorate. He was having nebulised saline and ventolin, another broncho-dilator. He was admitted to the Ayrshire Hospice as an emergency.
[4.94]Although he had not personally seen pathological material, Professor Friend had seen the report on the pathological material by Dr Keith Kerr, who stated:
"There is unequivocal evidence of squamous cell carcinoma in this biopsy. There is also evidence of moderate squamous dysplasia. The latter is part of the recognised spectrum of pre-malignant changes which occur in the bronchial mucosa during the development of carcinoma in the central bronchi. I have no doubt that this patient suffered from primary bronchogenic squamous cell carcinoma (squamous cell carcinoma of the bronchus)."
Professor Friend said that he was in no doubt that Mr McTear developed a primary bronchial carcinoma in 1992, and indeed the x-rays taken in 1991 might, with hindsight, have shown early signs of the disease. The clinical presentation and progress of the disease were entirely compatible with this diagnosis.
Evidence of Mr McTear taken on commission
[4.95]At the beginning of the proof, junior counsel for the pursuer, Mr Divers, read out passages from the transcript of the examination-in-chief of Mr McTear when evidence from him was taken on commission. From these passages, I take the following summary.
[4.96]Mr McTear said that he was born on 25 September 1944. He was married and had three children, of whom the oldest, Sandra, lived in the house. Both his parents were dead. His father died in about 1960 or 1961. He had been a smoker. He died of an infectious disease in a hospital in Paisley which treated chest complaints and other things. His mother died in 1963. Mr and Mrs McTear were married in 1964 when he was aged 20. His mother died just before they were married. She was a smoker. She died of cancer, but he did not really know what type of cancer it was because this was kept from them at that time. No one said anything to him to the effect that either his mother's death or his father's death might be related to smoking. It did not arise, it did not come up. His mother was in hospital for a long time before she died, for about a year and a half in the Royal Alexandra Infirmary in Paisley. She continued smoking to the end. He used to bring her cigarettes because she was smoking in the ward. She smoked ten Player's a day while she was in hospital.
[4.97]Mr McTear said that he thought that he himself started smoking in 1964. It was not his marriage that made him smoke, but he started smoking about the same time as his marriage, i.e. in about September 1964. He had prepared a written note of what he smoked, at the request of his legal advisers. In it he stated:
"I started smoking Bristol cigarettes, 10 per day in 1964 or there abouts. I change to John Player cigerettes, very soon after this, and continued with John Player Superkings untill I changed to Old Holburn Tobacco to try and cut down my consumtion of cigarettes, as I was smoking 60 cigarettes a day by then. The Tobacco change didn't work out as I was still smoking J Players as well as Tobacco, like when my wife and myself went out, we always bought cigarettes as well as we couldn't possibilly roll our own, in a theatre, Resturant, etc.
I have signed a release form for my medical records to be release. As for my ascendants, descendants, siblings, you would have to ask them for their permission."
[4.98]In his evidence Mr McTear elaborated on this. He said that he changed to John Player cigarettes a few months after he had started smoking in 1964. His mother always swore by John Player cigarettes and he was afraid that he just kept it going when he started being on Player's as well. He changed over to Old Holborn hand-rolling tobacco about two or three years before giving evidence, in about 1990 or 1991. He still kept going with John Player cigarettes. The hand-rolling tobacco was mainly for the house "and the cigarettes were in it somewhere". When he changed over to Old Holborn it was to try and cut down on the number of cigarettes he was smoking, about sixty per day at that stage. When he started smoking he was not smoking sixty per day, he worked his way up to that number. When he first smoked Bristol cigarettes he always smoked ten per day. He did not think they were strong enough, but things just seemed to go on and the next he knew he was smoking more than he intended. He described himself as the "proverbial chain smoker", he never had a cigarette out of his mouth. When he moved on to John Player Superkings in the 1960s, he was smoking forty at least per day. The amount varied, it might be fifty or sixty-six, but it was roughly about sixty on average. The amount he smoked built up over the years. In the 1970s and 1980s he was smoking broadly this number of cigarettes per day. This was when he changed over to Old Holborn tobacco.
[4.99]Asked "What made you start smoking cigarettes?", he said that he wished he knew, he did not know really. He supposed there was a lot of advertising about it at that time, and it was just that he fell for this advertising. All his friends smoked, so he just continued the same thing. He had had the odd cigarette but was never a serious smoker before he started in 1964. The advertising at the time "was telling you to buy certain brands of cigarettes and then, you know, if you upset your wife or anything, you could always pacify her and give her a cigarette, calm everything down, things like that."
[4.100]When he started smoking he was not aware of any warnings about the dangers of smoking at all, not aware of anything like that. He was not given any information by anyone that nicotine was a poison. "This is the thing, why did the Government not bring this thing out?" The manufacturers of John Player cigarettes did not give him any information that smoking could cause lung cancer. No one gave him that information at all. He did not get any information from the manufacturers that he could come to any harm or sustain any disease by smoking. They did not give him any information that smoking could become addictive. No one gave him any information that smoking could become addictive.
[4.101]Mr McTear said that he would catch the odd advertisement when it was in the cinema at the time that he started smoking. He did not find anything in the advertisements in 1964 that tobacco was addictive and it could cause lung cancer. If he had received this information in 1964 when he started smoking, he would definitely not have taken it up. He could be sure of that because of what he knew by the time he was giving evidence. He was thinking back to when he was aged 20 at the age of 48. At 48 he certainly would not take up smoking; "I am a reasonably sensible lad and I do not think I would have taken up smoking if I thought all these risks would be involved." He was not made aware of any of these risks in 1964.
[4.102]So far as he could recall the message being put across by the advertising of cigarettes to the general public was "man about town, sort of thing". "If you went for a drink, you always passed it round the whole company, so you would have your twenty cigarettes anyway, at least within the company. The advertisements made smoking glamorous." Mr McTear was asked to look at an excerpt from The Times of 22 February 1993, in which the author of the article stated:
"For years cigarette sales have been buoyed by undercurrents of advertising promises of eternal youth, success and sex appeal."
Mr McTear said he would agree with that. In using the word "glamorous", he meant that it was to do with young men and young women, that sort of thing. He would definitely agree with the statement because it was always promises, promises, promises. In the same excerpt from The Times there was a reference, under the heading "Facts on smoking", to health risks such as oesophageal cancer, heart disease and respiratory disease and that the annual death from smoking world-wide was three million. He was not made aware of any of these facts in 1964 when he started smoking, in no way. There was a photograph of a cigarette pack with a skull and crossbones on it and the word "death". If this had appeared on cigarette packets in 1964 he thought it would have brought the true meaning home, with a vengeance.
[4.103]Mr McTear said that if his mother died because of cancer induced by smoking, and he had been told that at the time of her death in 1963, it would have had an effect on whether he started smoking the next year. He knew his mother died of cancer, but they were never ever told what type of cancer or whatever. In fact, he said, it might appear that it was lung cancer she died of but they did not really know. He did know it was cancer, because it was "brushed under the carpet", and nobody was to speak about it, and that was it. Otherwise he would not have been smoking. If a doctor had said to him soon after his mother's death that it was fairly certain that her cancer was caused by her smoking, he would not have started smoking. He was very close to his mother and he would definitely not have taken up smoking if he knew that was what his mother died of.
[4.104]Mr McTear said that he was told in 1992 that he was suffering from lung cancer. His wife forced him to go to the doctor, his GP, Dr McCarroll. This was in about April 1992. He had to go for various tests. He went to Crosshouse Hospital and saw Dr Jones, a consultant there. A bronchoscopy was done and Dr Jones looked down his bronchial tubes. There were various other tests on blood and urine samples. This was in May 1992. This investigation disclosed the tumour in one of his bronchial tubes. He was told this by one of the doctors who worked for Dr Jones. At that stage he was given one course of chemotherapy by Dr Jones, and that was all. He was not given any radiotherapy. He was put on painkillers. At that stage he was not suffering pain, it just gradually came with the months.
[4.105] His painkillers were just the same by the time he was giving evidence. The pain had worsened as the months went on. By the time of giving evidence he was taking 700mg of morphine in the morning and the same in the afternoon and "all sorts of steroids" as well, three in the morning, three in the afternoon, and tablets for anaemia, he was told. He could not remember them all, there were more but he could not even give the names of them. He wore an appliance around his waist, though he did not have it on when giving evidence. It was to give electric shocks and was called a pulser. He pressed the pads where the pain was and it shot a small electric charge from a battery into it. It took his mind away from the pain and eventually he thought about the pulser more than thinking about how much pain he had. He had had it for about two months. It had been helpful to him. He usually wore it at night time, unless his pain was bad, when he wore it most of the day. He had trouble sleeping, it was an on-off sleep, he was always waking up trying to get back to sleep. That morning he had had a problem and the doctor had been called. He just could not breathe. The doctor took all the mucus off his throat, which he did not have before. This was the disease progressing. His throat was dry all the time.
[4.106]In addition to the session of chemotherapy in the summer of 1992, he also went down to Bristol. He attended a residential course at the Bristol Cancer Help Centre. He said that this centre operated on a holistic model. His wife went with him. He had also been receiving help from Cunninghame Cancer Care. They did very good work for him, looking after him. He went to Bristol in about October 1992. He also made contact with the Western General Hospital in Edinburgh. He was reading a lot of books on cancer and came across the name of Professor Smyth. He was doing tests on various drugs to try and combat cancer. Mr McTear thought he had nothing to lose, so he wrote to Professor Smyth and told him of his case. He invited him to Edinburgh and gave him a medical. He recommended that he should do radiotherapy to help his breathing at that time. He was very bad in breathing at that time. He had difficulty in breathing then, wheezing and things like that. The radiotherapy was done in Edinburgh at the end of November 1992. He travelled up and down every day with "the cancer people from Ardrossan". The treatment was helpful, it made his breathing a lot better. At the time of giving evidence it was just coming back again, so he had had a few months which he otherwise would not have had. When he received the radiotherapy he could breathe much more easily and speak quite well. It was easier to understand what he was saying then. At the time of giving evidence his breathing had been affected.
[4.107]Previously, in June 1991, the records disclosed that Mr McTear had been having problems and he had an x-ray then. He said he had no idea what this was about, the records would probably tell. He had a hiatus hernia, for which he was also having to take pills. The records disclosed that he was sent for an x-ray and a report was sent back about his heart and the side of his lung. He had had umpteen x-rays in these past two or three years. His cancer was in his left lung, and it would be that.
[4.108]As part of his employment history, in a passage not read out by Mr Divers, Mr McTear had given evidence about stopping working for the (RSAC) in the summer of 1991. He was asked whether this was anything to do with his health. He said: "No, we just went away on holiday, just stopped work. I was feeling a bit tired but I did not think it was anything to do with that." Asked whether it was fair to say that he had not been in regular employment with one employer, he said no, he had had an abundance of jobs. He had worked for most of his working life.
[4.109]Mr McTear was next asked whether he ever tried to stop smoking. He said that he tried various times. "I know when all these signs came on, things like that, my wife wanted me to give it up. I tried to give it up. It was not working. My wife actually preferred me smoking because I was not so grumpy and moaning and angry." He explained that he meant "these things on the cigarette packets", the notices which appeared in 1971, warnings by the Government that "smoking can damage your health". When these came out he tried to give them up. At that time he was smoking about forty cigarettes a day. When he tried to give them up "I was like a bear with a sore head". He gave up for seven to ten days. He was just grumpy with everything, everything was wrong.
"Smoking helped me. I mean, God forgive me, I enjoyed smoking at the time. In fact, I have given it up for a year, near enough, and I still want to smoke. That is how bad it is, to really want to smoke even although I have got all this happened to me."
Asked why he stopped then, he said he was scared and frightened. He used to cry. He had been told that he had cancer and there was nothing that could be done for it. He just wanted to live as long as he could "so I was as well giving it up while I can". He did not stop until he was told by the doctors that he had lung cancer.
[4.110]Asked whether he had tried to stop smoking before 1971 when the notices began to appear on cigarette packets, he said that he had not done so seriously. He still continued to try to give up smoking all through the years. When he was like a bear with a sore head, this affected family life. There were arguments going on all the time between his children and between him and his children, things like that. Things which should never have bothered him did. He thought he had consulted his doctor about trying to give up smoking. He was almost positive that he had seen Dr Muir, a way back. He thought he saw Dr Peggie at the clinic. These were his previous GPs. This was within the previous ten years. He and his wife had only lived at their present address for that time. Dr Peggie was talking about acupuncture and things like that. He thought he just discussed it. "I do not take to needles and things like that." Dr Muir was someone he had seen, when he lived in Paisley before moving to Beith. His mind was never on stopping smoking.
"I never ever thought about giving up smoking at any time. Honestly, no definitely, my mind was never on giving up smoking at any time. [...] What I mean is, I tried to give up smoking, I tried very hard, sometimes. The most I can remember, it was not just the once that I tried to give up smoking, this might have been going on four, five, six, maybe seven times, I tried to give it up but I have always failed eventually and took up smoking again."
Asked why he thought that was, he said: "Well, I like smoking and I take it it is addictive to me." The reason he stopped in 1992 was "pure scare, pure fright".
[4.111]In discussion both before and after the passages from the transcript of Mr McTear's examination-in-chief were read out, the possibility was raised that the cross-examination might be read out immediately afterwards, but Mr Jones indicated to me that reference would be made to the transcript during the proof as and when it was appropriate to do so, and no more was read out at that time. Some items of information elsewhere in this Part are derived from the cross-examination.
Evidence of Mrs McTear
[4.112]Mrs McTear said that she and Mr McTear lived together at 20 Cherrywood Drive, Beith before he died in March 1993. About a year before then, in 1992, he took quite ill. He gradually deteriorated. She needed to provide a lot of support. She had to tell him when to take tablets and things like that, all the medication.
[4.113]Mr and Mrs McTear were married on 25 September 1964 when he was 20 and she was 19. They had known each other since they were about 13 or 14, but met again when she was 17 and he was 18. They went out for about two years before they married. When they met up again in about 1962, his father was dead but his mother was still alive. She did not really know much about Mr McTear's family. She met his mother briefly before she died. She knew his father when they were children and she met a few of his aunts during the course of the marriage. She did not know much about the other relations at all.
[4.114]She said that Alfred McTear was a smoker. He smoked John Player cigarettes. He started off smoking Bristol cigarettes, because she thought that at the time Bristol was the only cigarette which could be bought in packets of ten, and then they gradually made the packets into twenties. He started smoking Player's cigarettes in 1964. She could remember him smoking briefly before they were married, she could not say exactly when. At the time they were married he was definitely smoking twenty or maybe forty a day, twenty at least a day. He was smoking John Player cigarettes at that stage. He smoked John Player King Size. He did try to give up smoking. She tried to persuade him, because she knew he was smoking about sixty a day. He thought that if he went on hand-rolling tobacco and rolling his cigarettes, that would reduce the smoking. But actually, this did not work and any time they went out they bought cigarettes as well, because she was a smoker too and obviously she would not smoke the hand-rolling tobacco while they were out. Rolling his own cigarettes did not really work because he smoked made-up cigarettes as well.
[4.115]Her memory was that when they were married in 1964, at the beginning Mr McTear was smoking John Player Special cigarettes. The number of cigarettes a day that he smoked gradually increased from twenty to forty on some days, and then in the late 1970s, maybe the early 1980s, he was up to about sixty a day. His smoking gradually increased. By the 1980s, when he was smoking about sixty a day, they were John Player King Size cigarettes, with filter tips. Between their marriage and his death Mr McTear tried to give up smoking on about three or four different occasions, but really without any success. He was very angry, like a bull with a sore head. He went to his doctor on several occasions, but she thought it was really just to talk about different methods to give up smoking. She did not really think he tried any of them. At the most he was probably able to give up for about two weeks.
[4.116]Mrs McTear was a smoker when they were married. She started at the age of 15 when she left school. At that time smoking was glamorous, "you were grown up if you smoked and that was the reason I started smoking." It marked the fact that she had left school. She did not recollect much at all about talk in the newspapers and media about the risks of smoking in the 1960s. She did not recollect that there was warning about possible health hazards, nothing at all then. There was advertising of tobacco products in the cinema and newspapers and on television; it all looked so glamorous. She thought the message they were trying to put out was that smoking could ease stress and things; if they were under a lot of stress, most people lit a cigarette.
[4.117]When they were married Mr McTear played football some weekends. He went to matches on odd occasions. Mrs McTear was asked to look at some advertisements. One of them showed a man and a woman. The caption referred to their meeting at a particular place at which "both had a Player's, both very happy". A further caption stated "Player's are honest to goodness cigarettes, firmly and skilfully packed with fine Virginian tobacco [...]". Another advertisement had the caption "When you've time to think of the pleasure a cigarette gives you, that's when you realise that of all the cigarettes only Player's please so much." Mrs McTear confirmed that there was no sign of any warnings about the dangers of smoking, or health risks, on any of these advertisements.
[4.118]Mrs McTear said that Mr McTear was referred to Crosshouse Hospital in May 1992. The GP, Dr McCarroll, had referred him. Mrs McTear persuaded him to go to the GP. He was not eating regularly and was losing weight and off-colour. She could see differences in him and she persuaded him to go. He was not getting pain at that stage. The GP took a sample because he was coughing up blood and things like that. The sample was to be tested for tuberculosis first, and then she said she would send him to Crosshouse Hospital to check for anything else. Mrs McTear waited for him at Crosshouse Hospital and when he came out the doctor said that he had cancer and that it was probably because he had been a smoker for so long. It was the doctor who had carried out the bronchoscopy. Mr McTear was not very pleased or happy about what he had been told. They said that the cancer was inoperable because it was too near the arteries to the heart and to have an operation would be dangerous. He was not told that right at the beginning. He went into Crosshouse Hospital again and the junior doctor told him that after they had checked everything. All they could offer was some chemotherapy and that would only shrink the cancer in size. He only had one course of chemotherapy, at Crosshouse Hospital in the summer of 1992.
[4.119]Mr McTear sought a second opinion and went to the Western General Hospital in Edinburgh. He had picked up a few leaflets in Cancer Research shops and reference was made to Professor Smyth, so Mr McTear wrote to him and as a result went to Edinburgh. The Professor recommended only radiotherapy for him. At this stage his health was getting worse, he was quite breathless and could not speak very clearly. Obviously the cancer was getting bigger and growing over his windpipe. He spoke very quietly and with great difficulty. They went to quite a few different hospitals, but she did not really remember going to the Beatson Institute in Glasgow. He was back at Crosshouse Hospital in January 1993, complaining of shortness of breath, and he had a collapsed lung. That happened suddenly. They had gone to see the GP and she referred him to Crosshouse. They also went to a centre in Bristol.
[4.120]Mr McTear tried quite a few different things to see if they would help, because he obviously wanted to live and not to give up. He was prescribed morphine to relieve the pain, and steroids to build him up and help him eat more. She could not really recall exactly when the pain started to become a serious problem. It was just a gradual thing, she thought it was only months after he was diagnosed, maybe in about September 1992. From then on he had to take morphine to control the pain. They had a Macmillan nurse, who came in the whole time he was ill, to offer support and answer any questions and help as much as possible. She would give medication if it was needed. She came for about three or four months before his death, once a week or sometimes twice a week if asked. Near the end Mr McTear was mostly bed-ridden. The bedrooms in their house were upstairs and it was a tremendous effort for him to get downstairs, so she had to help him. This lasted from January or February 1993 until his death. It was sometime after his emergency admission to hospital with a collapsed lung. The lavatory in their house was downstairs. He did struggle downstairs until during the weeks before his death he used a commode upstairs. This was in the very final stages of his illness. Mrs McTear was upset by Mr McTear's death. She said that she was close to him.
[4.121]Mrs McTear agreed that it was probably accurate to say that, as was averred by ITL, between 1959 and 1991 Mr McTear had about seventeen short-lived jobs with different employers and during the last ten years of his life he was only in employment for about ten months. She did not know that a number of his employers found his conduct unsatisfactory until "these documents came through". She did not really know anything about his time in the Army. It was correct that Mr McTear had a problem with alcohol and sought help from Renfrew Council on Alcohol. He had some criminal convictions but "that was mostly through alcohol". He went out for a drink, but just on the odd occasion, not every week. He had too much to drink maybe once a month, sometimes after three months or six months. It upset her that he did this. She asked him to seek help for his alcohol problems and they both went to Alcoholics Anonymous together to see if that would help. Even though he came home drunk on various occasions, she cared for him and kept hoping he would change, and she stayed with him. It was broadly correct to state that he had about thirty-six convictions for assault, breach of the peace, fire-raising and social security fraud and that sentences of imprisonment were imposed on eleven occasions.
[4.122]The present action was started by Mr McTear and continued by her as his executrix. Basically, she thought that his reasons for bringing the action were "to get back at the tobacco companies, and to get across to young people that smoking was dangerous." In an article in The Scotsman published in July 1992 Mr McTear was quoted as saying:
"I don't expect to get anything out of this. I'm not going to be here. What I am doing is for the youngsters. I want cigarettes banned altogether, not just here but in other countries. Cigarette companies are simply selling poison to make money."
Mrs McTear recalled that this was his attitude.
[4.123]Mr McTear was sent to the Ayrshire Hospice the day before he died in the early hours of the next morning. She was with him. He died from lung cancer. The doctors told her that the cause of the lung cancer was smoking. Her husband had said he did not want a post mortem examination to be carried out, so she agreed to his wishes. She did not know why he said that: he was just reluctant because he did not want his body to be cut up. She confirmed a statement in the medical records that there had been a discussion with her and her daughter about whether permission would be obtained for a post mortem examination to be carried out and they did not give permission for it because Mr McTear himself had not wanted it.
Cross-examination of Mrs McTear
[4.124]In cross-examination, Mrs McTear was asked first about the visit she and Mr McTear made to attend a course in Bristol in 1992. In his evidence Mr McTear was asked about the cost and said that Mrs McTear "dealt with all these things". She said that she normally dealt with bills and things like that; she usually handled the money. At the time of giving evidence on commission, Mr McTear had prepared a list of employers, listing sixteen employers, for whom he claimed to have worked over the years. She did not remember the preparation of this list. She did not give him help with any application forms, such as an application for employment with Cunninghame District Council; he filled them in himself. He did not discuss them with her, except that she maybe helped him with some of the dates. These were mostly about how long they had lived in Beith and at other addresses.
[4.125]When they were children she and Mr McTear were at different schools. She was at St James'. In his evidence taken on commission Mr McTear stated that he went to school at Mossvale which was a primary and junior secondary school between the ages of 5 and 15, leaving in 1959. Mrs McTear agreed that pupils had to leave a junior secondary at the age of 15. They did not sit examinations, but obtained a school leaving certificate. Camphill School was a senior secondary school, for a different area, where it was possible to stay on after the age of 15 and take lowers and highers, or later O Grades and subsequently O Levels. In the Cunninghame District Council application form, dated 17 February 1989, Mr McTear had stated that his education was at Camphill School from 1956 to 1960. Mrs McTear said that he might well have gone to that school because she did not know him then, she did not meet him again between the ages of about 13 and about 17, so he might have gone to that school before they got in touch again. When they were young, he went to Mossvale and she went to St James' and they lost touch until they left school. He told her then he was home from the Army. If he did attend Camphill School, this was the first day in her life that she had ever heard of that. In an application form for employment at the Hunterian Museum in Glasgow, dated 10 April 1990, Mr McTear stated that he attended Camphill School from 1956 to 1959 and gained O Levels in Maths, English and History, all at B grade. Mrs McTear said that he had never discussed these with her and confirmed that if he had gone to Mossvale School he could never have obtained them.
[4.126]Mrs McTear said that they met up again in about 1962 when he was home on leave from the Army, where he was serving in the Junior Leaders. She confirmed that this was from 1960 to 1962. She met him in 1962, they were engaged in 1963 and married in 1964. She did not think he was doing anything when they were engaged. He was home on leave because his mother was ill. She agreed that he could not have been home on leave from the Junior Leaders in 1963 if he left them in 1962. She only met him on different occasions and understood that he was home on leave. She wrote to him while he was away in Germany. She thought she wrote to him while he was at Catterick, but she did write to him in Germany. They were engaged in late 1963, just after his mother had died. When they were married in 1964 he must have been working for Brown & Polson. He did not ever tell her the sorts of things he was doing in the Army. She knew that he drove tanks or worked in tanks. He showed her the pictures.
[4.127]She was taken through details in the Army records of Mr McTear. According to these, Mr McTear was discharged from the Junior Leaders on compassionate grounds on 30 January 1962. She did not go out with him until later in 1962. She did not recall whether he went back into the Army after leaving the Junior Leaders. She agreed that he signed up for the Army in July 1962, but he never told her that this was for twenty-two years. She knew he was in the Army and intended staying in it and they were going to travel to different places. She was going to be an Army wife. She was only aware that he told her that he left the Army on compassionate grounds. He never mentioned that he had been in trouble when he was in the Army. She remembered him being back in the United Kingdom after being posted to Aden. She agreed that if he was still in the Army until 9 June 1964, his reason for leaving could not have been because his mother was ill and died in about August 1963. They were told that his mother died of cancer, but not what kind of cancer it was. They went to see his mother in hospital, about once or twice. She knew nothing about all the trouble Mr McTear had been in during his Army career, which was put to her in detail, for all the years until hearing about them in court that day.
[4.128]Mr and Mrs McTear were married on 25 September 1964, which was his twentieth birthday. They had decided to be married some months before. They were married in St James' Roman Catholic Church in Paisley. It was basically just a family gathering. They did not have a honeymoon. They had a meal in the local pub, attended by family members, and then went to the cinema. She probably took a week or perhaps two weeks off work and had a break with Mr McTear. His health was fine at the time. She confirmed that the records showed that on the day before they were married Mr McTear had complained to his GP of a strained back while lifting a machine and thereafter received sickness benefit until 30 September 1964.
[4.129]At the time that they were married, Mrs McTear was living with her parents. They read newspapers. All she could remember was that they probably read the Daily Record. They had a television in the house for quite a wee while before her marriage. They took a Sunday paper, either the Sunday Mail or the Sunday Post. They had a radio in the house. She presumed that her parents listened to the news but she could not really remember that far back.
[4.130]Mrs McTear said that her husband could have done more with his life and he was not happy because he did not. She agreed that she had told a journalist in about late 2001 or early 2002 that Mr McTear had plenty of jobs and would give them up to try something different when offered the chance and that he had the brains to do more, such as engineering. She told the journalist that the last job he had before he was diagnosed was with a telecommunications company. He was really enjoying it because he was good with electronics, but then the illness struck.
[4.131]Mrs McTear was asked about records of Brown & Polson showing that Mr McTear was employed by them from 31 May to 29 October 1965. She agreed that this established that Mr McTear was not working for Brown & Polson at the time of their marriage. On reflection, she thought that when they were married he was working at the airport.
[4.132]Mrs McTear was next asked about Mr McTear's criminal convictions. She was shown a press cutting about the conviction for breach of the peace in St Andrews in 5 July 1965. According to the report, he and some co-accused had spent the weekend in the cells between the offence and the conviction. Mrs McTear said that she did not remember her husband coming home and telling her he had spent a weekend in the cells, though probably he did. It was a long time ago. Mrs McTear said that she did not remember the conviction of 4 December 1965. Her husband would probably have told her about it then, but it was very difficult to remember back so many years. He got into trouble most of their married life and it was all alcohol-related. He only got into trouble through drink. He did not drink a lot all the time. They went out together a lot. On occasions when he got into trouble he had gone out on his own or with friends.
[4.133]He would go out on his own once a month or once every six months; it varied, he did not stick to any sort of pattern. Occasionally there would be six months between occasions when he went out drinking. When the children were of school age they went out as a family and went away for the day. He spent time with his children during the week when she was at work. The children were born in 1966, 1967 and 1968, so she was speaking about the period from the early 1970s through to the mid-1980s. He was unhappy because he could have achieved more with his life and that was the reason he went for a drink and that would help. Obviously he was intelligent but he could have done more with his life and he was unhappy about that so he drank. Pressed about her evidence that there could be six months between occasions when he went out drinking, Mrs McTear said that she did not say it was every six months, she said it could have been a month. Maybe it was a week, but then he would maybe go a month before he went out again. He could not deal with things and went out to drink hoping he would deal with the situation. Instead of getting better, things got worse. Her husband had a lot of convictions when they were young. She spoke to him about these things. He apologised and said things would get better. She stuck by him and hoped to work through all these things. He did eventually mend his ways, later on in life. When he was young he would say he was going to mend his ways and then he would get into trouble again.
[4.134]Mr and Mrs McTear's eldest child, Sandra, was born on 28 July 1966 and their son Alan was born on 8 August 1967. Mrs McTear said that she did not remember the conviction for assault on 4 November 1967, three months after Alan was born. Around this time he discussed with her re-enlistment in the Army. She could not remember whether he explained why he was not accepted. She would remember if he had told her that he was turned down because he had previously been discharged for misconduct. Mrs McTear did not remember anything about the conviction on 3 April 1968; she could not remember that far back. If she had children and was pregnant again and he was not working, they would have been entitled to money. She knew nothing about his getting money he was not entitled to. Their third child, Lesley, was born on 28 November 1968. Mrs McTear said repeatedly that she could not remember about the occasions when her husband was convicted, not because they were so many, but because they were so long ago. She did not remember that he was convicted for theft and other crimes of dishonesty, his offences were mostly drink-related. She agreed that if he stated in his application for employment at Hunterian Museum that he had been eleven years in the Army, that would have been untrue.
[4.135] She was asked about other employments and convictions and said repeatedly that she could not remember them. She did know he had a lot of convictions and a lot of jobs, but she could not remember specific things. She could not remember anything about any of his convictions over the years. She did not remember, she said, about the time when he assaulted her in the house. She hesitated when she was asked about the time Mr McTear assaulted Alan in the house and then said that she did know, she did remember that on these occasions he did these things, but she not recall specifically what happened then. She could remember that there had been a lot of incidents, but not exactly what happened, because of the time lapse. She did not remember that he came home one night and assaulted her. She did remember the time he came home one night and assaulted Sandra. She could remember him assaulting Alan. She could remember the fire-raising. She did not remember him trying to break the door down on Christmas Day.
[4.136]On 19 November 1976 Mr McTear was convicted at Paisley Sheriff Court and sentenced to be imprisoned for thirty days. Mrs McTear said that she remembered the case. Her husband had been claiming benefits for her on the basis of an untruthful statement that she was not working when in fact she was. Mrs McTear said that she did not know he had been doing this at the time. She had done nothing to cause him to claim benefits dishonestly. Her attention was drawn to a letter dated 20 January 1976 in which Mr McTear wrote that it seemed ridiculous that he should repay the money, "as it was my wife's fault that I got in this mess". Mrs McTear said that it might have been her fault. She had been working without telling her husband that she was. She did not have enough money to keep her children. She worked for Littlewoods Pools. She would go out in the morning while he was in bed and leave the children with an aunt. At first she would lie to Mr McTear about where she had been. She did not conceal her employment from him for the whole of the year in question. When Mr McTear learnt that she was working he continued falsely to claim benefit for her. She knew that he was doing this. In the course of subsequent correspondence about repayment of the benefits, Mrs McTear agreed on Mr McTear's behalf to having a sum deducted from sickness benefit which he was receiving.
[4.137]From 17 July 1978 to 25 April 1979 Mr McTear was employed by Plessey, but he ended the employment, she said, because of the travelling. Plessey were in Liverpool and he did not like to travel. She thought he had told her that he had been disciplined for drinking at work with Plessey. She would not have approved. He promised he would stop. She agreed that Mr McTear made an untrue statement in his application for employment at the Hunterian Museum, where he stated that he had been employed by Plessey from 1980 to 1988. She remembered that her husband also worked for Saveheat as a storeman for a few months. He also worked for Bostik in Germany for a few weeks, maybe a month, maybe in the late 1970s or the 1980s. There was no time when he worked in Germany for more than two years. He worked, she said in the United States for a few months, maybe in the 1980s. She could not remember when this was or where he went to. She agreed that this employment was not shown in the list prepared by Mr McTear before giving evidence on commission.
[4.138]Mrs McTear agreed that her husband continued to get drunk and get into trouble from time to time. She was asked about the incident which led to her husband being admitted to hospital on 2 May 1981 after sustaining burns to his right leg and hand. She said that this was not because he had come home drunk and tried to set fire to the house. He came home drunk, tried to light the paraffin heater and an accident happened because he was unsteady and drunk. Referred to newspaper reports about his subsequent conviction in November 1981, Mrs McTear said that her truthful recollection of what happened was that her husband tried to kill himself. They managed to put the fire out and their son helped Mr McTear because he had burned himself. They tried to reason with him when he came in drunk. When she found him with the paraffin, she tried to take it from him, but he nevertheless succeeded in starting a fire. She agreed, in light of this, that she had not told the truth when she said that it was an accident. On 25 November 1981 Mr McTear was put on probation for two years. One of the conditions of this was that he be of good behaviour.
[4.139]For a time after the fire incident Mr and Mrs McTear were separated. This was one of several occasions when they were separated. They were back together on 18 December 1981 when Mr McTear was drunk, wrecked furniture, tried to rip a lit gas fire from a wall and threatened their son Alan. This led to the conviction on 21 December 1981. Mrs McTear said that she was not happy about this incident. She could not remember all the occasions when she and Mr McTear were separated. She went back to him each time because he said that he would change and get help. Eventually in the late 1980s he went with her to Renfrew Council on Alcohol. Until then he did not change his ways. On 15 April 1983 Mr McTear was convicted of breach of the peace, although he was still on probation. On 14 December 1983 he was also convicted for breach of the peace. Mrs McTear agreed that these were both drink-related offences.
[4.140]In 1984 Mr McTear had a period of employment with Britax. His next employment was at the Hunterian Museum in 1990. In the list of employers Mr McTear had prepared there was a gap of six years between "Britax 1984, Chichester, machine operator" and "Hunterian Museum, Glasgow University, 1990, security officer". Asked about this at the commission, Mr McTear said that he probably would be unemployed for a while, because people could not get jobs. It was not so easy then as it had been to get jobs. He did not think he was unemployed for several years, he would say six, seven or eight months.
[4.141]Mrs McTear said that she could not recall exactly what happened between 1984 and 1990. Her husband was probably in prison for some of the time. She remembered that he was imprisoned for sixty days on 27 February 1984 for breach of the peace and assault. There were further convictions on 7 and 29 March 1984. Mrs McTear remembered that this was a bad period for his drinking. On 6 August 1984 he was convicted of breach of the peace and assault and sentenced to imprisonment. Mrs McTear remembered visiting him in Low Moss Prison and thereafter at Longriggend. She did not remember when he came out. On 16 July 1985 he assaulted their daughter Sandra by grabbing her by the hair, pulling her to the floor, kicking her, dragging her along the floor, pushing her onto a bath and banging her head on a bath, and committed a of breach of the peace. Mrs McTear said that she remembered this incident. Sandra was then 19 years old. She said that she could not really remember a lot of details. There were quite a few assaults, all drink-related. She said that she did not remember the incident on 9 August 1985, at a time when she was not allowing Mr McTear to come into the house, and he came to the door, rang the doorbell, banged on the door, shouted, swore, uttered threats, forced a piece of metal through the door and struck the door repeatedly with it. She agreed, however, that there was a time when she obtained an interdict against Mr McTear to have him excluded from the house. This was at a time when he was in prison. He was assaulting her and the children every time he got out of prison and she was scared.
[4.142]On 19 December 1985 Mr McTear was convicted of the assault and breach of the peace committed on 16 July 1985. Sentence was deferred. On 16 January 1986 he was again convicted of breach of the peace and sentence was also deferred. On 29 January 1986 he assaulted Mrs McTear by spitting on her and striking her on the face, and also committed a breach of the peace and resisted arrest. There was a period of separation thereafter, so Mrs McTear was not able to explain her husband's failure to appear for sentence. She agreed that he obtained employment with Britax on 24 March 1986. This was in Arundel. She did not know why he left this employment on 25 April 1986, being described as "unsuitable". She did not know why he came back to Scotland. She could not remember if they started living together again after that. She and the children did not visit him while he was working in Arundel. After some prompting, she said that she thought that she and the children all went to Chichester (which is near Arundel). They travelled by train, there and back in one day. She thought that Chichester was somewhere in the middle of England (when it is in fact on the south coast).
[4.143]On 15 May 1986 Mr McTear was sentenced to imprisonment and was sent to Low Moss Prison. He was again transferred to Longriggend. Mrs McTear visited him there. When he came out he came home to live with her. They talked about trying to get help for him. On 18 September 1986, however, he was again convicted of breach of the peace and sentenced to imprisonment. He went to Low Moss Prison. After this he probably mended his ways for a brief time. On 20 October 1986, however, he assaulted Sandra, pushed her to the ground and punched her about the head to her injury, and committed a breach of the peace. On 10 November 1986 he committed a further breach of the peace. On that day he was convicted of these offences and sentenced to imprisonment. He was again sent to Low Moss Prison. Mrs McTear did not remember that he was released after about two weeks pending an appeal, but went back because his appeal was refused. She agreed that he was in Low Moss on several occasions between 1984 and 1990. She remembered that after he came out of prison on 24 April 1987 there was another incident involving her and Alan. She had difficulty in remembering each incident. Mrs McTear agreed that on 30 April 1987, shortly after her husband had been released from prison, he assaulted her by pushing her onto a bed, seizing her round the neck and attempting to strike her with a wooden shaft, and also assaulted Alan by attempting to strike him with a wooden shaft. She said that Alan was trying to help her. After this incident her husband was remanded in custody. On 11 May 1987 he pled guilty and was sentenced to imprisonment for three months.
[4.144]Mr McTear was released in late June 1987. Thereafter they were not living together. Mrs McTear said that she did not recall the incident in which Mr McTear assaulted Alan, burnt him on the back with a lighted cigarette, grabbed hold of him and pushed his head through a window, all to his injury, and also committed a breach of the peace. He was convicted for this on 24 July 1987 and again sentenced to imprisonment for six months. Mrs McTear agreed that when he came out she persuaded him to go and see the doctor about his alcohol abuse, and they went there together. She thought it did him good for some time. She agreed, however, that on 25 December 1988 he committed a breach of the peace by playing music at an excessive volume, shouting and swearing. She agreed that he was "back on the alcohol again". On 24 January 1989 Mr McTear again assaulted Alan, turned him out of bed, and committed a breach of the peace. Mrs McTear said that she remembered this incident, which was again the result of drink.
[4.145]On 17 February 1989 Mr McTear applied for re-employment at Valley Arc. In this he stated that he had been employed by Plessey from 1982 to 1987. Mrs McTear agreed that this was untrue. He also claimed to have Army Certificates of Education Classes 1, 2 and 3. Mrs McTear agreed that it must have been clear to him that if it were discovered that he had not been employed by Plessey from 1982 to 1987, then the job offer could be withdrawn. Mrs McTear agreed that Mr McTear made untrue statements when he was interviewed for this employment. He was not in the Army for eleven years. He was not employed by Plessey from 1982 to 1987 and he was not made redundant from that employment. He was not employed in Germany from 1973 to 1974. He was not employed by Component Tools in the United States from 1974 to 1975. He was not employed by Scottish Cables in Renfrew from 1975 to 1979. He was not employed in Portsmouth for one year. Mrs McTear agreed that what was stated in the form presented a picture of somebody who had been in more or less continuous employment for the period from 1960 onwards, including the Army service he claimed to have, which was not true. He did not have, as he claimed, O Levels in mathematics, English and history. He did not have, as he claimed, an interest in pottery. It was untrue to say that he did not have a police record. It was untrue to say that he did not drink. It was not true that in the period from February 1986 to February 1989 he had three days off work for sickness. It was not true that he had never been dismissed from a job and had never been disciplined by an employer.
[4.146] He committed a breach of the peace on 21 February 1989. Mrs McTear said that this was an incident brought about by alcohol abuse, about ten days before Mr McTear told the interviewer that he did not drink. Mr McTear was eventually sentenced for the assault on Alan on 24 April 1989, having failed to appear for sentence on 3 March 1989, the day that he was interviewed for employment by Cunninghame District Council. Mrs McTear said that she remembered him going for his interview. She did not think it right that he failed to go to court.
[4.147]Mrs McTear was asked further questions about occasions when she said Mr McTear had travelled to obtain employment. She did not remember how long the journey took when she and the children went to meet her husband in Chichester or how many trains they travelled on. When she said that her husband went to work in the United States she thought it was the company he was working for who paid for his flight, but she could not remember the name of the company or where he was employed. They thought that Mr McTear's skills were worth their paying his fare over. He flew from Glasgow Airport, but she did not see him off.
[4.148]Mrs McTear remembered that her husband applied for employment with the Royal Mail in Dorking, Surrey and that he took up an offer of employment dated 6 June 1989. On 8 June 1989 he pled not guilty by letter to the complaint alleging a breach of the peace on 21 February 1989. Mrs McTear said that she could not remember that he was due to stand trial on 8 September 1989, and that he was convicted and fined on that date. He resigned from his employment at Valley Arc on 23 June 1989; Mrs McTear understood that this was in order to take up his employment with the Royal Mail. On 15 June 1989 he applied for employment with Burns International. In the employment form he stated that he attended Camphill School in Paisley and obtained O Levels in mathematics, English and history. He stated that he had never been interviewed as a suspect in a criminal case. Mrs McTear said she understood that this was a security officer's job and that he was to be working at night at shops and other places. He said that he had never been a "defendant" in a criminal trial, had never been arrested or convicted of an offence other than parking, and that he had no court charges then pending against him. Mrs McTear agreed that these statements were untrue. She also agreed that he made untrue statements that he had never served in the armed forces, that he had been employed by Plessey from 1981 to 1987 and left them because he had been made redundant, that he had never been suspended or dismissed or asked to resign from any position, had never been arrested, summoned or arraigned in a court, other than for a traffic misdemeanour, and that there had been no unfavourable incidents in the past through which his honesty might be questioned. Mrs McTear said that she did not know that Mr McTear had filled in the form with these untruthful answers, and would not have been happy about it if she had known. She agreed that, according to the form, any misrepresentation of the facts would be grounds for immediate dismissal.
[4.149]According to Mrs McTear, her husband worked for the Royal Mail in Dorking for a few months. They were living together at the time and it was difficult to recollect the length of time that far back. She thought it was longer than the three days shown in the records. He might have gone to Dorking and given up his job after three days and then just stayed away looking for something else. She agreed that his application for employment at the Hunterian Museum Mr McTear stated that he had been employed at Valley Arc from August 1988 to July 1989, and did not indicate any subsequent employment. The application form was dated 10 April 1990. His employment with Burns International started on 1 November 1989 and ended on 21 November 1989. The reason for termination was given as "under the influence of alcohol". Mrs McTear said that she did not really know anything about that, but he did tell her that he was dismissed for being under the influence of alcohol while he was working. She could not remember exactly what she said to him, but she was not very happy with it. She did not remember exactly what he said. She would have been displeased if he had been dismissed for drinking at work and would have told him so and he would no doubt have tried to say something to pacify her. There was no reason to think that he did not do what he had done in the past, which it was to say that he was sorry and he would not do it again. On 23 November 1989, however, two days after being dismissed by Burns International, Mr McTear committed a breach of the peace at his home address, an offence which included setting fire to a quilt. Mrs McTear said that she remembered this incident, which was drink-related again. Her husband took the quilt out of the house. He accused her untruthfully of seeing someone else. He was sorry when he had sobered up. After sundry procedure, he was fined £150 for this offence on 15 January 1991. Mrs McTear said that she did not help him pay his fines off all the time, he usually paid them himself. It sometimes came out of the housekeeping money. She did not remember about the last conviction, which was on 31 October 1990.
[4.150]Mrs McTear said that she did remember going with her husband to Renfrew Council on Alcohol on 19 July 1990 and being interviewed there. She was asked about statements recorded by the interviewer that "Alf feels his drinking is getting out of control" and "his wife admitted there had been a few problems over the last six months". She agreed that there had in fact been problems for many years, really from the start of the marriage, but she said that there had been more incidents in recent years. An appointment was made for them to go back on 2 August 1990, but according to the records Mr McTear cancelled this appointment as he was working seven days a week for the next three weeks. Mrs McTear said that she could not remember where he was working at that time. She remembered that he had been employed at the Hunterian Museum in the summer of 1990. There was trouble there later on. He told her that he had been out for lunch and had been drinking and was dismissed. She remembered that he had not gone to work the next day: this was probably because he had been drinking and not because he was ill. He did suffer from hangovers when he was drinking too much. He just stayed in bed, out of the way. He was usually grumpy and a bit tetchy, and Mrs McTear agreed that when the children were younger they could annoy him when he had a hangover. Mrs McTear remembered that there had been talk of her husband obtaining a full-time job at the Hunterian Museum, in place of his part-time job there, but nevertheless he had gone out for a drink at lunchtime. Mrs McTear could not remember why her husband did not attend an investigatory hearing on 14 August 1990, or that sick pay was being withheld.
[4.151]Mrs McTear was shown records relating to her husband's referral by his GP to Dr Lind in August 1990. She agreed with the statement that he had a long history of excessive alcohol intake but had never really tried to do anything serious about it. She agreed that, throughout these years of alcohol abuse, he and she appreciated the damage it was doing to the family and the damage it could do to his health. It was true that he was drinking every lunchtime as well as every evening, large quantities of beer and spirits. He would be drinking in the house, and less often in the pub. He would be drinking large quantities of beer and spirits. She was worried that during the years her husband was drinking he might do himself some physical damage. She remembered that in August 1990 her husband suffered from an anxiety state, but she did not really know what he was anxious about. She did not remember making a telephone call to the Hunterian Museum on 7 September 1990, after her husband had been reinstated, to say that he would not be able to take up his position again as he was off sick.
[4.152]Dr Lind's notes showed that Mr McTear told him on 9 October 1990 that he was a bout drinker, spending £70 to £80 on whisky and beer every weekend. Mrs McTear agreed that this was the pattern. He was getting the money when he was earning. He earned about £100 a week and blew it all on drink. Her husband enjoyed going to the pub. She did not know whether he enjoyed drinking or not. Mrs McTear noted statements made by her husband that his memory was away when he was drinking and that he was harming his wife and children, and agreed with the statement that after drink he had aggressive persecutory feelings. She agreed that, as stated by her husband in a certificate dated 21 October 1990, he was suffering from anxiety, blackouts and dizziness, and that this was connected with recovering from his drinking. She agreed that it was not a true statement by her husband in a letter to the Hunterian Museum dated 21 October 1990 that he was to go into hospital for tests for two to three weeks. She could not remember that a suggestion had been made by Dr Lind that her husband be admitted to a programme at Loudoun House starting on 29 October 1990. She agreed that if this was the arrangement it was not for "further tests". She did remember that there was an arrangement that he would go into Loudoun House on 29 October, and that was then re-arranged for 10 December, when he failed to turn up. She was not very happy about this. She agreed with the description of her husband at interview with Renfrew Council on Alcohol on 29 November 1990 as "undernourished and under par". She also agreed with a description of him at a subsequent interview on 13 December 1990 that he lacked responsibility in some ways, opted out of decision-making and then argued with her when she was in control. She also agreed with the description of her husband made following the interview on 17 January 1991: "No matter what you try to discuss with Alfred, he seems to have all the answers."
[4.153]She recollected that by 7 February 1991 he was, as stated, depressed and negative although he was not drinking. He had applied for about six jobs locally and down south. He did in fact obtain employment with the (RSAC) in early April 1991. Thereafter he was employed by John Churchill & Co in December 1991 and January 1992. At commission he described his employment at the Club as temporary. Mrs McTear said that he left because he was drunk one night and was summarily dismissed. She agreed her husband did not tell the true story at the commission when he said he left the job because he did not like it. She agreed that they did not go on holiday in the summer of 1991. In the application dated 13 August 1992 for financial assistance for the trip to the Bristol Cancer Help Centre, Mr McTear stated that he had been unemployed for two years. He also described himself as a social drinker who took alcohol occasionally. Mrs McTear agreed that these were not true statements.
[4.154]Mrs McTear was next asked about her own smoking history. She started when she was 15, after she left school. When she started smoking she first smoked Bristol cigarettes because it was the only type that could be bought in tens. Thereafter she went on to John Player cigarettes, when filter tips became available. The brand name was Sovereign. Thereafter she smoked John Player King Size or John Player Special. She stopped on several occasions and started smoking again, until she stopped altogether in February 1992 for health reasons. She said that she did not smoke more than about ten a day. Asked about an interview published in the Daily Record in early 2002, in which she stated that she was smoking twenty a day, she said that some days it could have been twenty, some it was ten. If she was not at work she would smoke more during the day. If she and her husband were going out they would buy a packet of twenty and smoke it between them, or she would smoke the whole packet. She agreed that she smoked roughly ten, maybe twenty a day. How much she smoked depended on the circumstances.
[4.155]Mrs McTear said that her husband smoked roll-ups (hand-rolled cigarettes) when they were living at Schaw Road between 1968 and 1980 and thereafter when they lived in Albion Street. He smoked roll-ups in the house most of the time, and cigarettes were really for when they went out. Roll-ups were cheaper. She would buy the tins of tobacco, which was Old Holborn. She did not remember that it was planned originally to sue not only ITL but also the manufacturers of Old Holborn. He did try to stop smoking on several occasions. He said it was difficult. Later she said that her husband did not smoke roll-ups because this was cheaper than buying cigarettes. She said that the idea was to try and cut down on his smoking. He thought it was time-consuming to roll them and he would smoke less. Most of the time she smoked she bought cigarettes and did not smoke roll-ups. It was cheaper in the long run to smoke roll-ups, it was possible to make forty from one tin of tobacco.
[4.156]Mrs McTear was brought up in a strict Roman Catholic home. She had an older sister and a younger brother. Her father was a strict non-smoker and a strict teetotaller. She remembered that her father had in fact smoked when he was younger and in the Navy. When he came out of the Navy and married he did not smoke. Her mother did not smoke or drink. Her parents would warn her not to drink. She would get into trouble if she came home smelling of drink. She would also get into trouble if she came home smelling of smoke. They advised her not to drink and she followed their example. They told her that smoking was bad and she should not do it. When she started smoking she concealed this from her parents and did not smoke at home because that would get her into trouble. They advised her that it was better not to smoke and not to drink, and she presumed that this was because it was bad for her. Her father died in about 1983 and her mother in 1996. After she and Mr McTear married in 1964 she visited her parents' house, but her husband did not very often. After she was married she did smoke in front of her parents. She agreed with the statement made by Mr McTear at the commission that it was "a big deal" to smoke in front of her father because she knew he did not approve. She now knew or believed that smoking was said to be addictive and that there were warnings on packets of cigarettes about health risks. These warnings first appeared in about 1971. They said that smoking was dangerous. This was a surprise to her when she first saw them. She knew before the warnings came on packets that smoking was generally thought to be bad for people.
[4.157]The first disease that Mrs McTear remembered being linked to smoking was lung cancer. She became aware of this through people talking about it and through newspapers, television and radio. She remembered that there was a cancer scare, everybody was talking about it and it was in all of the media. She was asked extensive questions based on newspaper reports, many of which are referred to in Part III of this Opinion. I do not propose to quote the detail of these reports, and I shall simply summarise what Mrs McTear said about her own awareness of issues relating to smoking and health. Under reference to a report in the Daily Mirror of 25 January 1953, she said that she remembered that people changed to filter cigarettes. She remembered that it was said that the problem with smoking was that it was bad for the lungs if cigarettes were smoked right down to the last puff. Reference was made to a report in the Daily Record of 30 June 1960. She agreed, under reference to a report in the Sunday Post of 23 October 1960, that there was discussion of the relation between the rise in the lung cancer death rate and the rise in the smoking habit. She remembered that it was being said that the risk of lung cancer was many times greater in heavy smokers than in non-smokers. Under reference to a report in the Evening Citizen of 30 June 1961 she said that she remembered statements about the great increase in lung cancer deaths over the previous ten years. She agreed that advice was being given that people should not start smoking and if they had already started they should either give up or at least cut down.
[4.158]Under reference to reports in the Daily Record of 28 June 1957, 31 March 1961 and 26 May 1961, Mrs McTear said that she remembered that warnings were being given that lung cancer was associated with smoking, particularly heavy smoking: this was consistent with her memory that the first disease she remembered being associated with smoking was lung cancer. She remembered that there were from time to time big publicity drives about smoking. She remembered that it was being said that the people most at risk were men who were heavy smokers, and women were at relatively less risk. She was aware that it was said that it was never too late to stop smoking, as this would reduce the risk. She remembered that in addition to lung cancer, people began to talk more and more about other diseases being linked to smoking, such as heart disease, tuberculosis and chronic bronchitis. Further reference was made to the Daily Mirror of 28 June 1957, the Daily Herald of the same date, The Observer of 14 January 1962, the Daily Express of 16 February 1962 and the Sunday Pictorial of 17 December 1962. Mrs McTear said that she remembered that when there was a big scare about smoking and health, one of the things that was being talked about was that the Government should take action to make cigarettes more expensive. She remembered that people talked about switching from cigarettes to pipes because they were supposed to be less dangerous. She remembered suggestions that cigarettes should not be smoked all the way down, so as to reduce the amount of tar that would accumulate in the lungs, and that it was better to give up than to carry on smoking.
[4.159]Under reference to a series of reports in the Daily Record of 16 February and 8, 13 and 14 March 1962, the Sunday Post of 11 March 1962, The Observer, the Sunday Pictorial and the Sunday Post of 18 March 1962, the Sunday Post of 20 May 1962, the Daily Record of 30 May 1962, 22 June 1962 and 3 December 1962 and the Evening Times of 14 November 1962, Mrs McTear said that what had caught her interest was the lung cancer scare. In answer to questions by me, she said that she was not aware of this when she started smoking in 1960. She did not really remember being aware of this until the warnings were on the packets. She did remember that there was this emphasis on lung cancer at the start, and that smoking might cause other diseases. She remembered it was being said that in Scotland bronchitis as well as lung cancer was a problem.
[4.160]Under reference to reports in the Paisley Daily Express of 4 March 1964, the Daily Record of 3 July 1963, the Sunday Mail of 12 January 1964, the Sunday Post of 12 January 1964, the Paisley Daily Express of 15 January 1964, the Sunday Post of 15 March 1964, the Daily Record of 25 June 1964 and the Paisley Daily Express of 8 November 1964, Mrs McTear said that she remembered publicity about an American report that smoking caused lung cancer and that there was no evidence that filter cigarettes reduced the health hazard. She remembered that it was said that women who smoked during pregnancy tended to have underweight babies. She did not smoke while she was pregnant but started again as soon as the children were born. She remembered that people started talking about heart disease being associated with smoking. She remembered that it was being stated in the press that everybody now knew what the risks were and that they had to take their own decisions if they wanted to carry on. She was aware of the link between low birth-weight babies, smoking and drinking. She was aware of reports about large numbers of lung cancer deaths in Scotland being caused by cigarette smoking. She remembered an anti-smoking campaign through advertisements and posters. She remembered that there was a time when there was talk of banning cigarette advertising on television. She and Mr McTear had a television when they were married in 1964. Reference was made to reports in the Evening Citizen of 8 January 1965, the Daily Record of 9 February 1965 and the Glasgow Herald of 19 June 1965. Mrs McTear said that she did remember the ban on cigarette advertising on television coming into force. She also remembered that it was being said that the problem was that there were chemicals in cigarettes which were thought to be harmful to smokers and to their babies if they were pregnant. Under reference to reports in the Evening Citizen of 16 May 1967 and the Daily Record of 17 May 1967 she said that she remembered that there were experiments being carried out to paint cigarette smoke condensate on the skins of mice.
[4.161]Mrs McTear was next asked about a series of reports in the Daily Record of 30 September 1968, 8 November 1968 and 31 March 1969, the Sunday Post of 11 May 1969, the Daily Record of 20 May 1969, the Sunday Post of 4 January 1970, the Daily Record of 7 January 1970 and 18 April 1970, the Sunday Post of 2 August 1970, the Evening Times of 19 August 1970, the Daily Record of 20 August 1970, 22 October 1970, 28 October 1970 and 4 November 1970, the Evening Citizen of 5 January 1971, the Sunday Mail of 10 January 1971 and the Daily Mail of 11 January 1971. She said that she was aware that it was being said that Scotland had a particular problem because of heavy smoking. She was aware of the link said to exist between this and Scotland's high lung cancer death rate, and that lung cancer was almost the most common cause of death in Scotland. She was aware that it was being said that if people gave up smoking then they would quickly return to good health. The Sunday Post was a paper she had taken for many years, though she preferred to read the Daily Mail. She got both papers and read the Daily Mail from cover to cover and whatever caught her eye in the Sunday Post. She was aware that there was a particular problem with lung cancer in the west of Scotland. She did not remember any relative or friend of her parents dying of lung cancer while she was young, or any of her neighbours after she was married. She only knew, from Mr McTear, that his mother died of cancer and learnt later that it was lung cancer.
[4.162]Mrs McTear said that she remembered it was being said that cigarette smoking was worse for health than industrial pollution. She also remembered that it was being said that in addition to the risk of lung cancer there was a risk of dying, most likely from a heart attack, before the age of 65: every cigarette cut life expectancy by ten minutes. She advised her children that they should not smoke. She was aware of a time when it was being said that cancer was beginning to affect more women, and that cigarette smoking was being described as a menace to health. She remembered that by 1971 smoking was being said to cause death and disease on an epidemic scale, through lung cancer, chronic bronchitis, coronary heart complaints and other diseases.
[4.163]Against this background, Mrs McTear said that she already knew by the time that warnings were first printed on packets that smoking was said to be a cause of lung cancer and other diseases. Reports like that in the Sunday Mail of 10 January 1971 would have made an impact on her at the time, even though she did not specifically remember them now. Asked about her previous evidence that she was not aware that it was being said that smoking could cause lung cancer until warnings came on cigarette packets in 1971, she said that she was aware about the dangers later, not in the 1960s, in the late 1960s - it was hard to explain. The first time that she was aware that smoking was said to be bad for health was in the late 1960s. She was made more aware when warnings came on the packets. She was reminded that she was pregnant with Sandra in late 1965 and when she went to the antenatal clinic they told her what she already knew, that smoking was bad for her baby.
[4.164]Mrs McTear was asked about a series of reports and advertisements in the Daily Record of 11 January 1971, the Sunday Post of 9 May 1971, 11 March 1973 and 25 March 1973, the Daily Record of 14 April 1973 and 14 June 1973, the Sunday Post of 1 July 1973, the Paisley Daily Express of 28 September 1973 and 26 October 1973, the Daily Record of 19 October 1973 and 26 October 1973, the Sunday Post of 24 March 1974, 9 March 1975 and 13 July 1975, the Daily Record of 23 February 1976, 7 April 1976, 10 May 1976, 11 November 1976, 24 November 1976 and December 1976, the Sunday Post of 9 May 1976 and 27 June 1976, the Daily Record of 20 April 1977 and 2 June 1977, the Sunday Post of 19 June 1977 and 25 September 1977, and the Daily Record of 13 July 1977 and 14 September 1977. All of these related to health education and anti-smoking campaigns. Mrs McTear said that she was aware that there were suggestions to help people stop smoking cigarettes. She agreed that it would not need warnings on packets to know from health education advertisements that smoking was said to be bad for health and that people should give it up. She remembered that there was a public campaign to persuade people to stop smoking. She remembered aids to stopping smoking, such as nicotine-flavoured chewing gum. She was aware that by 1973 there were calls for a ban on smoking in public places. She remembered that time after time the same messages about risks to health were being repeated in the press. This was the kind of thing that would have registered with her at the time. She could hardly miss full-page advertisements offering help to stop smoking or saying that parents should set an example to their children.
[4.165]Mrs McTear said that she saw a newspaper article in which it was stated that ASH were looking for test cases in which lung cancer victims were prepared to sue tobacco companies for their suffering. She told her husband about this, he was quite keen about it and they got in touch with ASH. ASH put Mr McTear in touch with Mr Fyfe of Ross Harper. They met Alison Hillhouse, the Director of ASH (Scotland) at that time, on a number of occasions, at ASH headquarters in Edinburgh. There were times when Mr McTear appeared on the radio and on television and was interviewed in the newspapers. This was usually arranged by Mr Fyfe or by ASH. When he was interviewed, Mr Fyfe and Ms Hillhouse would be there. She always went with him. It was not until later that he was quite poorly. She did not remember the sort of things that Ms Hillhouse said to her husband. She remembered that he was told that the nicotine in cigarette smoke was addictive, more addictive than heroin. She remembered Ms Hillhouse telling them about tobacco manufacturers advertising so that they would attract young people to smoke, and that they denied that there was any health risk to smoking, when all the time they knew that it was dangerous to smoke, and that smoking was addictive. Mr McTear had a "wall of death" at home, with newspaper cuttings about cigarettes, lung cancer and death. She was not aware that her husband was campaigning for ASH.
[4.166]When Mr McTear was diagnosed with lung cancer, he was given only a few months to live and was determined to do what he could to prolong his life. He gave up smoking at once and was not drinking at that time. Mrs McTear agreed that ASH must have known that Mr McTear would die and that she would continue with the present action. She did not, however, feel like a champion of the anti-smoking cause. She did remember saying that she felt that if one person stopped smoking because of the publicity about the case, then her husband's death was not in vain. "This became his purpose, I hope that it will become his greatest achievement." She remembered her husband appearing on television to launch a campaign to get the Government to act against tobacco and that ASH were campaigning with Mr Fyfe's firm to get lots of victims to raise actions. She remembered Ms Hillhouse saying that this action would be the end of the multinational tobacco industry as they knew it. She remembered Mr McTear telling a newspaper that when he started smoking thirty years earlier, John Player had failed to warn him about the dangers. She remembered him saying on radio that he was bringing this action just to get tobacco done away with, "in the hope that the young people do not have to go through the same course that I went through due to tobacco." After her husband died she started doing interviews, arranged by ASH and Mr Fyfe. In one interview, in late 2001 or early 2002, she said that she now knew that the tobacco companies were fully aware of the risks "but did nothing to warn us". During 2003 it was reported that she was looking for funding to support her in paying the court dues. As far as she knew, there had been no response. She remembered that her husband's position, as stated in an interview in July 1992, was that when he started smoking, that was the thing. He stated:
"If you were a man about town or something, you smoked the best cigarettes [...] and you really did not think about these warnings, because, I mean, you had been smoking for that long and it just never did you any harm."
[4.167]In re-examination, Mrs McTear said that her husband felt quite strongly about the matter and wanted to proceed with an action even though he was ill. She decided to continue with it after his death for the same reason that he started: to let young people know of the dangers of smoking so that hopefully they would not smoke. She was not very happy about the length of time the action had been in court, because it was very difficult for her to remember back. She applied unsuccessfully for legal aid and her legal team agreed to proceed on a "no win, no fee" basis. ASH provided her with information but there was no question of their paying for her case. At the end she was quite proud of her husband for doing this and thought that this might be the achievement of his life.
[4.168]Mrs McTear said that she was aware that in the early stages, in the 1950s and 1960s, the tobacco industry were denying what was being said by the doctors. She was aware that there was a controversy between the tobacco companies and the doctors. In addition to publicity about warnings given by doctors, there were newspaper advertisements placed by tobacco manufacturers for their products. She had never found any manufacturer's message on a cigarette packet giving any warning. Despite the Government health warnings which had appeared since 1971, she herself did not give up smoking until 1992. She started smoking at the age of 15 because it made her feel grown-up, older, and her friends were all smoking. This was really the attitude of those of her age. Mr McTear started smoking roll-ups in the late 1970s. He tried to stop smoking in the 1980s and went on to the rolling tobacco more then. On further reflection, after an adjournment, Mrs McTear said that her husband did not start smoking roll-ups until they moved to Beith in 1983, she was confused about the dates previously. In the 1980s he was smoking up to sixty cigarettes a day, of which about half were roll-ups and half were ordinary cigarettes.
Mr McTear's smoking history: additional evidence
[4.169]Proof of Mr McTear's smoking history depends principally on the evidence of Mr and Mrs McTear, narrated above. In addition, evidence relevant to Mr McTear's smoking history was given by three witnesses; I summarise it now.
[4.170]Ronald Green, who knew Mr and Mrs McTear in the period between 1970 and 1976, when he lived in the flat opposite them at 12 Schaw Road, Paisley remembered that Mr McTear smoked cigarettes, and his mental picture was that he smoked ordinary cigarettes, and roll-ups periodically.
[4.171]Mrs Jane Barlow, aged 77, lived in Schaw Road, Paisley, next door to Mr and Mrs McTear, from about 1976 for several years. She said that after she had ceased to live there she saw Mr McTear on television, saying that he had lung cancer caused through cigarettes. Her reaction was to wonder why he was doing that, when it was roll-ups he smoked. These were what she remembered him smoking. Although her recollection was not entirely clear, she must have lived next to Mr and Mrs McTear for about four years, until they moved away in 1980. She said that during that time she saw him smoking on fewer than ten occasions.
[4.172]Gordon Swinburn, aged 44, was the business support services manager at H.M. Low Moss Prison at Bishopbriggs, Glasgow. He was previously an administration officer there. He described the system by which prisoners who undertook work in the prison were able to have earnings credited to them which they could then spend in the prison shop on such things as tobacco. Mr Swinburn only had direct experience of the prison in the 1990s, but had made enquiries and found that it was possible for a prisoner's earnings in the 1980s to be about £3 or £4 per week. They were also allowed access to their own personal funds once a week, the permitted sum in the 1980s being £2. At the time of the proof the tobacco available in the shop was several brands of hand-rolling tobacco and packets of ten Kensitas, which was the only brand of manufactured cigarettes sold there. Mr Swinburn was, however, unable to provide information about what cigarettes might have been sold at Low Moss Prison earlier than the 1990s.
[4.173]I would add at this point that it is agreed between the parties by joint minute that:
"John Player Special Filter (also known as 'John Player Special Filter (International)' from 2/8/82) cigarettes were first introduced to the market on 5 April 1971 and withdrawn from the market in June 1988;
John Player King Size cigarettes were first introduced to the market on 10 April 1976 and withdrawn from the market in March 1990;
John Player Special King Size were first introduced to the market in November 1980 and have been available since that date; and
John Player Superkings were first introduced to the market on 18th August 1983 and have been available since that date;"
Submissions of counsel
(1)Mr McTear's credibility and reliability
[4.174]As will be seen, Mr McEachran did not seek to uphold Mr McTear as a witness whose evidence could be accepted in its entirety. He accepted that Mr McTear could be described as an unreliable witness, by which I took him also to mean that in some respects he was incredible. Mr Jones, however, mounted an all-out attack on Mr McTear's credibility and reliability. In the written submissions for ITL, which Mr Jones adopted as part of his oral submissions, it was argued that the evidence in this case disclosed that, in conducting himself throughout his adult life, Mr McTear's paramount motivation was to advance his own interests. He spoke the truth, he concealed the truth and he lied, according to the occasion and to his view of what best suited him at the time, uninhibited by conscience.
[4.175]Mr McTear misrepresented his educational qualifications on numerous occasions. He made untrue claims in his application form for employment at Valley Arc and repeated these at interview. He made untrue representations in his application for employment at the Hunterian Museum, and for employment with Burns International.
[4.176]He did not tell Mrs McTear the truth about being in trouble in the Army, or about his discharge. She knew nothing about these matters until she was asked questions about them in cross-examination. He lied about his Army career on different occasions in different ways: he disclosed the fact that he had served if he thought that this would be to his advantage, and concealed it if he thought that disclosure would be to his disadvantage. He misrepresented his Army career when interviewed for employment at Valley Arc. He denied having served in the Armed Forces when he applied for employment with Burns International. In the list of his employers which he prepared before giving evidence on commission, he referred to the Junior Leaders, but not to his subsequent Army service. It was clear that he took a deliberate decision not to disclose to the court that he had served in the Royal Scots Greys.
[4.177]He made misrepresentations to his GP, to his employers, and to the social security authorities. It was inconceivable that Mr McTear truly suffered back strain on the eve of his wedding and that it had slipped his memory and that of Mrs McTear when they were asked to recount the details of their marriage, particularly when specifically asked whether he had suffered any injury or illness at that time. What was much more likely was that, in order to have time off work to be married and have a break with Mrs McTear, Mr McTear lied to his employer and to his GP and lied also to the social security authorities in order to maintain his income.
[4.178]Mr McTear was convicted of theft, an offence of dishonesty, on two occasions, 5 March 1966 and 30 September 1970. He falsely stated when he was interviewed with a view to employment at Chrysler Motors on 15 November 1973 that he had not previously been employed by the company.
[4.179]During four periods, from 15 June 1974 to 20 July 1974, from 13 February 1975 to 17 February 1975, from 15 March 1975 to 24 March 1975, and from 31 March 1975 to 2 August 1975, Mr McTear claimed sickness benefit for various reasons. During these periods, he claimed dependant's benefit for Mrs McTear, who was in fact working and earning over the permitted amount. In the letter dated 20 July 1976 he said that it was Mrs McTear's fault that he "got into this mess". It appeared, therefore, that not only did he make a series of fraudulent claims over a period of more than a year, he tried to avoid the consequences by blaming his wife.
[4.180]Although he was employed by Plessey for only about nine months, from 17 July 1978 to 25 April 1979, Mr McTear falsely stated in his application for employment at Valley Arc dated 17 February 1989 that he had been employed by them from 1982 to November 1987; he falsely stated in his application for employment at the Hunterian Museum dated 10 April 1990 that he had been employed by them from 1980 to 1988 and was made redundant; in the list of his employers produced at the commission to take his evidence he falsely stated that he had been employed by them from 1978 to 1980, and that he left because he was made redundant; and he falsely stated in the application form for employment with Burns International dated 15 June 1989 that he had been employed by them from January 1981 until November 1987 and that he had left because he was made redundant.
[4.181]Mr McTear made misrepresentations to the court about his employment history, and concealed from the court his criminal record. He was employed by Britax in Arundel from 24 March 1986 to 25 April 1986, when his four-week probationary period as a hand-press operator came to an end and he was assessed as unsuitable. When giving evidence at the commission, he said that he was employed by this company for "a matter of months, six or seven months" and that he left because his family came down to visit him, and then they did not like where they were so they just came home, and he just stopped that job and just came home. In the list of employers produced by him at the commission he claimed to have been employed by Bostik in Oberusal, West Germany, as a machine operator in the early 1980s. At the commission he said that he was with Bostik for just a month, or two months at the most, and described it as a working holiday. The only other employment he mentioned on the list, before the job at the Hunterian Museum, was with Britax in 1984. When asked if he remembered what happened between employment with Bostik and employment with Britax he replied that he had a few jobs. He was also asked about what happened between his employment with Britax and his employment at the Hunterian Museum, and he said he probably would be unemployed for a while, because people could not get jobs. When pressed about this, he said that during the latter period he had had literally loads of various jobs. He was never overseas. The only time he was away from home was when he was in Chichester. There might well have been occasions when he was unemployed, but he had no real recollection of these, it was very difficult to phase them all into slots.
[4.182]In the whole circumstances it was submitted that, when asked to account for the time between 1984 and 1990, Mr McTear deliberately concealed from the court the fact that he had been imprisoned on six separate occasions between 1984 and 1987 and he lied when he claimed that these years were filled with spells when he had jobs of which he had no real recollection and spells when he was unemployed. At the date of the commission, his claims against ITL included claims for damages in respect of loss of employment and loss of earnings.
[4.183]Mr McTear made misrepresentations to his employers about his state of health, employment history, criminal record and alcohol abuse; he made further misrepresentations to the court; and further misrepresentations for financial gain. Having attended his GP on 7 November 1988 and having been diagnosed as suffering from bronchitis, on 28 February 1989 he completed a Cunninghame District Council medical questionnaire in which he denied a history of bronchitis. When he was interviewed by Isobel McCutcheon on 3 March 1989, in addition to falsehoods already referred to, he falsely told her that he had been employed by Hannomark in West Germany from 1973 to 1974 in telecommunications work, that he had worked for Component Tools in the United States from 1974 to 1975, that he worked for Scottish Cables in Renfrew from 1975 to 1979, that he was employed in Portsmouth on a one-year contract after leaving Scottish Cables, that he had never been dismissed from a job, that he had never been disciplined in a job, that he had never been in any trouble with the police and did not have a police record, and he had no problem with alcohol.
[4.184]It was submitted that it was clear that he lied about his employment history to make it appear that he had a record of continuous work. The truth was that between 1959 and 1991 he had about seventeen short-lived jobs with different employers and in the last ten years of his life he was in employment for a total of only about ten months. It was not a case of his having falsely claimed to have been dismissed from a job because he had forgotten this. At the commission, when he was asked whether moving from job to job was his decision, he replied that he had to move in some cases because he was sacked from a few jobs. Contrary to his representation that he had never been in any trouble with the police and that he did not have a police record, by 3 March 1989 he had been convicted of offences on thirty-four separate occasions and had been sentenced on seven occasions to a total of thirty-four months' imprisonment (not counting the sentence of three months imprisonment for wounding imposed at Newcastle-upon-Tyne Magistrates Court in December 1971, which was suspended for two years). He had also served two years on probation. Further, on the very day that he told Mrs McCutcheon this lie, he ought to have been at Kilmarnock Sheriff Court to answer one charge of assault and one of breach of the peace. Mr McTear was aware when he attended the interview that he was due to attend court.
[4.185]Far from having no problem with alcohol, his alcohol problem was manifest as early as 4 April 1964 when he was found drunk and disorderly by the Town Patrol in Fallingbostel, and from then on he had a string of convictions for alcohol-related offences. As Mrs McTear put it when giving evidence, "he got into trouble most of our married life and it was all alcohol-related". The complaint that he should have been answering at Kilmarnock Sheriff Court on 3 March 1989, when he was instead attending the interview with Mrs McCutcheon in Irvine, was drink-related. Prior to this, his most recent drink-related offence was committed on 21 February 1989, some ten days before he told Mrs McCutcheon that he did not have an alcohol problem and that he had never been in any bother with the police. He was disciplined for drinking at work while he was employed by Plessey. It was clear that by the time when Mr McTear was interviewed by Mrs McCutcheon, he himself had recognised that he had had an alcohol problem, because he had been to see Dr McCarroll on 7 November 1988 and she had advised a referral to a psychiatrist "re depression and [alcohol]".
[4.186]On 15 June 1989, in his application for employment with Burns International, Mr McTear falsely claimed that he had never been interviewed or a suspect in a criminal case, he had never been a defendant in a criminal action, he had never been arrested or convicted of an offence other than a parking offence, he had never been suspended or dismissed or asked to resign from any position, there had never been any unfavourable incident in the past through which his honesty might be questioned, and he did not have any court charges pending against him. He certified that this information was true. One week before this he had written to Kilmarnock Sheriff Court in answer to the complaint alleging a breach of the peace committed on 21 February 1989, and an intermediate diet was fixed for 14 August 1989 and a trial diet for 8 September 1989. He was ordained to appear on 14 August. His most recent conviction had been on 24 April 1989. In certifying that there had never been any unfavourable incident in the past through which his honesty might be questioned, he dishonestly concealed the fact that he had been convicted of theft on two occasions and of benefit fraud on one occasion. He was employed by Burns International from 1 November 1989 until he was dismissed on 20 November 1989 for being under the influence of alcohol while on duty. He did not mention his employment with Burns International in his list of employers prepared for the commission. At the commission he was asked what he did between 1984, when he left Britax, and 1990, when he was employed at the Hunterian Museum, and gave the untruthful reply referred to above.
[4.187]When Mr McTear applied for a job at the Hunterian Museum, he misrepresented his education and employment history and concealed his employment with Burns International. He started working at the Hunterian Museum on 30 April 1990, but after the incident on 11 August 1990, when he arrived back late from lunch under the influence of alcohol, he failed to report for work on 12 August 1990. On the next day he telephoned Mr Gray and told him that he had attended his GP earlier that day, but according to Dr McCarroll's records he did not attend at the surgery until 14 August 1990. He had accordingly not been to see Dr McCarroll on 13 August 1990, and he lied to Mr Gray. He left his employment at the Hunterian Museum on 31 October 1990. He mentioned employment at the Hunterian Museum in 1990 in the list of employers he prepared before the commission, and when asked about this at the commission he said that this was a short-term job, which was just for a year.
[4.188]Mr McTear was employed at the (RSAC) from 6 April 1991 to 4 July 1991, when he was dismissed for being under the influence of alcohol while on duty. At the commission he said that it was a good enough job as far as he was concerned, but a temporary job, which was why he stopped working there. Later he added that they just went away on holiday as he was feeling a bit tired. In cross-examination he said he did not like it, for a start; he was keen on nightshift but he was not keen on the job.
[4.189]His employment with the (RSAC) was the last shown on the list he prepared. He repeated in his evidence at commission on two occasions that this was his last employment, and he was unemployed thereafter. In fact he was employed by John Churchill & Co between December 1991 and January 1992, as evidenced by payslips that Mrs McTear produced after a court order was served on her. It was submitted that while at first sight it might seem curious that Mr McTear would fail to disclose to the court his employment with John Churchill & Co, in fact on 11 August 1992, seven months after he stopped working there, he applied for severe disablement allowance. One of the questions he had to answer in the application form was the date when he last worked. He stated that this was 20 June 1991. As a result of subsequent correspondence, Mr McTear went to see Dr McCarroll on 20 August 1992. She certified in a special statement that she examined him on 23 December 1991, 17 January 1992, 30 January 1992 and later dates and advised that he should refrain from work. Mr McTear sent this special statement to the DSS on 20 August 1992. When he gave evidence at the commission, he knew that he had falsely stated to the DSS that he had last worked in June 1991, and had claimed to have been unfit for work since 23 December 1991. He could not risk disclosing to the court that he had worked for John Churchill & Co in December 1991 and January 1992.
[4.190]The DSS was not the only body Mr McTear lied to after his diagnosis, in order to obtain money. On 13 August 1992 he applied for a bursary to attend as a patient at the Bristol Cancer Help Centre. In the application form he stated that he had been unemployed for two years. During the previous two years, however, i.e. from August 1990, he had been employed at the Hunterian Museum, at the (RSAC) and with John Churchill & Co.
[4.191]Mr McTear made misrepresentations to the court about his mother's cause of death. She died on 24 August 1963. When asked about this at the commission he said that she died of cancer, but he did not really know what type of cancer it was because it was kept from them at that time. It was submitted that it was implausible that the type of cancer from which his mother died was kept from him. He was his mother's only child. His father had died in 1961. Mr McTear had been given a compassionate discharge from the Junior Leaders in January 1962 because his mother was finding it very difficult to make ends meet at home without him. It was clear therefore that he regarded himself as responsible for his mother's welfare. He re-enlisted on 12 July 1962. Colonel Blacklock interpreted the Army records as meaning that he was sent home to the United Kingdom from Aden on 31 May 1963 because of a "compassionate problem", no doubt his mother's illness. He was taken on the strength of the regimental band and, when it became apparent that he was going to stay longer in Britain, he was transferred to the Ayrshire Yeomanry, which was the nearest regiment to him in Glasgow. He was, once again, taking responsibility for his mother's welfare. He registered her death. The immediate cause of death on the death certificate was stated to be "mediastinal tumour". As Dr Kerr explained, primary tumours in the mediastinum were relatively rare, but a squamous cell bronchial carcinoma might invade through the bronchial wall and into the mediastinum. Mr McTear had returned to Scotland to be with his mother. He knew that she had cancer. In all these circumstances, it was difficult to understand on what basis the hospital authorities would have felt justified in refusing to tell him what type of cancer she had or to explain to him what a mediastinal tumour was and how it had come about, so that it could be "kept from" him.
[4.192]In any event, the first part of the answer he gave in evidence was untruthful, that is to say that on 16 March 1993 he did not know what type of cancer she had. By letter dated 19 June 1992 he was referred to the Ayrshire Hospice by Dr McCarroll and as a consequence was seen at home on 24 June 1992, when a history was taken from him by Dr Kirsty Muirhead. He told her that his mother had died of lung cancer when he was 18. Dr Muirhead made a record of this. At the proof, in cross-examination, Mrs McTear was asked what Mr McTear's mother died from and she said they were told it was cancer, but nobody told them and they did not know what kind of cancer it was. Later in cross-examination she was asked whether she knew of anybody, apart from Mr McTear, who had died of lung cancer. As part of her response she referred to Mr McTear's mother and said that she knew now that it was lung cancer, she did not know at the time, and that she had learned that from Mr McTear. It was inconceivable that between 16 March and 23 March 1993 Mr McTear learnt for the first time that his mother had died of lung cancer. Accordingly, he deliberately lied to the court when he claimed that he did not know what type of cancer she had.
[4.193]For these reasons, the evidence demonstrated that Mr McTear was a thoroughly dishonest man. He was capable of theft, fraud, deceit and perjury, both by misrepresentation and by concealment, and his overriding motivation was gain for himself. It was accordingly submitted on behalf of ITL that the court should approach the evidence of Mr McTear with great care, and that nothing said by him should be accepted as true, unless it was against interest or corroborated by evidence from an independent source. The same submission applied to the evidence of Mrs McTear.
(2)Mrs McTear's credibility and reliability
[4.194]Mr McEachran submitted that ITL were not entitled to make criticisms of Mrs McTear as a witness. She gave evidence with a quiet dignity. It was obviously highly distressing for her to have her husband's mis-doings raked over with her, over three or four days of evidence. If she was not forthcoming about these, it was because it was human nature to play down distressing things. She tried to help the court with her evidence.
[4.195]Mr Jones submitted that in cross-examination Mrs McTear was asked many questions about the details of her life with Mr McTear. For the most part, she said that she was unable to recall detail. This might or might not have been true. It was submitted, however, that what emerged clearly was that her primary concern was to give answers that she considered might be supportive of her husband, rather than answers that were necessarily true. The clearest example of her tailoring her evidence in this way came when she was asked questions about Mr McTear's alcohol abuse. She initially said, in her examination-in-chief, that he went out for a drink, just on the odd occasion, not every week, and he would have too much to drink maybe once a month, and it was maybe three months, maybe six months, before he would go out again. She repeated this in cross-examination, when she denied that he drank all the time and drank a lot. Eventually, however, when shown the records of Dr Lind at Ailsa Hospital, in which Mr McTear was recorded as having said inter alia that he had been a bout drinker for many years, Mrs McTear finally agreed that this was accurate, and that he had a serious alcohol problem.
[4.196]In cross-examination Mrs McTear told the court that she and Mr McTear went to different schools and that he did not go to Camphill School. When asked about his statement, in the application for employment at Valley Arc, that he had attended Camphill School between 1956 and 1960, which she knew was not true, she said that he might well have gone to that school during a period when they had lost touch with each other during their teens. This demonstrated that her motivation was to say whatever she thought would avoid discrediting him. When asked about the wilful fire-raising incident on 2 May 1991, Mrs McTear initially said that this was an accident, because he was drunk when he came home and was unsteady. When pressed about this she said that she thought actually he had tried to kill himself, but they did not know that until later. Pressed further, she agreed that it became clearer and clearer that this was not an accident.
[4.197]Mr McTear claimed to have been employed in the United States. When interviewed by Mrs McCutcheon he said that he had worked for Component Tools there from 1974 to 1975. Mrs McTear accepted in cross-examination that this was untrue. Earlier, however, she said that Mr McTear had worked in the United States, though she could not say when, where, or what he was doing. She said that she thought he flew to the United States and that the company he was working for paid for the flight. He flew from Glasgow Airport but she did not see him off. It was submitted that it was impossible to believe that Mr McTear could have persuaded anyone that he had skills so valuable that he should be given a job in the United States and that he should be flown there at his employers' expense. If this had happened, he would have mentioned it in his job applications, his list of employers and in his evidence at the commission, when in fact he stated that he was never overseas during the period between 1984 and 1990. In any event, there was scant opportunity for him to take up employment in the United States in the 1980s, when regard was had to the history of criminal offences, sentences of imprisonment and periods of unemployment and employment mentioned above. The submission was that the explanation for Mrs McTear's evidence on this issue was that, knowing that Mr McTear had never worked in the United States, she guessed that the question was intended to discredit him, and answered in a way that she believed would support him.
[4.198]Submissions were made about the "Chichester day trip", at a time when Mr McTear was employed by Britax in 1986. It was submitted that Mrs McTear did not truly recollect a trip to Chichester. Had it happened, it would have been hard to forget. Mr McTear had assaulted her on 29 January 1986. In the complaint relating to this assault he was designed as "formerly of 60 Main Street, Beith" and "whose present whereabouts are meantime unknown". At the time he left to work for Britax, he was separated from Mrs McTear. The visit, which on her account involved the whole family, would mark their reconciliation. It was to be expected that if that had happened she would have remembered it when first asked about it. While she might have no more than an imperfect grasp of geography, it was to be expected that she would remember a round trip of over 800 miles, which on her account was completed in one day. In addition, there would have been journeys from Beith to the nearest mainline railway station and from Chichester where Mr McTear was living. It would have been an unexpected round trip: the intention had been to visit him, leaving him behind to continue in his employment with Britax when the visit ended. On Mr McTear's account, which Mrs McTear adopted, the decision that he should leave Britax was formed only after the family had arrived. That would have meant that Mr McTear would have had to pack and leave his accommodation immediately, to catch a train home the same day. If all of that had happened, it would have been a remarkable and unforgettable day. It was not until she saw that Mr McTear had claimed that the family had travelled to Chichester that Mrs McTear affected to remember the trip. Her reason for not having recollected it sooner, because Arundel had been named as the place, did not pass scrutiny. In answer to questions about Britax, unrelated to Arundel, she said earlier that she could remember whether or not she and Mr McTear were back together when he left Britax. She said that she did not know why he came back to Scotland.
[4.199]Accordingly, counsel submitted, I should approach her evidence with great care and nothing said by her for the benefit of the case or in support of her husband should be accepted, unless corroborated.
(3)Mr McTear's smoking history
[4.200]Mr McEachran invited me to make various findings in fact. Mr McTear died of lung cancer. He started to smoke in or around 1964. This was established by reference to passages in his evidence given on commission and in Mrs McTear's evidence. In cross-examination of Mr McTear it was not really challenged that it was about 1964 that he started smoking. This was a matter on which Mrs McTear's evidence could be relied upon. He started smoking because of peer pressure and advertising. He was a heavy smoker. Counsel said that this was not challenged. His smoking increased from forty per day in 1971 to about sixty per day in the late 1970s or maybe early 1980s.
[4.201]Mr McEachran also invited me to find that, in accordance with his evidence Mr McTear smoked cigarettes manufactured by ITL from 1964. He started with Bristols but very soon moved over to John Player cigarettes and remained with them until the end. Counsel invited me to accept that it was only in the last few years of his life that Mr McTear started smoking roll-ups made from Old Holborn tobacco and they constituted about half of what he smoked until he stopped in 1991. Accordingly, on any view, the great majority of the cigarettes smoked by him over the years were John Player cigarettes. He was a heavy smoker for over twenty-seven years before he contracted lung cancer. He was not aware of any health risks when he started smoking. This was his evidence, and the evidence of Mrs McTear. As he said, there were no Government health warnings then. Counsel also invited me to hold it proved that once he started smoking Mr McTear quickly became addicted to cigarettes, in the sense that it was difficult for him to wean himself off the habit of smoking.
[4.202]Mr McEachran accepted that the court would be entitled to say that Mr McTear was an unreliable witness, for the various reasons which were to be put forward by ITL, but this did not mean that a witness who had proved unreliable in the past was unreliable in everything. Mr McTear had been told by the doctors that he had lung cancer, he was angry and upset about that and he made a decision to sue the tobacco companies. It was not likely that he would "just invent a brand of cigarettes to sue". The evidence he gave really had the ring of truth about it. He was asked to write down for his solicitors what his smoking history was and he said that he started on Bristols for some months, then went on to John Player because his mother said these were good cigarettes to smoke. He continued smoking these until the end, although he did start smoking roll-ups at a later stage when he was trying to stop. There was no reason why he should invent a tobacco company whose products he had not smoked. It was not something he was likely to be unreliable about, and he was supported in this by his wife. He tried to stop on various occasions and in particular in 1971 when the warnings came on to the cigarette packets. He was not able to quit then because he became very grumpy and bad tempered and his wife did not like him like that.
[4.203]Counsel invited me to hold that Mrs McTear gave reliable evidence about the brands which her husband smoked. Mrs McTear's evidence could be relied on in relation to a matter like this, and it supported her husband's. She said that Mr McTear had smoked a little bit before they married in 1964. Thereafter he smoked John Player cigarettes almost from the beginning. He smoked twenty a day increasing to forty and sixty a day in the last fifteen years. Mrs McTear gave evidence about when her husband started smoking roll-ups, and after reflecting on the matter over lunch she said that he did not start using roll-ups until after they had moved to Beith in 1983. Her earlier evidence that he was smoking roll-ups at Schaw Road was incorrect. By the end she was worn down and some of the things she said about public awareness of the dangers of cigarette smoking she could not have known about because she was far too young. But it was not suggested to her in cross-examination that Mr McTear was not smoking John Player cigarettes: she was only cross-examined about when he started smoking roll-ups, and how many he smoked. So counsel said that he was entitled to submit that it appeared at that stage that it was not being challenged that he smoked John Player cigarettes. She accepted she knew there were health risks at the time she was pregnant in 1966 and in re-examination, after thinking about the matter over lunch, she thought that Mr McTear had started used roll-ups after they moved to Beith in 1983. It was for consideration how far some of the things she conceded about knowledge was because she was really aware back in the 1960s about what was in the newspapers or whether she was just worn down by the cross-examination.
[4.204]On the written pleadings for Mrs McTear, as analysed by Mr Jones, she offered to prove the following:
(a)Mr McTear started smoking in or about 1964.
(b)When he commenced smoking he was unaware that smoking could cause fatal diseases.
(c)After commencing smoking Mr McTear quickly became addicted to cigarettes.
(d)He continued to smoke until 1992.
(e)The brand of cigarettes he smoked was "John Players", manufactured by ITL.
(f)In 1964 and thereafter, these cigarettes were widely advertised by ITL and were supplied by them to various retail outlets throughout Scotland.
(g)Between 1964 and 1977 he smoked approximately twenty to thirty cigarettes per day. From 1977 to 1991 he increased his consumption of cigarettes to approximately forty per day.
(h)At no time prior to 1971 was any warning given by ITL to their customers, such as Mr McTear, that smoking was dangerous to health.
(i)From and after 1971 a notice stating "Warning by H.M. Government: Smoking can damage your health" was printed on packets of cigarettes manufactured by them.
(j)Mr McTear then became aware of the risks to health caused by smoking.
(k)In about 1971, following appearance of the notice, Mr McTear attempted unsuccessfully to give up smoking.
(l)Thereafter, he attempted on numerous occasions to give up smoking.
(m)He was unable to stop smoking, "due to his addiction".
[4.205]Mr Jones explained that ITL had no reason to challenge the averments, which were supported by acceptable evidence, that Mr McTear smoked, that he did so until 1992 and that over the years he increased his consumption (paras. (d) and (g)). ITL had admitted that their cigarettes were advertised in 1964 and thereafter and were supplied by them to various retail outlets throughout Scotland (para. (f)). At no time prior to 1971 was any warning given to their customers by ITL that smoking was dangerous to health, and from and after 1971 a notice stating "Warning by H.M. Government: Smoking can damage your health" was printed on packets of cigarettes manufactured by them (paras. (h) and (i)).
[4.206]ITL challenged the remaining averments. Of these, Mr McTear was the only witness in the case to speak to paras. (b), (c), (j) and (m). The following averments were spoken to by Mr McTear and, to an extent, by Mrs McTear: paras. (a), (e), (k) and (l). Counsel submitted that, for reasons that would be developed later, the pursuer could not succeed in this case unless she proved averments described in paragraphs (a), (b), (c), (e), (j), (k), (l) and (m). It was further submitted that the court should not hold any of these averments proved because neither Mr McTear nor the pursuer could be regarded as a credible or reliable source of any evidence that they might have believed was helpful to their case. This submission, counsel explained, was directed to the question whether it was proved that for the most part, or for any substantial period of time, Mr McTear smoked ITL's brands of cigarettes and, if he did, what quantity he smoked. It was also directed to the dates that Mrs McTear gave about public awareness. The question was not whether Mr McTear had ever smoked ITL's brands, but the contribution they made to his total consumption. The evidence for this was wholly lacking. The court might make a finding that at some time in his life Mr McTear smoked ITL's cigarettes, but this could not be related, for example, to the question of how much Old Holborn tobacco he smoked or indeed any other brands he might have smoked.
[4.207]In support of this, counsel made the following submissions. A factor which it was relevant to consider in assessing the credibility and reliability of both Mr and Mrs McTear in respect of Mr McTear's smoking history was the role of ASH in this litigation. One could see that the influence brought to bear by ASH was manifested in the answers given to certain questions by both of them. When asked why he did not give up smoking, for example, Mr McTear said that he took it he was addicted. In Mr Jones's submission, one could trace that right back to his involvement with ASH.
[4.208]The evidence was that Mr McTear answered an advertisement in a newspaper in which ASH were asking for smokers with lung cancer to come forward in order that a test case could be raised. Once Mr McTear became involved, ASH and their solicitors Ross Harper arranged television appearances for Mr McTear and Mrs McTear. There was no evidence as to how it was that Mr McTear came to be selected as the pursuer in a test case. He was put forward by ASH to launch a campaign for people to sue tobacco manufacturers and to get the Government to act against tobacco. ASH told Mr McTear that smoking was more addictive than heroin, that companies targeted children in their advertising and that manufacturers had denied a causal link between smoking and lung cancer, despite being fully aware of the risks. They told him that tobacco companies were "trying to capture young people through slick advertising". The motivation for the action was to get tobacco "done away with" and to stop young people and other families suffering the way the McTears had.
[4.209]In the application for legal aid on behalf of Mr McTear dated 13 January 1993 it was stated that legal aid was sought to raise an action against "Richard Lloyd and Sons (who manufacture Old Holborn tobacco) and John Player and Sons (who manufacture John Players [sic] cigarettes)". On 27 January 1993, in a radio interview, the terms of which were agreed by joint minute, Mr McTear's solicitor, Mr Fyfe, said in Mr McTear's presence:
"There would have been a problem if he had smoked several brands, but he did not. So for that reason, this case would be easier to win than others where several brands were consumed."
At his evidence given on commission Mr McTear was asked to confirm his smoking history, as recorded in the written statement quoted at para.[4.97]. According to his evidence, the period when "the tobacco change did not work out" started in 1990 or 1991, which was when he started rolling his own cigarettes, and ended when he stopped smoking in June 1992. In 1990 and 1991, however, he was attending Renfrew Council on Alcohol and Dr Lind for help with his binge drinking. The picture that Mr McTear painted, of going out with his wife to the theatre and restaurants during that period and so having to buy manufactured cigarettes, was simply not credible.
[4.210] Mr McTear made a conscious decision to start smoking when he was 20 years old. Mr McEachran had suggested that people did not just decide to start smoking, and Mr McTear simply drifted into it. But this was not the evidence: when he gave evidence on commission, Mr McTear said in cross-examination:
"Once you left school, it was up to yourself if you were a smoker or if you were not. John [Strathearn, a friend] smoked, I didn't smoke and it was only when I was 20 that I decided to smoke."
Mr McTear said that he changed to John Player cigarettes "months" after he started smoking in 1964. He was asked when he changed over to Old Holborn tobacco and he replied that it would be about two or three years before giving evidence in 1990 or 1991. He said that he was smoking forty John Player Superkings a day at least in the 1960s, it was roughly about sixty on average. In cross-examination, he said that after smoking Bristol he had always smoked John Player brands. He said that he could not remember at what time he was smoking different brands. Asked what specific brands he smoked he said that there were different types, one was Superkings, the kingsized ones in a blue packet, there was even one in a black packet called Specials. He said that he could not remember when he took to smoking Superkings. Mrs McTear bought the cigarettes. She knew he smoked Player's because his mother always thought they were good cigarettes.
[4.211]Mrs McTear's evidence was that Mr McTear started off smoking Bristol cigarettes and then when they married he was smoking John Player, "John Player King Size". It was a matter of agreement by joint minute that John Player King Size were first introduced to the market on 10 April 1976 and withdrawn in March 1990. Mrs McTear then gave evidence that she thought that at the beginning it was John Player Special he was smoking. It was agreed that John Player Special King Size cigarettes were first introduced into the market in November 1980 and were still available. She said that by the 1980s he was smoking about sixty John Player King Size a day. When it was put to her in cross-examination that John Player was a maker rather than brand, and she was asked what she would ask for in a shop, she said it was John Player King Size or John Player Special they asked for, that was on the packet. John Player Superkings, referred to in Mr McTear's evidence, were agreed to have been first introduced to the market on 18 August 1983 and were still available. So, counsel submitted, there was great uncertainty about what Mr McTear was smoking in the early years.
[4.212]There was also the problem about Mr McTear's consumption of roll-ups. In cross-examination Mrs McTear said that he was smoking roll-ups when they lived at Schaw Road, Paisley. They lived there between 1968 and 1980. This evidence was corroborated by Jane Barlow and Ronald Green. In re-examination, however, when Mrs McTear began to understand that what was required from her was a recollection consistent with what Mr McTear had said, which was that he had started smoking roll-ups in 1990, and after reflection during the lunch break, she said that it was not until they moved to Beith that he started smoking roll-ups. She remembered buying the tins of tobacco. She said that she was confused about the dates. Counsel submitted that I should not rely on evidence from Mrs McTear that her husband did not start smoking roll-ups until they moved to Beith. It was not until it had become obvious to her that Mr McEachran was at pains to establish that Mr McTear started smoking rolls-up later rather than earlier in his smoking history that she reflected over lunch and wholly altered her position to support his evidence. Her evidence that she was confused with the dates was not credible: she was able to place her recollection of things that had happened into the context of where she happened to be living at the time. The questions about the smoking of roll-ups were related to where they were living at the time.
[4.213]Accordingly, counsel submitted, there was no reliable factual evidence on which I could make any finding as to: (1) the date when Mr McTear started smoking products manufactured by ITL; (2) how long he smoked ITL's products; (3) how much of ITL's products he smoked from time to time; and (4) the proportion of ITL's products he may have smoked compared with other products such as hand-rolling tobacco and cigarettes produced by other manufacturers.
[4.214]It was not clear, counsel submitted, what finding I was being invited to make about the role of advertising in Mr McTear starting to smoke. The reason why Mr McTear started to smoke was not relevant to any issue determinative of the present case. The relevant issues were whether or not he was aware of the public health warnings about smoking when he started and, if not when he became aware of them; and whether or not, having started to smoke, he made any effort to stop once he became aware. His assertion that he fell for this advertising should not be relied on. It was more plausible that he took up smoking because all of his friends smoked. Counsel invited me to treat with caution the evidence from both Mr and Mrs McTear about the message said to be given out by advertising at the time when Mr McTear started smoking.
[4.215]Counsel submitted that it was likely that Mr McTear was already aware by September 1964 of the link between smoking and lung cancer. For reasons already set out, Mr McTear's evidence should be treated as being incredible and unreliable in respect of any matter which might serve his own interests, including his account of not having become aware of this link at the time when he started to smoke. In addition, it was agreed by joint minute that on 24 June 1992 Mr McTear told Dr Kirsty Muirhead of the Ayrshire Hospital that his half-brother, Robert McTear, had died of cancer. It was agreed that Robert McTear died in 1978 at the age of 50 of bronchial carcinoma. In his evidence given on commission, when he was asked about his half-brothers, Mr McTear did not disclose his knowledge of this. Counsel submitted that this was because Mr McTear thought that such disclosure would be detrimental to his case. Similarly, in June 1992, Mr McTear told Dr Muirhead that his mother had died of lung cancer when he was 18; he also told Mrs McTear this. Mr McTear was his mother's only son and registered her death. It was likely, counsel submitted, that he learned that his mother had lung cancer at or before the time of her death in 1963. Notwithstanding this, his evidence at commission was that his mother had died of cancer, but he did not really know what type of cancer it was, and no one had said anything to him to the effect that his mother's death might be related to smoking. Yet Mrs McTear gave evidence that she knew that Mr McTear's mother had died of lung cancer. In counsel's submission, Mr McTear was seeking in these passages to distance himself from any acknowledgement that he was aware that his mother died of lung cancer. His motive for doing this was a recognition that, if he admitted that he had been aware that his mother who was a smoker had suffered from lung cancer, he would simply be unable to sustain the position that he was unaware when he started smoking of the link between smoking and lung cancer.
[4.216]This could be related to the general public awareness of the link between smoking and lung cancer, and the evidence of Professor Hastings that Mr McTear would have known of the health risks at the time he started to smoke. What in fact happened, counsel submitted, was that, although Mr McTear was aware of the warnings, he simply was not prepared to abide by them or take them into account sufficiently and chose, against this background, to start to smoke. As he said in the course of his evidence, he did not take life seriously at all, and he never thought for one minute that he would end up in this situation.
[4.217]So far as Mr McTear's own awareness was concerned, there was evidence about the newspapers which were taken by him, Mrs McTear and their parents. There was no evidence to suggest that any of them were not typical of people of their time, place of residence and social background. Mr McTear's father took the Daily Record. When he was a young man his parents also took the evening papers, the Sunday Post, the Sunday Pictorial and the Paisley Daily Express. They got a television while he was still living with them and they had a radio. Mrs McTear's parents took more or less the same newspapers. They had a television quite some time before she left home and they had a radio. Her father took Roman Catholic magazines. When he was at school and before he went into the Junior Leaders Mr McTear read comics and when he was about 16 he read aircraft books. While he was in the Junior Leaders, the radio was always on and in addition there were separate television rooms for the two channels and newspapers, including Scottish newspapers were available. When Mr McTear came out of the Junior Leaders at about the age of 18, he read the Evening Times, the Evening Citizen, the Daily Record, the Reveille, the Sunday Post and the Sunday Mail. After his marriage in 1964 he read the Daily Record, the Evening Times, the Sunday Post and the Sunday Mail. In addition, Mrs McTear took women's magazines. Mr and Mrs McTear had a television from the time they first moved to their married home. They listened to the radio.
[4.218]This could be tested by reference to the awareness of Mrs McTear. Counsel submitted that on a fair reading of her evidence as a whole she was aware of the link between smoking and lung cancer by 1964. Her first memory was of there being a link between smoking and lung cancer, and this was consistent with the reporting of MRC 1957. It would not come as a surprise: her parents did not smoke, her father was an ex-smoker and was opposed to smoking, and they had warned her that smoking was bad for her. She recalled a switch from plain cigarettes to filters, which was happening as early as 1953, and that it was said that it was a particular problem to smoke right to the end of a cigarette, which was being reported in the press in 1960 and 1962. She was aware of USSG 1964 when it was published. She was advised about the risks of smoking during her first pregnancy, in 1964 to 1965. She recalled an anti-smoking campaign in Paisley, which it could be inferred was the campaign already referred to. She took women's magazines, which were covering smoking and health issues in 1964. She recalled a time when there was talk about banning cigarette advertising on television, which was an issue at about the time of the General Election in January 1964.
[4.219]Counsel submitted that even if Mr McTear was not aware of the risks in 1964 or whenever he started smoking, he did become aware of the health risks associated with smoking, no later than 1971, and in fact the evidence as to when in fact he did become of the health risks, if it was later than when he started smoking, was unclear. He did not say that he was unaware until warnings came on, he simply said that when warnings came on he decided that he would stop at that point.
[4.220]Even if I accepted that Mr McTear was unaware of the link between smoking and lung cancer when he started to smoke, I should reject his evidence that he would not have started to smoke if there had been warnings on packets or in advertisements that smoking could cause fatal diseases and was addictive. In his evidence given on commission he said that he was a reasonably sensible lad and he did not think he would have taken up smoking if he thought all these risks would be involved. For reasons already given, counsel submitted, Mr McTear should not be regarded as a credible and reliable source of any evidence that he might have believed was helpful to his case. It was likely that by August 1963 he was aware of the link between smoking and lung cancer. He contradicted his evidence that he was a reasonably sensible lad later in his evidence when he disclaimed the suggestion that he was sensible when he was younger. Far from being a reasonably sensible lad, counsel submitted, he was repeatedly punished during his Army career for breaches of Army discipline. By the time he had started smoking he had received two criminal convictions from civilian courts. When in the Army he had refused recommended medical treatment following an injury to his hand, notwithstanding being warned of the risks to his health. He had been dishonourably discharged from the Army as a result of his conduct, despite repeated warnings about it. He had lied to his doctor and to the social security authorities in order to obtain sickness benefit for the week of his wedding. Moreover, within two years of the date of his wedding, he was convicted of three offences. He had had three jobs, from each of which he resigned, in two cases after working for only ten days. He resigned from the second of these jobs four months after his eldest child was born, took up the third shortly after she was born and resigned from it after only ten days. He was not a man who at any stage of his life heeded warnings. He was rather a man who in general acted as he wished to act regardless of the consequences to himself or to others.
[4.221] It was unlikely that if a warning had appeared on cigarette packets or in cigarette advertisements that would have affected his decision to smoke. Even when it came to his evidence about having on occasions wanted to give up smoking, it was clear that having spoken to his doctor and having been given advice about measures to adopt, as Mrs McTear put it he did not really try any of them. Against this background, counsel submitted that it should not be held proved that a warning that smoking could cause fatal diseases would have caused Mr McTear not to smoke.
Discussion
(1)General
[4.222]Although I have not of course had the opportunity of assessing Mr McTear's demeanour as a witness, I have nevertheless learnt enough about him to be able to form an impression of his credibility and reliability. I would regard him as a profoundly dishonest man who readily lied in order to obtain advantage for himself. This conclusion is amply supported by the detailed submissions advanced by Mr Jones, which I accept, and which Mr McEachran did not attempt to counter except in relation to Mr McTear's evidence about his smoking history, to which I shall return. Mr McTear appears to have been able to adopt a plausible manner when he lied so that he was, for example, able to obtain employment on a number of occasions by lying about his previous history without this being detected at interview. His plausibility lay in telling people such as prospective employers what he thought they were likely to want to hear. He did not only lie to obtain pecuniary advantage. He concealed the truth from and lied to his own wife about himself, for example about his Army career and about what he intended to do to improve his drunken and violent behaviour towards her. It is not clear to me what the full range of his motives was in putting himself forward as the original pursuer in this action, but since it was an action in which payment of a sum of money to him as damages was concluded for, I see no reason to except it from the generality of my assessment of him as a person who would readily lie for gain. This makes it likely that he was prepared to say what he believed would suit the purposes of ASH as well as himself. Accordingly, I would not be disposed to accept his evidence about his smoking history, about which it would be to his advantage to lie, unless it were at least corroborated by evidence from Mrs McTear which I was prepared to accept as credible and reliable.
[4.223]I have had the opportunity of assessing Mrs McTear's demeanour as a witness, as well as the content of her evidence, which was given over several days. During her cross-examination by Mr Jones, Mr McEachran intervened to object to its length and detail. I repelled the objection (assuming it to be a relevant ground of objection), because the conduct of the cross-examination appeared to me to be entirely proper, not only for ITL's purposes, but also because it was in Mrs McTear's interests that she be given an opportunity to comment on matters which might be brought out in the evidence of subsequent witnesses. Notwithstanding this, at the hearing on evidence, Mr McEachran renewed this criticism, applying to it the expression "a form of abuse". He said that in her evidence-in-chief Mrs McTear admitted Mr McTear's bad employment record, his drink problems and his various convictions. In cross-examination she was taken over his bad employment record in detail, every conviction in detail, his drinking problems in detail, and this must have been a very distressing and harrowing experience for her. It took over three days. When I asked him whether he was alleging that there was anything improper about this cross-examination, Mr McEachran said that a little humanity would have helped. Mrs McTear had accepted the position about Mr McTear in her evidence-in-chief and there was not really much need to go into that much further. In a discussion the next day he withdrew the submission that there had been "a form of abuse" and apologised to Mr Jones.
[4.224]Looking back on this incident, I regret that I did not say something more vigorous than occurred to me at the time. Fair notice was given in the pleadings for ITL that detailed evidence would be led about Mr McTear's previous history, in particular in averments extending over about four pages, from p.26E to p.30E of the Closed Record. These averments were met with a bare denial. If they had been admitted in the same detail, Mr Jones might have felt able to conduct his cross-examination differently. As it was, however, he had no option but to do as he did, which is why I repelled Mr McEachran's objection. The broad way in which Mrs McTear was asked to comment on her husband's previous history in her evidence-in-chief was in my view quite inadequate to serve Mr Jones's legitimate purposes, which included testing Mrs McTear's credibility and reliability in relation to a number of events. I may add that I was left with the impression that there had not been discussion, as might normally be expected, with Mrs McTear in advance of the proof, and preferably before the Record was closed, about these averments; she certainly appeared unprepared for questions during cross-examination, for example questions about Mr McTear's Army record, which was the subject of averments at p.28C to E.
[4.225]In assessing Mrs McTear's credibility and reliability as a witness, I am prepared to accept, without treating it as a criticism of counsel, that she found the experience of giving evidence stressful and tiring. Making allowance for this, however, I regarded her as a poor witness. There appears to me to be much force in Mr Jones's detailed criticisms of her evidence, which I accept. She appeared to me to be willing far too readily to agree with counsel's questions without proper reflection. She was, no doubt understandably in the circumstances, concerned to present her husband's behaviour in as favourable a light as possible. To that end, she took refuge in forgetfulness. I accept that she may during her married life have wished not to remember his bad behaviour; it is hard to see how she could have managed to stay married to him otherwise. But I have to say that I found her to be an unreliable, and in some respects an incredible, witness.
(2)Mr McTear's smoking history
[4.226]The principal difficulty about the evidence of both Mr and Mrs McTear is in deciding what is established about the detail of his smoking history. I am satisfied, in the first place, that advertising had nothing to do with Mr McTear's reasons for starting to smoke. His evidence about the role of advertising, even on the printed page, has an air of glibness about it: he appears to me to have been saying what he knew he was expected to say as the pursuer in a test case. Mrs McTear's evidence does not appear to me to be capable of being viewed in any better light. Of course there was advertising of cigarettes at the time when he started smoking, but in my opinion the proper view of the evidence of both Mr and Mrs McTear is that he (and she) started smoking because it was socially acceptable and most young people started smoking as part of becoming adults. I do not regard advertising as having had any causative influence on Mr McTear.
[4.227]The next difficulty is in deciding how much of ITL's products Mr McTear smoked and when he smoked them. I am prepared to accept the evidence of both Mr and Mrs McTear that he smoked the John Player brand or brands of cigarettes manufactured by ITL for many years, as part of his consumption of cigarettes. Both Mr and Mrs McTear referred quite specifically to the John Player brand. It is, however, agreed by joint minute that John Player Special Filter cigarettes were first introduced to the market on 5 April 1971. There is no recorded use in the evidence before me of the "John Player" brand name before that date. Accordingly, Mr McTear cannot have started smoking the John Player brand of cigarettes in 1964 or shortly thereafter, as he and Mrs McTear both claimed. Their evidence on this matter cannot be right, and it is otherwise so vague that I am not prepared to hold it proved that it was ITL's products that Mr McTear smoked at any time prior to 1971.
[4.228] I am prepared to accept that he did smoke John Player brand cigarettes from the early 1970s onwards. I am not, however, prepared to accept that he smoked them exclusively until the last few years of his life, when he also smoked roll-ups made from Old Holborn tobacco. There was undisputed evidence from Ronald Green and Jane Barlow that he smoked roll-ups well before he claimed to have done. Indeed, Mrs McTear gave evidence to that effect, until she changed it after an adjournment. I found this a most unsatisfactory feature of her evidence. It appeared to me that she was motivated partly to bring her evidence into line with that of her husband, and partly to agree with Mr McEachran when he re-examined her on this point. An additional factor is that when he was in prison on several occasions during the 1980s Mr McTear may well not have had access to John Player brand cigarettes. I conclude therefore that he smoked a significant quantity of roll-ups made from Old Holborn tobacco along with his smoking of John Player brand cigarettes for many years, perhaps as many as twenty years, but I am not able to decide in what proportion he divided his smoking between John Player brand cigarettes and roll-ups. All I can say is that they both made a material contribution to his total consumption from about 1971 onwards.
[4.229]I discuss the topic of "addiction" to tobacco or to nicotine later in this Opinion, at paras.[6.202] to [6.208]. I propose to say a little about it at this stage. Much of course depends on the definition of "addiction". The pursuer offers to prove that tobacco is addictive in the sense that once individuals have started smoking it is difficult for them to wean themselves off the habit. Taking this as the definition for present purposes, I am prepared to accept that Mr McTear found it difficult to wean himself off his habit and in that sense could be described as addicted. I do not, however, accept that he was for this reason unable to stop smoking. On the contrary, he did stop smoking on occasions, one at least of which, in 1971, was for several days. The fact that it affected his temper, so that he was like a bear or a bull with a sore head, goes no further than to reinforce the view that he found it difficult to give up. When he started smoking again, on each occasion when he had tried to stop, he did so, in my view, because he chose to do so. And he gave up smoking, apparently without difficulty when he had an incentive to do so towards the end of his life.
[4.230]I am also satisfied that Mr McTear was aware, in common with the general public, well before 1971 of the publicity about the health risks associated with smoking, and in particular the risk of lung cancer. I accept the reasons advanced by Mr Jones for this. This was also the view of Professor Hastings at para.[5.325]. One important reason for doing so is that there is good reason to think that Mr McTear was well aware that his mother had died of lung cancer in 1963, so he would relate the publicity to his own family circumstances. In addition, Mrs McTear appears to me to have accepted that she was aware of the health risks at least by the time that she was pregnant with their first child in late 1964. I think it unlikely, from what I can tell of their relationship, that she would be aware of such a matter without his also being aware. It appears to me therefore that by the time Mr McTear is shown by acceptable evidence to have started smoking the John Player brand of cigarettes he was already aware of the publicity about the health risks. As with many other aspects of his life, he chose to ignore it.
PART V: THE EXPERT EVIDENCE
[5.1]I turn now to the evidence bearing on the pursuer's averments that cigarette smoking can cause lung cancer, that it did in fact cause Mr McTear's lung cancer, that tobacco is addictive (in the sense defined by the pursuer) and that Mr McTear was addicted to cigarettes. The burden of proving these averments rests, as I have said, on Mrs McTear. The evidence in question is principally that given by expert witnesses called for both parties.
The law applicable to expert witnesses
Submissions for ITL
[5.2]During his concluding submissions, Mr Jones referred to a number of authorities in which the proper approach to the evidence of expert witnesses was discussed. I propose to consider these at this stage, because they are relevant to some of the main issues which I have to resolve.
[5.3]In Lewis, Manual of the Law of Evidence in Scotland (1925), pp.47 to 49, it was stated:
"The term opinion evidence is generally used in the law of evidence in a technical sense, and indicates a species of evidence conveniently described as testimony of experts and regarded as admissible in certain circumstances, the particular limits of which cannot be rigidly defined. Whenever the subject-matter of inquiry is of such a nature that special knowledge is required in order that it may be understood by the tribunal which has to decide on conflicting views, evidence is admissible of ex post facto opinions and theories formed by witnesses possessing peculiar knowledge or skill in the matter in question. The evidence of skilled witnesses or experts is admissible wherever the inquiry involves decision on facts of a technical or scientific nature. The tests of its relevancy are (1) that the opinion is based on the principles of some recognised craft or science in relation to which the witness may be cross-examined on his opinion, and (2) that the subject-matter of the opinion is not such that the tribunal is bound to take judicial notice of it.
The admission of evidence of this description is on the principle recognised in the practice of appointing assessors to sit with the Court in certain cases involving specialised knowledge [...]. The function of such assessors is to supply the judge with the technical or scientific knowledge necessary to enable him to understand and appreciate the evidence given by witnesses in regard to matters beyond the sphere of ordinary knowledge. Such an assessor is neither a judge nor a witness, and there is no obligation on the tribunal to accept his view.
No rule can be laid down beforehand as to what persons may be regarded as qualified to give evidence of opinion, but there should be in the witness an extensive and accurate state of knowledge and experience of the subject involved, derived from study or practice, or both. The special features met with in dealing with this class of evidence as contrasted with the evidence of witnesses to facts in the limited use of the term may be summarised as follows:-
[...] (d)The published opinions of writers on the subject may be adopted by skilled witnesses and so made a part of their evidence. So also a skilled witness may be taken as concurring in his testimony with the opinion expressed in full by a preceding skilled witness."
[5.4]Mr Jones submitted, in light of this, that the purpose of opinion evidence was to help the Court to acquire special knowledge. So the evidence performed an educative function, which was a function of the witness, not some other source simply mediated through the witness as if he were no more than a conduit. Mr Jones further submitted that the words "the subject" referred to the subject in which the witness was skilled, so that while the witness might properly adopt passages from published material in the same field of expertise as his own, it was not open to him to import into his evidence passages from published material in another field. If the Court was to be given a proper understanding of the subject, the witness's evidence must be capable of being tested by cross-examination, which was not possible if the witness had to admit ignorance of the field in which the published material lay.
[5.5]In Davie v Magistrates of Edinburgh 1953 S.C. 34 a number of issues arose in relation to the expert evidence which had been led in that case. At p.40 the Lord President (Lord Cooper) rejected a submission that, where no counter evidence on the science in question had been adduced for the pursuer, the Court was bound to accept the conclusions of an expert witness for the defenders, saying that this view was "contrary to the principles in accordance with which expert opinion evidence is admitted". He went on to explain these principles, as follows:
"Expert witnesses, however skilled or eminent, can give no more than evidence. They cannot usurp the functions of the jury or Judge sitting as a jury, any more than a technical assessor can substitute his advice for the judgment of the Court [...]. Their duty is to furnish the Judge or jury with the necessary scientific criteria for testing the accuracy of their conclusions, so as to enable the Judge or jury to form their own independent judgment by the application of these criteria to the facts proved in evidence. The scientific opinion evidence, if intelligible, convincing and tested, becomes a factor (and often an important factor) for consideration along with the whole other evidence in the case, but the decision is for the Judge or jury. In particular the bare ipse dixit of a scientist, however eminent, upon the issue in controversy, will normally carry little weight, for it cannot be tested by cross-examination nor independently appraised, and the parties have invoked the decision of a judicial tribunal and not an oracular pronouncement by an expert."
At p.41, the Lord President said, in relation to the use made by the Lord Ordinary of passages in a publication referred to by an expert witness for the defenders, some of which inter alia not been put to the witness:
"I do not think that he was entitled to do so. Passages from a published work may be adopted by a witness and made part of his evidence or they may be put to the witness in cross-examination for his comment. But, except in so far as this is done, the Court cannot in my view rely upon such works for the purpose of displacing or criticising the witness's testimony."
[5.6]Mr Jones submitted that this reflected the principle, which also underlay the proposition that it was not open to an expert witness to rely on passages in published material which did not lie within his field of expertise, that the court could not have regard to any passage in any publication which had not been put to a suitably qualified expert in the course of his evidence. He also founded on a passage in the opinion of Lord Russell at p.42, who said, in rejecting a submission that the evidence of an expert witness required to be corroborated:
"The opinion expressed by an expert witness in any branch of technical science depends for its effect on, inter alia, his qualifications, skill and experience in that science. If it appears to be based on a sufficiency of research directed accurately and relevantly to a particular issue and to be so supported as to convince a Court of its fundamental soundness and applicability to the particular issue, a Court is entitled, although not obliged, to accept it, even if unsupported by any corroborative expert opinion. Secondly the defenders argued that in the absence of any counter evidence of expert opinion in the science professed by [the expert witness for the defenders] the Court is bound to take his opinion as conclusive, and as decisive of the issue. I am clearly of opinion that that argument must be rejected as being contrary to the principles by which the rules of evidence are regulated, and as constituting an unwarrantable encroachment on the judicial function of the Court. I respectfully agree with your Lordship's observations on that topic and would only had to the authorities cited by your Lordship a reference to Lewis on Evidence (at pp. 47-49)."
[5.7]It may be noted in passing that since the enactment of the Law Reform (Miscellaneous Provisions)(Scotland) Act 1968, s.9, in relation to personal injury actions, and the Civil Evidence (Scotland) Act 1988, s.1, in relation to all civil actions, there is in any event no requirement for corroboration, so there would be even less force now to a submission that the evidence of an expert witness requires to be corroborated. Apart from this, what was said in Davie v Magistrates of Edinburgh about the function of expert witnesses remains unaffected by any subsequent development in the law.
[5.8]Another textbook to which Mr Jones made reference was Wilkinson, The Scottish Law of Evidence (1986), pp.65 to 66, in which the author, under reference to the passage in the opinion of the Lord President in Davie which I have already quoted, stated:
"The point that Lord President Cooper was concerned to make is sometimes overlooked. The function of the expert is not to present ready-made conclusions but to provide the tribunal of fact with material on which it can reach its own conclusions. The decision on the various issues in the case, including the issues of fact in the resolution of which the expert may assist, is for the judge or jury. The expert must not usurp their function. On the basis of that perception, it has been said 'a question is inadmissible if its purpose is to elicit an opinion on the actual issue before the court'. The principle is reasonably clear and intelligible. Judges and juries have their functions and experts have theirs. The expert who crosses the line dividing these functions ceases to assist, and usurps. [...] While court or jury are to be furnished with criteria on which to make their independent judgment it is clear that that judgment is to be applied to conclusions which experts have themselves reached. The court will inevitably want to know how the expert has applied the criteria to the facts in order to reach his conclusion. There is, therefore, much ground which both the expert and court or jury must traverse together. The problem of whether a particular question or piece of evidence transgresses unacceptably on the province of judge or jury does not admit of an easy answer."
[5.9]Mr Jones went on to refer to further cases. In National Justice Compania Naviera S.A. v Prudential Assurance Co. Ltd ("The Ikarian Reefer") [1993] 2 Lloyd's Rep.68, Cresswell J. said at p.81:
"The duties and responsibilities of expert witnesses in civil cases include the following:
1.Expert evidence presented to the Court should be, and should be seen to be, the independent product of the expert uninfluenced as to form or content by the exigencies of litigation [...].
2.An expert witness should provide independent assistance to the Court by way of objective unbiased opinion in relation to matters within his expertise [...]. An expert witness in the High Court should never assume the role of an advocate.
3.An expert witness should state the facts or assumption upon which his opinion is based. He should not omit to consider material facts which could detract from his concluded opinion [...].
4.An expert witness should make it clear when a particular question or issue falls outside his expertise.
5.If an expert's opinion is not properly researched because he considers that insufficient data is available, then this must be stated with an indication that the opinion is no more than a provisional one [...]. In cases where an expert witness who has prepared a report could not assert that the report contained the truth, the whole truth and nothing but the truth without some qualification, that qualification should be stated in the report [...]." (I have omitted from this quotation references to other cases.)
This passage was quoted with approval by Lord Caplan in Elf Caledonia Ltd v London Bridge Engineering Ltd, 2 September 1997, unreported, at pp.224-225, where it was described as a "helpful and correct" formulation of an expert's duties.
[5.10]Lord Caplan also referred to John Pierce v Her Majesty's Advocate 1981 S.C.L.R. 783, in which a forensic scientist who had been called as an expert witness at a criminal trial had made an assumption, which was not justified, and he had not disclosed the making of the assumption to the court. The Lord Justice-General (Lord Emslie) (in a passage omitted in the report) said, in concluding that the witness had been discredited, not only as a scientist, but also as a witness upon the accuracy, fairness and objectivity and of whose evidence reliance could be placed:
"This was in our judgment, conduct on the part of an expert witness which demonstrated a complete misunderstanding of the role of scientific witnesses in the Courts, and a lack of the essential qualities of accuracy and scientific objectivity which are normally to be taken for granted."
[5.11]In Dingley v The Chief Constable, Strathclyde Police 1998 S.C. 548, 2000 S.C. (H.L.) 77, the Lord President (Lord Rodger of Earlsferry) at p.555 of the 1998 report referred to the opinion of the Lord President in Davie v Magistrates of Edinburgh, which he described as affording "[a]uthoritative guidance on the approach which a court should take to expert evidence". After quoting the above passage, he said:
"Perhaps the essential point is that parties who come to court are entitled to the decision of a judicial tribunal. Such a decision may take account of many rather intangible things such as the demeanour of witnesses and the way that they gave their evidence, but, whatever its components may be, such a decision must be reasoned. As Lord Cooper says, an oracular pronouncement will not do."
Lord Rodger also said that the Lord Ordinary required to test the experts' evidence and, having done so, to use those parts which he accepted and apply them to the facts of the case. If he did not do so it must be inferred that he misdirected himself. Lord Prosser said at p.604:
"I would wish to make two other general observations, before turning to the issues between the parties. First, there was a certain amount of evidence to the effect that certain views on causation were very widely held, or were no longer widely held. If a particular process of reasoning is widely accepted, then that I think may be persuasive for a court. But the fact that a particular view is widely held, without any persuasive explanation as to why it should be so held, and constitute a conclusion, does not appear to me to be a matter to which a court should give significant weight. Rather similarly, the fact that a particular view was or is held by someone of great distinction, whether he is a witness or not, does not seem to me to give any particular weight to his view, if the reasons for his coming to that view are unexplained, or unconvincing. As with judicial or other opinions, what carries weight is the reasoning, not the conclusion."
Submissions for Mrs McTear
[5.12]Mr McEachran, while not disputing the principles to be derived from the foregoing authorities, placed reliance on the decision of the Second Division in Main v Andrew Wormald Ltd 1988 S.L.T. 141, in which one of the issues in the reclaiming motion related to the entitlement of the medical witnesses in a case relating to asbestosis to rely on epidemiological literature. The Lord Justice-Clerk (Lord Ross) said at p.142:
"In my opinion, the medical witnesses in this case were entitled to refer to medical literature, and in particular they were entitled to refer to published papers by epidemiologists even though they themselves were not epidemiologists. All the medical witnesses in this case were experts in chest disorders. They were there thus fully entitled to have regard to medical literature bearing upon that subject. Of course, where a medical witness has made reference to the published views of epidemiologists, it must be kept in mind that these views of epidemiologists have not been subjected to testing by cross examination."
The Lord Justice-Clerk then referred to various authorities, including Davie and R. v Abadom [1983] 1 W.L.R. 126, in the latter of which Kerr L.J. said, at p.129:
"In the context of evidence given by experts it is no more than a statement of the obvious that, in reaching their conclusion, they must be entitled to draw on material produced by others in the field in which their expertise lie."
The Lord Justice-Clerk went on to say:
"I am accordingly satisfied that the medical witnesses were entitled to refer to the views of epidemiologists, and to adopt their views. On the other hand, it must be borne in mind that the authors of the articles were not examined as witnesses and were not cross examined. Furthermore, as Lord President Cooper observed in Davie, except in so far as a witness had adopted a passage from a published work, the court cannot rely upon the published work for the purpose of displacing or criticising the witness' testimony. Moreover, where a witness has adopted a particular passage from a published work, the court is entitled to determine whether the reasoning in the particular passage appears to be reasonable and convincing or not."
[5.13]Lord Dunpark, after reference to the authorities, concluded by saying, at p.143:
"The pursuers' doctors' evidence, based, it seems to me, primarily if not solely upon these epidemiological studies, was that the greater the exposure to asbestos dust inhalation, the greater the risk of contracting lung cancer; but that does not answer the crucial question, namely, whether asbestos exposure per se is a likely cause of lung cancer in the absence of any lung damage which could be associated with asbestos inhalation.
Nevertheless, I am of opinion that the relationship between asbestos exposure and lung cancer was sufficiently within the field of the pursuers' doctors to enable them professionally to refer to studies on this subject; but the real question is whether they drew the correct inference from them."
Lord McDonald said, also at p.143:
"It is, in my opinion, clear that an expert witness may in the course of his evidence, make reference to passages from a published work and adopt these as part of his evidence [...]. There are, however, limits to this practice. One is that the expert witness must first have testified specifically to his own direct experience in the field in question. Having done that he is entitled to supplement his evidence by reference to recognised published works [...]. It is essential, however, that the introduction of the literature be preceded by firm evidence from the expert as to his personal experience in the specialist field concerned. If this is not so there is a real danger that the literature becomes the primary evidence and is given a status it should not acquire unless spoken to by a witness directly responsible for its contents."
[5.14]Mr McEachran submitted that I should take from Main the proposition that an expert witness who was a clinician was entitled to have regard to epidemiological publications. It was plain common sense. Clinicians must look at the general information that was available. Main decided that where chest consultants gave evidence, they were entitled to refer to published papers by epidemiologists, because if they were confined to what they themselves had experienced, that would be ludicrous. They must be able to refer to what they read in the British Medical Journal "and things like that" as forming their overall opinions and information.
Discussion
[5.15]I do not accept that Main yields such a general proposition. Nor could it do so: the question is one of fact, not of law. It may well be that on the evidence in that case it was a correct conclusion to draw that published papers by epidemiologists formed part of the medical literature to which those particular medical witnesses were entitled to refer. But in the passages I have quoted there is repeated reference to the requirement that the published material must lie within the field of expertise of the witness. It therefore appears to me to be a question of fact to be decided on the evidence in a particular case whether or not published material which had been put to an expert witness did or did not lie within his field of expertise.
[5.16]I note, moreover, that in a passage in the Lord Justice-Clerk's opinion which is not reported in the published report, but is on pp.73-74 of the version provided to me from the reclaiming print, the Lord Justice-Clerk held that the reasoning of the Lord Ordinary in that case was flawed in respect that he appeared to have accepted what the pursuer's medical witnesses said about a report of the Industrial Injuries Advisory Council without himself applying any critical analysis to the passages in that document which were relied upon. The Lord Ordinary was not obliged to accept a passage referred to by one of the witnesses as the expression of reliable opinion, nor was he obliged to accept the witness's view that what was stated in the passage was correct: the Lord Ordinary was entitled and indeed bound to consider whether what was stated in it was convincing. In the Lord Justice-Clerk's opinion, the proper conclusion was that reliance could not be placed upon it in the context of that case. Among other reasons, one reason was that the authors of the report put forward, as a ground for believing that an association was likely to exist between asbestos exposure and lung cancer in the absence of intervening asbestosis, that research had shown that the incidence of lung cancer deaths among asbestos workers was directly related to total asbestos dust exposure. No detail was given regarding this research, and the result must be, the Lord Justice-Clerk said, that the basis upon which the conclusion of the report was based had not been established before the court. This of course was a view expressed in relation to the evidence in that case, but I have quoted it because it is a clear demonstration of the application to that evidence of the general principles relating to the evidence of expert witnesses.
[5.17]I accept Mr Jones's submissions on this matter. Having regard to all the authorities referred to above, I conclude that it is necessary to consider with care, in respect of each of the expert witnesses, to what extent he was aware of and observed his function. I must decide what did or did not lie within his field of expertise, and not have regard to any expression of opinion on a matter which lay outwith that field. Where published literature was put to a witness, I can only have regard to such of it as lay within his field of expertise, and then only to such passages as were expressly referred to. Above all, the purpose of leading the evidence of any of the expert witnesses should have been to impart to me special knowledge of subject-matter, including published material, lying within the witness's field of expertise, so as to enable me to form my own judgment about that subject-matter and the conclusions to be drawn from it. As will be seen, this is of particular importance in the field of epidemiology, since it is generally agreed that where an association is found, such as that between cigarette smoking and lung cancer, it is ultimately a question of judgment whether the evidence is sufficient to establish a causal relationship. I shall of course return to this theme later.
[5.18]Another matter which I propose to mention at this stage, and to which I shall also return, is the need for expert witnesses to be independent. I must decide in relation to each of the expert witnesses whether, and if so to what extent, he may have been acting as an advocate rather than providing independent assistance to the court. As I understand it, all the expert witnesses for the pursuer provided their services without remuneration. Three of them (Professor Friend, Professor Sir Richard Doll and Professor Hastings) were or had been connected in one way or another with ASH, and were clearly committed to the anti-smoking cause; and no doubt for this reason were prepared to give evidence gratis. This is not in itself a criticism of any of them, but it does in my opinion justify scrutiny of each of their evidence, so as to see to what extent they complied with their obligations as independent expert witnesses and how soundly based their views were. By contrast, all the expert witnesses for ITL charged fees for their services. This is generally the case: expert witnesses are usually professional people who would normally be expected to seek appropriate remuneration for research, preparation of reports and attendance at court. Mr McEachran put it to three of these witnesses that they were being "handsomely" paid for giving evidence. I have no basis for saying that any of their fees were not properly charged. In discussion at the hearing on evidence, Mr McEachran maintained that I had to be very careful with witnesses whose research was funded by the tobacco industry and who were paid handsome fees. There was the danger that this might induce bias, and I should look critically at such evidence. I do not accept as an a priori assumption that funding from the tobacco industry is tainted. Everything depends on the independence of the researcher and the quality of the research; and it may well be that ample funding leads to sound research. The question, however, remains for consideration whether the expert witnesses for ITL complied with their obligations as independent expert witnesses and how soundly based their views were.
[5.19]I would ask the reader to bear all these considerations in mind when turning, as I do now, to an account of the evidence given by the expert witnesses.
The evidence of expert witnesses: (1) Expert witnesses for Mrs McTear
Dr Sheila McCarroll
[5.20]Mr McEachran sought to rely on Dr McCarroll, Mr McTear's GP, for her opinion as an expert witness as well as for her evidence about Mr McTear's medical history (see paras.[4.67] to [4.84]). She held the qualifications of MB, ChB and had been a GP for eighteen years. In her letter of 20 November 2003 she wrote:
"All of the teaching I received over the years leads me to believe that this was as a direct result of smoking. [...]
I can certainly say from my experience as a doctor and all the teaching I have received, that my general view is that smoking does cause lung cancer and it is likely that Mr McTear died from lung cancer that was as a result of cigarette smoking."
[5.21]She said in evidence that the teaching she had received at medical school was categorically that smoking was the main cause of lung cancer. It was her considered view that smoking caused lung cancer and that it was likely that Mr McTear died from lung cancer caused by cigarette smoking. She believed that Mr McTear was a heavy smoker. She had had other patients who developed lung cancer, the majority of whom had been smokers. It was difficult to generalise, but probably most of them smoked at least twenty cigarettes a day. Many of them tried to give up, but most of them found it very difficult, she supposed because of the addictive nature of the substance. Dr McCarroll said that during her career as a GP there had been a constant public health message about smoking, which was: "Don't, because it is bad for your health". She was aware of this as a result of messages from the Government and constant advice from various sources advising people to stop smoking. She read medical journals, probably the British Medical Journal.
[5.22]Dr McCarroll was asked about Callum 1998. She said that she was aware of the publishers, the Health Education Authority. She would probably have had "something like this" in her surgery. She said that she was aware of statements in the publication that in 1995 smoking caused more than 120,000 deaths of people in the United Kingdom aged 35 years or more, that more than 80,000 men died on account of their smoking, that the United Kingdom death rate was 23% higher than it would have been in the absence of smoking and that nine out of ten lung cancer deaths among men were caused by smoking.
[5.23]Dr McCarroll was also asked about UKWP 1998, entitled "Smoking Kills". She said that this was the message she had been receiving in her surgery. She was aware of statements in the White Paper that the death rate in Britain from smoking related disease was more than 120,000 a year, that smoking was dangerous at any age but the younger people were when they started the more likely they were to smoke for longer and to die earlier from smoking, that tobacco was a uniquely dangerous product and that if introduced today it would not stand the remotest chance of being made legal.
Cross-examination of Dr Sheila McCarroll
[5.24]In cross-examination, Dr McCarroll said that her view that it was likely that Mr McTear died from lung cancer that was as a result of cigarette smoking was based on her understanding that smoking was the main cause of lung cancer and that Mr McTear was a smoker. She was taught at medical school that smoking was a major cause of lung cancer. For many years it had been a consistent public health message that smoking was a major cause of lung cancer. She had no reason in the course of her practice to examine that proposition critically. She had not made a detailed study of the epidemiological literature on the subject of smoking and lung cancer, or of the literature on the subject of carcinogenesis as it related to smoking and lung cancer.
[5.25]Dr McCarroll was asked about Peto and Doll 1992. In this communication the authors wrote:
"The recently proposed change in death certification rules, whereby deaths attributed to tobacco would no longer automatically be referred to a coroner, will lead to a number of death certificates attributing death to tobacco. There is, however, little reason to expect that it will be the correct number, for there are substantial scientific difficulties in assessing the external causes of any one particular death from the main chronic diseases to which the use of tobacco can sometimes lead. These difficulties can, of course, be circumvented by using appropriate epidemiological methods when assessing the proportion of deaths that is attributable to tobacco in a population. But for most deaths that were in fact due to tobacco there is no reliable way to know that those particular deaths were due to tobacco. Consider, for example, 1000 habitual smokers who die of myocardial infarction at about 65 years of age. Even though the epidemiologist may be able to say with confidence that about half of these 1000 deaths were due to tobacco, there would be no way for the medical practitioners certifying those deaths to know which ones to attribute to the habit. Should all be attributed, should none be attributed, or should about half be attributed - and, if half, which ones?"
In light of this passage, Dr McCarroll accepted that where there was a statistical association between smoking and a disease there would be no way for the medical practitioners certifying deaths to know which of the incidences of these diseases to attribute to the habit.
[5.26]Asked about her evidence that she had patients who found it difficult to give up smoking, Dr McCarroll said that she assumed that people who found it easy to give up smoking were unlikely to attend for advice about smoking. It had been the public health message for many years that smoking was difficult to give up, and indeed had been the public health message for some time that nicotine was addictive. She had no reason to examine these propositions critically and had not made any detailed study of the literature on the question of addiction and smoking.
Professor James Friend
[5.27]Professor Emeritus James Friend was aged 65. He graduated from Cambridge University with the degree of BA in 1959 and from Edinburgh University with the degree of MB, ChB in 1962. He became a Member of the Royal College of Physicians of Edinburgh in 1965 and a Fellow of that body in 1977. After holding posts at Edinburgh and Oxford, from 1973 until he retired in June 2002 he was Consultant in Thoracic Medicine, Grampian Health Board, and Aberdeen Royal Hospital NHS Trust. He was Clinical Professor in Medicine and Therapeutics at the University of Aberdeen from 1998 to 2002. In his CV he listed numerous publications of which he was author or joint author. Among his current appointments, he had been Chairman of the Government Scientific Committee on Tobacco and Health since 2000, a Member of the National Cancer Task Force of the Department of Health, also since 2000, and Chairman of the Tobacco Policy Review Group for Grampian Health Board.
[5.28]Professor Friend explained that as a consultant in thoracic medicine he had been in what was very much a full-time National Health Service post, looking after people with respiratory diseases in Grampian, Orkney and Shetland. This was a responsibility shared initially with only one other colleague, looking after the respiratory consultant needs of a population of over 500,000 people. In the course of his work he had come into contact with a great many patients with lung cancer. The primary diagnosis of lung cancer was usually made by respiratory physicians, and the treatment was usually conducted by other consultants. In any given year in the Grampian area the diagnosis of lung cancer was made in 300 to 400 patients. Initially he would have been involved in seeing perhaps half of these patients, 150 to 200 in a given year. Later on, as the staffing of his department increased, there were probably rather fewer that he saw personally, but still perhaps seventy or eighty in each year of the latter part of his career. So he estimated that he had seen about 3,000 patients with lung cancer during his clinical career in Aberdeen.
[5.29]Professor Friend said that the presence of squamous dysplasia was a pre-malignant change often found in heavy smokers who went on to develop lung cancer. He was not a pathologist, but in Aberdeen they would frequently take samples from patients with lung cancer in whom, in other areas of the lung biopsies, there was squamous dysplasia, a change which pathologists recognised as often being a prelude to malignant change. Squamous dysplasia was frequently found in heavy smokers with lung cancer. Although tumours of squamous type could originate from other tissues (such as skin, bladder or oesophagus), none of these would present as a secondary tumour in the lung in this particular way, with bronchial obstruction and haemoptysis as the initial developments, as they had been in Mr McTear's case. In his view a secondary tumour from another source would not have presented in this manner, and a primary tumour originating in the lung was without doubt the cause of Mr McTear's condition. In Professor Friend's view, Mr McTear was investigated and treated appropriately, but given that the tumour was not removable by surgery, his subsequent death was inevitable.
[5.30]On the question of causation, Professor Friend's opinion was that Mr McTear developed a primary lung cancer as a result of his smoking habit. The histological type of cancer diagnosed, of squamous cell type, was of the type where the association with smoking was particularly strong, as it was in so-called small cell carcinoma. This was his own experience as a consultant, that people with lung cancer who were smokers had, in the majority of cases, squamous cell or small cell carcinomas. The diagnosis of squamous cell lung cancer in non-smokers was exceptional, and it could be argued that some of these unusual patients might have contracted the disease through the inhalation of tobacco smoke in the home or at work, despite not being active smokers themselves. It was stated that Mr McTear had started smoking in around 1964 at the age of about 20 years, and appeared to have smoked up to sixty cigarettes daily from that time until he stopped smoking a number of weeks prior to the diagnosis of lung cancer, so that he smoked heavily for approximately twenty-eight years. (Professor Friend said that he would regard smoking more than twenty cigarettes a day as heavy smoking.)
[5.31]Tobacco smoke, he said, contains known carcinogens. A carcinogen was a chemical or a substance which had been demonstrated by a variety of techniques to cause malignant change in cells or tissues. The prevalence of lung cancer was closely related to the level of consumption, and epidemiological data provided clear links between historical smoking levels in different countries and lung cancer incidence. There was also a dose-response relationship between an individual's cigarette consumption and the risk of developing lung cancer. Professor Friend said that the literature demonstrated that, for instance, people who smoked less than ten cigarettes a day had a relatively lower risk of developing lung cancer, although it was in excess of the risk of a life-long non-smoker. The risk was further increased by smoking between ten and twenty cigarettes a day, and the highest risk of all was smoking more than twenty cigarettes a day. There was a clear relationship between the number of cigarettes smoked per day and the likelihood of developing lung cancer. This was demonstrated very clearly in the British Doctors Study, "which I am sure we will hear more about in later days". So someone like Mr McTear was at very high risk. Gender differences in lung cancer risk could also be largely explicable on the basis of smoking habits. In heavy smokers who ceased to smoke, the risk of subsequent development of lung cancer steadily diminished, so that within fifteen years of ceasing smoking, the risks of developing lung cancer were little more than in the life-long non-smoking population.
[5.32]Not all smokers would develop lung cancer; it had been estimated that about 16% of smokers who continued to smoke would develop lung cancer before they reached the age of 75 years. Although cigarette smoking was not the only risk for lung cancer, and occupational exposures to substances such as asbestos, various metals, hydrocarbons, radiation and diet had all been identified as potential risk factors, the proportion of lung cancer mortality attributable to smoking was estimated in RCP 2000, p.17, Table 1.2, to be 89% in males in the UK. In Callum 1998, for which data on mortality and smoking had been provided by the Office for National Statistics, the General Register Office for Scotland, the General Register Office for Northern Ireland and Northern Ireland Statistics and Research Agency, it was stated at p.26 that nine in ten deaths from lung cancer among men were estimated to have been caused by smoking, and Table 5.2 on p.27 gave a figure of 90% as the percentage of deaths from lung cancer in men estimated to be caused by smoking in the United Kingdom in 1995. Professor Friend said that the rate of lung cancer among men had been relatively static throughout the time that he had been in consultant practice, with a slight reduction latterly, but among women there had been a very observable increase in the prevalence of lung cancer. He believed that this increase was a consequence of the history of women's smoking habits. Many of them started smoking during and after the Second World War, whereas, for men, the habit became particularly prevalent during the First World War.
[5.33]Professor Friend continued by stating that smoking was considered to be a major cause of lung cancer, not merely a statistical association, and this view had been widely accepted by all the medical profession world-wide with only a tiny number of exceptions. There was a very extensive literature on the subject which left no significant room for doubt on the importance of smoking as a major cause of lung cancer. He had been the President of both the British Thoracic Society and the Scottish Thoracic Society, and of the 500 or 600 respiratory physicians in the UK, he had never met any who believed other than that smoking was a major cause of lung cancer.
[5.34]Professor Friend was asked to comment on a number of passages in IARC 1986. He was asked to notice that the monograph extended to about 400 pages, of which the list of references took up about sixty pages, referring to more than 1,000 publications. There were twenty-eight members of the working group, from a number of different countries. Professor Friend said he was not familiar with many of the names, and he did not know how they were selected, but the names he did recognise, mainly from the United Kingdom and Australia, were people whose reputation was enormously high and valued and who were respected academics. He thought that a document of this sort was very persuasive and important. The World Health Organization International Agency for Research on Cancer (IARC) had been established to examine issues related to cancer and had published over eighty separate monographs on a variety of issues on a worldwide basis. He would regard the monographs as of very high standing.
[5.35]Passages in the preamble to IARC 1986 were read out to Professor Friend. At p.15 the working group referred to the criteria which had been adopted by working groups whose deliberations resulted in monographs published by IARC. They continued:
"The objective of the programme is to elaborate and publish in the form of monographs critical reviews of data on carcinogenicity for chemicals, groups of chemicals, industrial processes and other complex mixtures to which humans are known to be exposed, to evaluate the data in terms of human risk with the help of international working groups of experts, and to indicate where additional research efforts are needed. These evaluations are intended to assist national and international authorities in formulating decisions concerning preventive measures."
[5.36]At p.16 the working group stated:
"The IARC Monographs are recognized as an authoritative source of information on the carcinogenicity of environmental and other chemicals. [...] The chemicals (natural and synthetic [...]) and complex exposures are selected for evaluation on the basis of two main criteria: (a) there is evidence of human exposure, and (b) there is some experimental evidence of carcinogenicity and/or there is some evidence or suspicion of a risk to humans."
[5.37]At pp.16-17 the working party stated:
"4.WORKING PROCEDURES
Approximately one year in advance of a meeting of a working group, a list of the substances or complex exposures to be considered is prepared by IARC staff in consultation with other experts. Subsequently, all relevant biological data are collected by IARC; recognized sources of information on chemical carcinogenesis and on-line systems such as CANCERLINE, MEDLINE and TOXLINE are used in conjunction with US Public Health Service Publication No. 149(8). Bibliographical sources for data on mutagenicity and teratogenicity are the Environmental Mutagen Information Center and the Environmental Teratology Information Center, both located at the Oak Ridge National Laboratory, TN, USA.
The major collection of data and the preparation of first drafts for the sections on chemical and physical properties, on production and use, on occurrence, and on analysis are carried out by Tracor Jitco, Inc., and its subcontractor, Technical Resources, Inc., both in Rockville, MD, USA, under a separate contract with the US National Cancer Institute. Most of the data so obtained refer to the USA and Japan; IARC attempts to supplement this information with that from other sources in Europe. Representatives from industrial associations may assist in the preparation of sections describing industrial processes.
Six months before the meeting, articles containing relevant biological data are sent to an expert(s), or are used by IARC staff, to prepare first drafts of the sections on biological effects. The complete drafts are then compiled by IARC staff and sent, prior to the meeting, to all participants of the Working Group for their comments.
The Working Group meets in Lyon for seven to eight days to discuss and finalize the texts of the monographs and to formulate the evaluations. After the meeting, the master copy of each monograph is verified by consulting the original literature, edited by a professional editor and prepared for reproduction. The aim is to publish monographs within nine months of the Working Group meeting. Each volume of monographs is printed in 4000 copies for distribution to governments, regulatory agencies and interested scientists. The monographs are also available via the WHO Distribution and Sales Service.
These procedures are followed for the preparation of most volumes of monographs, which cover chemicals and groups of chemicals; however, they may vary when the subject matter is an industry or life-style factor.
5.DATA FOR EVALUATIONS
With regard to biological data, only reports that have been published or accepted for publication are reviewed by the working groups, although a few exceptions have been made: in certain instances, reports from government agencies that have undergone peer review and are widely available are considered. The monographs do not cite all of the literature on a particular chemical or complex exposure: only those data considered by the Working Group to be relevant to the evaluation of carcinogenic risk to humans are included.
Anyone who is aware of data that have been published or are in press which are relevant to the evaluations of the carcinogenic risk to humans of chemicals or complex exposures for which monographs have appeared is asked to make them available to the Unit of Carcinogen Identification and Evaluation, Division of Environmental Carcinogenesis, International Agency for Research on Cancer, Lyon, France.
6.THE WORKING GROUP
The tasks of the Working Group are five-fold: (a) to ascertain that all data have been collected; (b) to select the data relevant for evaluation; (c) to ensure that the summaries of the data enable the reader to follow the reasoning of the Working Group; (d) to judge the significance of the results of the experimental and epidemiological studies; and (e) to make an evaluation of the carcinogenicity of the chemical or complex exposure."
Professor Friend said that this was an appropriate way to review in a responsible manner a large amount of data.
[5.38]At pp.17-18 the working group continued:
"The widely accepted meaning of the term 'chemical carcinogenesis', and that used in these monographs, is the induction by chemicals (or complex mixtures of chemicals) of neoplasms that are not usually observed, the earlier induction of neoplasms that are commonly observed, and/or the induction of more neoplasms than are usually found - although fundamentally different mechanisms may be involved in these three situations. Etymologically, the term 'carcinogenesis' means the induction of cancer, that is, of malignant neoplasms; however, the commonly accepted meaning is the induction of various types of neoplasms or of a combination of malignant and benign tumours. In the monographs, the words 'tumour' and 'neoplasm' are used interchangeably."
[5.39]At pp.18-23 the working group referred to experimental evidence, under headings relating to evidence for carcinogenicity in experimental animals and evidence for activity in short-term tests. At pp.23-24 the working group then discussed the evaluation of carcinogenicity in humans. In this passage, they stated:
"Evidence of carcinogenicity can be derived from case reports, descriptive epidemiological studies and analytical epidemiological studies.
An analytical study that shows a positive association between an exposure and a cancer may be interpreted as implying causality to a greater or lesser extent, on the basis of the following criteria: (a) There is no identifiable positive bias. (By 'positive bias' is meant the operation of factors in study design or execution that lead erroneously to a more strongly positive association between an exposure and disease than in fact exists. Examples of positive bias include, in case-control studies, better documentation of the exposure for cases than for controls, and, in cohort studies, the use of better means of detecting cancer in exposed individuals than in individuals not exposed.) (b) The possibility of positive confounding has been considered. (By 'positive confounding' is meant a situation in which the relationship between an exposure and a disease is rendered more strongly positive than it truly is as a result of an association between that exposure and another exposure which either causes or prevents the disease. An example of positive confounding is the association between coffee consumption and lung cancer, which results from their joint association with cigarette smoking.) (c) The association is unlikely to be due to chance alone. (d) The association is strong. (e) There is a dose-response relationship.
In some instances, a single epidemiological study may be strongly indicative of a cause-effect relationship; however, the most convincing evidence of causality comes when several independent studies done under different circumstances result in 'positive' findings. [...]
[I]t must be recognized that the probability that a given study can detect a certain effect is limited by its size. This can be perceived from the confidence limits around the estimate of association or relative risk. In a study regarded as 'negative', the upper confidence limit may indicate a relative risk substantially greater than unity; in that case, the study excludes only relative risks that are above the upper limit. This usually means that a 'negative' study must be large to be convincing. Confidence in a 'negative' result is increased when several independent studies carried out under different circumstances are in agreement. Finally, a 'negative' study may be considered to be relevant only to dose levels within or below the range of those observed in the study and is pertinent only if sufficient time has elapsed since first human exposure to the agent. Experience with human cancers of known etiology suggests that the period from first exposure to a chemical carcinogen to development of clinically observed cancer is usually measured in decades and may be in excess of 30 years."
Professor Friend said that this was in accordance with his experience.
[5.40]The working group continued:
"The evidence for carcinogenicity from studies in humans is assessed by the working group and judged to fall into one of four groups, defined as follows:
(1)Sufficient evidence of carcinogenicity indicates that there is a causal relationship between the exposure and human cancer.
(2)Limited evidence of carcinogenicity indicates that a causal interpretation is credible, but that alternative explanations, such as chance, bias or confounding, could not adequately be excluded.
(3)Inadequate evidence of carcinogenicity, which applies to both positive and negative evidence, indicates that one of two conditions prevailed: (a) there are few pertinent data; or (b) the available studies, while showing evidence of association, do not exclude chance, bias or confounding.
(4)No evidence of carcinogenicity applies when several adequate studies are available which do not show evidence of carcinogenicity."
[5.41]At pp.24-25 the working group discussed the relevance of experimental data to the evaluation of carcinogenic risk to humans. They stated:
"Information compiled from the first 38 volumes of the IARC Monographs [of which IARC 1986 was the then most recent] shows that, of the chemicals or groups of chemicals now generally accepted to cause or probably to cause cancer in humans, all of those that have been tested appropriately produced cancer in at least one animal species. For several of the chemicals [...], evidence of carcinogenicity in experimental animals preceded evidence obtained from epidemiological studies or case reports."
[5.42]In the general introduction, at p.38, the working group stated that the idea that lung cancer might be caused by smoking occurred to many people independently, particularly after it began to appear that the disease was increasing in incidence. Much of the early evidence, they stated, was occupational in character. Very little attention was paid to any of this evidence or to other case-control studies until 1950 when five case-control studies were reported, including Doll and Hill 1950. For four diseases, including cancer of the lung, the association with smoking had attracted a great deal of attention and had been investigated in many different ways. Case-control and cohort studies were, for the most, in complete agreement in differentiating the diseases and causes of death that were associated with smoking from those that were not. For six diseases, the evidence suggested that practically the whole of the difference in mortality between smokers and life-long nonsmokers was due to tobacco. These were listed in Part A of Table 1 on p.40. Reasonable proportions to attribute to smoking would be about 85% of the deaths due to cancer of the lung, chronic obstructive lung disease and aortic aneurysm, and 25% of the deaths due to ischaemic heart disease. Professor Friend did not comment on these statements.
[5.43]In Table 15, on pp.72 and 73, figures were given for proportions of tobacco use for various forms of tobacco consumption in selected countries in 1923, 1953 and 1973, in millions of kg. For the United Kingdom, the figures for cigarettes were 34.1, 90.2 and 103.9 in these three years.
[5.44]At p.126 a chapter on the chemistry and analysis of tobacco smoke was summarised in these terms:
"Tobacco smoke contains more than 3800 constituents. This section summarizes present knowledge as to the physicochemical nature of tobacco mainstream and sidestream smoke and the presence of specific agents in these aerosols. Emphasis has been placed on the formation and identification of biologically active agents in tobacco smoke that had been the subject of extensive laboratory studies; their amounts in the mainstream smoke of nonfilter cigarettes are summarized."
A list then followed of some of these agents.
[5.45]The next chapter discussed the biological data relevant to the evaluation of carcinogenic risk to humans. At p.194, in a part of the summary of the chapter relating to carcinogenicity studies in animals, the working group stated:
"Considerable effort has been devoted to developing experimental animal systems to study the carcinogenicity of cigarette smoke. Useful models have been developed for testing both whole smoke, by inhalation, and smoke condensate, by topical application.
Studies involving inhalation of smoke are hampered by difficulties in reproducing the exposure of humans. Technical problems occur in the generation of smoke and its delivery to animals; moreover, the respiratory systems of animals and humans differ. Rodents are obligatory nose breathers, and the structure of their nasal turbinates is more complex than that of humans. Unlike humans, experimental animals smoke involuntarily with shallow, hesitant breathing patterns. Other difficulties are caused by the toxicity of nicotine and carbon monoxide. Despite these problems, however, informative data have been obtained concerning the carcinogenicity of whole smoke and its gaseous phase.
In some experiments in mice, exposure to whole cigarette smoke resulted in the induction of lung tumours. In one study involving long-term exposure of rats to cigarette smoke, tumours of the respiratory tract were induced. In hamsters, various experiments demonstrated reproducibly the induction of laryngeal carcinomas. Studies in rabbits and dogs of whole cigarette smoke were inadequate for evaluation [...]."
[5.46]At p.197, under the heading "Observations in humans", the working group stated:
"Exposure to tobacco smoke can be determined by measuring biochemical or biological markers of tobacco smoke constituents or by measuring intake indirectly, eg, from butts or puffing patterns.
A general dose-response relationship is observed between the number of cigarettes smoked and the levels of tobacco-specific intake markers, such as nicotine, its metabolite cotinine and carboxyhaemoglobin. [...]
Tobacco smoke impairs lung defence mechanisms and affects some systemic aspects of the immune system. The consequences of these changes on tobacco smoke pathogenesis are currently unknown."
[5.47]Counsel next read out to Professor Friend passages from a chapter entitled "Epidemiological studies of cancer in humans". The chapter began, at p.199:
"Knowledge on the relationship between tobacco usage and a variety of human cancers depends primarily on epidemiological evidence."
Professor Friend said that this was his understanding. The passage continued:
"An immense amount of such evidence has been obtained, and, of necessity, only a small proportion can be referred to here. Cancers that are clearly related to smoking, described later in this monograph (i.e., cancers of the lung, upper respiratory and digestive tracts, lower urinary tract and pancreas) occur at lower rates of incidence (and mortality) in religious groups that proscribe smoking (particularly Seventh Day Adventists and Mormons) than in the corresponding national populations. Although many aspects of lifestyle differ in such populations, it seems probable that differences in smoking contribute substantially to the differences seen in smoking-related disease rates [...].
Case-control (retrospective) and cohort (prospective) studies first published in the early 1950s - though using different methodologies - are in qualitative, and approximately quantitative, agreement as to the risk among tobacco users for several types of cancer, among which lung cancer predominates.
The most readily comprehensible evidence, although often not the first nor the most detailed (which has commonly come from case-control studies), has been obtained in several large cohort studies, and they are, in consequence, referred to repeatedly in the sections that follow. Many of the case-control studies are described later in different sections of the monograph. To save unnecessary repetition, the large cohort studies are described and commented upon here:
Cohort studies on smoking and cancer
The first cohort studies to compare the risk of cancer among smokers and nonsmokers were begun in 1951. In most instances, smoking habits were ascertained through self-administered questionnaires. The cohorts studied were subsequently followed up to discover cancer deaths, or in some studies, incident cases of cancer. The design of those studies is summarized below and in Table 53."
Counsel drew attention briefly to some of the figures given in the table. The American Cancer Society Nine-State Study had a sample size of 204,547 men, the Canadian Study a sample size of 207,397 subjects, the British Doctors Study 34,440 men and 6,194 women and the American Cancer Society 25-State Study 1,078,894 subjects.
[5.48]At p.203, in a section of the chapter relating to cancer of the lung, the working group stated:
"The following section summarizes some of the epidemiological evidence on smoking-related factors that modify the incidence of lung cancer, assesses the proportion of lung cancer risk currently attributable to smoking in several different parts of the world, and shows how trends in the consumption of cigarette tobacco and changes from one type of cigarette to another relate to trends in the incidence of lung cancer in a few particular countries.
One factor that affects the estimate of relative risk in different studies is misdiagnosis of the disease. Although some patients with other disease may be misdiagnosed as having cancer of the lung [...], these account for only a small proportion of cases nowadays. About 94% of deaths attributed to lung cancer were confirmed by hospital diagnosis in a study based on the Third National Cancer Survey in the USA [...]. Among nonsmokers, however, lung cancer is so rare that misdiagnoses may, in studies that are undertaken without careful histological evaluation, appreciably change the measured rates of lung cancer among nonsmokers, thereby biasing the relative (though not necessarily the absolute) excess risk of the disease among smokers."
[5.49]Counsel drew attention to a few other brief passages in the same chapter. At p.206, under the heading "Duration of smoking", it was stated:
"One of the key features of the relationship between cigarette smoking and lung cancer is the relevance of duration of regular cigarette smoking to lung cancer onset rates. For example, using a statistical model fitted to data from the British male doctors study, Doll and Peto (1978) estimated that the excess annual incidence rates of lung cancer after about 45, 30 and 15 years of cigarette smoking were in the approximate ratio 100:20:1 to each other (Table 55)."
Passing reference was made to Table 5, and to Figure 8 on p.208, which was entitled
"Background and excess risks: lung cancer death rates among nonsmokers in relation to age (lower line) and among regular cigarette smokers, in relation to approximate years of smoking (upper line)". Professor Friend agreed with a statement by counsel that this graph showed that the risk rate for those who had smoked cigarettes since they were aged between 15 and 24 was much higher than for those who had never smoked regularly, and commented that the scale was logarithmic which, if anything, rather diminished the impact of the smoking.
[5.50]Counsel then passed to the chapter entitled "Conclusions and evaluations". At p.309, under the heading "Carcinogenicity in animals", the working group stated:
"Cigarette smoke has been tested for carcinogenicity in experimental animals by inhalation and by topical application of condensate and in other ways. Exposure of hamsters and rats to whole smoke results in the induction of malignant respiratory-tract tumours. Cigarette smoke condensate induces skin cancers in mice and rabbits after application to the skin, and lung cancers in rats after intrapulmonary injection. Cigarette smoke contains many chemicals known to produce cancer in animals and/or humans.
More tumours occur in animals exposed to both cigarette smoke and 7,12-dimethyl-benz[a]anthracene than to either one alone; the same is true for concomitant exposure to benzo[a]pyrene or radon daughters."
On p.311, under the heading "Human exposure", the working group stated:
"Approximately 80% of inhaled particles from cigarette mainstream smoke is deposited in the respiratory tract, the majority in the tracheobronchial region."
Professor Friend said that this was the area where Mr McTear got his lung cancer. He thought that what the working group meant was the area of larger airways, between the beginning of the trachea and the end of the little airways in the bronchial tree.
[5.51]On p.312, under the heading "Cancer in humans", the working group stated:
"Lung cancer is believed to be the most important cause of death from cancer in the world, with estimated total deaths in excess of one million annually. The major cause of the disease is tobacco smoking, primarily of cigarettes. Risk of lung cancer is particularly dependent on duration of smoking; therefore, the earlier the age at initiation of smoking, the greater the individual risk."
Professor Friend said that he agreed with this. The working group continued:
"Further, the longer the time period during which a major proportion of adults in a population have smoked, the greater the incidence and mortality from the disease in that population. Risk of lung cancer is also proportional to the numbers of cigarettes smoked, increasing with increasing cigarette usage."
Professor Friend said that this was his experience. The working group continued:
"In populations with a long duration and heavy intensity of cigarette usage, the proportion of lung cancer attributable to smoking is of the order of 90%. This attributable proportion applies to men in most western populations [...]."
Professor Friend agreed that this would include the United Kingdom.
[5.52]Counsel turned finally to the evaluations on p.314:
"There is sufficient evidence that inhalation of tobacco smoke as well as topical application of tobacco smoke condensate cause cancer in experimental animals.
There is sufficient evidence that tobacco smoke is carcinogenic to humans.
The occurrence of malignant tumours of the respiratory tract and of the upper digestive tract is causally related to the smoking of different forms of tobacco [...]."
Professor Friend said that he agreed with these statements.
[5.53]Counsel next asked Professor Friend to comment on passages in IARC 2004. (Such information as I have been able to establish about the documents that were lodged as part of No.97/4 of process is as follows. A working group met in 2002 to review "all significant published evidence related to tobacco smoking and cancer, both active and involuntary". Part 5, "Summary of data reported and evaluation" was published, along with a press release, in June 2002. The main text of the monograph, however, had not been published by the conclusion of the proof before me, but was published during 2004 while I was preparing this opinion. I have of course only taken account of the material which was in process and put to Professor Friend and subsequent witnesses for their comment.) In the press release it was stated that:
"While its [the working group's] conclusions unsurprisingly confirmed the cancer-causing effects of active smoking, which an earlier working group had considered back in 1986, it now concluded its evaluation of the carcinogenic risks associated with involuntary smoking, with second-hand smoke also classified as carcinogenic to humans."
Under the heading "Active smoking" the press release stated:
"In brief, the tobacco epidemic is big - one-half of all persistent cigarette smokers are eventually killed by a tobacco-caused disease. Half of these deaths occur in middle age (35-69 years), when those killed by tobacco lose on average 20-25 years of nonsmoker life expectancy. [...] Unfortunately, as we continue to examine the cancer risk caused by smoking we are learning that it is even greater than previously thought and more cancer sites are affected."
[5.54]In Part 5 reference was made in para.5.2 to human carcinogenicity data. In relation to cigarettes and cancer of the lung, it stated:
"Lung cancer is the most common cause of death from cancer in the world. [...] The major cause of lung cancer is tobacco smoking, primarily of cigarettes. In populations with prolonged cigarette use, the proportion of lung cancer cases attributable to cigarette smoking has reached 90%."
Professor Friend agreed that this confirmed the view reached by the IARC working group in 1986. The paragraph continued:
"The duration of smoking is the strongest determinant of lung cancer in smokers. Hence, the earlier the age of starting and the longer the continuation of smoking in adulthood, the greater the risk. Risk of lung cancer also increases in proportion to the numbers of cigarettes smoked."
At para.5.5 the working group's evaluation was:
"There is sufficient evidence in humans that tobacco smoking causes cancer of the lung [...].
There is sufficient evidence in experimental animals for the carcinogenicity of tobacco smoke and tobacco smoke condensates."
Professor Friend appeared to agree with these statements when counsel read them out.
[5.55]Returning to his report, Professor Friend referred to the averment on behalf of Mrs McTear that "cigarette smoking can cause lung cancer", and said that he agreed with this. He then commented on an averment for ITL that cigarette smoking had not been scientifically established as a cause of lung cancer. He said that he believed the epidemiological evidence was very strong and that it had been established beyond reasonable doubt. It was true to say that the precise mechanisms by which smoking caused lung cancer were not known, but that did not mean that the effect did not occur. The exact chemical or biological process by which it happened might not be known, but he had no doubt that smoking caused lung cancer. He was not a research scientist, but it was known that there were a number of materials in cigarette smoke which had a reputation for inducing cancerous changes in animals and these therefore had a reputation as being carcinogens. It was known that people who smoked were much more likely than nonsmokers to develop lung cancer. It was not known what was the mechanism by which that happened. There might be chemical changes on cell division, there might be other factors. The precise mechanisms were not known and it might not be the same mechanism in every person. People were all different and reacted differently. Clearly there were differences between people, and it was known that not everybody who smoked got lung cancer, but a lot did, and that was the medical concern. Cancer took a long time to develop in humans. One of the concerns about animal experiments was that many animals did not live more than two or three years and yet what was being considered in humans was a development of a disease which might require twenty or thirty years of smoking before it became a possibility, so there was a concern about how easily the animal experiments could be transferred to human experience.
[5.56]In Doll 1997 Sir Richard Doll said at p.25:
"In saying that a particular factor is a cause of disease, epidemiologists have in mind a situation in which, for example, prolonged cigarette smoking results in a rare disease becoming ten times as common as it would have been in the absence of smoking."
I asked Professor Friend whether he used the word "cause" in the sense in which Sir Richard said that epidemiologists would use it. Professor Friend said that he thought that what Sir Richard was saying did not mean that it was an obligatory cause but that it was a very important and common cause. A cause in a given individual could never be defined with total accuracy, but it was possible to state a probability of causation. He went on to say that in Mr McTear's case, he was a very heavy smoker and it was highly probable that his disease was caused by smoking. But this was not necessarily the only cause, and it was conceivable that some other cause might have been present in his case.
[5.57]At p.26 of Doll 1997, Sir Richard Doll said:
"In sum, the total effect of cigarette smoking appears to double the risk of deaths in middle and old age in both sexes. Some six per cent of the excess mortality in men is, however, due to diseases [...] caused by factors with which smoking is confounded and this might be thought to reduce the risk that the avoidance of smoking could avoid. In fact, it does not, for confounding can operate in both directions and confounding with the consumption of alcohol reduces the effect of smoking because alcohol reduces the risk of vascular disease and this, in developed countries, is the principal cause of death."
Professor Friend said that he would accept that view. He agreed with the suggestion that "if alcohol is brought into the picture, it does not increase the risk".
[5.58]Also at p.26, Sir Richard Doll said:
"In retrospect, it may be surprising that resistance to the idea that smoking caused so much disease was initially so strong. Three factors, at least, contributed to it. One was the ubiquity of the habit, which was as entrenched among male doctors and scientists as among other men and had dulled the sense that tobacco might be a major threat to health. Another was the novelty of the epidemiological techniques, which had not previously been applied to any important extent to the study of non-infectious disease. The findings were consequently undervalued as a source of scientific evidence. A third was the primacy given to Koch's postulates for determining causation. The evidence that lung cancer occurred in non-smokers was consequently taken to show that smoking could not be the cause and the possibility that it might be a cause was inappropriately doubted. The manner in which lung cancer was linked to smoking was not, however, unique. All the other major diseases related to smoking were found to be so by epidemiological enquiry and laboratory evidence of physiological effects that provided plausible mechanisms by which smoking might cause them was obtained only later and, in some instances, is still awaited."
Professor Friend said that he would agree with this. He said that he forgot the exact collection of Koch's postulates, but one of them was that it had to be possible to find a specific infecting organism as a cause for a condition and that that established a cause and effect. This was obviously appropriate for an infectious condition but it did not follow through automatically to a condition such as lung cancer where there might be many factors involved in the precise causation. By this, he meant that there might be many different compounds. He thought that this passage was a very good broad summary of the difficulty. It was remarkable that once the epidemiological evidence became known the proportion of doctors who smoked dropped progressively over the years.
[5.59]Sir Richard Doll concluded the lecture with this sentence, also at p.26:
"That so many diseases - major and minor - should be related to smoking is one of the most astonishing findings of medical research in this century; [...]."
Professor Friend said that he agreed with this comment. Smoking was now believed by the medical profession to be the most important cause of preventable ill-health and death in the western world.
[5.60]Professor Friend was next asked to read out the following passages from a statement dated 14 October 2003 on the website of the tobacco manufacturers Philip Morris USA:
"We agree with the overwhelming medical and scientific consensus that cigarette smoking causes lung cancer, heart disease, emphysema and other serious diseases in smokers. Smokers are far more likely to develop serious diseases, like lung cancer, than non-smokers. There is no 'safe' cigarette.
We agree with the overwhelming medical and scientific consensus that cigarette smoking is addictive. It can be very difficult to quit smoking, but this should not deter smokers who want to quit from trying to do so."
Professor Friend was not asked to comment on this passage. In answer to a question by me about the meaning of "addiction", he said that there were definitions which had been formed in America by a psychological institution. There was also the international classification, ICD-10. He would need to refer to these documents to be accurate, but a general definition included a degree of compulsion to continue using the substance even when there were established reasons not to do so on grounds of health, and also the difficulty in withdrawing from the substance and with some degree of withdrawal symptoms.
[5.61]Professor Friend was next asked for his opinion on Mr McTear's initiation to smoking. He said that although information on smoking as a cause of lung cancer became widely publicised during the 1960s, and particularly after the publication of RCP 1962, the advertising of cigarettes without health warnings, and publicity from a variety of sources casting doubt on the causative role of smoking in lung cancer, meant that the decision to start smoking was not altered by understanding of the health risks, and the consumption of cigarettes in the united Kingdom throughout the 1960s showed little change. He referred to data provided by the Tobacco Advisory Council. This suggested to him that there was little tendency for smokers to discontinue smoking during the 1960s on the basis of the evidence that was available to them. If they had been sufficiently made aware and persuaded of the harm that cigarettes could do to them there would have been a much more significant reduction in smoking at that time. There was of a course a very significant reduction during the 1970s and onwards, when information was available and when warnings were printed on cigarette packets as a result of the voluntary agreement between the Government and the tobacco industry. In his opinion, Mr McTear would not have been made sufficiently aware of the risks of cigarette smoking by the product information provided by the manufacturers in their advertising material and elsewhere at the time when he started smoking. So far as he was aware, ITL did not put out any product information which contained a warning of the dangers of cigarette smoking.
[5.62]Professor Friend was next asked for his opinion on genetic predisposition. He said that he understood that in the pleadings there was an argument being expressed that because a number of members of Mr McTear's family had suffered from cancer, there might be a case to say that Mr McTear was unusually susceptible to the development of cancer and therefore this would put him at much greater risk of developing it and thus diminish the role of tobacco in the causation of his condition. Through his own reading or his general understanding he had not become aware of any dominant evidence that genetic factors played a particularly important part in this particular form of cancer. They could play an important part in other cancers, but he had never in his professional career been made aware of any very strong genetic component to lung cancer development. Since up to a third of the population could expect to die of malignant disease, it would be necessary to know the total numbers of the family being assessed for cancer death, together with the smoking habits of those individuals, and the exact site of the cancer attributed as a cause of death, before any judgment could be made in Mr McTear's case on the question of a family predisposition specifically to lung cancer. In many families there was a social tendency for smoking to become the norm, so that the family members of a smoker were more likely to be smokers also, thus accounting for an apparent increase in lung cancer in some families. There was evidence in the present case that Mr McTear's parents were both smokers. It was much more likely that a person became a smoker if his or her parents were smokers. He was asked:
"If this genetic predisposition is a correct theory, is it inherent in it that someone would have to start smoking as well as having the genetic disposition?"
He said that this would be his belief. Asked whether "if it was the case that certain people have a genetic predisposition to developing lung cancer, they would have to start smoking before that greater risk increased", he said that this was in general so.
[5.63]Professor Friend next offered his opinion on the issue of addiction. He said that it might be argued that a smoker could, by free will, cease smoking at any time to reduce and abolish the increased risk of developing lung cancer. However, if the smoker were not free to discontinue smoking because a habit or addiction had formed, it might no longer be possible to stop smoking without unusual measures. Tobacco was now regarded by many authorities as fulfilling the criteria for an addictive drug. Mr McTear ceased smoking some weeks before he presented at Crosshouse Hospital with his lung cancer, but this was a relatively common occurrence, well known in clinical practice to Professor Friend and his colleagues in the speciality of respiratory medicine. Even heavy smokers might cease smoking as they developed lung cancer, either before they first developed symptoms and felt unwell or after symptoms developed. It was not known whether this resulted from the development of a physical aversion to tobacco use as the illness developed, or whether the first symptoms, such as coughing up blood, caused fear and apprehension which overcame even previous addictive behaviour.
[5.64]Professor Friend said that the British Thoracic Society had always conducted large-scale research projects. Among them were some that he was directly involved with, partly as a member of the committee which planned and executed the studies, but also because he had involved his patients in some of them. The study that he particularly remembered involved recruiting some 1,600 patients, mainly with chronic bronchitis or with recent myocardial infarction, and encouraging them to stop smoking as best they could. Four interventions were used: brief advice to stop smoking; the provision of literature about stopping smoking in addition to the brief advice; advice plus nicotine chewing gum to aid withdrawal from smoking; and advice, the leaflet, and nicotine chewing gum. Smoking habits were observed over the course of the subsequent twelve months and were assessed. They tried to verify that the patients had stopped smoking by biochemical measures of nicotine products in their urine. To their disappointment they found that, of this group of patients, who already had very persuasive illnesses which were attributed to smoking, the success rate was that 10% discontinued smoking at the end of one year. This was the same in virtually all the four groups. They concluded that it was very difficult to help people, even with very persuasive symptoms, to stop smoking. They were not very impressed as to the benefits of nicotine replacement therapy.
[5.65]Professor Friend concluded his report with these final comments:
"Tobacco smoking causes lung cancer.
Mr McTear developed squamous carcinoma of the lung in 1992 after smoking heavily for 28 years. The strong probability is that this disease was caused by smoking cigarettes.
At the time he started smoking in 1964 Imperial Tobacco continued to promote cigarettes by advertisement and other means without mention of any risk or danger, despite widespread publication of evidence of the links between smoking and lung cancer (and especially from 1962 onwards) of which they were fully aware.
Even when smokers become very aware of the health risks of smoking, the addiction is such that for many smokers (and particularly those who smoke heavily) they will continue to smoke."
Professor Friend said that he remained of the views expressed in this passage. He had read reports prepared by expert witnesses for ITL and they had not caused him to change any of his comments in any way.
[5.66]Mr McEachran next asked Professor Friend about passages in USSG 1988. When the report was transmitted to the United States Congress the Secretary of Health and Human Services wrote to the President:
"This report [...] examines the scientific evidence that cigarettes and other forms of tobacco are addicting. The issue of tobacco addiction has been addressed in previous Surgeon General's Reports and in the medical literature beginning in the early 1900s. Because of the recent expansion of research in this area, a thorough review of this topic is warranted. Despite the significant health risks of tobacco use outlined in previous reports, many smokers have great difficulty in quitting. This report concludes that such difficulty is in large part due to the addicting properties of nicotine, which is present in all forms of tobacco.
The report further concludes that the processes that determine tobacco addiction are similar to those that determine addiction to other drugs such as heroin and cocaine."
Professor Friend said that this was his understanding.
[5.67]In the foreword it was stated:
"Scientists in the field of drug addiction now agree that nicotine, the principal pharmacologic agent that is common to all forms of tobacco, is a powerfully addicting drug. [...] After carefully examining the available evidence, this Report concludes that:
- Cigarettes and other forms of tobacco are addicting.
- Nicotine is the drug in tobacco that causes addiction.
- The pharmacologic and behavioral processes that determine tobacco addiction are similar to those that determine addiction to drugs such as heroin and cocaine."
Professor Friend said that this was still the position.
[5.68]Attention was next drawn to the table of contents, which showed that there were chapters entitled "I Introduction, Overview, Summary and Conclusions", "II Nicotine: Pharmacokinetics, Metabolism, and Pharmacodynamics", "III Nicotine: Sites and Mechanisms of Actions", "IV Tobacco use as drug dependence", "V Tobacco use compared to other drug dependencies", "VI Effects of nicotine that may promote tobacco use" and "VII Treatment of tobacco dependence", and that the report extended to 639 pages. Professor Friend agreed that this was a substantial document.
[5.69]In the overview at pp.7-8 the report stated:
"The terms 'drug addiction' and 'drug dependence' are scientifically equivalent: both terms refer to the behavior of repetitively ingesting mood-altering substances by individuals. The term 'drug dependence' has been increasingly adopted in the scientific and medical literature as a more technical term, whereas the term 'drug addiction' continues to be used by NIDA [National Institute on Drug Abuse] and other organizations when it is important to provide information at a more general level. Throughout this Report, both terms are used and they are used synonymously.
The main conclusions of the Report are based upon concepts of drug dependence that have been developed by expert committees of the World Health Organization, as well as in publications of NIDA and the American Psychiatric Association. These concepts were used to develop a set of criteria to determine whether tobacco-delivered nicotine is addicting. The criteria for drug dependence include primary and additional indices and are summarized below.
CRITERIA FOR DRUG DEPENDENCE
Primary Criteria
- Highly controlled or compulsive use
- Psychoactive effects
- Drug-reinforced behavior
Additional Criteria
- Addictive behavior often involves:
-stereotypic patterns of use
-use despite harmful effects
-relapse following abstinence
-recurrent drug cravings
- Dependence-producing drugs often produce:
-tolerance
-physical dependence
-pleasant (euphoriant) effects
The primary criteria listed above are sufficient to define drug dependence. Highly controlled or compulsive use indicates that drug-seeking and drug-taking behavior is driven by strong, often irresistible urges. It can persist despite a desire to quit or even repeated attempts to quit."
[5.70]Professor Friend said that he recognised the features of addictive behaviour in many of the people he had met. This did not apply to every single smoker. There were considerably variable degrees of addiction, going all the way from people who had a totally compulsive addictive behaviour to smoke to people who could smoke casually at different times but did not need to smoke regularly. There were a significant number of people who had very compulsive behaviour towards smoking, and many of these became his patients. Asked whether that had anything to do with the number of cigarettes they smoked, he said that in general there was quite strong evidence to suggest that the larger number of cigarettes people smoked, the more heavily they were addicted to them. There had been a number of measures of how it could be decided how addicted people were to cigarettes, based substantially on the total number of cigarettes they smoked, but also how early in the morning they needed to have their first cigarette. The most addicted smokers would need to have their first cigarette within five minutes of waking up. People could almost be categorised into different levels of addiction by using an index of that sort, with a number of simple questions.
[5.71]The overview continued, on p.8:
"To distinguish drug dependence from habitual behaviors not involving drugs, it must be demonstrated that a drug with psychoactive (mood-altering) effects in the brain enters the blood stream."
Asked about this passage, Professor Friend said that it was known that nicotine entered the bloodstream remarkably quickly after inhalation. It was absorbed into the blood vessels in the lung and transmitted through the bloodstream. It could reach the centres of the brain within about fifteen to twenty seconds of the inhalation and immediately would afford the smoker a pleasurable feeling. Because it was a relief of a need which had developed in that centre of the brain, that centre of the brain enjoyed the experience of the relief of the appetite, and this occurred within a very quick period of the inhalation of cigarette smoke.
[5.72]At p.9 of the overview, the major conclusions of the report were set out:
"1.Cigarettes and other forms of tobacco are addicting.
2.Nicotine is the drug in tobacco that causes addiction.
3.The pharmacologic and behavioral processes that determine tobacco addiction are similar to those that determine addiction to drugs such as heroin and cocaine."
Professor Friend said that this was still the position today. One had to be aware that the pattern of addiction was not identical to that of cocaine or heroin. Each addictive drug had a slightly different emphasis on how it was used and how it affected behaviour and so on. But the actual principles of addiction were still the same in each of these, and he believed it was proper to categorise nicotine as an addictive drug for many people: not for everybody, but for many, many people who used it. Asked about people with a compulsion to eat chocolate or drink coffee, he said that for most of these compulsions there was less of a problem of withdrawal. The behaviour was not quite as compulsive as it was for things such as tobacco. For a tiny number of people there might be almost as major a compulsion as there was with things such as tobacco or heroin. He would agree with that, but it did not normally cause major withdrawal symptoms. He thought it might have more of a behavioural content than a physical dependency. Caffeine and similar compounds did not cause such an intense physical addiction, as a result of a chemical process which had been very carefully studied. He said:
"I am not an addiction specialist, I should state that at this stage, and I am not a psychiatrist, I have only had the opportunity to read some of this literature and therefore I am not a specialist in that field. But I do believe there are gradations, and - in different compounds - but I do believe that nicotine results in a very strong addiction for many people."
This was his personal experience, absolutely.
[5.73]Finally, reference was made to a passage at pp.10-11 of the report:
"There was no question at the time of [publication of USSG 1964] that nicotine was the critical pharmacologic agent for tobacco use, but its role was then considered to be more similar to cocaine and amphetamines than to opiates and barbiturates. Later in 1964 the World Health Organization dropped this semantic distinction between habituating and addicting drugs because it was recognised that habitual use could be as strongly developed for cocaine as for morphine, that social damage generally accompanied personal damage, and that behavioral characteristics of drug use could be similar for the so-called habituating and addicting drugs. In an effort to shift the focus to dependent patterns of behavior and away from moral and social issues associated with the term addiction, the term dependence was recommended.
It is now clear that even by the earlier distinction in nomenclature, cigarettes and other forms of tobacco are addicting and actions of nicotine provide the pharmacologic basis of tobacco addiction."
Professor Friend appeared to agree with this.
[5.74]Reference was next made to RCP 2000. Attention was drawn to the membership of the Tobacco Advisory Group of the Royal College of Physicians who prepared this report. They were a professor of respiratory medicine, the Director of ASH, a consultant cardiologist, the press and public relations manager of the Royal College of Physicians, a professor of health economics, a professor of health psychology, and a strategic research advisor with the Health Education Authority. Counsel also drew attention to the length of the main body of the report, which contained 189 pages.
[5.75]In the foreword, the President of the Royal College of Physicians wrote:
"This report addresses the fundamental role of nicotine addiction in smoking. It is now recognised that nicotine addiction is one of the major reasons why people continue to smoke cigarettes, and that cigarettes are in reality extremely effective and closely controlled nicotine delivery devices. Recognition of this central role of nicotine addiction is important because it has major implications for the way that smoking is managed by doctors and other health professionals, and for the way in which harmful nicotine delivery products such as cigarettes should be regulated and controlled in society."
Professor Friend agreed that this was the message that this report was giving out. He obtained a copy of it, because he thought it was so important.
[5.76]On p.xiii, among key points relating to physical and pharmacological effects of nicotine, it was stated:
"Nicotine receptors are present in the brain and many other organs vary markedly in their binding, activation and desensitisation characteristics
Cigarettes deliver rapid doses of nicotine to receptors in the brain
Animal studies provide strong and consistent evidence that nicotine is addictive"
Professor Friend said that this was in accordance with his understanding.
[5.77]On p.xiv key points relating to the psychological effects of nicotine and smoking included the statements:
"There is strong evidence of psychological dependence on cigarettes
The major psychological motivation to smoke is the avoidance of negative mood states caused by withdrawal of nicotine"
Professor Friend said that he could not help with this in a particularly technical sense, but only as an observer of many people who were smokers, who might, when they required a further dose of nicotine, either become agitated or feel flat and need to be aroused by nicotine. He thought people were very variable. He was no psychologist, but he thought the effects of nicotine on a regular smoker was to heighten alertness and improve mood, and that was why people enjoyed smoking. He would absolutely accept that if someone was habituated to nicotine, it brought pleasure to relieve the withdrawal effects by taking further nicotine in the form of a cigarette. This was his experience.
[5.78]Key points, also on p.xiv, on the question whether nicotine was a drug of addiction included the statements:
"Nicotine obtained from cigarettes meets all the standard criteria used to define a drug of dependence or addiction
Historically, and in contrast to addiction to opiates or alcohol, addiction to nicotine has not been recognised as a medical or social problem in Britain
Nicotine is highly addictive, to a degree similar or in some respects exceeding addiction to 'hard' drugs such as heroin and cocaine
Most smokers do not smoke out of choice, but because they are addicted to nicotine"
Professor Friend said that he agreed with these points. As to the last one, he agreed that this was so once smoking was fully established. The majority of people who started smoking were young and usually in their secondary school years. He did not believe that many people enjoyed their first cigarette or their second, but it had been stated that, within fourteen days of regular use of cigarettes, there might well be an addictive state present in many people.
[5.79]Key points on pp.xiv-xv under the heading "The natural history of smoking: the smoker's career" included the statements:
"Addiction to nicotine is established in most smokers during teenage years, in many cases before reaching the age at which it is legal to buy cigarettes
Teenagers who smoke one or more cigarettes per day demonstrate evidence of addiction similar to that seen in addicted adults, but addiction can be evident at lower levels of smoking
Addiction to nicotine is usually established in young smokers within about a year of first experimenting with cigarettes
A small proportion of smokers, approximately 5%, do not appear to be addicted to nicotine
Once addicted, most smokers are unable to give up smoking even when they develop disease caused by smoking and made worse by continued smoking
Only about 2% of smokers succeed in giving up in any year
About 50% of young adult smokers will still be smoking when they are 60"
Professor Friend said that he agreed with these points, which were in accordance with his experience.
[5.80]At p.100, the authors of the report stated:
"On current evidence, we can conclude that cigarettes are properly categorised among the most addicting substances as this form of nicotine delivery maximises the addictive effects of the drug. The fact that nicotine is of low abuse potential in controlled dosage forms such as the transdermal nicotine patch or nicotine gum supports the conclusion that the form of delivery is an important determinant of its addiction potential. Thus, tobacco-delivered nicotine is of great concern, with the cigarette of greatest concern of all tobacco products because of its high toxicity and addictiveness."
Professor Friend said that the point that was being made was that this remarkably quick delivery of nicotine to the brain, within seconds, gave a very immediate positive effect to the smoker, whereas with things like nicotine gum, which was chewed slowly, the nicotine was absorbed through the mouth, took some time to reach the brain and therefore only very gradually improved it. Nicotine patches were even more slow; the nicotine seeped through the skin and into the bloodstream over sixteen or twenty-four hours, depending on the construction of the patch. They did not give any immediate benefits to the smoker, but they might satisfy the needs of the nicotine receptors in the brain if they were taken in advance of smoking and therefore reduced people's demand for the quick and immediate response that they got from a cigarette smoked and delivering its load.
[5.81]Also on p.100, the authors stated:
"The pharmacological effects of nicotine are not identical to those of heroin, alcohol or cocaine - nor, for that matter, are the effects of cocaine identical to those produced by heroin. In its arguments that nicotine is not addictive, the tobacco industry has often argued [...] that nicotine is not addicting because it does not meet criteria that the tobacco industry itself has developed. In essence, these criteria appear to be those achievable only by a drug whose composite profile would be as intoxicating as ethanol [alcohol], would produce as severe withdrawal symptoms as ethanol or heroin, would have the euphoriant effects of cocaine, and would serve as a reinforcer for animals and naïve humans as readily as does cocaine.
Any one factor may be selected to argue that one of these drugs is more or less addicting than the others. However, this exercise makes it clear that addiction severity and society's level of concern about drug use are best evaluated by assessing several variables. We can, however, conclude, as was concluded in [USSG 1988], that:
'The pharmacologic and behavioral processes that determine tobacco addiction are similar to those that determine addiction to drugs such as heroin and cocaine.'
We can further conclude that tobacco dependence is a serious form of drug addiction which, on the whole, is second to no other."
Professor Friend said that he agreed with this passage. The report endorsed the findings of USSG 1988, so there had been no change in the thinking.
[5.82]At p.184 the authors stated:
"Although nicotine in the form of tobacco is a legal drug, it should not be regarded as pharmacologically benign. The classification of drugs as 'legal', 'soft' or 'hard' reflects public perceptions and current law enforcement practice, rather than constituting a useful pharmacological classification. In terms of addictiveness, nicotine delivered in tobacco smoke is a 'hard' drug on a par with heroin and cocaine. The status of nicotine as a seemingly innocuous legal drug, and attempts for many years by the tobacco industry to equate addiction to nicotine with addiction to substances such as coffee, colas or chocolate, have distracted attention from the highly addictive nature of nicotine in cigarettes."
Professor Friend said that this passage was correct.
[5.83]At pp.184-185 the authors wrote:
"Most people begin smoking and become addicted to nicotine as teenagers. This addiction may then cause tobacco use to continue long after an informed adult choice has been made to stop smoking on the grounds of a change in attitude to health, changed circumstances such as starting work in a smoke-free office, starting a family or other reasons. This characteristic of tobacco use - an attenuation of free choice initiated in childhood - is a central plank of the case for government intervention to control tobacco use through measures such as advertising bans, tax increases, anti-smoking communications and cessation support, and to regulate the availability and safety of nicotine products.
Nicotine addiction is closely linked to socio-economic disadvantage. Smoking prevalence is higher and nicotine use heavier among poorer smokers."
Professor Friend said that all of this was in accordance with his experience. It was also consistent with his experience that about two-thirds of smokers said that they would like to quit and about one-third tried in any one year, but only about 2% succeeded, as stated at p.186 of the report.
[5.84]Reference was next made to MRC 1957. In this statement the Medical Research Council drew attention to the very great increase in the death rate from lung cancer in then recent years. They commented that the trend indicated that the incidence had not yet reached its peak, that the figures were not to be explained as a mere reflection of introduction of improved methods of diagnosis, but they must be accepted as representing in the main a real rise in the incidence of the disease, only a small part of which could be attributed to the larger number of older persons living in the population. They concluded that on balance it seemed that atmospheric pollution played some part in causing the disease, but a relatively minor one. Heavy and prolonged smoking of tobacco, particularly in the form of cigarettes, was associated with an increased risk of lung cancer. In the view of the Council, the most reasonable interpretation of the evidence was that the relationship was one of direct cause and effect. Professor Friend said that he did not know what the reaction of the tobacco industry was to this statement, which was published when he was a very young medical student. He was taught at his lectures in Edinburgh on respiratory medicine that smoking was a cause of lung cancer.
[5.85]Counsel next asked Professor Friend about a number of passages in RCP 1962, which was published as a main report and a separate summary. In the summary, at p.S2, the introduction stated:
"Several serious diseases, in particular lung cancer, affect smokers more often than non-smokers. Cigarette smokers have the greatest risk of dying from these diseases, and the risk is greater for the heavier smokers."
Professor Friend said that this was consistent with his experience, and the conclusion had remained valid for forty years.
[5.86]At p.S3, under the heading "Smoking and cancer of the lung", the summary stated:
"There has been a great increase in deaths from this disease in many countries during the past 45 years [...]. Some of this increase may be due to better diagnosis, but much of it is due to a real increase in incidence. Men are much more often affected than women."
Professor Friend said that over long periods of time there had certainly been differences in diagnostic criteria, and the methods of diagnosis, and it was the case even now that the accuracy of death certification was affected by the reduction in the autopsy rate compared with previous decades. But he thought there would have had to be a very remarkable change in diagnostic procedure to have created such a dramatic increase in the rates of lung cancer, particularly in the ten years or so prior to 1962.
[5.87]The summary continued at pp.S3-4:
"Many comparisons have been made in different countries between the smoking habits of patients with lung cancer and those of patients of the same age and sex with other diseases. All have shown that more lung cancer patients are smokers, and more of them heavy smokers than are the controls. The association between smoking and lung cancer has been confirmed by prospective studies in which the smoking habits of large numbers of men have been recorded and their deaths from various diseases observed subsequently. All these studies have shown that death rates from lung cancer increase steeply with increasing consumption of cigarettes. Heavy cigarette smokers may have thirty times the death rate of non-smokers. [...] They have also shown that cigarette smokers are much more affected than pipe or cigar smokers [...] and that those who had given up smoking at the start of the surveys had lower death rates than those who had continued to smoke. [...] The lungs of smokers without cancer show changes of chronic irritation, of the sort which might precede cancer, more often than the lungs of non-smokers [...]."
Professor Friend said, in respect of the last sentence, that this was something he had observed in practice and he agreed with the statement.
[5.88]The summary stated, at pp.S4-S5:
"The association of lung cancer with cigarette smoking is generally agreed to be true but various possible explanations of this association other than that of cause and effect have to be considered. [...] None of these explanations fits all the facts as well as the obvious one that smoking is a cause of lung cancer. [...] There are a few facts which may be considered to conflict with this conclusion namely:-
(i)that lung cancer occurs in only a minority of smokers:
(ii)that death rates from this disease are lower in some countries than would be expected from their cigarette consumption:
(iii)that there is some conflicting evidence on the effects of inhalation of smoke:
(iv)that no animal has yet been given lung cancer by exposure to cigarette smoke. [...]
These facts are discussed [...] and none of them is found to contradict the conclusion that cigarette smoking is an important cause of lung cancer."
At p.S7 the following conclusions were stated:
"Cigarette smoking is a cause of lung cancer, and bronchitis and probably contributes to the development of coronary heart disease and various other less common diseases. [...] The risks of smoking to the individual are calculated from death rates in relation to smoking habits among British doctors [...]. The chance of dying in the next ten years for a man aged 35 who is a heavy cigarette smoker is 1 in 23 whereas the risk for a non-smoker is only 1 in 90."
Professor Friend appeared to agree with these passages, subject to the comment that it had been reported in IARC 2004 that there was now evidence that animals had been given lung cancer by exposure to cigarette smoke.
[5.89]Professor Friend was next asked about passages in the main report. He said that he believed that the intention was to make it palatable to politicians and others who might have some ability to take action on behalf of the public health. He had not ever read the entire report, but he had read summaries and was happy to rely on intelligent and sensible appraisal of these large reports. This report was referred to in journals read by doctors and was publicised in the general press. Counsel read out passages under the headings "Introduction", "History of smoking", "Present smoking habits", "Advertisement of tobacco goods", "The chemistry and pharmacology of smoking", "Smoking and cancer of the lung", "Increasing death rates from lung cancer", "Retrospective surveys", "Prospective surveys", "Pathology" and "Interpretation of the evidence". In para.32, at pp.20-25, there was discussion of the relationship between cancer of the lung and smoking, and explanations which must be considered before acceptance that the "obvious explanation of this association is that it is causal". In para.33, at p.25, the authors of the report stated:
"We are therefore left with the hypothesis that habitual cigarette smoking over many years is a cause, in the ordinary sense, of lung cancer. It is important to realise that the hypothesis is not that cigarette smoking is the only cause of lung cancer. The fact that the disease does, rarely, occur in non-smokers, and the effects of air pollution and various industrial hazards clearly indicate that other factors are concerned. Nor does the fact that only a minority of smokers develop lung cancer negate the hypothesis any more than does the fact that only a minority of persons exposed to tuberculous infection develop tuberculosis negate the hypothesis that exposure to infection is a cause of the disease. The minority response only indicates that other factors determine susceptibility."
[5.90]This was followed by further consideration of "several gaps and apparent discrepancies in the evidence". On p.26 the following passage appeared:
"37.Skin cancer can be produced in mice by applications of tar condensed from tobacco smoke but the results obtained by various investigators have not been uniform and exposure of animals to tobacco smoke in inhaled air has failed to produce lung cancers. Moreover, the amount of cancer-producing substances in the smoke itself does not seem likely to be sufficient to account for the large number of cases of cancer associated with the habit.
38.These facts are sometimes used to support the statement that there is no proof that lung cancer is cause by cigarette smoke; but this would imply that the cause of human disease can only be demonstrated by animal experiment. If tobacco smoke had been shown to cause cancer in animals the causative hypothesis would have been strengthened, but it can still stand without this report."
Professor Friend agreed, as he had already done, that research reported in IARC 2004 now provided this support. He said, however, that he believed that animal experiments could not be directly related to human experience. Animals were very different organisms from human beings. But he believed that in a way the exposure experiment had already been undertaken in man and that we were now witnessing its effects.
[5.91]At para.41, on p.27, the following conclusion was stated:
"The strong statistical association between smoking, especially of cigarettes, and lung cancer is most simply explained on a causal basis. This is supported by compatible, though not conclusive, laboratory and pathological evidence namely (a) the presence of several subjects known to be capable of producing cancer in tobacco smoke; (b) the production of cancer of the skin in animals by repeated application of tobacco tar; and (c) the finding, in the bronchial epithelium of smokers, of microscopic changes of the kind which may precede the development of cancer. The conclusion that smoking is an important cause of lung cancer implies that if the habit ceased, the death rate from lung cancer would eventually fall to a fraction, perhaps to one fifth or even, among men, to one tenth of the present level."
At para.86, on p.43, the report stated, under the heading "Smoking as a cause of disease":
"The most reasonable conclusions from all the evidence on the association between smoking and disease are: that cigarette smoking is the most likely cause of the recent world-wide increase in deaths from lung cancer, the death rate from which is at present higher in Britain than in any other country in the world [...]."
Professor Friend appeared to agree with these passages. He was also asked to note that the list of references at pp.59-70 contained 216 entries.
[5.92]Counsel next made extensive reference to passages in USSG 1964. He drew attention to the fact that the report extended to 387 pages. Reference was made to passages in Chapter 1 under the headings "Historical notes and chronology" and "Establishment of the committee" and in Chapter 2 under the heading "Conduct of the study". In Chapter 3 the committee set out their criteria for judgment, with sub-headings "Criteria of the epidemiologic method" and "Causality". Under the first of these sub-headings, on p.20, the report stated:
"When coupled with the other data, results from the epidemiologic studies can provide the basis upon which judgments of causality may be made.
In carrying out studies through the use of this epidemiologic method, many factors, variables, and results of investigations must be considered to determine first whether an association actually exists between an attribute or agent and a disease. Judgment on this point is based upon indirect and direct measures of the suggested association. If it be shown that an association exists, then the question is asked: 'Does the association have a causal significance?'
Statistical methods cannot establish proof of a causal relationship in an association. The causal significance of an association is a matter of judgment which goes beyond any statement of statistical probability."
Professor Friend said that he agreed with this.
[5.93]In Chapter 4 summaries and conclusions were set out. Under the heading "Kinds of evidence", reference was made on pp.26-28 to animal experiments, clinical and autopsy studies and population studies. Further passages appeared under the headings "Evidence from the combined results of prospective studies" and "Associations and causality". At pp.30-31, under the latter heading, it was stated:
"In this inquiry the epidemiologic method was used extensively in the assessment of causal factors in the relationship of smoking to health among human beings upon whom direct experimentation could not be imposed. Clinical, pathological, and experimental evidence was thoroughly considered and often served to suggest an hypothesis or confirm or contradict other findings. When coupled with the other data, results from the epidemiologic studies can provide the basis upon which judgments of causality may be made."
On p.31, under the heading "The effects of smoking: Principal findings" and the sub-heading "Lung cancer", it was stated:
"Cigarette smoking is causally related to lung cancer in men; the magnitude of the effect of cigarette smoking far outweighs all other factors. The data for women, though less extensive, point in the same direction.
The risk of developing lung cancer increases with duration of smoking and the number of cigarettes smoked per day, and is diminished by discontinuing smoking. In comparison with non-smokers, average male smokers of cigarettes have approximately a 9- to 10-fold risk of developing lung cancer and heavy smokers at least a 20-fold risk. [...] Cigarette smoking is much more important than occupational exposures in the causation of lung cancer in the general population."
Professor Friend said that this was in accordance with the conclusions of RCP 1962.
[5.94]Chapter 9 related to cancer, and a passage relating to lung cancer began at p.149. Among sub-headings, reference was made to retrospective studies and to prospective studies. Among the latter, reference was made on p.162 to studies by Doll and Hill and by Hammond and Horn. On the same page it was stated:
"All the prospective studies thus far have shown a remarkable consistency in the significantly elevated mortality ratios of smokers particularly among the 'cigarettes only' smoking class. Of special interest is the fact that in a number of the studies the magnitude of the association between cigarette smoking and total death rates has increased as the studies have progressed. This has particularly been true for lung cancer. [...]
With reference to the smoking and lung cancer relationship, each of the seven prospective studies has thus far revealed an impressively high lung cancer mortality ratio for smokers to non-smokers."
Reference was made to Table 5 on p.164.
[5.95]When counsel asked Professor Friend about this, the following exchange took place between me and the witness:
"Lord Nimmo Smith:Professor, I am just wondering what I should be making of this part of your evidence. Are you in a position to express any expert opinion about epidemiological studies?
A.I would not claim to be an epidemiologist but I have been very impressed by these studies, particularly the Doll and Hill study, which [...] was conducted in a very simple manner on British doctors - where every doctor on the British Medical Register was written to and asked about their smoking habits - and, ever since then, Doll and Hill, and latterly Doll himself, have really sat receiving the death certificates of the doctors who participated in that study. And [...] the paper reported here represents the early results, but he has continued to accumulate those results and they have been utterly consistent. I find that very persuasive, although, as I say, I am not an epidemiologist, but they seem very convincing to me.
Lord Nimmo Smith:I am just wondering what to make of it, because Mr McEachran is reading out quite long passages to you and you say 'Yes' from time to time. When you say 'Yes', does that mean you see that [this] is what is written on the page, or does it mean also that you accept it as accurate?
A.I would say what is stated in the document is in accord with my clinical experience and with my beliefs from a reading of the literature, but I have not had an in-depth reading of the literature [...] in the way a professional epidemiologist would have had."
[5.96]In view of this, I do not propose to do more than refer briefly to further passages read out by Mr McEachran from Chapter 9, in which there was discussion of reasons for forming the judgment that the association between cigarette smoking and lung cancer was one of cause and effect. At p.196 conclusions were stated:
"1.Cigarette smoking is causally related to lung cancer in men: the magnitude of the effect of cigarette smoking far outweighs all other factors. The data for women, though less extensive, point in the same direction.
2.The risk of developing lung cancer increases with duration of smoking and the number of cigarettes smoked per day, and is diminished by discontinuing smoking. [...]"
Professor Friend said that what he found particularly persuasive was the fact that the risk of lung cancer diminished steadily when people had discontinued smoking. Once people had stopped smoking for around fifteen years, their risk of developing lung cancer approximated to that of life-long non-smokers: he found that, personally, a particularly persuasive outcome.
[5.97]Reference was next made to RCP 1971. Counsel noted that this report extended to 148 pages. Professor Friend said that he thought that it was produced in frustration by the medical profession at the lack of change in the nation's smoking habits, and perhaps partly a lack of change in corporate attitudes by the Government and others. Reference was made in this regard to paragraph 1.3 of the Introduction. In Chapter 4, "Smoking and cancer of the lung", the report stated at p.48:
"Many countries have set up authoritative committees and commissions to study the cause of this modern scourge [lung cancer]. All have concluded that it is almost entirely due to cigarette smoking. A small number of individuals have challenged these expert conclusions, and some have publicised their criticisms. This may explain why nearly nine out of every ten smokers in this country believe that 'experts disagree' about this question, and that cigarette smoking has not yet been proved to be the main cause of lung cancer."
Professor Friend said that he was a junior doctor at the time, but his memory was very clearly that there were one or two sporadic opponents of the widespread belief that smoking caused lung cancer, who sought to oppose "these immensely prestigious and worthy and experienced committees", but their opinions were not widely held in the medical or scientific professions. He thought that the public did get much conflicting advice, and were confused by it, but he had no evidence for this.
[5.98]The report proceeded to recapitulate the facts on which the conclusion that cigarette smoking caused lung cancer was based. There was discussion of criticisms of and alternatives to the causal hypothesis, before the conclusion was stated in para.4.29 at p.64:
"The quantitative association between cigarette smoking and the development of lung cancer is most simply explained on a causal basis and no other explanation accounts for the facts."
Professor Friend agreed that the Royal College of Physicians therefore still accepted the causal relationship between cigarette smoking and lung cancer.
[5.99]Finally, reference was made to RCP 1977, which was published in the form of a main report and a summary. In the summary it was stated that cigarette smoking was still as important a cause of death as were the great epidemic diseases of the past. The evidence of its dangers was becoming increasingly clear, but, although the dangers were more widely recognised, measures to combat them remained pitifully inadequate. Total expenditure by the Government on anti-smoking activities in 1975 to 1976 was £1 million compared with the £80 million spent on promoting tobacco sales. Professor Friend said that he thought that represented direct expenditure by the Government on campaigning and health information. He imagined there was quite a lot of endeavour on the part of individual doctors and nurses at that time towards individual patients. Reference was also made to passages relating to the reduction in incidence of lung cancer among British male doctors, most of whom had given up smoking. This was suggested as one of the reasons why the association between cigarette smoking and lung cancer should be regarded as causative. Professor Friend described RCP 1977 as "a very brief report" (apparently because he had only in mind the summary and not the main body of the report, which extended to 128 pages), and said that it sought to bring the subject to attention again.
Cross-examination of Professor James Friend
[5.100]Mr Jones began his cross-examination of Professor Friend by asking about his sources of information. He said that his report was principally based on Mr McTear's medical records. He probably read the report of the commission to take Mr McTear's evidence after he had prepared his own draft report, but he did not incorporate material from it into his final report. This was primarily a clinical report and also based on his thinking over a professional lifetime of treating patients with lung cancer. The latter part of his report changed partly as a result of his reading a number of the productions which had subsequently been lodged with the court, particularly UKHC 2000, and of course he had always been aware of the four RCP reports (RCP 1962, RCP 1971, RCP 1977 and RCP 2000), as well as USSG 1964 and USSG 1988. He had also read some of the expert reports which had been lodged on behalf of ITL.
[5.101]Although no mention was made of it in his evidence-in-chief, Professor Friend's CV stated that he had been a member of the executive committee of ASH Scotland, its acting chairman from October 1992 to February 1993, and a board member from 1995 to 2000. He said that he was not currently a member or a director of this organisation, but he contributed to it financially in a modest way. ASH was established at a time when there was increasing concern about the epidemic of deaths from smoking, in order to improve public education and to present the medical arguments. There was no such thing as membership of ASH. People subscribed to journals published by ASH and might contribute donations to it, and thus might be described as supporters. He was not aware whether supporters were invited to attend annual general meetings, though he had attended meetings in Edinburgh when he was a director and acting chairman.
[5.102]ASH, he said, was set up in about 1971 by very eminent physicians in the Royal College of Physicians in London, following the publication of RCP 1962 and RCP 1971. ASH Scotland was set up in 1973 under the auspices of the Royal College of Physicians of Edinburgh. Sir John Crofton was instrumental in that process. ASH Scotland campaigned for the implementation of effective tobacco prevention and cessation strategies, to raise awareness of nicotine as an addictive substance and to regulate the activities and products of the tobacco industry. ASH Scotland believed the most effective way to take forward the tobacco control agenda in Scotland was to work in partnership with other public health agencies, voluntary organisations and statutory bodies.
[5.103]Professor Friend said that did not know whether ASH Scotland was said in 1992 to be supporting Mr McTear's action. He had been in contact with Mr Cameron Fyfe, Mrs McTear's Glasgow solicitor, on one occasion at his office about six weeks previously. He did not know that Mr Fyfe had been engaged by ASH. Counsel asked about a statement by Mr Fyfe on the radio:
"We can only cite witnesses who are prepared to give evidence free of charge. But, having spoken to one or two experts on health, one or two doctors, they have told me they are prepared to consider that and that, if they think they can give evidence which might help the public, help the public health, then they will do that."
Professor Friend said that he imagined that he must be one of these doctors. He thought the initial contact he had about the case was a telephone call from somebody in the office of ASH Scotland in Edinburgh, who asked if he would be willing to give evidence and, if so, whether they could give his name to the solicitors involved. He said he was willing to consider this and that was how he became involved.
[5.104]Professor Friend was asked about passages in Hastings et al. 1998. He said that he knew Professor Hastings, having met him on a number of occasions at meetings related to tobacco and health, the first such meeting having taken place about twelve or fifteen years previously. He had heard of the term "media advocacy". At p.54 the authors wrote:
"Two broad ways of using media advocacy to tackle health inequalities are considered in this sub-section: media advocacy to direct attention towards the general issue of health inequality caused by poverty, and media advocacy to combat one specific phenomenon of particular relevance to low-income groups, tobacco marketing."
Professor Friend said that this was broadly his understanding of what media advocacy was, but he was not an expert in this field.
[5.105]The article continued by stating that since the publication in 1980 of the Black Report, which examined the relationship between poverty and ill health, the medical profession through the Royal College of Physicians and the British Medical Association, and other bodies, had all been "active advocates fighting health inequality by issuing regular authoritative reports, applying sustained pressure on politicians and civil servants, issuing policy statements and staging conferences and media events." Professor Friend agreed that he would like to think of himself as an active advocate fighting health inequality.
[5.106]At p.55 the authors of the article stated that much of the serious attention now being given by the United Kingdom Government to the subject of inequalities in health might be attributable to successful media advocacy throughout the 1980s and 1990s. Professor Friend said that one of the purposes of media advocacy was to put pressure on the Government to act. On the same page, under the heading "Combating tobacco marketing", the article stated:
"A widespread application of media advocacy is in scrutinizing and lobbying against the health-damaging behavior of health promotion's competitors, the alcohol and tobacco industries [...]."
Professor Friend accepted that this was a widespread application of media advocacy; he thought it was very right and proper that those who were committed to improving the public health would wish to assist it by ensuring that harmful products did not achieve undue promotion.
[5.107]The text continued:
"The bans and restrictions on tobacco advertising in many countries are attributable to a consistent stream of research and publicity about its effect on smoking prevalence, and the current wave of litigation in the US is dependent on careful examination and revelation of the industry's marketing activity [...]."
Asked whether he agreed that litigation was seen within the context of media advocacy and campaigning against health inequalities as a legitimate weapon in the arsenal, Professor Friend said that he had not seen it in that way. His concern was to help people to be healthy. He did not have a prime purpose himself in encouraging litigation, but he believed that the continuation of the promotion of cigarettes was harmful to the public health. He did not know enough about media advocacy to be able to say whether litigation was seen as a legitimate weapon. He understood it to be an aim within the concept of media advocacy, as stated in the same passage, "to expose the industry's activity to public and political scrutiny, thereby encouraging more restrictions on it."
[5.108]Professor Friend said that he had dipped into Crofton and Simpson 1992. He had probably not read a passage in a chapter entitled "Tobacco and legal action", in which it was stated that litigation both by and against tobacco companies had had a major influence in the fight against tobacco.
[5.109]The next publication Professor Friend was asked to consider was Wallack 1990, in which it was stated at p.154 that media advocacy was the strategic use of mass media for advancing a social or public policy initiative. It did not directly attempt to change individual risk behaviour but focused attention on changing the way the problem was understood as a public health issue. Professor Friend agreed that this was a strategy of which he was aware, and said that it was perfectly proper. The publication also contained the statement, at p.159:
"The goal is to empower the public to participate more fully in defining the social and political environment in which decisions affecting health are made."
Professor Friend said that he believed that this was an approach which ASH had adopted. He could not speak for ASH and had never been a big player in it, but he believed that the way one achieved changes in individual behaviour was by creating awareness of more generalised issues such as risks to health. He had never read any documents referring to the strategy of ASH, he had only been aware of its general direction and purpose.
[5.110]At p.159 of the publication it was stated:
"Creative epidemiology is the use of new scientific evidence and existing data to gain media attention and clearly convey the public health importance of an issue. It does not imply an improper use of data or misleading presentation of the facts [...]. Creative epidemiology frames data to be interesting for the media and more understandable and meaningful to the general public."
Professor Friend said that he understood the approach, which was to make the complexities of epidemiology more understandable to the general man in the street. He agreed that a document headed "Smoking and lung cancer fact sheet" which had been lodged on behalf of Mrs McTear was an example of this. This document, which was dated February 1990, started with the statement:
"Every year in this country about 110,000 people die because they smoked cigarettes. It's as bad as a jumbo jet crashing every day of the year, killing all the passengers. [...] Every two hours someone dies from lung cancer in Scotland - the highest rate in the world."
Professor Friend agreed that this was an example of the same technique, to make the figures a little more engaging.
[5.111]Professor Friend was asked about some passages in Friend 1991. In this editorial, he wrote:
"Tobacco smoking is now a major public health problem and although most people (apart from the tobacco companies) admit the link between smoking and disease, few (including many doctors) are aware of the scale of the problem. A quarter of smokers will die early because of their habit, a total of 110,000 deaths annually or 300 daily - more than four times the number of deaths from all accidents, suicide, drugs and alcohol, and acquired immunodeficiency syndrome [AIDS] put together. [...] Children are more likely to start smoking if they believe that smoking is an accepted adult habit in the community. [...] The usual answer is to say that health education in schools needs to be increased, but although many programmes have been devised there is little evidence that those who start smoking have any concern for their future health in, say, 20 years time. [...] Despite all this, there is a hope that as smoking becomes gradually less acceptable even as an adult habit and smokers are seen as victims rather than sophisticates the habit will seem less attractive to children. [...] Can doctors help? From our close and depressing knowledge of the effects of smoking we are the best placed to demand the abolition of tobacco promotion and the prohibition of sales to children and to inform people about the scale of the problem [...]. Doctors have a special responsibility to oppose the tobacco companies, who seek to replace all those who die from tobacco with new smokers and to increase their markets in the developing world."
Professor Friend said that he still held the views which he had expressed in 1991. He continued to believe that doctors had a special responsibility to oppose the tobacco companies. These companies were selling a product which was known to be harmful to health, and he thought it was entirely proper that the medical profession should make that statement.
[5.112]In Van Teijlingen and Friend 1992 Professor Friend and his co-author wrote at p.486 that several studies indicated that the smoking behaviour of the mother had a stronger influence than the father's on the likelihood of smoking by the children. Those with older brothers and sisters, who were more likely to be smokers themselves, were more likely to start smoking than those who had only younger, non-smoking siblings. Outside the home other influences were also important. For instance, the acceptability or otherwise of smoking in the community at large, in public places, and at school, and whether smoking or non-smoking was the norm. The importance of advertising in encouraging smoking could not be underestimated. It was astonishing that a product capable of causing lethal disease in a quarter of its users could still be advertised. The arguments in favour of an advertising ban were incontestable on ethical grounds. Success in the battle to reduce the disease and death caused by smoking would depend on public opinion supported by political action. At p.488 the authors stated:
"Doctors can make a major contribution in several ways, in particular because 'the general public regards doctors as the best and the most credible source of health information.'"
Professor Friend said that he still held the views expressed in this editorial. He believed that doctors could and should be health advocates. The tobacco industry were the real enemies, because the health problems created by tobacco had been perpetuated through their activities.
[5.113]In his report, Professor Friend had quoted from a report by Dr Keith Kerr on the pathological material taken from Mr McTear. In this passage, Dr Kerr reported that there was evidence of moderate squamous dysplasia, part of the recognised spectrum of pre-malignant changes which occurred in the bronchial mucosa during the development of carcinoma in the central bronchi. Professor Friend added in his report the statement that the clinical presentation and progress of the disease were entirely compatible with this diagnosis. The presence of squamous dysplasia was a pre-malignant change often found in heavy smokers who went on to develop lung cancer. When asked about this, he explained that he had worked all the time in close communication with respiratory pathologists and they had discussed virtually all the reports for each patient as they came through. He became well accustomed through his clinical practice to know that this change of squamous metaplasia was a common finding in patients who were heavy smokers and who subsequently developed bronchial carcinoma. So this statement came from his clinical experience, instructed by his pathological colleagues. He said that he believed that dysplasia was one of a number of changes which might be found on histopathological examination of a sample from the lung, but this was a question which should be asked of a pathologist. He suggested that counsel should not pursue the question of squamous dysplasia further with him. He was familiar with the term. It was a common part of the reporting by pathologists which he had seen many times. He felt entitled to make the comment in his report from regularly finding these phrases in pathological reports. He suggested that Dr Kerr be asked about the question whether the presence of squamous dysplasia was a pre-malignant change often found in heavy smokers. He accepted that such changes could be found in the lungs of those who had not been diagnosed with squamous cell carcinoma. He did not know that it could be found in the lungs of those who had succumbed to influenza.
[5.114]Professor Friend was asked in this regard about passages in Winternitz et al. 1920. He said that he was aware of the pandemic of influenza in 1918. The authors reported on their pathological findings at autopsy on persons who had died of this disease in New Haven, Connecticut. Asked about certain findings reported by the authors, Professor Friend said that he was aware that any irritative process was bound to cause histological change. He had not at any stage suggested that squamous metaplasia was unique to cancer. They also reported that epithelial proliferation in many cases invaded the surrounding lung tissue and a typical histological picture resulted of an infiltrating, malignant, epithelial neoplasm. Professor Friend agreed that this fitted the description of the progression of cancer. The authors also stated that in a number of cases epithelium proliferation had been so extensive that it could not be differentiated histologically from an invasive, malignant neoplasm. There was no reason to believe that malignancy might not result from the continuous stimulation of the epithelium to proliferate, in the chronic inflammatory process of the lung in influenza. Professor Friend said that when it was written this was perhaps commensurate with knowledge at the time, but he thought it was irrelevant to modern practice. He accepted the observations but not the interpretation. At no point had the authors said that there was any evidence of a malignant neoplasm in persons who had suffered from influenza.
[5.115]Professor Friend was next asked about the statement in his report that the diagnosis of squamous cell lung cancer in non-smokers was exceptional and it could be argued that some of these unusual patients might have contracted the disease through the inhalation of tobacco smoke in the home or at work, despite not being active smokers themselves. In his opinion, and that of a number of other authorities, passive inhalation of tobacco smoke might cause lung cancer in non-smokers. He was saying this as a matter of fact, on a review of the literature which had been carefully compiled by the Scientific Committee on Tobacco and Health which reported in 1998. He had not cited this literature in his report.
[5.116]Professor Friend said that he was aware of Enstrom and Kabat 2003. He had read the summary of this paper and had dipped into the rest. The objective of the study was to measure the relation between environmental tobacco smoke, as estimated by smoking in spouses, and long term mortality from tobacco related disease. The design was that of a prospective cohort study covering 39 years, the subjects being 118,094 adults in California enrolled in late 1959 in the American Cancer Society Cancer Prevention Study, who were followed until 1998, with particular focus on the 35,561 never smokers who had a spouse in the study with known smoking habits. The authors concluded that the results did not support a causal relationship between environmental tobacco smoke and tobacco related mortality, although they did not rule out a small effect. The association between exposure to environmental tobacco smoke and coronary heart disease and lung cancer might be considerably weaker than generally believed. The authors explained how they had arrived at the age adjusted relative risk, with 95% confidence interval, for never smokers married to ever smokers compared with never smokers married to never smokers, and that no significant associations were found for current or former exposure to environmental tobacco smoke before or after adjustment for confounders. They also referred to meta-analyses of epidemiological studies. Asked about this latter expression, Professor Friend said that he was not an epidemiologist, but he believed it to be a valid technique of assessing an issue. So far as the conclusion reached by the authors was concerned, he drew attention to the funding source for the study, about which there was a statement at p.1060. This was that the latter part of the study was supported by a research organisation that received funding primarily from United States tobacco companies. He said he thought that this called into question the integrity of the interpretation of data by the authors. He believed that there had been a history over a number of years where the papers which had emerged from tobacco-sponsored research had always approached the problem with a particular slant. His lack of trust revolved around the reluctance of the tobacco industry to accept the clear association and causal role of tobacco in causing lung cancer. He accepted that a paper submitted for publication in the British Medical Journal, as this had been, would be subjected to peer review.
[5.117]Professor Friend said that he believed that he was aware what were the duties to the court of an expert witness. He said that they were to respond to questions within his range of expertise and to comment on the basis of his experience and knowledge. He did not think that he was fully aware that it had been judicially stated in England and in Scotland that among the duties of an expert witness was to bring to the attention of the court material which was contradictory of that witness's position. At this particular point in his report, since he was not asked to address the issue of passive smoking and it had no particular relevance to this case, he did not feel it was necessary.
[5.118]Asked about the statement that tobacco smoke contained known carcinogens, Professor Friend agreed that there were many known carcinogens in the environment. One would be concerned to know their concentration and perhaps their method of exposure or site of exposure in the human body. Whether there should be concern about carcinogens would depend on, amongst other things, the dose. The carcinogens he had in mind were a number of products which included nitrosamines, benzo[a]pyrene, polonium and others, but he was not a chemist and did not know more than that. He was referred to Wynder and Wright 1957a. He said that he had not heard of Wynder before he began reading some of the papers in connection with this case. In this paper the authors stated that several recent investigations had demonstrated condensed cigarette tar to be carcinogenic to the skin of several strains of mice as well as to that of rabbits. In view of these results, it became of interest to determine the nature of the carcinogen or carcinogens responsible for these observations. For this reason a combined chemical and biological study programme was undertaken in 1952. Professor Friend said that he was not sure that he could offer any expert advice on this sort of topic. He was not a toxicologist, he was a serving clinician. The authors reported that the benzo[a]pyrene content of the total tar as well as of the active fractions was far too low to account alone for the positive results. So far, no carcinogens had been identified in large enough quantity in tobacco tar or its fractions to account for the observed activity. Current efforts were directed towards the identification of carcinogens not yet identified which might be the most important ones in tobacco tar. Professor Friend accepted that this was being said about benzo[a]pyrene in 1957.
[5.119]Professor Friend was next asked about Passey 1962. He did not know who Passey was. The paper stated that he was Emeritus Professor of Experimental Pathology at the University of Leeds, and was writing from the Chester Beatty Research Institute at the Royal Marsden Hospital in London. He suggested that lung cancer might well be a sequel to tissue damage of a non-specific nature rather than to the specific action of carcinogens. On the topic of smoking, he stated:
"It is now accepted that smoking increases the risk of lung cancer, and that the heavier the smoking the greater the risk. But nowhere has it been claimed that the heavy smoker is stricken with cancer earlier than the light smoker. If lung cancer in smokers is a result of direct carcinogenic action, one would certainly expect this to happen; for experiment has shown beyond question that a potent carcinogen induces tumours early."
Professor Friend said that those with opposing views were now no longer present, in the sense that there were only a tiny minority of people who did not accept that smoking caused lung cancer. Asked what was wrong with the question posed by Passey, he said that he was not sure and he could not answer the question whether the statistics clearly suggested that heavier smokers developed lung cancer earlier than light smokers. What he did know was that people who started smoking younger were more prone to develop lung cancer than those who started smoking at a later age. The question posed by Passey was respectable. He did not know that experiment had shown beyond question that a potent carcinogen induced tumours early. He said:
"I should emphasise [that] I am not a toxicologist, I am not an epidemiologist, I am a clinician who obtains information about the cause of disease from my reading elsewhere."
[5.120]In USSG 1964 at p.58 reference was made to assays of tobacco smoke tars for carcinogenicity by mouse skin painting. It was reported that the total tar from cigarettes had about forty times the carcinogenic potency of the benzo[a]pyrene present in the tar. The other carcinogens known to be present in the tobacco smoke were, with the exception of dibenzo[a.i]pyrene, much less potent that benzo[a]pyrene and were present in smaller amounts. Apparently, therefore, the whole was greater than the sum of the known parts. This was a "puzzling anomaly". Asked about this, Professor Friend said that he did not know whether this anomaly was ever finally resolved by the use of experimentation or otherwise.
[5.121]Reference was next made to Lijinsky 1971. Professor Friend said that he had not heard of Dr Lijinsky, who was stated to have held research fellowships at various institutes before becoming Professor of Biochemistry at the University of Nebraska Medical Centre in Omaha. Dr Lijinsky said that the increasing interest in the nitrosamines as a class of carcinogens derived largely from the failure to relate other types of cancer-causing agents with human cancer. It was impossible to correlate the infinitesimal amount of benzo[a]pyrene and other polynuclear compounds in tobacco smoke with the rather high incidence of lung cancer among cigarette smokers. Most of the known types of carcinogenic agents were very restricted in the number of organs and tissues of animals in which they induced tumours. Professor Friend said that he had not known of this before coming to give evidence.
[5.122]In USSG 1964 at p.229 it was stated that the amount of known carcinogens in cigarette smoke appeared to be too small to account for their carcinogenic activity. Professor Friend was asked about Falk et al. 1964. He had not heard of these researchers and said that it was literature he was quite unfamiliar with. In this paper the authors discussed the inhibiting effect of chemically-related compounds on the carcinogenic potency of carcinogenic agents. They stated that of the various properties of environmental carcinogenic agents studied thus far, the one with the greatest apparent deficiency in data was that concerned with the relationship of chemical carcinogens to other chemical compounds formed simultaneously with them, or introduced into the environment from other sources. These data were particularly pertinent in attempting to assess the quantitative role of carcinogens present in polluted urban air and cigarette smoke in the pathogenesis of lung cancer. It had been recognised for a considerable time that weak and strong carcinogens might either summate their effect or exert an inhibiting effect upon one another. The authors concluded their study by stating that the activity of carcinogenic hydrocarbons could be inhibited by closely-related pure compounds or by crude mixtures, including a spectrum of polycyclic aromatic hydrocarbons when both carcinogen and anti-carcinogen were administered simultaneously. Though this effect was maximum when the agents were administered simultaneously, inhibition could also be observed when the anti-carcinogen was administered several days before or after the administration of the carcinogen. Professor Friend said that he was not aware of this conclusion. It was quite outwith his area of expert knowledge.
[5.123]In Peto and Doll 1985, with the authors of which Professor Friend said that he was familiar, it was stated that governments could reduce tobacco consumption and the amount of tar delivered by cigarettes without affecting personal freedom. Thirty years of laboratory research had yet to identify reliably the important carcinogenic factors in cigarette smoke. Consequently, it was necessary to discover by epidemiological observation whether the switch to lower tar cigarettes materially reduced the risks of lung cancer. Beyond noting this, Professor Friend was not asked to comment on this paper.
[5.124]In Goldstein 2001 the author stated that the lack of cancer tumorigenicity of ingested benzo[a]pyrene contrasted with the extensive body of information that demonstrated the efficacy of benzo[a]pyrene for inducing skin tumours in mice when applied directly to skin. Polycyclic aromatic hydrocarbon metabolism was different in different organs. Mouse skin had some metabolising enzymes in common with mouse liver but lacked others. For benzo[a]pyrene, tumorigenicity in skin following a topical administration did not predict tumorigenicity in lung following ingestion. Polycyclic aromatic hydrocarbons were always found as complex mixtures, but most laboratory studies were conducted using a single chemical. Results from studies with a single agent might not predict results when that agent was part of a mixture of other chemicals. Benzo[a]pyrene in the presence of other polycyclic aromatic hydrocarbons in a mixture formulated to approximate their relative abundance in an environmental coal tar did not induce tumours, whereas benzo[a]pyrene by itself did. One interpretation was that the other polycyclic aromatic hydrocarbons reduced the tumorigenic effectiveness of benzo[a]pyrene. If this was generally true, the actual potency of benzo[a]pyrene in environmental polycyclic aromatic hydrocarbons might be much less than the potency determined in studies of benzo[a]pyrene alone. Professor Friend said that he did not know that polycyclic aromatic hydrocarbon metabolism was different in different organs. As he had said earlier, work in animals could not be directly transferred to human experience. He accepted as a matter of general science that results from studies with a single agent might not predict results when that agent was part of a mixture. He had no view on the finding that benzo[a]pyrene in the presence of other polycyclic aromatic hydrocarbons in a mixture as described in the paper did not induce tumours. It was stated in IARC 1986 that tobacco smoke contained forty known carcinogens. Professor Friend agreed that there was nothing in that publication which contradicted what was written in Goldstein 2001 about the need to think about the action of constituents in complex mixtures.
[5.125]Professor Friend was next asked about the statements in his report that the prevalence of lung cancer was closely related to the level of consumption, that epidemiological data provided clear links between historical smoking levels in different countries and lung cancer incidence, and that there was a dose-response relationship between an individual's consumption and the risk of developing lung cancer. No references were given in support of this passage. Professor Friend said that the assertion came from the many reports which he had referred to in his earlier evidence, the reports of the Royal College of Physicians and the United States Surgeon General. During his career he imagined that he had read some of the papers that were presented to the Royal College of Physicians, but certainly not all of them. A practising physician's duty was to distil what was available from the readily accessible medical literature and to follow his practice accordingly. He had been happy to rely on reports produced by learned people for whom he had a high regard.
[5.126]He agreed that "prevalence" referred to the level of disease observed at a given point in time without regard to any time period. His assertion that there was a dose-response relationship between an individual's cigarette consumption and the risk of developing lung cancer was justified substantially by his readings of the results of Doll and Hill's study on British doctors. It was true that Doll and Hill were not concerned with any individual, but with populations of people. An individual in that population could be assessed as having a higher risk depending on their smoking habit. It was true that one individual might smoke twenty cigarettes a day and be diagnosed with lung cancer after twenty years, whilst another individual might smoke fifty a day and never develop lung cancer. An individual might not smoke and yet be diagnosed with lung cancer after ten years. The probability of developing lung cancer, he insisted, was increased by his smoking habit. He was using the word "individual" in contradistinction to a whole population in a given country.
[5.127]Professor Friend agreed that it was ultimately a matter of judgment whether it could be concluded that an increasing strength of association with increased levels of smoking that was observed in populations was a cause and effect relationship. He did not know whether he could answer the question whether if that relationship were one of cause and effect, one would expect that increasing levels of smoking would result in an earlier age of diagnosis of lung cancer. He was not aware that researchers had repeatedly found that the age of diagnosis of lung cancer was unrelated either to level or to duration or smoking. He believed other researchers might have found otherwise, but he was not familiar with the detailed literature in that area. He believed that the statement that those who started smoking earlier and therefore who smoked for a longer period of time were more prone to develop lung cancer at an earlier stage came from the public health material, but he could not state precisely where. He did not know whether it was correct that age of diagnosis of lung cancer was not dependent even on whether or not the person smoked at all.
[5.128]Professor Friend was referred to Pike and Doll 1965. In this paper the authors stated that from their results it was evident that Passey's two principal results - that neither the amount smoked nor the age at starting made any substantial difference to the "period" average age at onset of the disease - were valid also for the "lifespan" average under the conditions in which lung cancer was produced in man and followed directly from the observed relationships between age-specific mortality rates and the duration of smoking. Professor Friend agreed that the authors of this paper appeared to agree with Passey 1962.
[5.129]Herrold 1972 stated that the statistical data concerning smoking revealed that a high percentage of lung cancer occurred in smokers. Only a small percentage of heavy cigarette smokers developed lung cancer. In one study, only 9.9% of heavy smokers - those who smoked one or more packs of cigarettes per day - had lung cancer. The other 90.1% who were heavy smokers did not develop lung cancer but died from other causes. Professor Friend said that he broadly agreed with these statistics, though he concluded that it was more like 16% of heavy smokers who developed lung cancer. Herrold 1972 stated of the histologic sections which the author had reviewed that there was no correlation found between the histologic type of primary lung cancer and the amount of tobacco smoked among the "current smokers of cigarettes only". The age at death from lung cancer in this smoking category was not related to the age at which smoking started, the number of years of smoking or the number of cigarettes smoked per day. Professor Friend said that he had no basis for challenging this conclusion: he was prepared to accept it as a statement of the evidence at the time that the paper was printed. He believed that there was a body of knowledge which might have accumulated since 1972 which might provide the answer to the question whether there was any work which contradicted Herrold's conclusions, but he could not point to it.
[5.130]Professor Friend said that he did not agree that if the dose-response relationship he referred to was one of cause and effect, it would be expected that there would be a higher incidence of lung cancer among those who inhaled than among those who did not. He did not believe that inhalation was an assessable factor in smoking. Not enough was known about the distribution of tobacco smoke in the lungs of "declared inhalers" and those who did not inhale. It was a very complex relationship. How cigarette smoke particles were deposited in the lung depended on many other factors. He was asked about Doll and Peto 1976. In this paper the authors reported on twenty years' observations on male British doctors. In questionnaires the doctors who smoked were asked whether they thought they inhaled the smoke. The authors stated at p.1530 that the results showed a notably higher mortality among men who said they inhaled than among men who said they did not for chronic bronchitis, emphysema and pulmonary heart disease, for ischaemic heart disease at young ages, and for other conditions closely associated with smoking, but not for cancer of the lung, cancers of the oesophagus and other respiratory sites, or for any other group of diseases. Indeed, the mortality rate for lung cancer was lower among inhalers than among non-inhalers. This last result corresponded to that in a retrospective study by Doll and Hill published in 1952. Professor Friend agreed that the authors of this paper had thought it was worthwhile to ask about inhalation and had felt able to draw conclusions from the evidence they were given. They also confirmed earlier work, recorded in Doll and Hill 1950. In this paper the authors stated that one anomalous result of their inquiry appeared to relate to inhaling. It would be natural to suppose that, if smoking were harmful, it would be more harmful if the smoke were inhaled, but in fact it did not seem to make any difference whether the patient inhaled or not. In the present state of knowledge, it was reasonable to accept the findings and await the outcome of research into the effect which any alteration in the rate and depth of respiration might have on the extent and site of deposition of the carcinogen.
[5.131]Professor Friend was next asked about the statement in his report that epidemiological data provided clear links between historical smoking levels in different countries and lung cancer incidence. He cited no papers in support of this. He said in his evidence that he had read books and other material which had in the past led him to believe this and he was making a statement based on his knowledge accumulated over a period of time. He could not say what these publications were. His purpose in making these statements was to express his views as to the causation of Mr McTear's condition, based on his clinical experience. He agreed that what he had to say about epidemiological data about historical smoking levels in different countries was not derived from his clinical experience.
[5.132]Professor Friend was asked about Doll 1953. In this paper it was stated that no figures were available for assessing the incidence of lung cancer in Britain other than the mortality statistics of the Registrars-General. These statistics were subject to the inaccuracy inherent in the certification of causes of death. Not all workers were agreed on the conclusions to be drawn from the increase in the reported mortality since 1900. Rigdon and Kirchoff 1952, for example, continued to believe that the increase was wholly spurious. At a then recent international symposium it was agreed that a significant part of the increase was absolute and represented a real increase in the number of people suffering from cancer of the lung. Doll regarded this conclusion as reasonable. At p.523 he stated:
"How much of the increase is real after standardizing for age and sex remains uncertain. The extent of the change in the last five years, when the importance of the disease has been recognized and facilities for diagnosis have been readily available, suggests that the real increase is likely to be large. I believe it may well be more than half. On the other hand, I would think it certain that some of the increase is nosological and some is due to the therapeutic advance which prevents death from pneumonia before the presence of the underlying growth is evident."
Professor Friend agreed that it was clear that it could not be accepted that the whole of the apparent increase between 1900 and 1953 was real and that some believed it was completely artefactual. He accepted that others would be free to express different views, based on their judgment, from those of Doll.
[5.133]Professor Friend was next asked about Burch 1983. In this paper the author stated that so far as he was aware there was no inherent reason why the association between smoking and lung cancer, in spite of its strength in Caucasoid populations, should not reside in the genome. A dose-response relation was important to the hypothesis that the association between smoking and lung cancer was one of cause and effect. But if heavy smokers were genetically predisposed and light smokers were not, the association with lung cancer would be relatively weak among the group of light smokers and strong among the group of heavy smokers, and an apparent dose-response relation would be observed. Professor Friend said that he agreed with this hypothesis. Burch went on to refer to a "pure" causal hypothesis in which the association would be free from biological interference. He contrasted this with a "pure" constitutional hypothesis which predicted that the association between smoking and lung cancer depended, not on smoking levels, but on the strength of the associations between predisposing genotypes. He pointed to anomalies in various studies. At p.826 he stated:
"The existence of a weak correlation between national rates of mortality and smoking is consistent with a causal component but it is also consistent with a pure constitutional hypothesis and no causal action. However, for this type of evidence to be definitive it would be necessary to ensure comparability of death certification for lung cancer and, when testing the causal hypothesis, to have a good theory of the mechanism whereby cigarette smoking causes lung cancer so that explicit assumptions about temporal relations between the two could be adopted. One of the most unfortunate features of [the causal hypothesis] is that no good theory of mechanisms is available that is consistent with the salient features of epidemiologic evidence [...]."
Professor Friend said that he agreed with the approach proposed by Burch.
[5.134]Reference was also made to Doll and Hill 1954, in which the authors stated that the great majority of the observed facts accorded with the causal hypothesis, but the picture was not yet complete. It was necessary to know, in particular, why the mortality from the disease in the United States was so low relative to the past consumption of cigarettes and why the association which appeared to exist between cancer of the larynx and cigarette smoking had not been reflected in an increase in the incidence of cancer of the larynx comparable to that believed to have occurred with cancer of the lung. Professor Friend agreed that Doll and Hill recognised that there was a relatively low mortality from lung cancer in the United States, compared with England and Wales. Burch 1983 referred to a report of an inconsistency between the age-standardized mortality from lung cancer in Finnish men being about double that in United States white men, whereas cigarette consumption in Finland in 1950 was about half that in the United States. Professor Friend agreed that this was another apparent inconsistency which did not provide a clear link between historical smoking levels in different countries and lung cancer incidence. As he understood it, the reports prepared by the Royal College of Physicians and other bodies stated otherwise, but he accepted that this was what was stated in this paper.
[5.135]Professor Friend agreed that when the Royal College of Physicians came to prepare their reports they had to exercise a judgment on causation. If they had good evidence of a strong statistical association between an exposure and a disease, he would expect them to incline towards warning the public to avoid the exposure. If the exposure was seen by some as having little or no social benefit, then it was easier to form the view that the public should be advised to avoid it. That was absolutely fair as a statement. One would expect the public health community to attempt to persuade the public to avoid the exposure by giving a clear and consistent message and to express the view that the association that they had found was causal. This was on the basis that if the association was not causal but there were no social benefit in the exposure, then it could not do any harm and might do some good to persuade people to avoid the exposure. It would not be consistent with putting out a clear message in an attempt to persuade people to avoid the exposure if one were to clutter the message with references to doubts and ambiguities in the material. He believed, however, that in much of the material many of these uncertainties were addressed and an opinion was given. At the end it was necessary to give a clear and persuasive opinion.
[5.136]Professor Friend was next asked about his statement that gender differences in lung cancer risk could also be largely explicable on the basis of smoking habits. Reference was made to Fisher 1959. He said that he had heard of Sir Ronald Fisher and believed him to have been the father of modern statistical methods. In this pamphlet, Fisher said that it was possible to enquire whether or not the rate of increase in lung cancer in men was the same as that in women. Whereas the smoking habits of men had not changed very dramatically over the previous fifty years, yet the smoking habits of women had changed a very great deal. On making that comparison, it appeared that lung cancer was increasing considerably more rapidly - absolutely and relatively - in men than it was in women, whereas the habit of smoking had certainly increased much more extensively in women than in men. Professor Friend said that he thought that Fisher was correctly stating the facts at the moment. Fisher continued by stating that there was in fact no reasonable ground at all to associate the secular increase in lung cancer with the increase in smoking, as had been done with dramatic eloquence. Professor Friend said that he did not agree with this, because Fisher did not address the time-course of the increase in smoking in women and its relationship to the increased prevalence of lung cancer in women. When Fisher was writing in 1959 he would not have been aware of the full increase in prevalence among women which took place subsequently.
[5.137]Reference was next made to more papers by Burch. In Burch 1974a the author, who then had a personal Chair in the Department of Medical Physics at the University of Leeds, referred to the different conclusions reached in reports such as RCP 1971, on the one hand, and Sir Ronald Fisher on the other. He said that having at one time accepted that most cases of lung cancer were caused by smoking, the evidence forced him to change his mind. In a table he plotted the proportion of population by sex at apparent risk with respect to lung cancer, and annual cigarette consumption per adult male or female, during the period from 1890 to 1970. He said that the thirty years gap in cigarette consumption between men and women was of inestimable value in testing hypotheses of cigarette-related secular change in the incidence of disease. If the curve for women in the figure was shifted thirty years to the left to allow for the thirty-year lag in their smoking habits compared with those of men, the synchronism of change predicted by the causal hypothesis was absent. Burch 1975 reported that data for England and Wales 1901 to 1970 were analysed by quinquennia. Their characteristics did not support a causal hypothesis of the association between cigarette smoking and lung cancer. Professor Friend said he had not read this paper. He was relying on other data in expressing a contrary view to that of Burch. He believed that Burch's opinion was not shared by others at the time and was not shared now by the vast majority of physicians in practice. He himself did not agree with the broad conclusions because of the information that he had read in other places, in reports by the Royal College of Physicians and other reports.
[5.138]In discussing an association between a habit and a disease, Burch stated that it was not widely appreciated that a negative association between the habit and the disease need not preclude the hypothesis that the habit caused the disease. A strong constitutionally-based, negative association could, in principle, overwhelm a weaker, positive causal association. Professor Friend said that he was not sure if he fully understood the sentence. Asked: "Shall we go to an epidemiologist?", he said, "Yes".
[5.139]Burch referred to the work of Tokuhata and Lilienfeld 1963, showing that the prevalence of smokers among the first-degree relatives of non-smoking lung cancer probands was significantly higher than among the corresponding relatives of non-smoking matched controls. Professor Friend was not aware of that work. Burch stated of it that in conjunction with other evidence, this finding implied an association between at least one of the genotypes that predisposed to smoking and at least one of the genotypes that predisposed to lung cancer regardless of any causal connection. In his paper, Burch said that for lung cancer in men the secular increase was much too large to be explained in terms of the increase in cigarette smoking. Secular increases in lung cancer rates had occurred in both sexes, although almost synchronously, and the increase in men far exceeded that in women. Asked whether he agreed that it appeared that Burch did not accept the proposition that gender differences in lung cancer risk were to be explained on the basis of smoking habits, Professor Friend said that his difficulty was in understanding the graphical presentation of his investigation, in which he was not an expert. The paper concluded with the statement that difficulties abounded in the interpretation of cancer statistics, especially those for lung cancer, a disease for which the clinical diagnosis was unreliable. The verdict in Fisher 1959 would be as clear in retrospect as it then was in logic. The data so far did not warrant the conclusions based upon them. Professor Friend said that he was not able to help with the question whether or not the data, or the conclusion that lung cancer was almost entirely due to cigarette smoking, stood up to critical analysis.
[5.140]In his report Professor Friend stated that cigarette smoking was not the only risk for lung cancer and occupational exposures to substances such as asbestos, various metals, hydrocarbons, radiation and diet had all been identified as potential risk factors. When asked about this, he agreed that alcohol consumption was another such risk factor. He was referred to Pollack et al. 1984. According to the abstract of this paper, the relation between alcohol consumption and the subsequent occurrence of the five most frequent cancers in a cohort of Japanese men in Hawaii was analysed in a prospective study. The analysis, which was adjusted for the effects of age and cigarette smoking, revealed a positive association between consumption of alcohol and rectal cancer. A significant positive relation between alcohol consumption and lung cancer incidence was also found, accounted for primarily by an increased risk among subjects who consumed larger amounts of wine or whiskey, as compared with the risks among nonconsumers of these beverages respectively. No significant relation between alcohol consumption and the incidence of the other three cancers was found. Professor Friend agreed that this was material which went to show that alcohol consumption was a risk factor for lung cancer, adding that it obviously depended on the degree.
[5.141]Professor Friend also agreed that low socio-economic status was also a risk factor for lung cancer. He was referred to Hein et al. 1992. In this paper the authors stated that during the previous decade a number of studies had demonstrated that in addition to there being an increased risk of lung cancer in smokers, as had first been observed in 1950, the existence of social inequalities added to the risk of lung cancer. The Copenhagen male study in a long-term follow-up provided data that made it possible to study the interaction of different forms of smoking, different socio-economic backgrounds and future risk of lung cancer. They concluded that substantial social inequalities existed in the risk of lung cancer. Smoking men belonging to the lowest social classes had a three times higher risk of lung cancer than men belonging to the upper social classes. These inequalities could not be explained by baseline differences in smoking habits, nor in available information of occupational exposure to dust, fumes and insulation materials. They concluded that the substantial social inequalities in lung cancer could only to a minor degree be explained by social class differences in tobacco smoking habits.
[5.142]Reference was also made to Van Rossum et al. 2000. This related to a follow up of civil servants from the first Whitehall study. Professor Friend said that he was not aware of this. The objective of the study was to test the hypothesis that the association between socio-economic status and mortality rates cut across the major causes of death for middle-aged and elderly men. The authors found that after more than twenty-five years of follow-up on civil servants aged 40 to 69 years at entry to the study, employment grade differences still existed in total mortality and for nearly all specific causes of death. The main risk factors, among them smoking, could only explain one third of this gradient. The authors concluded at p.183 that socio-economic differentials in mortality still persisted at older ages for almost all causes of death. Together with more general socio-economic factors, working conditions themselves might affect a broad range of health inequalities among middle-aged men. In addition, social differentials influenced most causes of disease and these effects continued through retirement. Professor Friend agreed that this was another study which vouched what he understood to be the case, that low socio-economic status was a risk factor for lung cancer. He added that the study appeared to reflect gradations among white collar workers.
[5.143]Professor Friend said that he was not aware that stress and depression had been associated with lung cancer. He was asked to consider Knekt et al. 1996. This study related to the association between depressiveness and the subsequent incidence of lung cancer in the nationally representative mini-Finland health survey. The authors found that the relative risk of lung cancer between depressive persons and individuals with a normal depressive score was 3.32 with a 95% confidence interval. Neither adjustment for the potential confounding factors of age, education, geographic area, smoking, alcohol consumption, body mass index, serum cholesterol, leisure time exercise, general health, and use of anti-depressant medication, nor exclusion of cancer cases occurring during the first four years of follow-up, notably altered the results. The authors stated that there was a strong interaction between depressiveness and smoking. It was possible that depressiveness modified the effect of smoking on lung cancer risk, either by biological mechanisms or by affecting smoking behaviour.
[5.144]Professor Friend said that he believed he was aware that differences between urban and rural living were a risk factor, and that living in West Central Scotland was a risk factor for lung cancer. He was referred to Gillis et al. 1988b. In this study a general population cohort of men from Renfrew and Paisley were followed. Analysis of cigarette smoking and lung cancer (incidence and mortality) relation was undertaken in order to establish whether unusual results found in a previous case-control study of cigarette smoking and lung cancer in Glasgow could be confirmed. Lung cancer incidence and mortality rates increased markedly for exposure categories up to an average consumption of fifteen to twenty-four cigarettes per day. Above this level, the rates increased only marginally. Expressing these rates relative to that estimated in the never-smoked group and comparing them with the relative risks estimated in the case-control study revealed a similarity in terms of both the shape and the level of the dose-response relation. The authors concluded at p.47 that it was not just the West of Scotland smoker who was at an increased level of risk, compared with his equal smoking counterpart elsewhere, but the West of Scotland non-smoker might also experience a higher than expected lung cancer risk. The flattening of the dose-response relation seen in the case-control study had not been explained by any of the smoking characteristics examined. The results of the cohort study led the authors to believe that this flattening was a genuine representation of the smoking and lung cancer relation in the West of Scotland. The reasons for this were less obvious. Professor Friend agreed that this study was in line with what he understood to be the position, that living in the West of Scotland was a risk factor for lung cancer.
[5.145]Professor Friend was next asked about his statement that the proportion of lung cancer mortality attributable to smoking was estimated in RCP 2000 to be 89% in males in the United Kingdom. He was referred to a statement in Callum 1998 that in the United Kingdom in 1995 nine out of ten lung cancer deaths among men and three in four among women were caused by smoking and that smoking caused 30% of all deaths from cancer. He agreed that the figure for deaths from lung cancer attributable to smoking in RCP 2000 was derived from Callum 1998. In RCP 2000 the figure was 89% for men. RCP 2000 gave estimated figures for 1997. For men, the numbers of deaths from lung cancer estimated to be caused by smoking were stated to be 90% and for women 73%, a total of 84%. UKWP 1998 stated that smoking caused 84% of deaths from lung cancer. Professor Friend said that he did not know how it had been estimated that 89% of lung cancer deaths in men were caused by smoking. He agreed that smoking was not given as a cause of death where a person who had been a smoker died from lung cancer.
[5.146]Counsel attempted to put an example to Professor Friend of how an estimate might be arrived at. Professor Friend said: "I do not know what statistical methods you would use. You would need to ask a statistician." Counsel put an example to Professor Friend which involved the determination of the prevalence of an exposure in a population and the calculation of an attributable fraction. Professor Friend said that this was not a technical phrase that he was aware of, but he could understand what it might mean. Counsel then put an illustration which involved the calculation of an attributable fraction. Professor Friend said that he would prefer to say that this was not part of his expertise and that the data he used in his report were derived from other reports which he took as being valid. Counsel then asked Professor Friend about an illustration which assumed that there existed the same statistical association between a disease and exposure to another substance, leading to the same attributable fraction. Professor Friend agreed that this model was not disease-specific or exposure-specific, it was just a mathematical model. Pressed further, however, he said that he believed that he was being taken beyond his level of expertise and he would prefer that this be taken up with one of the other expert witnesses, in particular Sir Richard Doll. He did not know that he was qualified to give an answer to the consequences of calculating attributable fractions where there was a statistical association between a disease and exposure to more than one risk factor. He believed that he would invite a statistician who was experienced in techniques to examine these very issues, to examine the evidence, and this was indeed what, in his view, had happened. "Experienced statisticians of the status of Sir Richard Doll have assessed all of these aspects, and I am not competent to make further analysis of that sort of data."
[5.147]Counsel asked Professor Friend about passages in Rothman and Greenland 1998. At p.13, the authors, both professors of epidemiology, referred to "the naïve view that every case of disease has a single cause". They continued:
"In fact, since diet, smoking, asbestos and other factors interact with one another and with genetic factors to cause cancer, each case of cancer could be attributed to many separate component causes. There is a tendency to think that the sum of the fractions of disease attributable to each of the causes of disease should be 100%. For example, in their widely cited work, The Causes of Cancer, Doll and Peto (1981: Table 20) created a table giving their estimates of the fraction of all cancers caused by various agents; the total for the fractions was nearly 100%. Although they acknowledged that any case could be caused by more than one agent (which would mean that the attributable fractions would not sum to 100%), they referred to this situation as a 'difficulty' and an 'anomaly'. It is, however, neither a difficulty nor an anomaly, but simply a consequence of allowing for the fact that no event has a single agent as the cause. The fraction of disease that can be attributed to each of the causes of disease in all the causal mechanisms has no upper limit: For cancer or any disease, the upper limit for the total of the fraction of disease attributable to all the component causes of all the causal mechanisms that produce it is not 100% but infinity. Only the fraction of disease attributable to a single component cause cannot exceed 100%."
Professor Friend said that he agreed with the proposition that each case of cancer could be attributed to many separate component causes. He agreed with the argument as set out in the remainder of this passage, but he suggested that the questions be directed to an epidemiologist. He did not know that he had expertise to give a full response. Counsel put to him that it was a matter of logic rather than science. Professor Friend said that he thought it was a matter more of science and the interpretation and application of statistical method to data. He could not say what within the proposition was special to the field of epidemiology rather than arithmetic and logic.
[5.148]On the same page, Rothman and Greenland wrote:
"[E]very case of every disease has some environmental and some genetic component causes, and therefore every case can be attributed both to genes and to environment. No paradox exists as long as it is understood that the fractions of disease attributable to genes and to environment overlap with one another."
Professor Friend said that he quarrelled with the statement that every case of every disease had some environmental and some genetic component causes, but he agreed that lung cancer was a case where there were both genetic and environmental components.
[5.149]Professor Friend was next asked about passages in Gori 1989. According to the abstract of this paper:
"Unlike infectious diseases of the past, diseases prevalent in modern industrialized societies have multifactorial origins whose complexity so far has defied an integrated scientific understanding. Their epidemiologic investigation suffers from the conceptual inability of formulating plausible causal hypotheses that mimic a complex reality, and from the practical difficulties of running elaborate studies controlled for multifactorial confounders. Until biomedical research provides a satisfactory understanding of the complex mechanistic determinants of such diseases, epidemiology can only field reductionist causal hypotheses, leading to results of uncertain significance. Consensual but rationally weak criteria devised to extract inferences of causality from such results confirm the generic inadequacy of epidemiology in this area, and are unable to provide definitive scientific support to the perceived mandate for public health action."
Professor Friend said that he agreed with the statements in the first three sentences, and that what was being discussed in the fourth sentence was a division between definitive scientific support and the perceived mandate for public health action. He said that the argument was that the public health community had a responsibility to prevent disease where they felt that there might be some action which could prevent it. If it seemed probable, even though not absolutely proven, that a particular situation was causing damage, it was perfectly proper and indeed to be expected of public health authorities that action be taken. This was so where there was a strong association between an exposure and a disease, and the exposure could be removed without any harm. If the exposure was one with no social benefit, then it would be perfectly legitimate to advocate its removal. Since the Second World War there had been more funding for epidemiological work because this was a developing speciality which was shown to be of value in the control of disease.
[5.150]At p.267 Gori stated:
"[E]pidemiology can be expected at best to identify factors associated with a given disease, but whose causality remains hypothetical. In the future, biomedical research may discover classes of prime molecular mechanisms that trigger a disease, and the factors necessary to its progression. This could then identify the pathogenic potential of various external insults after additional insight into their internal transformations, and thus allow epidemiology to determine how decisive or partial is their causal contribution to disease."
Professor Friend said that he would not take issue with this passage. At pp.267-268 Gori continued:
"Until then, epidemiology can have only a very modest role, and yet epidemiologists are the only ones that have spoken with certainty about causes of cancer, cardiovascular, and other chronic diseases."
Professor Friend said that this was a legitimate view for the author to hold.
[5.151]At p.270 Gori referred to a statement by Rothman (in an earlier edition of the work that became Rothman and Greenland 1998) that there was no upper limit to the sum of the many causes of disease: the total of the proportion of disease attributable to various causes was not 100% but infinity. Gori wrote that theoretically this statement could be given when all the so-called causes of lung cancer were in fact necessary parts of each possible set of distinct causative chains, but the contrary was evident. Observation showed that people developed lung cancer even in the absence of one or many of the putative causal factors identified. Professor Friend agreed that this was a correct proposition. He was referred to similar passages in other papers. In Doll 1990 the author stated that it could properly be said that two factors might each be separately responsible for, say, 80% to 90% of the risk of developing a particular type of cancer, while the avoidance of both would have little more effect than the avoidance of one. In Cole and Merletti 1980 the authors stated that the population attributable risk percent (PARP) might serve several useful functions, for example for purposes of health education, if a reasonably valid and precise estimate could be developed, but it was inherently a statistic which was very difficult both to estimate and to interpret. The PARP was difficult to estimate with validity because it was highly derived from two more fundamental statistics, the exposed proportion of the population and the relative incidence risk. Professor Friend said that he agreed with these authors about the difficulty of making such an estimate. In Chang et al. 2001 the authors assessed the associations and population attributable risks of risk factor combinations and ischaemic heart disease mortality in the United States. They used logistic regression models to assess the association of risk factors with ischaemic heart disease in two studies, examining eight modifiable risk factors. Professor Friend agreed that, from the figures given, the total risk factor was 100%.
[5.152]Professor Friend was next asked about the statement in his report that in his opinion Mr McTear would not have been made sufficiently aware of the risks of cigarette smoking by the product information provided by the manufacturers in their advertising material and elsewhere at the time when he started smoking. He said that he had conducted no research apart from the fact that he was aware that warnings were not placed on packets until 1971. He was also aware that there was some information about the public arena to imply that not a lot of people were aware of the health risks of smoking at that time. He could not remember the source for this. He was not aware when he prepared his report that every single statement in it had to be supported by a reference to the literature. He was asked about a report in Hansard for 14 December 1959 in which the Minister of Health, Mr Walker-Smith, stated:
"I am aware of the continuing increase in the number of deaths from lung cancer though there is some evidence that the rate of increase is slowing down. So far as smoking is concerned, the Government's intention is that the possible consequences should be made widely known to the public and I believe this to be largely achieved."
Professor Friend said that he was not aware of this statement.
[5.153]He was also asked about a report in Hansard for 19 December 1960 when the Minister of Health, Mr Enoch Powell, said in answer to a question:
"There is good evidence that people in this country are widely aware of the risks involved in smoking. The health education measures of local authorities are largely directed to the young and should ensure that this awareness is maintained and intensified. I consider this approach to the problem is the right one. [...] I have no reason to think that the facts are not reaching the public, and not reaching the younger members of the public, but they must be regarded as responsible people who take their own decisions."
Professor Friend said that he had no reason to doubt the accuracy and truth of the Minister's answer.
[5.154]On 30 January 1964, as reported in Hansard, the Prime Minister, Sir Alec Douglas-Home, in answer to a question, said that he thought that the Government had taken a lead and action. Local education and local health authorities did a great deal, and 440,000 posters carrying the slogan "Cigarettes cause lung cancer" had been distributed for display. "I do not think that there is any excuse for anyone not to know the connection between cigarette smoking and cancer." Professor Friend said that he took issue with this, on the basis of his reading. He was not aware of any survey which had been conducted at that time into awareness of the issue. To convince him, it would be necessary for a detailed survey to have been conducted into the awareness of individuals who were contemplating smoking.
[5.155]Professor Friend was next asked about his statement that it seemed clear that ITL would have been aware that cigarette smoking could cause lung cancer prior to 1964. He agreed that to be accurate one could say that ITL would have been aware prior to 1964 that there was a statistical association between cigarette smoking and lung cancer. He accepted that whether or not the association was causal was a matter for judgment. He agreed also that not only did the United States Surgeon General declare that the question of causation was a matter of judgment, a number of scientists, well beyond 1964, judged that the relationship was not causal and were prepared to speak out in scientific papers and in the scientific press.
[5.156]Professor Friend was next asked about the views he had expressed about genetic factors and lung cancer. He had already acknowledged that genetic factors might play a part in the development of lung cancer. He was asked whether, epidemiologically, a particular family history of lung cancer had been shown to be statistically associated with an increased risk. He said he was not very sure of the particulars of that relationship. He said that he had no qualification to assist the court on matters of genetics, he was not a specialist in this field, his information was based on a reading of texts and other sources. These were textbooks of respiratory medicine, a European Respiratory Society monograph and so on. He acknowledged that there was in this an established possibility of a genetic impact and that was what he had said in his report. "As I said earlier [...] I was unaware that every statement in my report had to be backed up by a written reference to the primary literature." It would have made a "stronger argument" if it had been backed up by some research into the primary literature.
[5.157]Asked about the expression "stronger argument", he said that he understood his function was to provide a specialist opinion on the nature of Mr McTear's illness, its management and its probable causation, and to give a clinical opinion as from a clinician who was experienced in the management of this disease. His opinions were derived from epidemiology. In this section they were derived from genetics. He was aware that other expert witnesses would be presented who could speak to the epidemiological and other aspects of the case. So he did not feel he needed to go into any depth in that part of his report, "because I felt the court might be able to question them in more detail." He was not an experienced expert witness. He appeared as an expert witness in the area in which he was an expert, but he had already declared the areas in which he was not an expert.
[5.158]Asked about the passage in his evidence-in-chief in which he agreed with the suggestion that: "If this genetic predisposition is a correct theory, is it inherent in it that someone would have to start smoking?", he said that this was an incorrect answer and he would now say no. "I think you will understand the length of the examination and the inevitable fatigue of the brain during the course of an interrogation of this sort". In his evidence-in-chief he agreed with the suggestion that if certain people had a genetic predisposition to developing lung cancer, they would have to start smoking before that greater risk increased. Asked about this, he said that he found the whole issue confusing to discuss and he did not find himself able to answer that.
[5.159]Reference was made to Tokuhata and Lilienfield 1963. At pp.298-299 the authors reported that they carried out a comparison of the lung cancer mortality between a group of relatives of lung cancer probands and a control group by taking into account the effects of sex, age, category of relatives and cigarette smoking simultaneously. They found that there was an excess mortality from lung cancer in all categories of the former group, including both smokers and non-smokers. The overall difference in lung cancer mortality for all relatives considered was statistically significant, which suggested that the relatives of lung cancer probands had a significantly increased risk of dying from lung cancer regardless of the history of cigarette smoking. This relationship was more clearly present among the male relatives, particularly brothers, than among the female relatives.
"In addition, the observed number of lung cancer deaths was nearly 4 times greater than expected among those case relatives [relatives of lung cancer probands] who did not smoke cigarettes, whereas it was about 2 times greater than expected among those case relatives who smoked cigarettes."
Professor Friend said that he was not aware of this particular study, but he would certainly absolutely accept that there might be cases of lung cancer which were not associated with smoking and which might run in families, but he did not believe such cases were common. He agreed that lung cancer might not happen often, but if it did then there might be a high expectation that a family member would contract lung cancer.
[5.160]Professor Friend said that he was not familiar with Samet et al. 1996. In this paper it was reported that a positive history of lung cancer in a parent was strongly associated with lung cancer risk in the cases studied. The odds ratio estimate of 5.3 was adjusted for cigarette smoking by the subjects and should not reflect concordance of the smoking habits of parents and children. Other epidemiologic studies and clinical series had also indicated aggravations of lung cancer. Professor Friend agreed that this confirmed his general understanding that lung cancer could run in families, after adjustment for smoking. In Dong and Hemminki 2001 the study population included 5,520,756 offspring and their parents from 2,112,616 nuclear families. Standardised incidence ratios were calculated to analyse the risks for cancers in offspring by parental cancers and by sibling cancers. For twenty concordant sites, including the lung, all offspring and sibling risks were significantly increased. At four concordant sites standardised incidence ratios were high when both a parent and a sibling were affected: in the case of the lung, the ratio was 13.65. Professor Friend said that he had no reason to disagree with these findings. Ooi et al. 1986 reported on an analysis for family members of 336 deceased lung cancer probands and 307 controls. After control for the confounding effects of age, sex, cigarette smoking and occupational and industrial exposures, relationship to proband remained a significant determinant of lung cancer, with a 2.4-fold greater risk among relatives of probands. Overall, male relatives of probands had a greater risk for lung cancer than did their female counterparts, and the risk was fourfold for parents of probands as compared with parents of controls. Professor Friend said that he had no reason to call into question this conclusion. In Gauderman et al. 1997 at pp.208-209 the authors stated:
"The results from these analyses support previous findings that a major gene plays an important role in lung cancer risk. An additional finding not previously observed is that there is no apparent interaction between the putative lung cancer gene and smoking."
Professor Friend said that he did not have enough expertise to make a judgment upon this statement.
[5.161]Asked whether he stood by the statement in his report that in lung cancer there was only limited evidence for familial susceptibility, Professor Friend said that he did because that was his reading of the summary literature. There was evidence, and he had accepted in his statement, that there might be a genetic component. His reason for standing by this statement was that the evidence was in some degree in conflict with the finding of the increase of lung cancer over the years, the synchronicity of the development of lung cancer prevalence among men and women being at a different rate, and that was a rather surprising finding. Counsel pointed out that "we are back into epidemiology again"; Professor Friend said that he admitted readily that he was not an expert, but that was his reading of the epidemiological literature and of the reports of eminent advisory bodies such as the Tobacco Advisory Group of the Royal College of Physicians, the reports of that college and the Surgeon General's reports. But there was no reference to the underlying scientific papers. Asked whether the papers relating to the genetic component were considered to be the mainstream, the best available science, and authoritative, he simply did not know from his reading of the scientific papers. He agreed that his pronouncement that "if present, such a factor might have only very modestly increased Mr McTear's risk of developing lung cancer, but smoking would have remained the dominant cause of his disease" was made without any knowledge of the relevant scientific literature and without a knowledge of the primary literature. There could not be anything, even in the public health reports, that told him anything about Mr McTear.
[5.162]Professor Friend was next asked about his statement that tobacco was now regarded by many authorities as fulfilling the criteria for an addictive drug. He derived that view from the public health reports, and also from his observations of patients who smoked. He had no professional qualifications in psychology, psychiatry or the speciality of addiction science. He had never treated a patient suffering symptoms of withdrawal from heroin, but had observed somebody suffering from withdrawal from heroin. He agreed that such a person would regard withdrawal as an important aspect of their condition.
[5.163]Professor Friend was asked at length about Chapter 13 of USSG 1964, pp.349-356, entitled "Characterization of the tobacco habit". At pp.350-351 reference was made to definitions created by the World Health Organization Expert Committee on Drugs Liable to Produce Addiction in a report published in 1957, which were stated to be "accepted throughout the world as the basis for control of potentially dangerous drugs". Drug addiction was defined in these terms:
"Drug addiction is a state of periodic or chronic intoxication produced by the repeated consumption of a drug (natural or synthetic). Its characteristics include: (1) An overpowering desire or need (compulsion) to continue taking the drug and to obtain it by any means; (2) A tendency to increase the dose; (3) A psychic (psychological) and generally a physical dependence on the effects of the drug; (4) Detrimental effect on the individual and on society."
Drug habituation was defined in these terms:
"Drug habituation (habit) is a condition resulting from the repeated consumption of a drug. Its characteristics include: (1) A desire (but not a compulsion) to continue taking the drug for the sense of improved well-being which it engenders; (2) Little or no tendency to increase the dose; (3) Some degree of psychic dependence on the effect of the drug, but absence of physical dependence and hence of an abstinence syndrome; (4) Detrimental effects, if any, primarily on the individual."
The summary at pp.354-356 contained the following passages:
"The habitual use of tobacco is related primarily to psychological and social drives, reinforced and perpetuated by the pharmacological actions of nicotine on the central nervous system, the latter being interpreted subjectively either as stimulant or tranquilizing dependent upon the individual response. [...]
The tobacco habit should be characterized as an habituation rather than an addiction, in conformity with accepted World Health Organization definitions, since once established there is little tendency to increase the dose; psychic but not physical dependence is developed; and the detrimental effects are primarily on the individual rather than society. No characteristic abstinence syndrome is developed upon withdrawal. [...]
Medical perspective requires recognition of significant beneficial effects of smoking primarily in the area of mental health.
These benefits originate in a psychogenic search for contentment and are measureable only in terms of individual behavior. Since no means of quantitating these benefits is apparent the [Advisory Committee to the Surgeon General] finds no basis for a judgment which would weigh benefits versus hazards of smoking as it may apply to the general population."
[5.164]During this passage of his cross-examination Professor Friend said that he thought that the effects of nicotine differed considerably in those who had never come into contact with it and those who regularly consumed it. He believed that some of the pleasure that was derived from the inhalation of nicotine by regular smokers came from the restoration of nicotine levels. He reached this conclusion from his reading of USSG 1988 and RCP 2000, and not the underlying science. He did not take issue with a statement that smokers and users of tobacco in other forms usually developed some degree of dependence upon the practice, some to the point where significant emotional disturbances occurred if they were deprived of its use, but he was not sure what was meant by a further statement that the evidence indicated this dependence to be psychogenic in origin. He was aware that over the years the public health authorities had altered the definition of addiction to the point where tobacco, which was not considered to be addictive in 1964, was now said in RCP 2000 to be addictive. He was no expert in this field, but he did not believe that the development of tolerance was obligatory on the development of a dependence. While withdrawal from heroin and cessation of smoking were not alike, he had observed many people who had attempted to stop smoking and who found it an extremely difficult and unpleasant experience, with physical symptoms so intolerable that they would wish to continue smoking. These symptoms were not comparable in severity to the symptoms to be observed in a heroin user suffering from withdrawal symptoms. His position was that there was a wide spectrum of tobacco use and the symptoms of withdrawal. He accepted that many people did not have difficult symptoms when they withdrew from smoking, but a number did, and these were often quite overpowering, particularly for instance in the case of heavy smokers who for some reason were totally deprived of the ability to smoke cigarettes. He agreed that in contrast to drugs of addiction, withdrawal from tobacco never constituted a threat to life. He did not agree that this fact indicated the absence of physical dependence. While the observations had not changed since 1964, the perception of the medical profession had as a result of further experience. He agreed that by applying the World Health Organization definition as it stood in 1964, the tobacco habit should not be characterised as an addiction. What had changed since then was the definition of addiction, so as to include the tobacco habit.
[5.165]Professor Friend was asked about a number of passages in Frenk and Dar 2000. Chapter 13, "Epilogue", started at p.174, under the heading "Is nicotine an addictive drug? Conclusion":
"This book reviewed and evaluated the evidence for the Surgeon General's influential declaration [in USSG 1988] that 'Cigarettes and other forms of tobacco are addicting,' that 'Nicotine is the drug in tobacco that causes addiction,' and that 'The pharmacologic and behavioral processes that determine tobacco addiction are similar to those that determine addiction to drugs such as heroin and cocaine.' Although this assertion has been almost universally adopted by the scientific community, government agencies, the media and the public, we found that it is not sustained by empirical evidence. Instead, our analysis of the research to date indicates that if nicotine contributes to the persistence of smoking, it is not due to its purportedly gratifying psychoactive properties but rather to its contribution to the 'taste' of inhaled smoke and perhaps to placebo effects and acquired (secondary) reinforcing properties in experienced smokers. Thus, nicotine's role in maintaining the smoking habit bears no similarity to the role played by genuinely addictive drugs such as heroin, barbiturates, alcohol or other drugs to which nicotine is routinely compared."
Professor Friend said that he was not in a position to challenge this conclusion as a matter of science.
[5.166]He was asked about a number of other passages in the book. At p.177 the authors wrote:
"[T]he flaws we found in the nicotine research literature are of such magnitude and occur in such a regular fashion that they demand an explanation. A partial list of the methodological shortcomings compiled in this book includes:
- Systematic exclusion of subjects from statistical analyses
- Absence of saline control groups for injected drugs
- Result-biased selection of number of sessions to test manipulations
- Absence of statistical comparisons [...]"
Professor Friend was asked whether these passages caused him to wonder whether he should accept the views of the Tobacco Advisory Group of the Royal College of Physicians without further looking into the matter for himself by reading the material on which they relied. He said that he would have to read both documents (by which I understood him to mean USSG 1988 and RCP 2000) much more intensely than he had done. He would be interested to do this in the future as a result of seeing what Frenk and Dar said.
[5.167]Professor Friend was asked about passages in DSM-IV. He agreed that the diagnostic criteria in this manual were not intended to be applied to the effect of a substance, but were intended to be applied in the diagnosis of an individual by those capable of exercising clinical judgment about that individual's presentation. In a passage in the introduction entitled "Use of DSM-IV in forensic settings" the authors wrote, at p.xxxiii:
"In determining whether an individual meets a specified legal standard (e.g., for competence, criminal responsibility, or disability), additional information is usually required beyond that contained in the DSM-IV diagnosis. This might include information about the individual's functional impairments and how these impairments affect the particular abilities in question. It is precisely because impairments, abilities, and disabilities vary widely within each diagnostic category that assignment of a particular diagnosis does not imply a specific level of impairment or disability.
Nonclinical decision makers should also be cautioned that a diagnosis does not carry any necessary implications regarding the causes of the individual's mental disorder or its associated impairments. Inclusion of a disorder in the Classification (as in medicine generally) does not require that there be knowledge about its etiology. Moreover, the fact that an individual's presentation meets the criteria for a DSM-IV diagnosis does not carry any necessary implication regarding the individual's degree of control over the behaviors that may be associated with the disorder. Even when diminished control over one's behavior is a feature of the disorder, having the diagnosis in itself does not demonstrate that a particular individual is (or was) unable to control his or her behavior at a particular time."
Professor Friend agreed that this was in general terms the correct approach to take.
[5.168]Professor Friend was next asked about Hindmarch 1998. (Mr Jones told me that this paper was given at "a conference of people who are interested in the chemistry of tobacco".) In this paper the author examined the extent to which nicotine could be regarded as addictive. At p.22 he stated:
"The results of this exercise confirm that nicotine is clearly delineated from drugs such as heroin, cocaine and alcohol and that addiction is not a tenable label by which to explain tobacco use.
An alternative classification system is offered which examines the effects of psychoactive compounds on skills of everyday living. This approach is used to provide objective evidence indicating that nicotine has small positive effects upon the individual and their interaction with the environment which are clearly different from the effects found with drugs of abuse."
Professor Friend said that he regarded the statement in the last sentence as acceptable. The author went on to discuss the "basic, almost philosophical, controversy" in any attempt to define addiction which related to the dichotomy between free will and determinism. Professor Friend said that he recognised this dichotomy. Asked whether smoking deprived the smoker, or some smokers, of responsibility for his or their actions, he said:
"Yes and no. I believe there are some smokers who are unable easily, by free will, to change their behaviour. [...] I believe that they are responsible but they may not be able to exercise their full responsibility."
He placed what he called addiction to smoking between the extremes of free will and determinism.
[5.169]Hindmarch concluded, at p.28:
"[N]o matter how addiction is defined and, no matter what level or sphere of discourse is chosen, it is apparent that tobacco smokers do not fit the same criteria as users of other substances, be they medicines, social substances or drugs of abuse. The major distinguishing feature of tobacco smokers is that their drug using activity is pleasurable and the principal effects of their chosen substance are those of a mild improver of a cognitive and psychological performance and behaviour."
Professor Friend said that he did not know the literature well enough to be able to comment on this passage. He was not expert enough to be able to say one way or the other whether he supported it.
[5.170]Professor Friend was next asked about a passage in his examination-in-chief when he said that in general there was quite strong evidence to suggest that the larger number of cigarettes people smoked, the more heavily they were addicted to them. He said that he was not able to point to the evidence on which he relied in support of this proposition. He was referred to BTS 1990, a report of studies organised by a sub-committee of the Research Committee of the British Thoracic Society. Professor Friend had been a member of the sub-committee. The effects of various smoking cessation strategies were studied in two multi-centre trials with new patients attending hospital or a chest clinic because of a smoking related disease. In the first trial (Study A) the effect of the physician's usual advice to stop smoking was compared with the effect of the same advice reinforced by a signed agreement to stop smoking by a target date within the next week, two visits by a health visitor in the first six weeks, and a series of letters of encouragement from the physician. The second trial (Study B) compared (1) advice only, (2) advice supplemented by a signed agreement, (3) advice supplemented by a series of letters of encouragement, and (4) advice supplemented by a signed agreement and a series of letters of encouragement. Among other results, it was reported in respect of Study A, at p.837: "The number of cigarettes smoked per day bore no relation to success in stopping smoking." Of Study B, it was reported at p.838: "Outcome did not appear to be affected by [...] daily cigarette consumption." Reminded of this, Professor Friend said that in this study, that was the case. Asked whether he accepted that the available science indicated that there was no relationship between amount smoked and ability to quit, he said that he thought he would need to go further into the literature and he was not privy to all the details of that. "If I had been better prepared, I would have been, but I am not."
[5.171]Reference was also made to Lennox et al. 2001, of which Professor Friend was one of the authors. The paper reported on a study, the objectives of which were to develop and evaluate, in a primary care setting, a computerised system for generating tailored letters about smoking cessation. Analyses were adjusted for age, sex, level of social deprivation, heaviness of smoking, time to first cigarette of the day, and initial stage of change. At p.1398 it was reported that sex, age, and heaviness of smoking were not associated with cessation, but there was a significant inverse association with level of social deprivation. Reminded of this, Professor Friend said he remembered that this was one of the outcomes of this study.
[5.172]The next passage of cross-examination related to Professor Friend's statement during his evidence-in-chief that he agreed with the statement in Doll 1997 that following RCP 1962 and USSG 1964 the idea that smoking was a major cause of lung cancer ceased to be seriously challenged. Professor Friend said that he was aware that challenges took place, but he was also working in a setting of many doctors with an interest in this and there seemed to be general agreement that smoking was a major cause of lung cancer. So this was based on his own experience and his own reading at the time when he was a junior medical doctor.
[5.173]He was asked about passages in Doll 2002. At p.500 Doll referred to the claim, first published in Doll and Hill 1950, that cigarette smoking was a cause, and an important cause, of lung cancer. This had been criticised by Sir Ronald Fisher in a number of publications, including Fisher 1959. One of Fisher's criticisms was that there might have been some common factor that was responsible both for the individual's smoking habits and his or her risk of developing disease (i.e. confounding). At p.505 Doll said that this point was by far the most important of those made by Fisher, for confounding was certainly a theoretical possibility. He continued:
"It was [...] several years before it was possible to rule out a genetic explanation by the changes that took place in whole populations when sections of them gave up smoking (Doll and Peto 1976), and by the findings in monozygotic twins with different smoking habits [...]."
Professor Friend agreed that according to this passage it seemed that a man of the eminence of Sir Ronald Fisher did not accept the causal hypothesis and even in Sir Richard Doll's memoir the debate was not laid to rest until 1976. He thought the debate would continue to take place over a period of time. He agreed that Sir Ronald Fisher's point was a serious challenge to the causal hypothesis.
[5.174]Finally, Professor Friend was asked about evidence given by a number of witnesses to sub-committees of Committees of the United States House of Representatives. In Sommers 1972, Dr Sheldon C Sommers, Chairman of the Scientific Advisory Board to the Council for Tobacco Research, a physician specialising in pathology and Clinical Professor of Pathology at Columbia University College of Physicians and Surgeons and University of Southern California School of Medicine, gave evidence which included this statement, at p.96:
"[S]tatistical mathematics can never prove cause and effect. All they show is a relationship requiring further study, usually experiments in animals, to find out the meaningfulness biologically of this relationship. I really believe that among the active researchers in these fields, there is no great preponderance of feeling that cigarette smoke is carcinogenic."
Professor Friend said that he supposed that this was a very reasonable challenge to the causal hypothesis, but he would not call it serious. There were a number of challenges that came from individuals, but the great body of medical opinion supported Sir Richard Doll's original contention. He agreed that he was really talking about a head count. It did not mean that if there were enough people on one side, then that side won, but this did have an influence on one's understanding of the arguments. If a substantial number of eminent authorities came to a certain conclusion, that was bound to outweigh one's understanding of what a small number of individuals might contest in opposition to that view. This was not regardless of the merits of their argument, which must be taken into account. He acknowledged that there might have been many eminent people who did not accept the causal hypothesis after 1964.
[5.175]In Sommers 1976 Dr Sommers said at p.269:
"Now, as to lung cancer, there is a statistical association between cigarette smoking and lung cancer. But at present the nature of the association or whether it is causal are not known. The test of the original Surgeon General's report [USSG 1964] deals with the difficulties of assigning causality, but the summary and conclusions brush these aside, and assign a causality not demonstrably evident in the text. It is widely known that a statistical association is not by itself proof of causation. A statistical association may point to experiments that will help to determine whether there is cause involved."
Professor Friend said that he had not read sufficient of the United States Surgeon General's reports to enable him to express a view on Sommers's conclusion. He agreed that a statistical association was not by itself proof of causation and might point to experiments that would help to determine if a cause was involved. Sommers continued:
"Animal experiments to my knowledge have not succeeded in the production of so-called human type lung cancers in a significant percentage of any species tested."
Professor Friend said that these cancers were squamous cell and small cell cancers. He was not able to point to any scientific paper produced since 1976 that indicated any change in this state of affairs and that showed squamous cell carcinoma being produced in any species.
[5.176]In Furst 1982 Dr Arthur Furst, Director Emeritus of the Institute of Chemical Biology at the University of San Francisco, said at p.512:
"For many years, I tried to induce lung cancer in animals with cigarette smoke, with no success, despite the most sophisticated smoking machines available. Not only were my colleagues and I unsuccessful, but so was every other investigator. There have been a very small number of published reports of lung cancers occurring in experimental animals during smoke inhalation experiments. Anyone attempting to interpret these as showing that smoking causes lung cancer must understand that animals, like humans, do spontaneously develop lung cancer even in the absence of any suspected carcinogen."
Professor Friend said that he recalled reading in one of the United States Surgeon General's reports a treatment of animal inhalation experiments, but not in detail. He seemed to recall that they felt there was a small amount of evidence of induction of tumours in animals but not so much by inhalation. He had repeatedly stated that he did not believe that animal experimentation was a necessary part of making the connection between smoking and lung cancer. Animals were such an entirely different species and the possible duration of exposure to smoke was much shorter than in man. He accepted that biological plausibility was amongst the criteria that the United States Surgeon General's Committee set itself for determining causation. He thought that biological plausibility included the painting of some tar onto the skin of animals and the knowledge that some of these compounds did appear to have carcinogenic effects. He was not saying that he did not take anything from the animal skin-painting experiments, but he did not think they were a necessary part. It was not his evidence that they demonstrated biological plausibility. Asked whether, if animal inhalation studies were undertaken, particularly with animals in which it was known that squamous cell carcinoma of the lung occurred spontaneously, positive results from smoking experiments would be claimed to point towards biological plausibility, he said that he was again being taken into areas where he had no competence or expertise.
[5.177]Furst continued:
"Based on my own research and familiarity with the literature, I have concluded that no reliable, reproducible animal studies have shown that the inhalation of cigarette smoke causes lung cancer. I might add that skin-painting experiments are inappropriate for studying the question of tobacco smoke and cancer. We must insist that animal experiments simulate, as closely as possible, the human experience - and skin-painting, as well as certain other experimental techniques, fail to mimic adequately human inhalation."
Professor Friend said that he would not take issue with this. Furst then continued:
"The animal data are significant negative evidence. They basically contradict the popular interpretation of the epidemiological data. Why? We must have good research to find out."
Professor Friend said that Furst was entitled to hold that view. He thought that serious scientists had always challenged the causal hypothesis as the explanation for the association between cigarette smoking and lung cancer.
[5.178]In Eysenck 1982 Professor Hans J Eysenck, Professor of Psychology at the Institute of Psychiatry, University of London and Psychologist in the Maudsley and Bethlem Royal Hospitals in London, stated at p.444:
"More convincing proof is required before the theory [that cigarette smoking causes lung cancer, coronary heart disease and many other diseases with which it is statistically linked] can be accorded a more advanced status. But further than that, there are numerous facts suggesting an alternative theory, and these facts cannot easily be integrated with the causal theory."
Professor Friend said that Eysenck was perfectly entitled to express these views. Eysenck went on to discuss the alternative theory first suggested by Sir Ronald Fisher that genetic factors were important in causing lung cancer, that genetic factors were active in causing people to maintain the smoking habit and that possibly the same genetic factors might be involved in both these trends, thus producing the observed correlation between smoking and cancer. Professor Friend accepted that there were eminent scientists who as late as 1982 continued to disagree that there was a causal connection between cigarette smoking and lung cancer.
[5.179]In Booker 1982 Dr Walter M Booker, Professor Emeritus of Pharmacology at Howard University, stated at p.573 that there was by no means unanimity in the scientific community that cigarette smoking could be incontrovertibly labelled as causal. Despite what those in the legislative arena might believe, the cause or causes of cancer of the lung (and other organs) remained unknown. Professor Friend said that he agreed with these statements. He also agreed that if the epidemiology was left to one side, the cause or causes of cancer of the lung remained unknown. He added, however, that he would wish to include in that broad statement about epidemiology the evidence of the reduction of lung cancer risk after cessation of smoking. Once people stopped smoking, their risk of developing lung cancer diminished over the subsequent fifteen years. He agreed with a further statement by Booker that both smokers and non-smokers contracted cancer and other diseases often associated with cigarette smoking, and it was still not known why.
[5.180]In Hickey 1982 Dr Richard J Hickey, a Senior Research Investigator in the Department of Statistics of The Wharton School, University of Pennsylvania, said at pp.619-620:
"It should be recognized that statistical associations are mathematical quantities. When properly obtained, they may suggest possible causal relationships, but they can never prove such relationships. Human conditions such as cancer, heart disease, spontaneous abortions, stillbirths and birthweight deficiencies are all basically biological and biochemical problems, not mathematical or statistical problems. When ill, one visits his physician, not his statistician."
Professor Friend agreed that this was an engaging way of putting it.
[5.181]In Eysenck 1983 the author stated, at p.445:
"Much of the evidence cited in favor of the causal theory is statistical, but many statisticians have severely criticized the evidence on statistical grounds. Such suggested proofs as the correlation between smoking and lung cancer within a given country are evidence of correlation, not of causation; one of the first lessons the budding statistician learns is that correlation does not imply causation."
Professor Friend said that this was a fair observation. At p.449 Eysenck said:
"In summary, I would like to state that the causal theory of smoking as being responsible for lung cancer and coronary heart disease, while it has found many supporters, is far from being established, and has many gaps, anomalies and contrary findings to contend with; these are too frequently glossed over and dismissed as unimportant, when in reality they may be found to discredit the causal theory in whole or in part.
An alternative theory, based on genetics and implicating [personality] factors, is much less well developed, more complex, and at present not too well known to oncologists; nevertheless there are many well-established facts which suggest that in part if not in whole it can account for the major findings."
Professor Friend agreed that these passages showed that in 1983 scientists were supporting the constitutional explanation rather than a causal explanation.
[5.182]In Langston 1982 Professor Hiram T Langston, Clinical Professor of Surgery (Emeritus) at Northwestern University Medical School and Chairman of the Department of Surgery at St Joseph's Hospital in Chicago said at p.659:
"Cancer of the larynx or voice box is also statistically linked with smoking. Because cigarette smoke passes through the larynx on its way to the lung, the larynx is exposed to at least the same concentration of smoke as are the lungs. Were the smoking-causation hypothesis valid, one would expect to see a rise in laryngeal cancer similar to the rise in lung cancer. Yet, the data show that there has been little change in the incidence of laryngeal cancer over the past decades."
Professor Friend said that he was aware that this was an anomaly also pointed to within the United Kingdom data. At p.663 Langston said:
"I do not agree that cigarette smoking is the major cause of lung cancer, because I believe very strongly that we do not know the cause or causes of cancer of the lung. Charges that smoking causes lung cancer are so familiar that very few people may realize that there is strong evidence to the contrary. I find that evidence to be persuasive. In my estimation, the smoking hypothesis is an oversimplification."
Professor Friend said that he had already acknowledged that ultimately a conclusion on causation as an explanation for the association between smoking and lung cancer was a matter of judgment.
[5.183]In Kupper 1982 Dr Lawrence L Kupper, a biostatistician specialising in epidemiology and environmental health and currently Professor of Biostatistics in the School of Public Health, University of North Carolina at Chapel Hill, said at pp.655-656:
"The belief that smoking is a cause of lung cancer can be questioned in light of the documented sources of bias attendant with epidemiologic studies of the smoking-lung cancer relationship.
Statistical associations between smoking and lung cancer, as reported in the various studies described in the Surgeon General Reports, have been interpreted to mean that a causal relationship does exist. In the absence of well-designed animal and laboratory studies elucidating the meaning of these reported associations, such a quantum jump from association to causality is invalid. Indeed, the self-selection bias itself (not to mention all the other possible sources of error) is sufficient to cast doubt on the causality claim."
Professor Friend said that he understood by this latter statement that Kupper was referring to the fact that smokers chose to smoke and in that sense they were self-selected. While he might not agree with it, he accepted that this was a perfectly reasonable and responsible argument to put forward.
Re-examination of Professor James Friend
[5.184]In re-examination, Professor Friend was asked to note that when Sommers gave evidence, there were members of the sub-committee who took issue with what he had to say. When pressed, Sommers said that his personal belief was that the causative relationship with cigarette smoking to lung cancer was not proved; the data available did not support the conclusions. Cigarette smoking might be a cause of lung cancer, but he did not think this had ever been proved. Professor Friend said that the conclusions of IARC 1986 had never been challenged, notwithstanding the views previously expressed by Sommers and others.
[5.185]Professor Friend was also asked to note that in Doll 2002 it was stated, at p.505:
"Why Fisher took the view he did and adhered to it so strongly [...] is difficult to understand. It has been discussed in detail in a perceptive article by Stolley (1991), who cites the following passage from the memoir that Yates and Mather (1962) wrote for the Royal Society after Fisher's death: 'In his own work, Fisher was at his best when confronted with small self-contained sets of data, and many of his solutions of such problems showed great elegance and originality. He was never much interested in the assembly and analysis of large amounts of data from varied sources bearing on a given issue.' - and it was, of course, precisely the analysis of such data that allowed us to reach the conclusion that cigarette smoking was an important cause of the disease. According to Sir Walter Bodmer, a graduate student of Fisher's who visited him shortly before his death, he had, however, come to accept that smoking was a 'co-factor' in the production of lung cancer and had intended to make a public statement of his revised decision had he survived [...]."
Professor Friend agreed that it appeared that at the end of his career Fisher was going to change his view. Counsel also asked Professor Friend to note, under references to passages he read out from Doll 1974, that Sir Richard Doll had responded to Professor Burch's arguments.
[5.186]Reference was made to BTS 1990. Professor Friend said that six months was an appropriate period to elapse before checking whether someone had given up smoking, but one year was even better because some people who stopped after six months started again in his experience. He was also asked questions about Lennox et al. 2001 (of which, it will be recalled, he was one of the authors). He explained that the numbers involved in this study were fewer than those in the previous one because the patients in general practice were involved opportunistically as they attended the practice, whereas in the previous study the patients had all come to the hospital with pressing symptoms and might perhaps have been more inclined to stop smoking following the advice they received there. Asked to explain the words "a significant inverse association" in the statement that sex, age and heaviness of smoking were not associated with cessation, but there was a significant inverse association with the level of social deprivation, he said he thought it was intended to mean that those with a major social deprivation had a lesser success in discontinuing smoking than those who were socially well supported. Counsel asked him about Table 1 on p.1397, entitled "Results of logistic modelling of validated smoking cessation" in which figures were given for unadjusted and adjusted regression ratios and P values. Professor Friend said that he was not sure that he could help with what was meant by a regression ratio or adjustment. He said that the P value was a term to describe whether such a finding could have occurred by chance. He could not explain what various figures meant. He suggested that there was a comparison of the success rate in people involved in the study who were in social class 1 compared with those in social class 5.
[5.187]Asked about Tokuhata and Lilienfeld 1963, Professor Friend said that in order to determine whether there was a genetic component to lung cancer, in cases where a non-smoking member of a family, other members of which smoked, contracted lung cancer, it would be necessary to eliminate the possibility that passive smoking had caused the lung cancer. He agreed that cases of lung cancer might run in a family, but he did not believe them to be common. The vast majority of patients he had seen with lung cancer had been smokers or had had members of their families who smoked. But certainly a number - a very small number indeed - would have developed primary lung cancer with no personal or environmental smoking habits. It depended somewhat on the histological type. Adenocarcinomas were at one stage regarded as being roughly equally present in smokers and non-smokers, but he thought that in recent times this had changed. He had never personally come across a family of non-smokers who had an extensive family history of lung cancer.
[5.188]Notwithstanding the material put to him in cross-examination, Professor Friend said that he continued to believe that tobacco smoking was a very important cause of lung cancer: not the only one, but the most important cause. The strong probability was that in the case of Mr McTear this disease was caused by smoking cigarettes.
Professor Sir Richard Doll
[5.189]Professor Sir Richard Doll, aged 91, had not provided a CV and reference was made instead to items in his entry in Who's Who. He said that he was still at work and gave lectures. He had recently returned from lecturing in Japan. He was awarded the OBE in 1956. He was made a Knight in 1971 and a Companion of Honour in 1996 for services to medicine. He became a Fellow of the Royal Society in 1966. His current post was Honorary Consultant, Cancer Research UK Cancer Studies Unit, Radcliffe Infirmary, Oxford, a post he had held since 1983. He was an honorary member of the Clinical Trial Service Unit and Epidemiological Studies Unit, Nuffield Department of Clinical Medicine, University of Oxford. He was Warden of Green College, Oxford from 1979 to 1983, the first head of this college. He had been instrumental in its establishment as a college with a special interest in clinical medicine. He qualified in medicine at St Thomas's Hospital Medical School, University of London. In the course of his subsequent career he was Regius Professor of Medicine at the University of Oxford from 1969 to 1979. Previously he was Teacher in Medical Statistics and Epidemiology at University College Hospital Medical School, London, from 1963 to 1969. He explained that he had been an epidemiologist from 1946 onwards, which required some knowledge of medical statistics, and this was an honorary title given to him when he took his Medical Research Council Statistical Research Unit to University College Hospital Medical School. He had been a member and chairman of a number of committees and sub-committees and had received a number of honours. He had been awarded honorary degrees by fourteen or fifteen universities. Among honorary fellowships, he was an Honorary Fellow of the Royal College of General Practitioners, the Royal College of Surgeons and the Royal College of Radiologists. He was a Fellow of the Royal College of Physicians. He had been awarded a number of prizes and gold medals, including the Gold Medal of the British Medical Association and the Royal Medal of the Royal Society. He said that he had not published many books, but had published just over 500 articles, mainly on the aetiology of lung cancer, leukaemia and other cancers. Some of his early papers were on clinical therapeutics, because he worked as a clinician as well as an epidemiologist for about twenty years.
[5.190]Sir Richard was next asked to consider IARC 1986. He agreed that this monograph was more than 400 pages long. He was chairman of the working group which wrote it. He did not know how the members were selected. IARC chose people on the advice of its own staff, and sought to have representatives from many different countries. He knew personally about half the members of the working group. They were leaders in their field. DL Davis, Director of the Tobacco and Health Research Institute at the University of Kentucky, was the principal person to have done chemical analyses of tobacco smoke in the United States. N Gray was Director of the Anti-Cancer Council of Victoria, Australia, which had been working for many years on publicising the harmful effects of smoking and getting the Victorian Government to do something about it. HJ Evans, of the MRC Clinical and Population Cytogenetics Unit at the Western General Hospital, Edinburgh, was a leading biologist working on chromosomes. Y-T Gao, Director of the Shanghai Cancer Institute, had done some work in confirming the same findings in China as in Britain. T Hirayama was a leading Japanese epidemiologist and had organised a very big cohort study, bigger than the one Doll and Hill had organised on British doctors, somewhat smaller than the big American studies, on some 280,000 Japanese residents, getting details of their smoking habits and following them up to find out what diseases they developed. AB Miller, Director, Epidemiology Unit, National Cancer Institute of Canada, at the University of Toronto, was the leading epidemiologist in Canada. S Moolgavkar was a statistician in the United States, very interested in time-exposure relationships between cigarette smoking and lung cancer. NP Napalkov was Director of the Research Institute of Oncology in Leningrad, and was a basic scientist whom Sir Richard knew well. R Peto was Sir Richard's colleague at Oxford and was now Director of the Clinical Trial Service Unit and Epidemiological Studies Unit, Nuffield Department of Clinical Medicine, University of Oxford. MAH Russell, Reader in Addiction, Institute of Psychiatry, The Maudsley Hospital, London, was a psychiatrist with a special interest in addiction. L Teppo, of the Finnish Cancer Registry, was a leading epidemiologist from Finland. NJ Wald, Department of Environment and Preventive Medicine, the Medical College of St Bartholomew's Hospital, London, had been a member of Sir Richard's department in Oxford and became Professor of Preventive Medicine at St Bartholomew's. EL Wynder, President of the American Health Foundation in New York had published a report with very similar findings to those of Doll and Hill 1950, associating cigarette smoking with lung cancer, though in that initial report he only suggested that it might be a cause, he did not regard the evidence as conclusive. Sir Richard was unable to recall some of the other members of the working group.
[5.191]Sir Richard agreed that the working procedures of IARC were as set out at pp.16-17 of IARC 1986 quoted in Professor Friend's evidence at [para.37]. One of the topics considered by the working group was epidemiological studies of cancer in humans. In their conclusions and evaluations, at p.312, they stated:
"Lung cancer is believed to be the most important cause of death from cancer in the world, with estimated total deaths in excess of one million annually. The major cause of the disease is tobacco smoking, primarily of cigarettes. Risk of lung cancer is particularly dependent on duration of smoking; therefore, the earlier the age at initiation of smoking, the greater the individual risk. Further, the longer the time period during which a major proportion of adults in a population have smoked, the greater the incidence and mortality from the disease in that population. Risk of lung cancer is also proportional to the numbers of cigarettes smoked, increasing with increasing cigarette usage. In populations with a long duration and heavy intensity of cigarette usage, the proportion of lung cancer attributable to smoking is of the order of 90%. This attributable proportion applies to men in most western populations; in populations in which women are increasingly using cigarettes, the attributable proportion in women is also approaching this level."
Sir Richard said that this was the conclusion of all twenty-seven members of the working group, with no dissent.
[5.192]At p.314 the working group set out their evaluations:
"There is sufficient evidence that inhalation of tobacco smoke as well as topical application of tobacco smoke condensate cause cancer in experimental animals.
There is sufficient evidence that tobacco smoke is carcinogenic to humans.
The occurrence of malignant tumours of the respiratory tract and of the upper digestive tract is causally related to the smoking of different forms of tobacco [...]."
Asked whether, after all the work they had done, this was quite a modest way of putting their conclusions, Sir Richard said that it made them clear for any reader to understand. So far as he was aware there had never been any challenge to these evaluations.
[5.193]Asked to comment on IARC 2004, Sir Richard explained that the monograph had not yet been published: publication was expected in early 2004. He was aware that a press release had been published, but said that he had to claim ignorance that part of the report, containing the summary of data reported and evaluation, was also available. He agreed that it looked as if this part of the report had been published on the Internet, which was something he was not really accustomed to dealing with himself. He agreed that the statement in IARC 2004 that the major cause of lung cancer was tobacco smoking, primarily in cigarettes, and that in populations with prolonged cigarette use, the proportion of lung cancer cases attributable to cigarette smoking had reached 90%, was consistent with IARC 1986. His attention was drawn to para.5.3, in which it was stated:
"The most compelling evidence for a positive carcinogenic effect of tobacco smoke in animals is the reproducible increase observed in several studies in the occurrence of laryngeal carcinomas in hamsters exposed to whole tobacco smoke or to its particulate phase."
He said that this was part of the material that he dealt with. At para.5.4 it was stated:
"Tobacco smoking is addictive, and nicotine has been established as the major addictive constituent of tobacco products."
He said that this was a conclusion which the working group had reached, though it was not a new one. In the evaluation at para.5.5 it was stated: "There is sufficient evidence in humans that tobacco smoking causes cancer of the lung [...]", and the overall evaluation was that: "Tobacco smoking and tobacco smoke are carcinogenic to humans." Peto was the only person whom Sir Richard could recall, apart from himself, who had been involved in the preparation of both IARC 1986 and IARC 2002. All the members of the working group which produced the latter were leading people in their fields, he said.
[5.194]Sir Richard's attention was next directed to a biennial lecture delivered by him at Green College in 1997, entitled "Tobacco: A medical history", the text of which was reproduced in UKHC 2000, Vol.II, pp.19-35 as Appendix 1 to a memorandum by the Health Education Authority: Doll 1997. In this lecture Sir Richard reviewed the medical history of tobacco, with particular reference to the question whether cigarette smoking caused lung cancer. Asked about the current teaching in medical schools and medical textbooks, he said that he had not read a recent medical textbook, but he knew from talking to senior colleagues that they taught the extreme dangers of cigarette smoking, and its importance as a cause of lung cancer.
[5.195]He described 1950 as a watershed, because five case-control studies were reported in that year. All of them showed a close association with smoking. Two studies stood out because of their size. One had been initiated by Wynder in 1948, on the basis of knowledge that the burning of tobacco would lead to the formation of cancer-causing chemical compounds. Analysis of results obtained from interviewing patients led to the conclusion that excessive and prolonged use of tobacco, especially of cigarettes, seemed to be an important factor in the induction of bronchogenic cancer. The results were published by Wynder and Graham in 1950.
[5.196]Of the other, which was published by himself and Professor Bradford Hill, also in 1950, he said (at p.23):
"In the other, which had been initiated by the British Medical Research Council's conference in 1947, detailed consideration of the possibility of confounding, the consistency of the findings in different studies, the biological relationships with amount and duration of smoking, the size of the estimated relative risk, and the relationships over time and place and for each sex led the authors to conclude that (I quote) 'cigarette smoking is a factor, and an important factor, in the production of carcinoma of the lung' (Doll & Hill, 1950).
Reaction to findings
This conclusion was accepted by Sir Harold Himsworth, who had become secretary of the Medical Research Council, but not generally by medical or statistical scientists and certainly not by the British Department of Health's Standing Advisory Committee on Cancer and Radiotherapy [...]. Most accepted that an association had been shown, but not that it implied cause and effect. Some, however, were even more sceptical, including Berkson [...] the leading American medical statistician who suggested that the findings were an artefact due to the combination of lung cancer and smoking leading to a greater chance of a patient's admission to hospital than when the disease occurred in a non-smoker. Other sceptics were the representatives of the tobacco industry, who, in Britain, sought an interview with the Medical Research Council and were referred to Professor Hill. The conclusion that cigarette smoking was a cause of disease was, they argued, unsustainable for three reasons: the international correlation between cigarette consumption and the mortality from lung cancer of about 0.5 was too low, smoking histories were too unreliable to use as a basis for an association with disease, and lung cancer, in any case, was obviously due to atmospheric pollution. To this Hill replied that a correlation of the size observed with crude international statistics was, in his experience, unusually high and supported a causal relationship rather than the reverse: that if smoking histories were unreliable, this would have weakened a true association rather than have created a false one; and if they had thought that atmospheric pollution was the main cause of lung cancer they should go away and prove it, for Hill and I couldn't."
[5.197]Sir Richard said that the theory that atmospheric pollution was the main cause of lung cancer was the one which was most widely held when the study was started and one that he and Hill were very conscious of trying to test in it. About twenty years earlier the idea that tobacco might be a cause had been considered and some English pathologists had tried unsuccessfully to produce cancer in animals with tobacco tar and decided that tobacco could not be a cause of human lung cancer because of this. It was subsequently shown they had not applied the tar for long enough to produce the effect. He and Hill kept their minds open to all the things that they thought could possibly be an explanation and tried to investigate them all. Very rapidly it became clear that the only one that stood up was tobacco smoking. At the outset, if he had to put money on it, he would have said it was something to do with motor cars and road tar, which was known to contain powerful human carcinogens. In their survey they could not find any relationship whatsoever with frequency of exposure to car exhausts or length of time spent on roads.
[5.198]In the lecture, at p.24, Sir Richard discussed the evidence that led to wide acceptance of major harm from smoking. He started by referring to the early cohort studies. He stated:
"Evidence of a different type was, however, clearly needed, if reactions were to be changed, as, for example, by recording the smoking habits of large numbers of people and following them up to see if the risk of lung cancer could be predicted from the information about the individual's level of smoking."
Sir Richard said that Professor Bradford Hill, who taught him epidemiology, taught him that the scientist's responsibility was always to try to disprove his own work, not to try to look for evidence in support of it. He had the idea that if they learnt about the smoking habits of British doctors and divided them according to the amount smoked, they would see if they could disprove the relationship between cigarette smoking and lung cancer by following up the non-smokers and the heavy smokers. Of course, he said, the opposite happened: it greatly strengthened the conclusion. The study concluded on 1 November 2001, fifty years after they started obtaining information from British doctors and following them up, with frequent reports about changes in smoking habits over time.
[5.199]The lecture continued:
"The evidence from the 'cohort' study of British doctors mounted quickly, and within two and a half years the findings with regard to lung cancer had confirmed those predicted from the case-control studies. This is shown in Table 8, which gives the relative mortality rates for different levels of smoking, as estimated from the final results of the British case-control study based on 1,357 deaths from lung cancer in men [...], and the first results of the cohort study based on only 36 such deaths [...]. With so few deaths in this second study, the confidence limits of the mortality rates were wide, but even so the trend in mortality with smoking was significant [...].
Altogether, however, 789 deaths had been recorded and it was possible to examine the relationship between smoking and several other diseases. [...]
Two years later these results were confirmed with larger numbers [by Doll and Hill, writing in 1956]. More importantly, they were also confirmed in the much larger study that the American Cancer Society had started in 1952 specifically, as the principal investigator told me, to disprove the relationship between smoking and lung cancer that had been observed in the case-control studies [...]."
Sir Richard said that this principal investigator was Hammond, who believed that the relationship was incorrect and strongly believed in the disproof, but within a couple of years he found he was wrong and admitted this. The lecture continued: "The results, based on nearly 5,000 deaths in the 190,000 American men followed for two years, are shown in Table 9 for lung cancer [...]." These investigators concluded inter alia that regular cigarette smoking caused an increase in the death rate from cancer of the lung.
[5.200]The next passage of the lecture related to proof of causation. It started:
"The conclusion that cigarette smoking was a major cause of the disease had not been easy to accept, as the evidence was observational in humans and unconfirmed by animal experiment."
Sir Richard said that this was the position in the 1950s. There had been animal experiments since then which had shown that tobacco tars were carcinogenic. The direct demonstration of carcinogenicity to the lung had not really been possible because experiments which had been started were stopped on humane grounds. They did not wish to expose the animals to tobacco smoke, it was considered improper to do so. But that had never been a significant objection to a carcinogen being a cause of cancer. IARC had on several occasions concluded that a carcinogen caused cancer in humans without experiments to produce the same cancer in animals.
[5.201]The lecture continued by stating that two leading statisticians remained unconvinced. One of these, in the USA, was Berkson, who wrote in 1958 that he was disturbed that the relationship with smoking held to some extent across the board with a variety of conditions.
"In Berkson's opinion this raised the suspicion that there must be something wrong with the method of enquiry and he suggested that they were the result of the interplay of various subtle and complicated biases or that they had a constitutional basis, people who were non- or relatively light smokers, being the kind who were biologically self-protective and that this (I quote) 'correlated with robustness in meeting mortal stress from disease generally.'
In making this criticism, Berkson [...] took no account of the great difference in the relative risks of different diseases among heavy cigarette smokers compared to non-smokers, varying in Doll & Hill's [...] study from 24 to one for lung cancer to 1.01 to one, [nor] of the fact that tobacco smoke was not a pure chemical entity, but a mixture of many chemicals, subsequently shown to number more than 4,000."
Sir Richard added that of course, as we knew now, there were other specific chemicals in tobacco smoke that specifically caused some of the cancers that were caused by smoking, so it was scientifically perfectly straightforward now that smoking did have so many effects.
[5.202]The lecture continued:
"In the UK, Fisher, the most eminent theoretical statistician worldwide, was disturbed that the original finding (Doll & Hill, 1950) that smokers with lung cancer reported inhaling less often than smokers without the disease [...] weighed against causation, unless it were also concluded that (I quote) 'inhaling cigarette smoke was a practice of considerable prophylactic value in preventing the disease' [...] and he argued that secular changes in smoking habits could not be related to the increase in lung cancer since 'lung cancer has been increasing more rapidly in men relatively to women' and that 'it is notorious, and conspicuous in the memory of most of us, that over the last 50 years the increase of smoking among women has been great, and that among men (even if positive) certainly small' [...].
Neither objection was valid. The effect of inhaling was impossible to predict without knowing where the smoke droplets would be deposited and this was uncertain because tobacco aerosols swell under warm and moist conditions and might, if inhaled deeply, deposit in the alveoli rather than on the bronchi [...]. Doll & Hill [...], moreover, found that while inhaling was associated with a diminished risk of cancer in the large bronchi, it was associated with an increased risk of developing cancer in the periphery of the lung, which made biological sense."
Sir Richard explained that most lung cancers occurred near to where the bronchi separated from the trachea at the top end of the lungs, but some occurred right out in the very small bronchi near the periphery. When reviewing the records of all the patients with lung cancer, he had kept a note of whereabouts in the lungs the cancers occurred. When they did their second analysis with a greater amount of data, they found that when subjects said that they inhaled, this was associated with a greater risk of cancer right out in the periphery, in the small bronchi approaching the alveoli, whereas the opposite was true of the cancers right up near the trachea in the big bronchi.
[5.203]The lecture continued:
"As for the evidence of secular changes, Fisher [...] was just wrong; for he had ignored the cohort effects whereby the risks among successive cohorts are determined not only by their recent smoking history but also by their smoking habits in the distant past. When comparisons are made at appropriate ages and times, the trends in the sex ratio of the disease mimic the trends in cigarette consumption by sex over the relevant periods [...]."
Sir Richard said that Peto and he showed that very clearly in some later analyses they were doing for another purpose.
[5.204]Sir Richard said that he understood that Fisher had changed his mind just before he died. A friend of Sir Richard's, Sir Walter Bodmer, now Principal of Hertford College, Oxford, and previously the head of the Imperial Cancer Research Fund, had been a statistical student of Fisher's and he called on Fisher shortly before he died in Australia. According to Bodmer, Fisher said that he recognised that he had been wrong and was intending to publish a statement to that effect, accepting that cigarette smoking was a co-factor in the production of lung cancer. It was the evidence that had led him to change his mind.
[5.205]The lecture continued, at p.25:
"Difficulty in reaching a conclusion about a causal interpretation of the evidence also arose, because different people gave different meanings to 'cause'. In saying that a particular factor is a cause of disease, epidemiologists have in mind a situation in which, for example, prolonged cigarette smoking results in a rare disease becoming 10 times as common as it would have been in the absence of smoking. Cigarette smoking is not then a necessary cause nor a sufficient cause; but it can be an important cause (as few people would have developed the disease if they had not smoked) and this is not contingent on the absence of other causes. What was claimed was that for several diseases causation in the sense described was proved beyond reasonable doubt. The detailed evidence that led to this claim has been reviewed many times and I note here only the extraordinary strength of the association with lung cancer, with increased risks of more than 20 fold in heavy cigarette smokers which alone made the alternative explanation of confounding virtually impossible, the diminution of risk with cessation of smoking, and the consistency of the findings with different methods of investigation and in different countries and different cultures."
Sir Richard said that it was his position that causation had been proved.
[5.206]The lecture continued:
"During the 1950s, this epidemiological evidence, which had been supplemented by many other studies, was supported by the experimental demonstration that tobacco tars were carcinogenic when applied regularly for a long time to the skin of laboratory animals [...] and by the identification of known carcinogens in tobacco smoke [...]. Expert committees appointed to review the evidence were consequently able to reach positive conclusions. Between 1956 and 1959, the Netherlands Ministry of Social Affairs and Public Health (1957), the British Medical Research Council (1957), a study group appointed jointly by the US National Cancer Institute, the National Heart Institute, and the American Cancer Society (Study Group on Smoking and Health, 1957), the Swedish Medical Research Council (1958), and the US Public Health Service (Burney, 1959) all reported that cigarette smoking was a cause of lung cancer, and a year later an expert committee of the World Health Organization (1960) did so too."
So beside Sir Richard's own cohort studies, he said, these various bodies were reaching the same conclusion.
[5.207]The lecture then turned to the topic of the public acceptance of causality. In it Sir Richard said:
"Despite their provenance these reports had little lasting impact on the general public and the situation did not change materially until after the reports by the Royal College of Physicians of London in 1962 and the Advisory Committee to the US Surgeon General in 1964. The first was short and aimed at interested laymen. The second was long and detailed and was particularly newsworthy, because the tobacco industry had been privileged to veto any member of the Committee who had publicly expressed any views about the subject. Both reports nevertheless agreed that smoking was a major cause of lung cancer. [...]
Following these reports, the idea that smoking was a major cause of lung cancer ceased to be seriously challenged. Even the tobacco industry in the UK agreed not to deny the causal relationship on the advice of Geoffrey Todd, their senior statistician. Todd had been a representative of the industry who had visited Doll and Hill in 1952 and had sought to persuade them that their conclusion was wrong; but he had become convinced that it was right. In the USA, however, the industry continued to maintain that all that had been shown was a statistical association and the causality had not been scientifically proven: that is, until recently when the smallest manufacturer broke ranks and accepted that smoking was a cause of the disease."
[5.208]Asked when it was generally accepted in the scientific community that cigarette smoking was a cause of lung cancer, Sir Richard said that this was in the late 1950s, by the end of the reports that he had referred to. The MRC 1957 effectively settled the issue as far as England was concerned. But the public of course did not pay much attention to these reports, because, when the media reported the conclusions of, say, the Medical Research Council, they also always reported a statement by some representative of the tobacco industry that the issue was controversial and that it could not be regarded as proven. This of course was very misleading to the general public. It was not until the early 1970s, 1972 to 1973, when the media became convinced and, for example, television announcers would no longer smoke cigarettes, that the British public started reacting much more sharply to the evidence and a lot more people started giving up smoking.
[5.209]Asked whether ITL had scientists who were advising on these issues in the 1950s, Sir Richard said that he did not know who they had apart from their statistician, Todd. They should have had scientists, he could not recall their names. They did not have any epidemiologists, certainly.
[5.210]At p.26 of the lecture, in a passage relating to the current knowledge of the effects of cigarette smoking, under the heading "Harmful effects" Sir Richard said:
"The morbid effects that are caused in part by cigarette smoking are listed in Tables 10-13. Those that are five or more times more common in cigarette smokers than in non-smokers are marked with an asterisk".
He was asked to look at Table 10, in which there was an asterisk against lung cancer (among other cancers). Under the heading "Total effect on risk of death" Sir Richard said:
"In retrospect, it may be surprising that resistance to the idea that smoking caused so much disease was initially so strong. Three factors, at least, contributed to it. One was the ubiquity of the habit, which was as entrenched among male doctors and scientists as among other men and had dulled the sense that tobacco might be a major threat to health. Another was the novelty of the epidemiological techniques, which had not previously been applied to any important extent to the study of non-infectious disease. The findings were consequently undervalued as a source of scientific evidence. A third was the primacy given to Koch's postulates for determining causation. The evidence that lung cancer occurred in non-smokers, was consequently taken to show that smoking could not be the cause and the possibility that it might not be a cause was inappropriately doubted. The manner in which lung cancer was linked to smoking was not, however, unique. All the other major diseases related to smoking were found to be so by epidemiological enquiry and laboratory evidence of physiological effects that provided plausible mechanisms by which smoking might cause them was obtained only later and, in some instances, is still awaited."
Sir Richard said that laboratory evidence was not available. He stood by everything that he had said in the lecture and by all the articles that he had written relating to lung cancer and its association with smoking.
Cross-examination of Sir Richard Doll
[5.211]Mr Jones started his cross-examination of Sir Richard by asking him about a passage in USSG 1964, at p.20:
"Statistical methods cannot establish proof of a causal relationship in an association. The causal significance of an association is a matter of judgment which goes beyond any statement of statistical probability."
Sir Richard said that this statement was correct and he agreed that it was a question of judgment whether a causal relationship was proved beyond reasonable doubt, on the basis of all the evidence. A conclusion had to be formed on the evidence as a matter of judgment, as in a court of law. In addition to the strength of the association all other relevant evidence had to be considered by an epidemiologist, in the same manner as a judge would do.
[5.212]Sir Richard said that he and Hill started thinking about their retrospective study in 1947, began work on it in 1948 and began writing it up in 1949, before it was published as Doll and Hill 1950. He gave up smoking in 1949 because he thought that the evidence that cigarette smoking caused lung cancer was sufficiently strong. He stopped without difficulty after having been a smoker for about twenty years. Sir Richard concluded in 1950 that smoking causes lung cancer in women. His wife smoked about forty cigarettes a day and found it very difficult to stop. She reduced the amount regularly year after year and still ended up smoking about forty a day. She eventually stopped, several years later; Sir Richard helped her by bribing her.
[5.213]Sir Richard was asked about Doll 2000, in which he gave an account of the work which led to the publication of Doll and Hill 1950 and its reception at the time. At p.5 he wrote:
"The paper obtained much less publicity than we had expected. Senior clinicians and cancer research workers advising the Ministry of Health were, for the most part, unconvinced of the causal relationship and they advised against publicizing the findings for fear of scaring people. Further evidence of a different type was clearly needed if our conclusion was to be taken seriously and this, we thought, could be obtained by seeking information about people's smoking habits and then following them up to see if the mortality from lung cancer varied, as we predicted it would, with the amount they smoked."
Sir Richard said that this was how he recollected it.
[5.214]He was next asked about Doll 1998, in which he wrote, at p.98:
"To Doll and Hill, it seemed clear that evidence of a different type would have to be obtained, if [critical] reactions to the findings in the case-control studies were to be changed."
Accordingly, they decided to obtain evidence from a prospective "cohort" study of British doctors. At p.99 he wrote that with the publication of the results of prospective studies by Doll and Hill in 1954 and 1956 and by Hammond and Horn in 1954, "scientific opinion rapidly changed". Two leading statisticians, however, remained unconvinced. Berkson in the USA had initially suggested that the first results of the two studies might be biased. In Sir Richard's view, Berkson was wrong. At p.100 he wrote:
"Fisher, in the UK, was the other outstanding statistician who questioned a causal interpretation. In his view, Doll and Hill's original finding that reports of inhaling by smokers with lung cancer (62% of whom reported inhaling) were less common than by smokers without lung cancer (67% of whom did so) weighed heavily against causation, unless it were also concluded that 'inhaling cigarette smoke was a practice of considerable prophylactic value in preventing the disease'. He preferred instead the idea that there was some common factor that was responsible both for the individual's smoking habits and his risks of developing the disease, which Fisher postulated was genetic, and he supported his hypothesis by showing that the smoking habits of monozygous pairs of twins were more similar than those of dizygous pairs and (on small numbers) appeared to be similar irrespective of whether they had been raised together or apart. [...] Neither objection was, in fact, valid."
At p.103 he referred to RCP 1962 and USSG 1964 and wrote:
"Following these reports, the idea that smoking was a major cause of lung cancer ceased to be seriously challenged, except by the tobacco industry outside the UK (where it had been quietly accepted) and by a few eccentric individuals such as Burch who, however, raised no material objections."
Asked by counsel for the identity of other "eccentric individuals", Sir Richard spoke of an Irishman, an American and an English psychiatrist; he could not remember their names or those of any of the others. He said that by "material objections" he meant objections which most scientists took seriously. Sir Richard agreed that this passage was similar to that in Doll 1997 at p.25, referred to earlier.
[5.215]Sir Richard was next asked about Sir Ronald Fisher. He said that he had done some genetic work but no epidemiological work. Fisher had suggested that the results of the epidemiological studies could be explained by there being some genetic factor which caused people both to want to smoke and, quite independently, cause cancer of the lung. Sir Richard said that it seemed a pretty bizarre idea to him and to a lot of people. He was not aware of any epidemiologist, anybody experienced in his field, who took it seriously. There could have been some American geneticists who took him seriously, but how they came to do it he could not imagine.
[5.216]Fisher 1959 was a pamphlet incorporating letters by Sir Ronald Fisher to the editors of the British Medical Journal and Nature in 1957 and 1958, two lectures published by the Centennial Review in 1958 and a previously unpublished passage on inhaling. Sir Richard agreed that Fisher had achieved a formidable reputation amongst statisticians for his pioneer work in this field during the previous forty years. His particular achievement had been in the development of statistical methods appropriate to biological research. During his brilliant career in academic and research work, many honours had come to him. He had been awarded the Royal, Guy, Darwin and Copley Medals of the Royal Society, of which he was a Fellow. He was a Foreign Associate of the United States National Academy of Science, a Foreign Honorary Member of the American Academy of Arts and Sciences, a Foreign Member of the Royal Swedish and Royal Danish Academies of Sciences, and a Foreign Member of the American Philosophical Society. He held degrees from the Universities of Ames, Chicago, Harvard, Calcutta and Glasgow; he was a Fellow of Gonville and Caius College, Cambridge, and a former Arthur Balfour Professor of Genetics in the University of Cambridge. He was a very eminent geneticist. He had also been Galton Professor of Eugenics in University College, London. He had a reputation for frank and outspoken contributions to many statistical debates.
[5.217]Sir Richard disagreed with the statement about Sir Ronald, under the heading "The author" (in a passage from which most of the foregoing information is derived): "This pamphlet is a fair-minded assessment of the value of the statistical evidence relating to the incidence of lung cancer in smokers." Sir Ronald thought that he himself was "fair-minded", but nobody else did. He was the leading theoretical statistician of his day, and an eminent geneticist, but that did not make him right. In his researches Fisher had obtained data from Doll and Hill's 1950 case-control study but, according to Sir Richard, he would not accept the data from the 1952 publication.
[5.218]At p.21 Fisher wrote:
"Before I stop, in fact, I hope I shall make it clear that there is a case for further research, and I shall only mention two areas which would seem to be profitable for investigation. I would stress the importance of what could be done comparatively easily with rather little expense, namely, to ascertain unmistakably what the facts are about inhaling. If inhaling is found to be strongly associated with lung cancer, it would be consonant with the view that the products of combustion, wafted over the surface of the bronchus, might induce a pre-cancerous and thence a cancerous condition. But if there is either no association at all or a negative association, we should have to reject altogether that simple theory of the causation of cancer."
Sir Richard said that of course Fisher was ignoring a lot of published data and he was quite wrong in making that conclusion in any case. He refused to look at the data when he made that remark. Sir Richard agreed, however, that this was the view that Fisher expressed.
[5.219]At p.22 Fisher wrote:
"For my part, I think it is more likely that a common cause supplies the explanation. Again, we do not know. I do not put forward any explanation as proved, but as requiring investigation. The obvious common cause to think of is the genotype. We are all different genotypes. [...] If one studies cancer in mice [...], if one examines any of the many [...] inbred lines of mice [...] - if you take, then, any two such lines of differing genotypes, they will, I believe, invariably be found to differ in the frequency, in the age incidence, and in the type of cancer which those mice suffer from. Consequently if there is any genotypic difference between the different smoking classes, we may expect differences in the type or frequency of the cancers that they display."
Fisher then went on to develop a proposal for a line of research directed to the possibility that there was a genetic component which distinguished the different smoking classes: non-smokers, cigarette smokers, pipe smokers and cigar smokers. Sir Richard said that this was a suggestion which Fisher was entitled to make, but he regarded it as a long shot. He himself did not think that it was worth researching but research was done to test it. His view was that it was not a sufficiently worthwhile proposal to spend money on. He and Hill had found, for example, that when doctors gave up smoking the incidence of lung cancer in the population was reduced. If it had been a genetic factor, the fact that some gave up smoking would not have affected the overall incidence. So they had evidence quite soon that it just was not a worthwhile topic to study. He had concluded in his own mind that it was smoking that caused lung cancer.
[5.220]At p.39, Fisher wrote:
"The association observable between the practice of cigarette smoking and the incidence of cancer of the lung, to which attention has been actively, or even vehemently, directed by the Medical Research Council Statistical Unit, has been interpreted, by that Unit, almost as though it demonstrated a causal connexion between these variables.
The suggestion, among others that might be made on the present evidence, that without any direct causation being involved, both characteristics might be largely influenced by a common cause, in this case the individual genotype, was indeed rejected with some contempt by one writer, although I believe that no one doubts the importance of the genotype in predisposing to cancers of all types.
It seemed to me that, although the importance of this factor had been overlooked by the Unit in question, it was well within the capacity of human genetics, in its current state, to examine whether the smoking classes to which human beings assign themselves, such as non-smokers, cigarette smokers, pipe smokers, cigar smokers, etc., were in fact genotypically differentiated, to a demonstrable extent, or whether, on the contrary, they appeared to be genotypically homogeneous, for only on the latter view could causation, either of the disease by the influence of the products of combustion, or of the smoking habit by the subconscious irritation of the postulated pre-cancerous condition, be confidently inferred from the association observed."
Sir Richard said that this was a view which Fisher was entitled to take and, when it was taken, it was shown to not be relevant.
[5.221]Fisher continued on pp.39-40:
"The method of inquiry by which such differentiation can be recognised is the same as that by which the congenital factor has been demonstrated for several types of disease, namely, the comparison of the similarities between monozygotic (one-egg) and dizygotic (two-egg) twins respectively; for any recognizably greater resemblance of the former may be confidently ascribed to the identity of the genotypes in these cases."
Sir Richard said that this was a view that Fisher was entitled to take. Fisher then referred to information provided by researchers in Germany about the results of an inquiry into the smoking habits of adult male twin pairs. He wrote, on p.40, that in all cases the monozygotic twins showed closer similarity and fewer divergences than the dizygotic. He continued:
"There can therefore be little doubt that the genotype exercises a considerable influence on smoking, and on the particular habit of smoking adopted, and that a study of twins on a comparatively small scale is competent to demonstrate the rather considerable differences which must exist between the different groups who classify themselves as non-smokers, or the different classes of smokers. Such genotypically different groups would be expected to differ in cancer incidence; and their existence helps to explain such oddities as that pipe and cigar smokers should show much less lung cancer than cigarette smokers, while among the latter, the practice of inhaling is associated with less rather than with more cancer of the lung."
Sir Richard said that he did not accept that Fisher was entitled to form a view on the matters of genetics that he addressed because he had not looked through all the human evidence on lung cancer. It was just a theoretical concept in which he had not taken into account the existing evidence. He was not entitled to express the view contained in the last sentence quoted above. Counsel made it clear that his questions were directed to Fisher's views about genetics, not about inhaling. Sir Richard said that Fisher was proved to be wrong, but he suspected he was wrong in any case. It was not a view that would be at all widely accepted by geneticists at the time that genotypically different groups would be expected to differ in cancer incidence. He described Fisher as an "ignorant geneticist" in expressing this extreme view which other geneticists would not have taken. In relation to smoking, Fisher was an ignorant geneticist.
[5.222]Sir Richard was then asked about Dr Joseph Berkson. He said that Berkson was concerned that both the American Cancer Society and his and Hill's study found that there was a relationship between smoking and a whole range of diseases, not just lung cancer and heart disease, and he said that this was a very surprising thing and must make one think that there was something wrong with the study. He did not take into account the fact that the risks for the different diseases were very different, some greatly increased risks and some very small increased risks, and he did not take into account the fact that tobacco smoke contained many, many different chemicals and perfectly reasonably might affect many different diseases. Hill said that it was as if Berkson had said that milk could not spread an infectious disease when, in those days it did spread many infectious diseases, such as diphtheria, typhoid fever and scarlet fever and therefore it could not cause any of them because it caused a lot. Sir Richard said that this was a good argument of Bradford Hill's. He agreed that milk did spread a large number of infectious diseases. He described Berkson's views as "silly nonsense".
[5.223]Sir Richard agreed that Berkson worked at the Mayo Clinic, Rochester, Minnesota and was an Associate Member of the Institute of Biological Research at Johns Hopkins University, Baltimore, Maryland. He was a very distinguished statistician, eminent in his field. He was Professor of Biometry in the University of Minnesota and at the Mayo Clinic he was Head of Biometry and Statistics. Berkson 1959 was a paper by him referring to the cohort studies of the British doctors and Hammond and Horn's study of 200,000 Americans. At p.448 Berkson wrote:
"Firm opinions have been published to the effect that, on the basis of accumulated evidence, it is scientifically established beyond reasonable doubt, that smoking is an important cause of cancer of the lung. I am a member of a committee that has sponsored some of the most important of the published studies and, owing to this circumstance, have felt the responsibility to make a fairly careful study of this evidence. My own conclusions are quite different.
In the first place, virtually all the evidence is obtained from statistical studies in the ordinary connotation of the term 'statistical.' We are not dealing with the results of laboratory experiments, or even with placebo-controlled clinical trials."
Sir Richard said that he disagreed with this because by 1959 there was experimental evidence from animals and there was the detection of benzo[a]pyrene in tobacco smoke. Benzo[a]pyrene was a very strong carcinogen but, at best, was only a minor cause of lung cancer. He would not call it a weak carcinogen in any circumstances. The amount present in tobacco smoke, however, was not sufficient to cause very large risks. It was one of the strongest carcinogens known to humans, but present only in small quantities. He did not believe that it was the component of tobacco smoke which caused the great majority of cases of lung cancer.
[5.224]Berkson continued:
"Nor is the conclusion based on a synthesis, by a 'chain of reasoning,' of relevant scientific knowledge from many different sources. Such statistical evidence, for a question like the identification of a cause of a disease, at best, can be only presumptive."
Sir Richard said that Berkson was wrong there again. Berkson continued:
"But even as statistical investigations, I do not find the published studies so sound or convincing as they apparently have widely been assumed to be. In the studies that have been called 'retrospective,' as well as in those called 'prospective,' I find questionable and even paradoxic elements."
Sir Richard said that he was not entitled to that view. On the same page Berkson suggested for consideration three explanations of the observed associations. The second of these was:
"The observed associations have a constitutional basis. Persons who are non-smokers, or relatively light smokers, are the kind of people who are biologically self-protective, and biologically this is correlated with robustness in meeting mortal stress from disease generally."
Sir Richard said that Berkson was here putting forward a constitutional hypothesis.
[5.225]In Berkson 1960 at p.968 reference was made to Dr Harold Dorn. Sir Richard said that Dorn was employed by the National Cancer Institute in the US and was Secretary of the International Organization of Cancer Societies. When Sir Richard knew him he was a statistician employed by the Public Health Service. Berkson wrote:
"I spent considerable time with Dr Dorn and with some veteran experimental workers of the Public Health Service and have corresponded with others. I cannot speak didactically of their views, but I can say that they seemed in general agreement with mine, as regards the tentative character of the evidence. Surely, I had the impression that Dorn believes that much more work in pharmacology, pathology, and other associated sciences must be done before anything definite can be said with regard to the explanation of the statistical findings."
Sir Richard said that while Berkson had this impression, it was not the impression he himself had from talking to Dorn. Berkson continued:
"Certainly, the word 'cause' does not appear in any of his writings on the subject, and he has recently expressed himself elaborately on the complexities of interpreting statistical results for their etiological significance."
At p.969 Berkson wrote:
"As I have repeatedly pointed out, the prospective studies show more excess deaths among the smokers from other causes than from lung cancer, and these other causes are distributed among all classes of disease. If the statistical results are not spurious but reflect some real biological effect, this points to a generalized, not a local, effect. I have presented a plan [in Berkson 1959 and other papers] for an experimental epidemiologic study to explore this lead. Why has not the Public Health Service set up this experiment, or some modification of it?
Sir Ronald Fisher, who has been critical of the analysis of the English data on smoking and lung cancer [in Fisher 1959], early remarked, 'The question seems to be a serious one; when is serious investigation going to begin?' His question is timely even now."
Sir Richard said that he disagreed with Berkson. Further research was done, though Sir Richard thought the evidence was quite strong enough to show that it was not necessary. A lot of money was spent on it and it showed what he expected it would show.
[5.226]Reference was next made to Berkson 1964. In this paper Berkson explained that he had prepared written questions and answers as a basis for a televised interview which he had been asked to give. He subsequently rescinded his acceptance of the invitation to appear on the programme because "the broadcasting people would select the parts actually to be presented." The written questions and answers he had prepared were incorporated in the paper. At p.327 Berkson explained why he had expressed doubt that "some statistical studies have shown fairly conclusively that smoking is the chief cause of lung cancer". He wrote:
"The way you have put the question reflects a widespread misunderstanding regarding the facts. You have heard the adage that the most misleading sort of untruth is a half truth. If it is said that these studies showed smokers to have a higher death rate from lung cancer than nonsmokers, this is about a 15% truth. What these studies disclosed is that, in the populations under investigation, the smokers have a higher death rate from all causes together - lung cancer, other cancers including, for instance, cancer of the pancreas, of the bladder and of the prostate, heart disease and diseases other than any of these - in short, all classes of disease. Lung cancer constituted only about 10 to 15% of the total excess deaths. The problem presented by these findings has been put as well as need be by Cuyler Hammond, the senior author of the American Cancer Society's reports, from whom I quote:
'In my opinion, the most important finding in all these studies is that overall death rate increases with the amount of smoking. I want to emphasize that I said "overall death rate," not "lung cancer." The relationship between smoking and lung cancer should be viewed in the light of this broader picture.'"
Sir Richard agreed that at the time Berkson made these observations, he was entitled to do so on the basis of the American Cancer Society Study, and that Hammond was also entitled to say what Berkson quoted him as saying.
[5.227]On p.328, after referring to the statistics from the studies by Hammond and Horn and by Dorn, Berkson wrote:
"We are not concerned with indicting or exonerating smoking [...] but to try to find the scientific explanation of these statistical results. The idea that cigarette smoking causes all these many deaths from all these many causes does indeed seem seriously questionable. There is not any scientifically known pharmacologic or physical explanation for so widespread and multifarious an effect. If we extrapolate the results to the general population, we must believe that there are some 250,000 deaths annually from smoking-induced diseases, without any of them having been individually noted as such from independent clinical or pathologic evidence. Only by their numbers are they known."
Sir Richard said that this had been done by other methods since. This was one of the first observations that indicated that smoking was responsible for so many more diseases, and it took quite a long time to establish which ones smoking actually caused and which were statistical flukes. The American Cancer Society finding about an increase in the death rate from cancer of the prostate turned out to be just an odd finding which was not repeated in other studies. But of course, he said, in subsequent years the explanation for these findings all became clear. Counsel pointed out that he was asking Sir Richard to look at the texts in the context of the time in which they were written, and he was not asking whether any of the views held good today in the light of subsequent knowledge.
[5.228]At p.329 Berkson wrote that it was the distinct and real possibility that the results stemmed from a statistical fallacy in the data. He had put forward several other explanations:
"Another explanation, which has been advanced also by other scientists, is that the difference in death rate from all causes reflects a constitutional difference between smokers and nonsmokers. The ideas is that nonsmokers or light smokers are of a constitutional type marked by self-protective habits, and one aspect of the constitutional makeup is that they have generally lower death rates. [...]
The findings of Seltzer seem especially pointed. An anthropologist, he investigated the morphologic characteristics of 922 college students as reflected in a number of anthropometric measurements, in relation to their smoking habits as determined 13 years after graduation. He found, not only that the indices of body build clearly differentiated the smokers and nonsmokers, but that smokers were clearly differentiated according to type of smoking. He concluded:
'Smoking behavior appears to be in part a reflection of the biological or genetic makeup of the individual.'"
Sir Richard agreed that Berkson was here suggesting a possibility, but did not feel able to say whether the suggestion was sensible without reading the whole paper. These statements were very complex. Seltzer was the American he had referred to earlier as being one of the "eccentrics".
[5.229]Sir Richard was next asked about Yerushalmy 1962. He agreed that Yerushalmy had been a statistician at the National Institute of Health in the United States, that in the early 1940s he assumed the Directorship of the Division of Statistical Research of the Children's Bureau in the US Department of Labor, and that, after working as a statistician in the Public Health Service, in the late 1940s he joined the University of California at Berkeley and was Professor of Biostatistics at that university. At p.212, under the heading "Specificity of association", Yerushalmy wrote:
"The main doubt about the validity of the epidemiologic evidence stems [...] from the fact that the groups possessing or not possessing the characteristic under suspicion have been self-selected. Consequently, the association which has been established epidemiologically between the factor F and the disease D-1 may not reflect a causal relationship between F and D-1, but be due to other factors and characteristics by which the two groups differ. To fix the ideas - the association observed between cigarette smoking and cancer of the lung may indicate a cause-effect relationship, but it may also be due to differences between smokers and non-smokers in characteristics other than smoking. It is at least possible that these other factors and characteristics, rather than smoking per se, are behind the observed association. It is therefore necessary to search for methods of investigation which would help elucidate, if not eliminate this dilemma."
Sir Richard said that he knew Yerushalmy's views, but he had not read the article and would rather not comment on it until he had had an opportunity of reading it. Counsel pointed out that he was asking Sir Richard about his evidence that nobody had seriously challenged the causal relationship between cigarette smoking and lung cancer. Sir Richard said that counsel was picking out the two or three who did, and Yerushalmy certainly would be one he would expect to have done so; he was a statistician who did not know a great deal about epidemiology.
[5.230]At p.214, under the heading "Cigarette smoking and health", Yerushalmy wrote:
"A strong association has been demonstrated between cigarette smoking and cancer of the lung. Many studies, both retrospective and prospective, have confirmed the fact that a larger proportion of persons who suffer from cancer of the lung are cigarette smokers than is true of a comparable group not suffering from this disease. Similarly, cigarette smokers have a higher death rate from cancer of the lung than non-smokers. Moreover, heavy smokers suffer higher mortality from cancer of the lung than light smokers and past smokers who stopped the habit have lower rates than those who continue to smoke [...]."
Sir Richard said that he agreed with these statements.
[5.231]Yerushalmy continued:
"The investigations by which these associations were established presented at first some interesting and subtle sampling problems which could have biased the results. These were discussed by a number of investigators, especially Berkson [...]. However, if the association were due entirely to these sampling biases they would not have persisted for many years after the initiation of the investigation. The fact that cigarette smokers continued to have higher rates in the second and third year of observation would indicate that the association between cigarette smoking and cancer of the lung is not a resultant of these sampling peculiarities alone. Consequently, the association itself is accepted as definitely established. The question turns to the interpretation of this association in terms of causation."
In the next paragraph, Yerushalmy wrote:
"The main difficulty in evaluating such association stems from the fact that the individuals observed have made for themselves the crucial decision whether they are smokers, non-smokers, or past smokers."
Sir Richard said that he did take objection to this, but really could not comment further without reading the whole article. At pp.220-221 Yerushalmy wrote:
"These findings can perhaps more easily be explained on the basis that smoking acts as an index to differentiate smokers from non-smokers on a number of different characteristics rather than as indicating a causal relationship."
Sir Richard said that he could not comment on this: he could not understand what Yerushalmy was saying until he had read the paper.
[5.232]Sir Richard was also asked about Yerushalmy 1972. At p.279 it was stated:
"A comparison of smokers and nonsmokers showed that the two differed markedly along several environmental, behavioral, and biologic variables. [...] These findings raise doubt that cigarette smoking acts as an exogenous factor which interferes with the intrauterine development of the fetus. The findings give equal support to the hypothesis that smokers represent a group of people whose reproductive experience would have duplicated the observed patterns whether or not they smoked. In other words, the observed differences in incidence of low-birth-weight infants may be due to the smoker, not the smoking."
Sir Richard said that although he was not familiar with the paper, he was familiar with Yerushalmy's general view on the effect of smoking on birth weight and he generally agreed with him. He did not feel able to make more detailed comments without an opportunity of reading the paper. I gave Sir Richard an opportunity to read the two Yerushalmy papers, and having read them he subsequently agreed that Yerushalmy also was a worker who questioned the causal hypothesis.
[5.233]Counsel next asked Sir Richard about HJ Eysenck. He said that he was familiar with the name. He was the psychiatrist Sir Richard had referred to earlier. He died in 1977. He did a lot of research for the tobacco industry. He was on Sir Richard's list of eccentrics; indeed he would go further and come straight out, he was a liar. They had direct experience of that with him saying one thing on one day and then denying and saying the opposite the next day. He was a psychologist and a Professor at the London Institute of Psychiatry, he worked at the Maudsley Hospital and at the Institute of Psychiatry for most of his professional life. He was editor-in-chief of a journal, the name of which Sir Richard could not remember. He was one of the leaders of clinical psychology as a profession in Britain. He had a particular interest in researching the role of personality types, explored concepts of introversion and extraversion and was particularly interested in the relationship between personality types and the development of lung cancer. He challenged the causal hypothesis (that cigarette smoking caused lung cancer), and then he withdrew, and then he challenged it again and then he withdrew. "If you got him in front of the public and cross-examined him, he would withdraw and then he would go back again and say the same thing a week later." There was a deathbed recognition of where he received his funding. Sir Richard agreed that he was suggesting that Eysenck's integrity was compromised by the source of his funding. He knew that Eysenck had written a lot of papers.
[5.234]Eysenck 1965 contained an introductory passage which concluded with this sentence:
"Above all, Dr Eysenck's book is an urgent plea for more fundamental research and for recognition of the fact that the issue is far more complicated than most official and journalistic statements would have us believe."
Sir Richard said that he would not pay any attention to what Eysenck said in relation to that. At p.15 Eysenck wrote:
"This book is concerned then with the relationships between three variables: smoking, disease, particularly lung cancer and coronary thrombosis, and personality. All the evidence to be considered is circumstantial; there is no direct evidence which does not rely on statistical investigation and logical interpretations. These are difficult matters and it is very easy to go wrong. As Dr R Doll, himself one of the scientists most prominently associated with the promulgation of the theory that smoking causes cancer, has pointed out:
'When the nature of the disease makes it impossible to carry out logically conclusive experiments there is always room for honest difference of opinion. In the case of smoking it is particularly hard to envisage how a conclusive experiment could be carried out and no such experiments have been made.'
Doll goes on to quote a famous saying of Claude Bernard, to the effect that 'There are no false theories and true theories, but only fertile theories and sterile theories.'"
Sir Richard did not recall having said this, but agreed that he might well have done. He did not take exception to it.
[5.235]At pp.50-51, in a chapter entitled "The critics hit back", Eysenck wrote:
"The work of Doll and Hill in England, of Horn and Hammond in America, and of all the other investigators who have taken up the trail of the disease-producing effects of cigarette smoking, has, of course, not gone unchallenged. I shall not in this chapter deal with all the arguments that have been advanced in an attempt to rebut their conclusions. Many of the criticisms are themselves unsound, and it would be a waste of time to discuss them in detail. Others, while reasonable at the time when they were made, have since been answered by the original authors, either in further analyses of their data, or by new studies. In going through the writings of Doll and Hill, and of Horn and Hammond again for the purpose of this book I was struck, as I had been when I had read them originally, by the great care which had been taken in the carrying out of these investigations, by the way in which the authors took note of published criticism and tried to answer it by adducing further factual information, and by their wholly admirable refusal to be side-tracked from strictly scientific argument. I believe that the case which they make out can be criticized but that is merely to say that scientific investigators, even the most eminent, are only human; whatever the truth of the criticisms here presented the work of these investigators will always remain as a fine example of scientific detective work."
Sir Richard said that he did not disagree with any of this, though he described the concluding part of the passage as "a bit smarmy".
[5.236]At p.75, in a chapter entitled "Personality and constitution" Eysenck wrote:
"We have already referred several times to the so-called constitutional theory of lung cancer and smoking, i.e. the hypothesis first put forward by Sir Ronald Fisher that people of a certain constitutional type are particularly prone to lung cancer and are also particularly predisposed to take up cigarette smoking. In this form the theory is too weak to be very useful because it is so indefinite that no specific test can be conducted to support or disprove it."
Sir Richard said that this was not actually true: studies were done to test it and in fact disproved it. The studies of monozygous twins that were carried out in Sweden, the United States and Finland all showed that it just was not true. Few people took Fisher's suggested hypothesis seriously. Eysenck was one of them. Sir Richard challenged his good faith and also pointed out that what Eysenck suggested had been demonstrated to be untrue. He could not be sure whether this was so when the book was published in 1965.
[5.237]Eysenck went on:
"What is maintained in effect is that there are certain types of people who smoke; that this type of person has acquired his particular personality through hereditary causes, and that this particular type of person is also more likely to develop cancer."
Sir Richard said that this was shown to be untrue and Eysenck knew it perfectly well, though perhaps not in 1965. Pressed on this, Sir Richard said that he did not say that in 1965 Eysenck knew it was untrue and it was misleading if he did say that. He repeated it later at a time when it was known to be true, at about the period when there were proceedings at the Royal Statistical Society in 1978, when there was more evidence. Eysenck continued: "Clearly, therefore, psychological studies are needed to link up both smoking and cancer proneness with specific personality types." Sir Richard said that it was wrong of Eysenck to make that suggestion. He agreed that he himself had no expertise in the concept of personality in psychology.
[5.238]Asked about Eysenck et al. 1960, a report of a study commissioned by the Tobacco Manufacturers' Standing Committee and published in the British Medical Journal, Sir Richard said that he must make it clear that he did not accept any of Eysenck's proposed findings "in the light of knowledge we gained later about his behaviour". He was corrupted, though Sir Richard could not say whether this was so in 1960. Sir Richard had not read this paper. He was not prepared to look to see what Eysenck and his colleagues had said so that he might be asked for his view on it, because he would not believe it.
[5.239]Sir Richard agreed that Professor Philip Burch was one of the people he described as "eccentrics". He was Professor of Medical Physics at the University of Leeds and was Director of the Medical Research Council Environmental Research Unit, but "not for long, because I attended a meeting at the Medical Research Council in which he sought funds for such a unit and he was flatly turned down". He was not aware of Burch having had a unit, but was aware of having "described himself as some such title". So far as he knew, Burch did not get support for such a unit. What Burch wrote should be regarded with some care. He wrote "a terrible lot", and some of it was "nonsense".
[5.240]Counsel pointed out to Sir Richard, under reference to Burch 1964, that the author was writing at that time from the Medical Research Council Environmental Radiation Research Unit at the Department of Medical Physics, University of Leeds. Sir Richard agreed that Burch was a member of that unit at the time, under a professor at Leeds, but said that he was talking about a time when Burch sought to be the Director of the unit and that was what the Medical Research Council turned down.
[5.241]Sir Richard's attention was next directed to a debate which was conducted on the pages of New Scientist in 1974. It started with Burch 1974a, which began:
"In their 1971 report, the Royal College of Physicians stressed:
'Many countries have set up authoritative committees and commissions to study the cause of this modern scourge [lung cancer]. All have concluded that it is almost entirely due to cigarette smoking.'
On the other hand, the late Sir Ronald Fisher, who has been described as the greatest statistician who ever lived, feared that this conclusion would be seen in retrospect to be a 'catastrophic and conspicuous howler'. Where then does the truth lie? With a statistician-logician-geneticist of genius, or with 'authoritative committees and commissions'?
During the past year or so I have reiterated Fisher's views in The Lancet and supplemented them with new analyses. Surprisingly, these arguments and demonstrations have provoked few responses and nothing to challenge Fisher's position. Having at one time accepted that most cases of lung cancer are caused by smoking, I shall outline in this article some of the evidence that forced me to change my mind."
Sir Richard said that by this time he had not responded to Burch because there was no controversy with him, he just made wild statements which people ignored. Of course it was quite untrue that Fisher's position had not been disproved, it had been by 1974. Sir Richard did not enter into debates with Burch. He had ignored him intentionally.
[5.242]At p.463 Burch wrote:
"For the reasons outlined here, and for many others that limitations of space do not allow me to describe, I am unable to sustain the hypothesis I once held: that lung cancer 'is almost entirely due to cigarette smoking'. At the same time, I am unable to refute Fisher's constitutional hypothesis which offers a plausible and well supported interpretation of numerous otherwise paradoxical findings."
Sir Richard agreed that the scientific method required that a hypothesis may be enunciated and then the scientist worked to try to disprove the hypothesis, and that this method was being invoked by Professor Burch.
[5.243]Burch's article was followed, on p.463, by a reply by Sir Richard, Doll 1974, which he said that he had been advised to write. The response to it was Burch 1974b, which generated correspondence in the letters pages, where among other letters were two by Burch, Burch 1974c and Burch 1974d. In the last of these, Burch wrote:
"[...] Fisher's constitutional hypothesis is, in principle, eminently falsifiable: many testable consequences follow from it. If 'smoking genotypes' generally associate positively with 'lung cancer genotypes', then appropriate studies of the first-degree relatives of (a) lung cancer probands and (b) suitably matched controls should reveal such associations. For example, the frequency of smokers among the first-degree relatives of non-smoking lung cancer probands should be higher than among the corresponding relatives of non-smoking matched controls. This and other predictions of Fisher's hypothesis have all been verified by Dr George K Tokuhata [...]."
Sir Richard agreed that Burch was here suggesting a methodology to test the hypothesis, but he added that there were "heaps of other methodologies" and that actually the hypothesis was untestable because it did not account for an increase in the disease; genotypes do not change, so it was never a starter.
[5.244]Sir Richard was next asked about Carl C Seltzer. He said that Seltzer was one of "a rather peculiar group of people who took some odd views". He did not accept the causal hypothesis, and a lot of other things as well. Sir Richard was unable to recall what had led him to describe Seltzer as one of a rather peculiar group of people, but he confirmed that he was one of the people he had previously described as "eccentrics". In Seltzer 1963a the author reported on a study of 922 college men relating their morphological characteristics as students to their subsequent histories of smoking thirteen years after graduation, in order to ascertain the extent to which the different classes of nonsmokers, cigarette smokers, pipe smokers and cigar smokers were phenotypically and genotypically conditioned. Significant differences in physique were found between smokers and nonsmokers and in accordance with the form of smoking adopted. Smokers were consistently greater than nonsmokers in height and weight and in the dimensions of the head, face, shoulders, chest, hip, leg and hand. He claimed that the findings delineated constitutional differences between smokers and nonsmokers and among the several varieties of smokers. Smoking behaviour thus appeared to be in part a reflection of the biological or genetic make-up of the individual. At p.644 Seltzer wrote:
"Given the strong likelihood of a constitutional factor in smoking behavior, consideration should also be given to the possibility of a constitutional factor in patients with lung cancer. (This would bear upon the subject of the association of smoking and cancer of the lung.)"
[5.245]Sir Richard said that while it was a view that he always held that consideration should be given to the possibility of a constitutional factor in patients with lung cancer, he accepted only to a trivial extent that this would bear upon the subject of the association of smoking and lung cancer. This was because of the increase in the incidence of the disease, so even if there was some constitutional factor it was relatively unimportant. Asked whether there were some who still did take issue with the proposition that there had been an increase in the incidence of the disease, Sir Richard said: "There was still a Flat Earthers Society at that time." Those who suggested that the reported increase in the incidence of the disease might be artefactual were Flat Earthers. There was no question that part of it was certainly artefactual, but by that time the suggestion that it was wholly artefactual was quite unacceptable. He had gone on record as saying that he accepted that part of the increase at least was artefactual, without question, and that one simply had to exercise one's judgment about how much. Here there was a thirty- or forty-fold increase in incidence that was not artefactual, and the incidence increased differently in the two sexes and in different countries. In the early years there were some who thought differently from him, and Seltzer must have, but it was a pretty extreme position for him to take in 1963.
[5.246]Seltzer continued:
"That there is a relationship between constitution and disease is generally accepted in medical circles. [...] Accordingly, a logical line of future research is indicated. Attention should be focused on an investigation of constitutional characteristics in patients with lung cancer."
Sir Richard said that this was unreasonable; the hypothesis was a non-starter because of the increased incidence, but nevertheless it was done, with tobacco industry support, quite properly.
[5.247]In Seltzer 1963b, in reply to a correspondent who had written that his speculations would be used by promoters of cigarette smoking as ammunition in their campaign against efforts to control "this addiction", Seltzer wrote:
"[D]oes Dr Flick wish to hold researchers personally responsible for what promoters, publicists, and others might do with their published works?"
Sir Richard said that this was a fair comment.
[5.248]The last paper by Seltzer which was referred to by counsel was Seltzer 1967. Seltzer had been asked by the committee responsible for a conference to review the status of knowledge of the subject of human constitution and genetics as related to smoking. He found that very little new information had been added to this area since the appearance of USSG 1964. At p.324 he noted "that a recent reevaluation of the Harvard Study [Seltzer 1963a] by Livson and Stewart has failed to undermine its basic results." Sir Richard said he had not been at the conference and was not clear what was being referred to.
[5.249]Reference was next made to KA Brownlee of the University of Chicago. Sir Richard said that he had heard of Brownlee, who was a statistician of British origin, and a fellow of the Royal Statistical Society of London, who had gone to work in the United States. In Brownlee 1965 he contributed an invited review article on USSG 1964 to the Journal of the American Statistical Association. At p.733 the author wrote:
"The fact that the hypothesis that cigarette smoking is a cause of cancer appears by and large to be in conformity with the data, and hence that this hypothesis is acceptable, does not rule out the possibility that there are other hypotheses also in conformity with the data. [...] The main alternative to the smoking-causes-cancer hypothesis is the genetic hypothesis, and there are several odd pieces of information that give plausibility to it."
On the same page there was quotation from a paper by Sir Ronald Fisher. Sir Richard accepted that Brownlee was someone who, in 1965, was not prepared just to accept the causal hypothesis, and who turned to Fisher and apparently took his views seriously.
[5.250]Burch 1978 was a paper read before the Royal Statistical Society in that year, followed by a discussion of the paper by some of those present and contributions subsequently received in writing. According to the summary:
"Methodological problems that arise in epidemiology are briefly reviewed. Associations between smoking and lung cancer, and their connexion with sex and country, are described. Secular trends in recorded mortality from lung cancer in England and Wales, 1901 to 1970, are derived from the Registrar General's statistics. Estimates are made of the expected trends assuming that the associations found between the various types of smoking and lung cancer reflect causation. Observed and expected trends conflict. The secular trends in mortality from lung cancer in British male doctors are also examined. From the foregoing and other types of evidence it is argued that no definitive conclusions can be reached, as yet, about the extent of any causal link between smoking and lung cancer. It is very doubtful, however, whether the entire association observed between smoking and lung cancer in occidental males should be interpreted in causal terms."
Sir Richard said that this was consistently Burch's view.
[5.251]At p.438, in para.2.1, Burch said:
"Epidemiology, like astronomy, is largely an observational rather than an experimental science and hence the scope for planned and controlled intervention by the investigator is usually either limited or absent."
Sir Richard said he did not disagree with this. In the same paragraph Burch said: "We cannot randomize for smoking." Sir Richard said that it was correct to say that as a general approach one could not randomise for smoking; attempts had been made to do so, not very successfully. At para.2.2 Burch said that many studies had shown that cigarette smokers differed, on the average, from non-smokers with respect to morphology (reference to three papers by Seltzer), personality (reference to papers by Heath, Lilienfeld, Eysenck and Thomas et al.) and genetic markers. Sir Richard said that he did not know the papers to which reference was made in respect of genetic markers, but he did know that no genetic markers had been recognised for lung cancer. At para.8.4, on p.456, Burch said that, having once shared the view that lung cancer was almost entirely due to cigarette smoking, he found himself forced back to the verdict in Fisher 1959 that "the data so far do not warrant the conclusions based upon them". Sir Richard agreed that this was a familiar theme of Burch.
[5.252]The first contributor to the discussion of Professor Burch's paper was Professor P Armitage of Oxford University, whom Sir Richard described as a close colleague of his with whom he had collaborated. At p.458 Armitage said:
"Professor Burch's own views have been widely publicized in the past, although this is the first time they have been presented in a paper to the Society. He expresses a hope [...] that rigorous methods of statistical inference will help to resolve the issues that concern him. In this I think he is mistaken, unless one takes a much wider view of the principles of statistical inference than is customary. The issues seem to me to be concerned with the reliability of sources of data, the possible effects of confounding variables and the plausibility of alternative biological hypotheses. These problems are basically for the epidemiologist, rather than the statistician, to grapple with [...]."
Sir Richard agreed that what Armitage was saying here was not that what Burch proposed was nonsense, but that it might be misguided. At p.460 Armitage concluded:
"It will be clear that I am not wholly in sympathy with Professor Burch's point of view, but he has provided a clear statement of his case and given us an opportunity to review it in detail."
[5.253]The next speaker was Dr PD Oldham of the MRC Pneumoconiosis Unit in Glamorgan; Sir Richard said he knew of him, describing him as a very solid, middle-of-the-road statistician with a lot of epidemiological experience. After referring to Doll and Hill 1950, Oldham said, at p.460:
"The consequence is that, 28 years later, we still do not know how cigarettes cause lung cancer, nor even, if we are particularly rigorous in our use of scientific logic, whether they do."
Sir Richard said that this was not a statement with which he would have disagreed. At p.462 Oldham said:
"In one respect at least I find myself in wholehearted agreement with the author [Burch], and believe that this would have been shared by Fisher. This is in the ridicule with which he describes the steady flow of theories of the causation of diseases based on epidemiological associations. There is nothing wrong with this method of formulating hypotheses, but too often the authors of such studies succeed in implying that a tenable hypothesis, developed from a careful epidemiological survey, is a proven one. Attribution of this step, by the public, to a statistical argument is a certain means of discrediting our science."
Sir Richard said that he thought that this was true.
[5.254]Professor HJ Eysenck spoke next. Sir Richard said that he would not be interested in his contribution. Asked to give his reasons for this attitude, Sir Richard said that, leaving aside the fact that Eysenck did not admit that his research was funded by the tobacco industry, which only came out after his death, it was the way in which he would change his opinions in a debate. When you were debating with him, and if you gave him good clear evidence of something, he would agree with you and then he would go back in the next meeting or in a television broadcast and say the opposite. This was why he could not take him seriously. So far as Sir Richard was concerned Eysenck concealed the fact that he was funded by the tobacco industry until after his death and this was dishonourable and quite probably tainted his views. If he had acknowledged that he had been funded by the tobacco industry, it would have made a difference; one would have known where one was then. In major research, the source for the funding should always be disclosed. Sir Richard did not know that the fact that Eysenck had been funded by the tobacco industry in the years between 1963 and 1967 was a matter of public record; all he could say was that he did not know it, nor did any of his colleagues.
[5.255]At p.462, GJA Stern of Imperial College, London, whom Sir Richard did not know, said:
"The author seems to confirm Fisher's objections to the dogma that smoking causes lung cancer. Fisher's point that inhaling correlates negatively with lung cancer is important, as is the rather suspicious silence and apparent reluctance to investigate this matter adequately on the part of medical statisticians."
Sir Richard said that this was quite untrue, it was investigated in detail, he himself had advanced a suggestion to explain the inhalation anomaly, and did some experiments with the use of radioactive isotopes to see where tobacco smoke went, but the experiments failed. At p.463 Stern said:
"Fisher observes that lung cancer has increased far more in women. This, and Professor Burch's analysis, makes the Royal College of Physicians' claim that the secular trend argument is the chief reason for rejecting a genetic hypothesis hardly believable. The identical twin analysis seems rather to demonstrate an important genetic component."
Sir Richard said that he did not agree with any of this; Stern was just incorrect about the increase in women.
[5.256]Professor H Gwynne Jones of the University of Leeds, whom Sir Richard knew, said at p.463:
"This paper represents a very valuable bringing together of the strands of a complex but empirically based argument by which Professor Burch has consistently failed to modify medical opinion concerning the relationship between smoking and lung cancer. Nevertheless, in my view, the popular causal theory is clearly falsified in true Popperian fashion by his careful analysis of secular trends, sex differences and smoking habits. Equally clearly, any direct influence of smoking on the aetiology of lung cancer is shown to be minimal."
Sir Richard said that he rejected this, it was just nonsense. Gwynne Jones continued:
"On the other hand, Professor Burch does present an admittedly complex biological model of diseases of this type which derives from quite different sources but is consistent with all the data reviewed. This model certainly merits more attention than he has so far received."
Sir Richard said that he would disagree with this. This was the model he was referring to earlier, considered by a special committee of the Medical Research Council and rejected. So his own disagreement was backed up by the committee.
[5.257]Sir Richard was asked to note that Dr CC Seltzer of Harvard University attended the meeting and made a contribution to the discussion which was supportive of Burch's approach. Dr Frank Hansford-Miller of the Inner London Education Authority expressed gratitude to Burch for opening up the question of the causative factors of lung cancer and suggested that the search should be started for causes other than smoking which Burch had shown must make a far bigger contribution than smoking. Sir Richard agreed that this speaker supported Burch. The last substantive contribution to the discussion was made by Joy L Townsend of the University of Essex, who reached a different conclusion from that of Burch.
[5.258]Among the written contributions, at p.468 was one from Professor AR Feinstein of Yale University, whom Sir Richard described as an eminent but peculiar scientist who tended to have a different view to anybody else on any subject. He was well known for this. He was a Professor of Medicine and Epidemiology at the Yale School of Medicine and was Director Emeritus of the Robert Wood Johnson Clinical Scholars Programme at Yale. He had "a clutch" of honours and awards. He was a professional critic and a professional author. Sir Richard was honestly not sure whether Feinstein was a sincere critic. He knew him quite well and had spoken in his department, but had difficulty making up his mind about him. "He liked to do things because it was naughty, I think."
[5.259]Feinstein wrote:
"The history of medical science contains many instances of thoroughly accepted, paradigmatic 'gospel' that was later rejected as fallacious. During the past century, statistical evidence was used to support many ideas about causes of disease that were eventually discarded as erroneous. Among such ideas were the beliefs that cholera was due to high atmospheric pressure, that pellagra was infectious, and that retrolental fibroplasia was produced by a vitamin deficiency. Recalling the long history of pitfalls in medical aetiological reasoning, cautious scientists may wish to keep at least a slightly open mind about the currently well-accepted hypothesis that cigarette smoking causes lung cancer. Although supported by a large collection of positive evidence, the hypothesis is not as securely established as the vigour with which it is argued by epidemiological authorities."
Sir Richard said that he did not accept this as a legitimate view. If he took the view, which he had expressed, that the evidence was proved beyond reasonable doubt, he did not have any doubt about that. Feinstein went on to write about "loose strands in the fabric of the argument", which he enumerated; Sir Richard said that they were not loose now. It was incorrect of Feinstein to state that "about 8 - 10% of patients with lung cancer have never smoked cigarettes"; this was not true of men, it was true of women at that time.
[5.260]Counsel next asked Sir Richard about Passey 1962. He said that he knew this paper well. Malcolm Pike and he wrote an article following it, pointing out the fallacies in Passey's argument. Passey challenged the causal hypothesis, but Sir Richard regarded the challenge as extremely fallacious. He added that Passey "unfortunately died of lung cancer". Passey was a pathologist by the time he wrote the article. Like Sir Richard, he was ageing. He had been interested in the cause of lung cancer for many years. He had done some experiments in animals in the 1920s with tobacco tar and had failed to produce cancer of the skin in mice, and Sir Richard thought that had influenced him. He did produce skin cancer in mice with lots of things, but he did not succeed in doing it with tobacco tar. At the time of writing he was Emeritus Professor of Experimental Pathology in the University of Leeds. In the article, Passey suggested that lung cancer might well be a sequel to tissue damage of a non-specific nature rather than to the specific action of carcinogens. He continued, at p.107:
"The smoker (Doll and Hill 1950) and the townsman [...] are more prone to lung cancer than the non-smoker and the countryman. We know that tobacco smoke and the air of our industrial towns contain small quantities of the polycyclic aromatic hydrocarbons [...], some of which are carcinogenic. Hence it is natural to suppose that cancer of the lung is the result of these carcinogens. But is this necessarily so? May not lung cancer be the result of altered conditions arising out of disease or damage of the respiratory system in which carcinogens need have played no part?"
Sir Richard said that this was rather a bizarre question.
[5.261]Passey continued:
"This damage may have been induced by (a) the irritating properties of tobacco or other smoke, (b) chronic respiratory disease, or (c) other injuries. Perhaps that is all that one can or should say; but if pressed I could, with some reluctance, add a suggestion that the altered conditions which appear to be important, are those associated with the presence of excess of mucus, and its accumulation and stagnation."
Sir Richard agreed that this was the view expressed by Passey in 1962. At p.111 Passey stated, as part of his conclusions:
"Lung cancer is not the result of carcinogens. It is a 'natural' form of cancer - the result of changed conditions in a damaged respiratory system."
Sir Richard agreed that Passey was prepared to express this view publicly in The Lancet in 1962.
[5.262]Asked to look at Hinshaw and Garland 1963, Sir Richard said that this was an American textbook which he had not seen before. He was asked to note that in the preface it was stated that in the six years since the first edition of the book was completed there had been developments, including the accumulation of much experience with bronchogenic carcinoma. These developments had necessitated extensive revision as well as the inclusion of entirely new material in the second edition. Chapter 20 was entitled "bronchogenic carcinoma". It started, at p.340:
"Bronchogenic carcinoma is of paramount interest to every physician and to every student of the cancer problem. While the causes are unknown, there are more stimulating theories and fragments of etiologic evidence than is true of many other forms of cancer. An increasing incidence of the disease challenges each physician to maximal efforts of prevention and control. Sex and age incidences suggest where we might find the condition with greatest frequency."
At pp.343-344 the authors stated, under the heading "Etiology" and the sub-heading "Cigarette smoking and lung cancer":
"There is a widespread belief that excessive smoking is the major cause of human lung cancer. If and when this opinion is verified, it will be the duty of physicians to warn persons against heavy cigarette smoking. The authors are keenly conscious of their responsibility in attempting to summarize the evidence on both sides of this important and controversial issue."
At p.346, under the heading "Evidence that lung cancer is not due to excessive cigarette smoking" and the sub-heading "Experimental evidence" the authors wrote:
"Despite literally hundreds of careful and prolonged experiments designed to produce lung cancer by exposure of mice or rats to prolonged breathing of cigarette smoke, no bronchogenic carcinomas have been produced."
Sir Richard, having noted the earlier passages, said that this passage was correct.
[5.263]The authors continued:
"The epidermis of the mouse is not the same as the epithelium of the human bronchus; the cigarette smoke condensate applied to the mouse was in very high concentrations, quite dissimilar to the concentration of polycyclic hydrocarbons in inhaled cigarette smoke. Incidentally, the condensate contains no substance demonstrated as being carcinogenic to man."
Sir Richard said that this last statement was untrue in 1963, they got it grossly wrong.
[5.264]Sir Richard said that he had heard of Dr R H Rigdon. In Rigdon 1965 he said that he was a physician who taught and practised pathology and was an experimental pathologist. For the previous fifteen years he had been interested in lung cancer. At p.600 he stated that he was unable to transfer data about cancer, as obtained from experimental animals, to man. Sir Richard said that this was a view he himself held, and he thought most people did the opposite, they transferred observations made in animals to the human situation. He had always personally been sceptical of the justification for doing so. In the next paragraph Rigdon said that genetic factors must be considered in cancer. Sir Richard said that this was not a controversial view, but it was a very minor factor. Rigdon continued:
"The cause of cancer is not known. By this we mean that we do not know why a cell in the body of one person will become a cancer and the corresponding cell in another person will not become a cancer."
Sir Richard said that he thought that at the time this was true.
[5.265]At p.601 Rigdon said:
"I hope that it is obvious from my remarks why I was classified in the Surgeon General's report [USSG 1964] on cigarette smoking on p.179 as 'though accepting the existence of an association, have questioned its significance in terms of a causal hypothesis.' In regard to the Surgeon General's report on smoking and health, I think it is an excellent summary of one side of this controversy. If equal time and effort had been given to the opposite view by this committee, I think the report would have been twice the size and would have been a report that scientists in the future could review to see really what the state of knowledge was in 1963."
Sir Richard said that of course he disagreed with Rigdon about this.
[5.266]In the next paragraph Rigdon said that he would consider a statement on cigarette labels that "Cigarette smoking may be dangerous to health" to be consistent with the facts as they were known, but also a number of other products such as peanuts and charcoal broiled steaks should be similarly labelled because they might contain carcinogenic substances. Sir Richard said that he did not think that this was a justifiable remark because there was a different quantitative effect.
[5.267]Rigdon was referring to different things, some very tiny and theoretical and some very large and evident. Rigdon continued:
"To summarize my views, may I say that, first, I believe that there is no satisfactory experimental evidence to establish a connection between cigarette smoking and lung cancer. Cancer of the lung has not been produced experimentally in any animal by the inhalation of cigarette smoke. The fact that tobacco tars will produce a tumor on the skin of a specific strain of mouse does not, in my opinion, lead to the conclusion that cigarette smoke will produce cancer in the lungs of man. As I continue my work in the field of experimental carcinogenesis, I find puzzling variations in the responses observed from one species of animal to another with respect to the development of cancer. This is why I say that data concerning cancer in animals should not be considered proof of a similar effect in man."
Sir Richard said that he agreed with Rigdon in this passage.
[5.268]In Rosenblatt 1969 the abstract stated:
"An eminent clinician takes a stand that indicts the concept of an absolute increase in bronchogenic carcinoma. He presents compelling arguments, pointing to the progressive decline in rate of increase concurrent with the growth of more accurate diagnosis. The author examines critically the paradoxical trends, inaccuracy of mortality statistics, faulty certifications of death and unrealistic classifications of malignancy that have combined to lead, more hysterically than historically, to the 'illusion'."
Sir Richard said that there were those who would have shared Rosenblatt's opinion in the 1950s, but he found it surprising that as late as 1969 there was anyone who took that view.
[5.269]The article concluded, at p.38:
"The prodigious increase in lung cancer during the past three decades is not due to the exposure of the population to an alleged carcinogen but is the natural consequence of the widespread use of diagnostic techniques not previously available. The intense interest in lung cancer has also produced a tendency toward over-diagnosis of the disease on the basis of radiologic, biopsy, and cytologic findings which are often not substantiated by autopsy."
Sir Richard said that he took issue with the proposition contained in the first sentence in this passage; practically everybody did, this was a "very far-out viewpoint" to be expressed as late as 1969. Asked about the tendency towards over-diagnosis on the basis of these findings, Sir Richard said that they did studies in the UK and there was some over-diagnosis, but there was also a compensatory under-diagnosis, and they just about cancelled each other out in the studies they did on autopsies and clinical diagnoses. So while it was true there was an over-diagnosis, it was also true there was under-diagnosis. With notice he could point to the studies in question.
[5.270]Referred to Wells and Feinstein 1988, Sir Richard said that he was also interested in detection bias in the diagnostic pursuit of lung cancer. At p.1025 the authors wrote:
"These results, which clearly demonstrated the existence of detection bias in the diagnostic pursuit of lung cancer in living patients, are entirely consistent with what has previously been noted at necropsy. The necropsy results showed that lung cancers are particularly likely to be undetected during life in patients who do not cough, are women, and do not smoke."
Sir Richard said that this was not consistent with what he had found.
[5.271]The authors continued:
"The existence of the pattern is not surprising. Physicians are particularly likely to suspect lung cancer and to plan a diagnostic workup if the disease has produced appropriate pulmonary manifestations (such as cough) and if the patient is in a demographic category (such as male sex or cigarette smoker) in which the disease is thought to have a relatively high incidence."
Sir Richard said that this was contrary to his experience, but it seemed to be the result of the investigation of these authors.
[5.272]Wells and Feinstein continued:
"On the other hand, despite an apparent economy in the ordering of tests, detection bias can have three important adverse effects. [...] A third consequence of detection bias is the effect on statistics for the cigarette smoking-lung cancer association. The magnitude of this association will be falsely elevated if the lung cancers are often not suspected and not diagnosed when present in nonsmokers. Although our results show a striking bias in the ordering of sputum Pap [Papanicolaou] smears for the antemortem diagnosis of lung cancer, the total effect of detection bias in the cigarette smoking-lung cancer relation cannot be quantified from our study."
Sir Richard said that he tried to quantify it in his. They continued:
"Separate research is needed to determine the effect of this bias when physicians order the many additional technologic tests used in diagnosing lung cancer today."
Asked whether he had reason to doubt the results of Wells and Feinstein's work, as reported in this article, Sir Richard said that all he could say was that it did not apply in the UK.
[5.273]In USSG 1964 at p.179 it was stated that a number of investigators, although accepting the existence of an association between lung cancer and smoking, had questioned its significance in terms of a causal hypothesis. A number of references were given for this statement. One of these was a paper by Cohen and Heimann (1962) entitled "Heavy smokers with low mortality", which Sir Richard had not read. Another was by Eastcott (1956), entitled "The epidemiology of lung cancer in New Zealand". Sir Richard remembered this paper, but did not know that Eastcott was a proponent of the constitutional hypothesis. Another reference was Haag and Hanmer (1957), entitled "Smoking habits and mortality among workers in cigarette factories". Sir Richard did not know this paper. Another reference was to Little (1969). Sir Richard recognised Little as "the man that worked for the tobacco industry". This, he said, eventually invalidated views that he might hold, because initially he was regarded as a good experimentalist, but later there came to be "some very odd questions about his work". This was for more reasons than because he was funded by the tobacco industry, but Sir Richard could not recall the details of what Little did. He agreed that Little had been managing director of the American Society for the Control of Cancer, now known as the American Cancer Society. He accepted that he had been President of the University of Michigan, but did not know about other posts he had held. He knew that he had been regarded as a senior scientist, that was really all that he could say. He became Scientific Director of the Council for Tobacco Research in the United States. It was not this feature that caused Sir Richard to doubt his views, but his subsequent behaviour in that position. Sir Richard only had second-hand knowledge about this, but sufficient for him to form a view about Little's views.
[5.274]Reference was next made to Tokuhata 1972. Sir Richard was aware of Dr George Tokuhata, who had worked with Lilienfeld at Johns Hopkins University. He was Director of the Division of Research and Biostatistics of the Pennsylvania State Health Department and held adjunct appointments as Professor of Biostatistics at the University of Pittsburgh Graduate School of Public Health and Associate Professor of Community Medicine - Epidemiology at Temple University College of Medicine. At p.5, having stated that despite the fact that statistical methods could not establish proof of a causal relationship in an association, USSG 1964 had concluded that cigarette smoking was a major causal factor in human lung cancer, Tokuhata continued:
"However, a number of investigators, though accepting the existence of a statistical association, have questioned its significance in terms of causal hypothesis. Some of these doubts have been on the basis of a possible genetic underlay which might determine both smoking and lung cancer. Others have supported some type of constitutional theory or have claimed that the observed associations are 'spurious' because of selection biases in the design of study. Also, many experiments on inhalation of cigarette smoke in animals have failed to produce a single cancer similar to the most prevalent type of lung cancer in humans." (I have omitted the references in the original.)
Sir Richard did not take issue with this as an accurate historical account, but said that the statement about biases was made by Berkson, who did not continue to make it because he recognised it was wrong.
[5.275]At p.17 Tokuhata wrote:
"Although [the] smoking habit is considered by many observers as being influenced by environmental factors, there is sufficient evidence to suggest that genetic factors may also play a significant role in the induction of such habits [...]. At present neither the acquired nor the inherited factor in smoking is completely understood."
Sir Richard agreed that genetic factors might play a statistically significant role, though a small one, and did not take issue with the second sentence in this passage.
[5.276]At pp.27-28 Tokuhata referred to Fisher's "common genotype" hypothesis, and wrote:
"Fisher's theory has been challenged by some investigators on the ground that the twin data on which his argument was based were biased, and that the history of cancer in twins whose smoking habits are known has not been documented sufficiently. More data on smoking habits and medical histories are needed regarding other siblings, offspring, and parents. Our data on the familial study of lung cancer and smoking, as discussed earlier, are not consistent with the 'common genotype' hypothesis."
Sir Richard agreed that Tokuhata was taking Fisher's hypothesis seriously; he would have expected him to, from the work he did. His work, however, was not consistent with the hypothesis. Reminded that he had given evidence earlier that Tokuhata was a statistician who did not know much about epidemiology, Sir Richard said that this was at the time he wrote his first paper. He became experienced and eventually he did know quite a lot about the subject.
[5.277]The next published work on which Sir Richard was asked to comment was a discussion by WC Hueper of Fletcher 1966. Sir Richard said that he was familiar with Hueper and that he was the founding chief of the environmental cancer branch of the American National Cancer Institute. He did a great deal of work on cancer-causing agents in the environment. There were other people who did not perhaps get as much credit as Hueper did, but he did a great deal on it. The discussion by Hueper started:
"I am afraid that I am one of the ignorant or biased individuals who have not been persuaded as yet that from 80 to 95% of all lung cancers affecting males are induced by cigarette smoking. Among the various types of so-called scientific evidence often advanced in support of this well promoted concept and possessing, in my opinion, rather dubious scientific merits is the proposition that the well-known and startling differences in lung cancer incidence prevailing in Great Britain and the United States are attributable to the fact that the English cigarette smoker inhales larger amounts of carcinogenic chemicals than the American one because he smokes his cigarette to a smaller butt which contains an accumulation of carcinogenic matter."
Sir Richard remembered that this was postulated as one of the contributory factors about this time. He did research on it himself, based on actually measuring the lengths of the butts.
[5.278]Hueper continued:
"The argument is based entirely on statistical data measuring coincidental factors. As a matter of fact epidemiologic studies on variations in lung cancer incidence of numerous metropolitan areas in the United States have established that there exist within different regions of similar character in the United States fluctuations of lung cancer incidence which are even more striking than those reported for English and American populations."
Sir Richard said that he would think that was true, though he did not know the evidence. Hueper continued:
"It surely cannot be maintained that the cigarette smoking habits as far as the length of the cigarette butt is concerned are significantly different in different parts of USA."
Sir Richard said he had thought this was quite reasonable; he did not have the data for it and it was not something he would wish to postulate himself.
[5.279]In the next paragraph, Hueper said:
"It is moreover a fallacy to contend that there exists among American scientists any degree of unanimity as to the role which cigarette smoking plays in the causation of lung cancer."
Asked whether he agreed that Hueper was in a position to have a view on this matter, Sir Richard said not actually on cigarette smoking. He really did not look into that evidence. He knew Hueper well and he was very careful in his many observations on occupational hazards. But he attended committees with him and talked to him about this problem and he really did not understand it at all. He did not question Hueper's view about the lack of unanimity among American scientists.
[5.280]Hueper then said:
"The opponents of the cigarette theory are merely less vociferous than its proponents and have less official and organized support."
Sir Richard said this was nonsense. Hueper said:
"They do not appreciate moreover the repeatedly advanced accusation that their scientific judgment is colored either by their chain smoking habit or, worse, by some financial considerations supplied by cigarette companies. I am speaking here from personal experience.
The obviously exaggerated estimates as to the causal role of cigarette smoking in regard to lung cancer tend also to defeat quite effectively compensation claims of workers afflicted with well-recognized occupational lung cancer and to paralyze the organization of a well-balanced program of investigation and control of pulmonary cancer hazards."
Sir Richard said that this was the point he was making earlier about Hueper's enthusiasm for occupational hazards, which he grossly exaggerated. Asked whether this was another scientist who was simply calling for the application of the scientific method and more research into the question, Sir Richard said that he would not say that in relation to Hueper. Asked whether this was because of Hueper or because of the words quoted here, he said that it was because of Hueper. Hueper continued:
"It is time that the bandwagon atmosphere which has controlled for some time the campaign of the lung cancer causation from cigarette smoking be abandoned for a more sober and realistic approach to this serious problem."
Sir Richard said that this was not a view to which Hueper was entitled.
[5.281]Sir Richard was asked about further passages in Fletcher 1992. At p.535 the interviewer asked:
"I seem to recall from Sir Richard Doll that the Ministry kept asking the MRC to do more research to confirm the findings [of Doll and Hill 1950], and the MRC refused because they said that they were satisfied with the conclusion and no more research was needed. What made you start thinking that you should do something like getting the Royal College of Physicians to publish a report?"
In his reply Fletcher referred to having lunch with George Godber, Deputy Chief Medical Officer, who
"made it clear to me that his chief, Sir John Charles (the Chief Medical Officer), was dead against the Ministry being involved in any action on smoking because he thought it would cause trouble. I asked him if he thought it would help if we asked the Royal College of Physicians to produce a report on smoking, sort of side-stepping John Charles."
Sir Richard said that he knew this was true, he had personal knowledge about the position of Sir John Charles.
[5.282]Fletcher went on to explain how Sir Robert Platt, who had just become President of the Royal College of Physicians, decided that the College should become involved and formed a committee, one of whom was Fletcher, who edited the report, RCP 1962. Sir Richard said that the idea was to make clear to Members of Parliament what the evidence was: they were the audience. In the interview Fletcher said that from the beginning he realised that the voice of doctors expressed through the report must influence the politicians, they were the ones who had to act. There was tremendous coverage of a press conference to advertise the report; the media recognised that what was new was that a group of practising doctors were saying that smoking was dangerous. Asked (at p.536) what the response of the politicians was, he said:
"Neglect. Enoch Powell was Minister of Health and he agreed that the Ministry of Information should produce some posters, but he said that any action on this must be taken by local authorities through their health education money."
[5.283]Sir Richard was asked to note the following passage in RCP 1962, pp.53-55, under the heading "Possible action by the Government":
"112. Some decisive steps should be taken by the Government to curb the present rising consumption of tobacco, and especially of cigarettes. This action could be taken along the following lines:-
113.Public education. Much more imagination, effort and money should be devoted to drawing the attention of the public to the hazards of smoking. Special attention should be paid to effective education of schoolchildren, but use should also be made of every modern method of advertising, including posters, press notices and short items on radio and television. The attention of parents should continually be drawn to their responsibility for dissuading and discouraging their children from smoking. Such public education might also advise safer smoking habits for those whose addiction is too strong to be broken. Appropriate surveys of smoking habits should be organised periodically to ensure that accurate information about the effects of education by various means, especially of schoolchildren, is obtained in order to discover and implement the most effective of them.
114.An educational campaign among children might be supported by more effective restrictions on the sale of tobacco to children. [...]
115.Restriction of advertisement of tobacco. Any increase in public education concerning the risk of smoking would at present be in conflict with the vast expenditure on advertising tobacco. While it may be doubted whether advertisement does much to initiate the smoking habit, and it is predominantly designed to attract smokers towards the advertiser's particular brand rather than to increase overall consumption [...], legislation to prevent or at least to restrict the advertisement of a habit which causes such widespread injury to health would be reasonable and would provide evidence of official acceptance of the reality of the hazard. [...]"
Other proposed measures were wider restriction of smoking in public places, taxation, smoke analyses on cigarette packets and anti-smoking clinics.
[5.284]Sir Richard was asked about a confidential Cabinet Office Report by a committee of officials who had been asked to consider the legal and administrative implications of the recommendations of RCP 1962. In this report the committee made various recommendations about education of the public, sale of tobacco to children, tobacco advertisements, smoking in public places, taxation, smoke analyses on cigarette packets and anti-smoking clinics. Sir Richard said that he had not seen the report (which was marked "confidential"), and would rather not express an opinion, in light of it, on whether he shared Fletcher's view that the Government's response to RCP 1962 was "neglect". He vaguely recalled that the Government had circularised local health and education authorities, calling on them to make the conclusions of RCP 1962 widely known in order to advance public education, but this was not a subject he had really been personally concerned with; his concern had always been with the science of the matter, not with what was done about it.
[5.285]Counsel then turned to a different topic, the evidence given by Sir Richard to the effect that experiments had shown that tobacco tars were carcinogenic to the animals exposed to them. In Wynder et al. 1955 at p.448, under the heading "significance of animal-cigarette research", the authors wrote:
"The ultimate proof of whether or not a given agent causes cancer in man rests exclusively on clinical, statistical, and incidence data obtained from man. [...] An animal experiment cannot significantly add and certainly cannot detract from these human observations. The purpose of the laboratory experiment is chiefly to identify active carcinogenic components which must be in cigarette tar. Such a procedure can only be done through laboratory investigations. It can only be assumed that the carcinogen(s) isolated for the animal will also be the carcinogen active for man."
Sir Richard said that there were differences of opinion about animal experiments, and it was not everybody's belief that a carcinogen isolated for an animal will also be active for man, but it was his belief.
[5.286]In Wynder 1959 the author wrote, at p.317:
"The importance of laboratory work is not to prove that smoking is a cause of cancer in man. Such proof can only come from human epidemiological investigation."
Sir Richard said that he believed that. IARC did not, but now he believed it. Wynder continued:
"Laboratory research can, however, contribute to and give a logical explanation for the human findings."
Sir Richard accepted that experiments on rats, mice, hamsters and various other animals continued beyond experiments on dogs, which he said were stopped on humane grounds because of objections to the methodology of using a tracheostomy for smoke inhalation.
[5.287]Reference was next made to Stewart and Herrold 1962. Sir Richard said that he knew Stewart very well. He was at the Laboratory of Pathology at the National Cancer Institute in Bethesda, Maryland. The paper began:
"Were it possible regularly to induce pulmonary cancers in laboratory animals by exposure to inhalation of cigarette smoke, this would constitute good evidence that cigarette smoking could cause cancer of the lung in man."
Sir Richard said that he would not agree with that wholly, but it would contribute to the evidence.
[5.288]RCP 1962 stated at p.26, para.37:
"Skin cancer can be produced in mice by applications of tar condensed from tobacco smoke but the results obtained by various investigators have not been uniform and exposure of animals to tobacco smoke in inhaled air has failed to produce lung cancers."
Sir Richard said that this was correct, squamous cell carcinomas had not been produced, though Wynder had produced adenocarcinomas. RCP 1962 continued:
"Moreover the amount of cancer-producing substances in the smoke itself does not seem likely to be sufficient to account for the large number of cases of cancer associated with the habit."
Sir Richard said that he did not agree with this because he did not think they knew all the carcinogenics, it was probably an unwise statement. It would have been correct if the statement had been that the amount of benzo[a]pyrene present was not sufficient, but it did not recognise that there were so many other carcinogens in tobacco smoke, the effects of which had to be taken into account. That was not done at the time.
[5.289]IARC 1986, in the chapter entitled "Conclusions and evaluations", stated at p.309:
"Cigarette smoke has been tested for carcinogenicity in experimental animals by inhalation and by topical application of condensate and in other ways. Exposure of hamsters and rats to whole smoke results in the induction of malignant respiratory-tract tumours."
Sir Richard was taken to the passage of the report which related to this conclusion. At p.127 the report stated:
"Although the evidence for carcinogenicity of tobacco smoke emerged first in humans, there was need for an inhalation model in experimental animals in which the carcinogenicity of different types of tobacco and tobacco products could be studied. The availability of animal models also permits the comparison of different products and the investigation of various modifying factors in the development of respiratory cancer. [...] The discovery that inhalation of tobacco smoke caused carcinomas in the larynx of hamsters established a model system in which the carcinogenicity of tobacco smoke for hamsters has been confirmed repeatedly [...]. Few bioassays have been conducted, however, in longer-lived mice, rats and dogs, because of low priority and high cost; therefore the spectrum of possible tumour responses in animals to inhalation of tobacco smoke is little known."
[5.290]On succeeding pages papers relating to experiments on mice, rats, hamsters, rabbits and dogs were reviewed. The papers relating to an experiment on dogs were by Auerbach and others and by Hammond and others, both published in 1970. IARC 1986 noted that in this report of an experiment, in which groups of male beagle dogs, trained to inhale cigarette smoke through tracheostomata, were exposed to smoke from different types of cigarette, while a non-exposed group served as controls, no data were given on specific smoking parameters or measures of exposure. It was also noted that a small number of control dogs were used and there was an unusually high incidence of lung tumours in these animals, since these were tumours that rarely occurred spontaneously in dogs. The focal inflammatory lesions usually found in the lungs of animals exposed to smoke were not mentioned in the report. Examination of the upper respiratory tract and other organ systems was not reported. The authors' interpretation of the photomicrographs as representing neoplasia was considered to be not entirely convincing. Sir Richard agreed that some aspects of the dog experiment were "getting the thumbs down" from the IARC working group (of which he was chairman).
[5.291]At p.194 of IARC 1986 it was stated:
"Studies involving inhalation of smoke are hampered by difficulties in reproducing the exposure of humans. Technical problems occur in the generation of smoke and its delivery to animals; moreover, the respiratory systems of animals and humans differ. Rodents are obligatory nose breathers, and the structure of their nasal turbinates is more complex than that of humans. Unlike humans, experimental animals smoke involuntarily, with shallow, hesitant breathing patterns. Other difficulties are caused by the toxicity of nicotine and carbon monoxide. Despite these problems, however, informative data have been obtained concerning the carcinogenicity of whole smoke and its gaseous phase."
Sir Richard said that he believed these statements to be correct.
[5.292]The report continued:
"In some experiments in mice, exposure to whole cigarette smoke resulted in the induction of lung tumours."
Sir Richard agreed that these were not described as "malignant" lung tumours. The report also stated:
"In one study involving long-term exposure of rats to cigarette smoke, tumours of the respiratory tract were induced."
Again, he agreed that these tumours were not said to be "malignant". By contrast, the report stated:
"In hamsters, various experiments demonstrated reproducibly the induction of laryngeal carcinomas."
Sir Richard agreed that these were stated to be malignant. The report continued:
"Studies in rabbits and dogs of whole cigarette smoke were inadequate for evaluation. No treatment-related tumour other than in the respiratory tract has yet been produced by smoke inhalation in experimental animals."
Sir Richard was asked to contrast the statements on p.194 with the statement on p.309:
"Exposure of hamsters and rats to whole smoke results in the induction of malignant respiratory-tract tumours."
Sir Richard agreed that it was implied on p.194 that the tumours of the respiratory tract were not malignant. He said that he would need to look at the original paper.
[5.293]He was referred to Dalbey et al. 1980, which related to the chronic inhalation of cigarette smoke by rats of a particular strain. The authors stated that their choice of the rat was heavily influenced by the induction of squamous carcinomas in the respiratory tract after intratracheal instillations of relatively small amounts of polycyclic hydrocarbons or after bronchial implantation of pellets containing cigarette smoke condensate. Sir Richard agreed that the rats had been chosen because of the ability to induce squamous carcinomas in their respiratory tracts. Sir Richard was asked to consider Table 2 on p.386, in which percentages were given for rats with tumours at specific sites. There were columns for the untreated and sham-exposed groups of controls, and for the smoke-exposed rats. One rat, representing 1% of the combined controls, had a tumour of the respiratory tract, while seven rats, representing 9% of the smoke-exposed group, had this tumour. A footnote stated that the figures for the smoke-exposed group were (statistically) significantly different from combined controls at P<0.05. In the text it was stated:
"We observed 10 respiratory tumors in 7 smoke-exposed rats. Nasal tumors occurred as 1 early adenocarcinoma and 1 squamous cell carcinoma. The pulmonary tumors were 5 adenomas, 2 alveologenic carcinomas, and 1 squamous carcinoma."
Sir Richard was asked how many of these ten tumours were malignant and how many were not, including the nasal ones, and he said there were five.
[5.294]The article continued:
"One alveologenic carcinoma was observed in controls. Two pulmonary adenomatoid lesions were observed in the controls and 1 was found in the smoke-exposed group. Also, 1 large, highly keratinizing squamous carcinoma was found in the head, including the nasal cavity, in each of 2 rats, 1 from the control group and 1 from the smoke-exposed group. These tumors are not included in Table 2 because their origin could not be determined. [...] Besides the description of laryngeal neoplasms in smoke-exposed hamsters [...], the present work is the only study in which an unequivocal tumor response in the respiratory tract resulted from long-term tobacco smoke exposure."
Sir Richard agreed that the authors were here not contending for an unequivocal "malignant" tumour response. He accepted that this was the only rat study in which statistically significant numbers of tumours were produced.
[5.295]The authors continued:
"The tumors in the respiratory tracts of smoke-exposed rats consisted of 5 adenomas and 5 adenocarcinomas, alveologenic carcinomas, or squamous carcinomas as compared to 1 alveologenic carcinoma in the control animals. This amounted to 10 tumors in 80 smoke-exposed animals as opposed to 1 tumor in 93 controls. All but 2 of the tumors in the smoke-exposed animals were in the lungs. Previous studies on increased tumor incidence in rats after tobacco smoke exposure had been much less definite."
[5.296]The authors concluded, on p.398:
"In summary, our studies with SPF F344 rats showed that significant damage could be induced in various parts of the respiratory tract by lifetime exposure to tobacco smoke. This damage consisted of hyperplastic and metaplastic epithelial lesions in the upper airways and of focal alveolitis and alveolar fibrosis in the lungs. The incidence of respiratory tract tumors was significantly elevated in smoke-exposed rats."
Sir Richard agreed that the authors did not contend that the incidence of malignant tumours in the respiratory tract was significantly elevated in smoke-exposed rats. If they were intent on attempting to induce carcinomas in the respiratory tract, one would expect them to say if they had succeeded. But of course, he said, the adenomas were regarded as a preliminary stage in this sort of experiment. They were a stage towards the development of, and frequently in these studies taken as equivalent to, malignant tumours. He accepted, however, that the authors did not contend that the adenomas were in any sense malignant, they contended that the incidence of respiratory tract tumours was elevated, of which five were benign and five malignant.
[5.297]Counsel asked Sir Richard to consider the guidelines set out in McConnell et al. 1986, bearing in mind that they were published after the meeting of the IARC working group which produced IARC 1986. In this paper the authors stated that a question frequently raised in the work of the National Toxicology Program (NTP) was whether certain neoplasms should be combined for overall assessment of rodent carcinogenesis data. If there were neoplasms in the same organ or tissue, or in different organs or tissues in which the morphology of the tumours was comparable, combining or not combining them might affect the carcinogenic evaluation of a given chemical, because combining them might produce statistical significance when not combining them would not:
"For example, 4 benign and 4 malignant neoplasms of the same cell type are found in a group of 50 treated animals versus none in 50 control animals. When the incidence data are analyzed separately, the increase in benign and malignant neoplasms does not reach significance with the use of Fisher's exact probability test [...]."
On p.286, Table 1 set out guidelines for combining neoplasms in the F344 rat and a particular strain of mouse. Among the guidelines relating to the respiratory system, it was stated that in the nasal cavity squamous cell neoplasms and glandular cell neoplasms should not be combined, and in the lung squamous cell neoplasms and broncheoalveolar neoplasms should not be combined. Sir Richard agreed that if the guidelines were applied to the results shown in Dalbey et al. 1980, one adenocarcinoma and one squamous cell carcinoma found in the nasal tract would not have been combined with the other tumours, the squamous carcinoma and the alveologenic carcinomas of the lung would not have been combined, and tumours of the bronchi would not have been combined with those found in the peripheral lung. Sir Richard added the comment that IARC did not necessarily adopt these guidelines.
[5.298]Counsel asked Sir Richard about the hamster studies. Reference was first made to Dontenwill et al. 1973. At p.1791 the authors wrote:
"[I]n earlier investigations, we could not observe carcinoma infiltration in the cartilage of the trachea or the larynx. Tumor growth spread almost always between the bridges of the cartilage and the area of the pars membranacea."
Sir Richard agreed that this related to neoplasms of the larynx in hamsters. At p.1801 the authors wrote:
"We were chiefly interested in the substances in the particulate phase of the smoke. Since man inhales via the oral cavity, it may be assumed that, in spite of complete inhalation, only about half the smoke particles remains in the respiratory tract. As already explained, part of the smoke is exhaled with the next expiration, and a further portion is carried away by the lung clearance mechanisms. Because of the intervals of 58 seconds between each 2-second inhalation, inhaled smoke particles can be removed by exhalation and lung clearance."
Sir Richard said that this was correct, and there was nothing he regarded as contentious in this passage.
[5.299]The authors continued:
"The situation in animals was completely different with our experimental techniques. The animal breathed from a vacuum-free system a smoke-air mixture that remained at a constant ratio of 1:15. The animal was continuously exposed to this mixture for 10-minute periods not more than 3 times a day. After a few breaths, the lungs were totally filled with the equivalent smoke-air mixture.
Since the inhaled mixture was constant, there was no interval between successive smoke inhalations and hence no cleansing exhalation or intervals for lung clearance to take place. The hamster normally has a respiratory frequency of 75 breaths/minute. According to previous investigations, respiratory frequency increased during exposure to smoke. On the assumption that the hamster's respiratory frequency was 100/minute during exposure to smoke, the animal inhaled the smoke-air mixture ≈ 1000 times during the 10-minute exposure with almost no lung clearance during that time. Since the flow characteristics of air in the upper regions of the respiratory tract are different in the golden hamster and in man, the highest deposition of smoke particles per surface unit occurred in the region of the larynx. The concentration there was ≈ 300 times that in the lungs and bronchi [...] under theoretical conditions of an equal distribution of smoke at the surface.
The dose per surface unit has a significant and important influence on the effects. Also, clearance is more difficult in the region around the larynx where the epithelium is not ciliated, and the laryngeal squamous epithelium is possibly more sensitive than the cylindrical epithelium of the bronchi and trachea [...]. Interpretation of all the factors shows that it is almost impossible to calculate an exact dose comparison between man and experimental animals. However, the effective dose acting on the larynx of the experimental animal is many times greater than the effective dose per surface area in the respiratory tract of man. These calculations do not affect the comparison between 2 experimental groups for which the same methods and techniques were utilized to show which dose of type of modified cigarettes had a stronger or weaker effect."
Sir Richard agreed that in this paper there was no report of carcinoma of the lung or any part of the respiratory tract other than the larynx in the hamsters which had been exposed to cigarette smoke in this experiment. He agreed that, subject to intervention in the course of the experiment, cancer involved growth, invasion, metastasis and finally death of the experimental animal. He further agreed that while the paper gave an explanation as to why it was thought that laryngeal carcinoma was induced in the experimental hamsters, there was no explanation as to why laryngeal carcinoma had not been induced in mice or rats exposed to inhalation.
[5.300]Reference was also made to Dontenwill et al. 1977, in which the authors carried out a further study on the effects of chronic cigarette smoke inhalation in Syrian golden hamsters. At p.11 of a translation from the German, prepared for the purposes of the proof, the authors stated that in summary the findings of the second smoke-exposure experiment confirmed the results of the first experiment to a large extent.
"The results show that inflammatory, pre cancerous and tumorigenic effects depend in number and intensity upon the dose and time. A reduction in the quantity of inhaled condensate reduces the frequency of inflammations and tumors in the respiratory tract."
Sir Richard agreed that, according to this paper, the authors had again succeeded in inducing laryngeal cancers in hamsters. This was subject to the suggestion that the strain of hamsters used in the experiment might be a relevant factor.
[5.301]Counsel next asked Sir Richard about Bernfeld et al. 1974, which was also referred to in IARC 1986. The article started by referring to the work of Dontenwill et al. 1973, in which "randombred Syrian golden hamsters" were used. The authors used a model system which they stated, at p.1150, differed from that reported by Dontenwill et al. in several important respects, using two groups of inbred hamster lines. At p.1150 they stated:
"The point of greatest practical importance to emerge from our work is the striking differences among various lines of hamsters with respect to susceptibility to acute toxic effects of smoke and to hyperplastic response of the larynx to smoke. Animals of the inbred BIO 15.16 line have both the highest resistance to smoke or nicotine toxicity and the greatest laryngeal susceptibility - qualities greatly increasing the sensitivity of the model. Further studies with larger numbers of animals will be necessary to ascertain the significance of the laryngeal changes in different strains."
While noting these statements, Sir Richard said that he thought that questions about them should be put to one of the pathologists on the IARC working group. Although he had been chairman of the working group, he did not set himself up as an expert on the subject-matter of these papers.
[5.302]Finally, Sir Richard was asked about benzo[a]pyrene. He agreed that this substance was produced by everything that was burnt and was present in the air that was breathed. As he had previously said, smoking thirty cigarettes a day was not equivalent to exposure to a strong carcinogen. He had also said that whether cigarette smoke acted even as a weak carcinogen was more difficult to determine, though it was necessary to be careful in the use of these terms, because the quantity of a carcinogen was a factor as well as its strength or weakness: "The poison is in the dose."
[5.303]Sir Richard agreed that he was giving evidence without fee (but in the hope of having his fares covered) in order to help the public health as well as to help the court. He had been a supporter of ASH over the years and was not sure whether he was president of it (though in fact he was).
Re-examination of Sir Richard Doll
[5.304]In re-examination Sir Richard said that by the late 1950s only a very small minority of scientists did not accept that cigarette smoking caused lung cancer. The standard of proof he looked for was proof beyond reasonable doubt. In the case of infectious diseases, Koch's postulates were applied to establish proof of causation. It was inappropriate to apply these postulates to chronic diseases, which required a very much more difficult procedure. A mass of evidence had to be taken into account, chance, bias and confounding had to be excluded and one then had to go on to look at the positive evidence in support of causality. Bradford Hill had drawn up nine guidelines, which grew out of his and Sir Richard's study of smoking and lung cancer. On the basis of such evidence, one could only say that one believed that a relationship was a causal relationship beyond reasonable doubt. One could not go further than that. In the case of occupational hazards, if a chemical agent was removed and the disease from which the workers were suffering disappeared, the causal relationship was confirmed. As regards smoking, if smoking was reduced, the diseases due to smoking became less common. "So what you have to do is decide that something is proved beyond reasonable doubt and then test it in practice, that your conclusion is correct." This was the standard he had used throughout his career as an epidemiologist.
Professor Gerard Hastings
[5.305]Professor Hastings, PhD, BSc, aged 49, was Professor of Marketing at the University of Strathclyde. He had been Director of the Centre for Social Marketing and the Centre for Tobacco Control Research there since 1987. He said that the Centre for Social Marketing was previously known as the Advertising Research Unit and was founded in 1980 by his predecessor. Once Professor Hastings had taken over the directorship, in 1992, to reflect the broadening of its advertising to look at the marketing process more generally, its name was changed to the present one. The Centre for Tobacco Control Research was founded in the late 1990s, with funding from the charity Cancer Research UK and other non-profit and Government organisations. He said that the two research centres really provided a channel for his research activity as an academic, which was an important part of his job.
[5.306]Professor Hastings served as Head of Department in the Department of Marketing from 1996 to 1992. From 1980 to 1987 he was a Research Fellow in the Advertising Research Unit. From 1978 to 1980 he was a Research Executive with Purchaser and Consumer Studies Ltd, a market research agency in London. He said that, having done a degree which covered social research methods, it was a natural progression to go and try and put some of those theoretical skills into practice in market research. Purchaser and Consumer Studies Ltd was a small company, working for a variety of different clients, mainly in the fast moving consumer goods area, and was interested in advertising and marketing. His first degree was in sociology and social research and his doctoral subject was social marketing. In his CV he listed numerous publications, including Government and other reports, of which he was author or joint author.
[5.307]Among his public and other appointments, Professor Hastings had been Special Advisor to the House of Commons Select Committee on Health and United Kingdom representative on the Comité Scientifique et Technique du Fonds Communautaire du Tabac. He explained that this was a European Commission body that was concerned with the control of tobacco products, and he had been asked by the Department of Health in London to take on that role. He was a member of the Health Technology Board for Scotland, and had been the Chair of the Evaluation of the CRC Care Education Research Group, which had been put together to see whether a particular research centre was doing a sensible job, an instance of academic peer review. He had been Assessor for the Department of Health Smoking Research Initiative, as a member of the panel who commented on tenders on research to do with smoking. He had been Convenor of the Health Education Authority Expert Group on the Mass Media and Social Depravation. He explained that this was one of a series of working groups which had been set up to look at the issue of the "health divide", a phenomenon of particular note in the United Kingdom where degree of deprivation and health status were strongly correlated. He was a founding member of the International Network of Tobacco Control Organisations. He said that these were research organisations, involved in doing research on tobacco control issues. It was an attempt to try to avoid duplication of effort and share learning and generally take forward concerns and research in this area on an international basis. As an example, they at Strathclyde were the leaders in the United Kingdom in an international study of adult smokers looking at their response to different policy interventions of one sort and another. The research was being done simultaneously in Canada, the United States and Australia and there were principal investigators in each country. It was very difficult to measure the effect of national policy. The classic way in which one would measure such effects would be to have some sort of control group, and it was difficult to find a control group in Britain for example. He was the invited expert at the Government Tobacco Summit. He described this as "very exciting". It was when the present Government first came into power and they had a strong commitment to do things about the problems of smoking. If they were to have a serious public health agenda, then tobacco had to be dealt with as well as possible, because it contributed such a big toll. The Government had called the summit to talk through the issues and "get learning from overseas". UKWP 1998 was one of the things that came out of it. Tobacco had to form a big part of any public health strategy.
[5.308]Professor Hastings said that in addition to having been Special Advisor to the House of Commons Health Committee on the Tobacco Industry and the health risks of smoking, he was currently Special Advisor in connection with an inquiry into obesity. He offered advice to the Committee about what things they should be investigating, what they should be concerned about, and who might be called as witnesses. The process operated by the Committee calling in people who were expert in the field and asking them questions and to provide written statements and written evidence. They needed to collect that evidence together, synthesise it and draw conclusions from it. The role of the expert was to advise them in that process and suggest, for example, questions they might ask of the witnesses. His advice had been about tobacco advertising and marketing. He suggested to the Committee what documents they should seek from the advertising agencies that worked for tobacco companies, such as creative briefs and market research reports.
[5.309]Professor Hastings's report continued:
"The health evidence about tobacco was therefore well known and publicised by the 1960's. For Mr McTear, however, the effects of this health information have to be balanced against three powerful counter-veiling [sic] forces emanating from the industry in general and Imperial Tobacco in particular:
1.Tobacco advertising
2.Health risk denial
3.A reluctance to introduce health warnings"
[5.310]Professor Hastings, who was born in 1954, remembered that his father smoked a pipe and, although his parents were very concerned for the health and welfare of their children, it did not seem to occur to them that this was an odd thing to do. He was asked about an article in The Herald by Ron Ferguson, dated 9 October 2003. In it the writer stated that attitudes to smoking had changed dramatically within the past three decades. He grew up at a time when nearly everybody smoked. Both his parents smoked, as did most of the adults he knew. His friends and he were determined to be fashionable when they started smoking. "To be a non-smoker was to be a freak with a headache." Professor Hastings agreed with the idea that young people in particular would take up a habit because it looked cool and fashionable. This was still true of young people in their relationship to tobacco. There was a glamour that people could associate with tobacco. The generation of moods and association was so much part of the promotion of tobacco, and tobacco advertising had long been predicated on "those sorts of levers" of encouraging the smoking process. Also the ubiquity of tobacco smoke and smoking was important. It was now recognised that one of the key policies one could adopt in order to reduce tobacco consumption was to control smoking in public places and in the work place.
[5.311]A few years previously they had done some research into smoking in deprived areas. There was a strong correlation between social class and smoking, which had been increasing over the years, and "the further down the social grade you are, the more likely you are to smoke." There was a concern that the very poorest in the multiply deprived areas had much inflated smoking prevalence levels, and because of that they were commissioned to do a survey in Castlemilk in Glasgow, which was one such area. They found that smoking rates there were about 56%, rather than 25% to 30% as they were in the population as a whole. One of their research techniques was to talk to people in focus groups. It was difficult to find non-smokers. There were ex-smokers who typically had some sort of health reason for not smoking. Previous research had been done by Alan Marsh earlier in the 1990s. He put the prevalence of smoking among poorer people down to "the sheer disappointment of being poor in Margaret Thatcher's Britain." He tied it in very closely with the problems of having very low aspirations, hopes and capabilities. Professor Hastings said he did not know about the reference to Margaret Thatcher, but he thought the principle was a good one. He had done focus groups in Jarrow in Northumberland with single mothers in very straitened circumstances, and tobacco provided one of the few pleasures they had in a life that was otherwise fairly bleak. "So it seems perverse but it does seem to provide people with some sort of support and tobacco promotion has actively exploited that."
[5.312]Advertising had now gone, he continued, but for many years there had been strong promotional efforts put into the cheapest brands to try and make people feel better about smoking what were really very cheap cigarettes and, therefore, inevitably lower quality cigarettes, to reassure them that they were OK and it was a reasonable thing to do.
[5.313]Professor Hastings's report continued:
"At the time Mr McTear took up smoking the tobacco companies, including Imperial Tobacco, were putting enormous resources into the marketing of their products. A combination of advertising, point of sale material, price promotions and pack design were used to enhance the attractiveness of the product. As now, this material emphasised images and associations rather than hard fact, building positive and powerful brand identities like Player's."
[5.314]Professor Hastings was asked to comment on some documents relating to expenditure on advertising. ITL had prepared, for the purposes of the proof, a table showing their expenditure on advertising and marketing in the UK on cigarettes and cigarette hand-rolling tobacco in each of the years 1960 to 1975. For the year ending 31 October 1960 the amount was £8,182,748, and for the year ending 31 October 1975 it was £15,802,000. In RCP 1962, p.6, para.10, it was stated:
"There have been impressive increases in expenditure on the advertising of tobacco goods in recent years. [...] During a period (1955-1960) when total expenditure on advertising had not quite doubled, expenditure on tobacco advertising has increased threefold. The total expenditure in 1960 was approximately £11,000,000."
Professor Hastings commented that expenditure by ITL made up quite a large percentage for that total in 1960, "so they were big players in the advertising market."
[5.315]RCP 1971, pp.16-17, para.1.11 stated:
"Substantial competition between the major manufacturers dates chiefly from 1955, when leaf supplies became more plentiful after post-war scarcity. Since then, expenditure on advertising of other goods has not quite doubled, while expenditure on tobacco advertising has more than trebled. After the end of July 1965, advertising of cigarettes was banned on television, and subsequently there was a moderate rise (greater than the increase in sales) in advertising of pipe tobacco and cigars. There were few gift-coupon schemes till 1963, but expenditure on this form of sales promotion is now larger than that devoted to direct advertising [...]."
[5.316]Reference was made to Table 1.1 on p.17, where figures were given for the UK expenditure on sales promotion of cigarettes, tobaccos and cigars in the years from 1955 to 1968, with totals both actual and adjusted for the increase in cost over the years, taking 1960 as the base for this purpose. Professor Hastings said that he supposed that an index of media costs, which could vary from general inflation, had been used for the adjusted totals. To compare what was being spent by the tobacco companies on promotion with what was being spent by the Government, it was necessary to look at the actual costs. He also commented that after 1965 expenditure on cigarette advertising as a whole continued to rise, notwithstanding the ban on television advertising, and there was now a lot of research evidence that this was precisely why partial bans on advertising simply did not work. The continued television promotion of pipe tobacco and cigars seemed slightly extravagant, when compared with the increase from sales, and one had to assume that part of the agenda here was to promote the idea of smoking and tobacco use.
[5.317]On p.18 of RCP 1971, in para.1.12, it was stated that despite the prohibition of television of advertising, the total expenditure on advertisements in 1968 amounted to £17 million and on coupon schemes to over £35 million, making a total of £52 million. At p.20, in para.1.15, this figure was contrasted with the £100,000 per annum spent by the newly established Health Education Council on publicity about the dangers of cigarette smoking. Professor Hastings commented that there was clearly an enormous divergence in the buying power of the two sides of the debate, and indeed that disparity had continued down the years.
[5.318]In RCP 1977, at p.20, it was stated:
"Expenditure on tobacco sales promotion by advertising in various ways and by gift coupons in cigarette packs has risen steadily in recent years through something in excess of £80 million in 1975 [...]. Until 1973, these increases just kept pace with the falling value of the pound, but by 1975 the pound had fallen so steeply in value that the effective expenditure appeared to have fallen too."
Reference was made to Table 1.1a on p.22, in which the total estimated advertising and promotional expenditure, including expenditure on coupons and sports sponsorship, was £82.9 million in 1975. This was made up of £25.4 million on advertising in the press and through posters, television and cinema, £52.5 million on coupons and £5 million on sports sponsorship, the latter figure being an estimate provided by ITL. Professor Hastings said that he thought that this expenditure of £5 million was in addition to the ITL figure of £15,802,000 referred to above. This was an example of compensating for restrictions on main media advertising. RCP 1977, in Table 1.1b on p.22, gave figures for Government anti-smoking publicity expenditure. In the year 1975 to 1976 expenditure by the Health Education Council was £707,000 and by the Scottish Health Education Unit was £223,000.
[5.319]Professor Hastings was next asked about a series of advertisements. During the course of this, objection was taken on behalf of ITL on the ground that there was no record for any line of evidence going to the general nature of cigarette advertising and any line of evidence going to the effects of cigarette advertising. Article IX of condescendence starts:
"The defenders have spent millions of pounds since 1960 in the promotion of smoking of their cigarettes and tobacco. They have instructed their advertisers to project an image of cigarette smoking where it is seen by the general public as 'very much the thing to do' and as a means of reducing stress. They instructed their advertisers to project it as a completely safe thing to do."
In the course of discussion about this objection, Mr McEachran sought leave to amend the pursuer's pleadings by adding averments in these terms:
"The defenders' advertising since 1960 has projected an image of cigarette smoking where it is seen by the general public as 'very much the thing to do' and as a means of reducing stress. A combination of advertising, point-of-sale material, price promotions and pack design have been used to enhance the attractiveness of the product. The material emphasises images and associations rather than hard fact, building positive and powerful brand images for their products. The defenders' tobacco advertising since 1960 has encouraged people, including Mr McTear, to take up and continue smoking."
This motion was opposed, and after further discussion I came to the view that the proposed amendment came too late and I refused the motion. I then sustained an objection to the line of evidence, on the ground that there was no record for it.
[5.320]This decision clearly gave difficulty to both Mr McEachran and Professor Hastings, and on a number of occasions, in the face of repeated objections, questions were asked or answers were given which appeared to me to ignore my decision. I made it clear that I would pay no heed to evidence about the matters referred to above for which there was no record. The summary of Professor Hastings's evidence which follows omits reference to such evidence.
[5.321]Professor Hastings said that it was highly likely that ITL would have employed advertising agents in the period from 1960 onwards. It was likely that they would have been given instructions as to how to proceed by ITL. There was a great deal of money involved and there would be planning documents which would be carefully thought through, and options would be researched to target audiences to make sure they were doing what they hoped they were doing. Asked whether inferences could be drawn from tobacco advertisements as to the sort of instructions ITL were likely to have given their advertisers, Professor Hastings said that he thought it was fairly apparent that they must have been seeking to attach certain values to the product, particularly values relating to the brand. Much as was done today, careful, creative briefs would be developed and careful designs would be used to get across, not overt messages, but associations between a product and certain values. The process of seeking to attach particular values would not only be the subject of instruction, but also careful research, particularly with the target groups for that material. Advertising was built on an understanding that communication was not a one-way process, it was not just about an active communicator telling things to a passive audience who then responded in a particular way, the consumer was actively involved in the process of communication and therefore good advertising was designed, using careful research, to ensure that language, images, feelings and associations were being used that would resonate with the target group.
[5.322]Professor Hastings was asked to comment on some documents obtained from ITL's advertising agency relating to creative briefs for the advertising of two new brands of cigarettes in the late 1990s, Richmond and Regal. He said that the need was not just to produce a physical cigarette with tobacco and paper, but also to imbue that with brand value. Branding was something that pervaded all areas of fast-moving consumer goods these days. It was a recognition that people bought things, not just for their physical practical use, but because they wanted to satisfy emotional needs, to express themselves, to show that they were fashionable, up to date, rebellious or whatever it might be. The documents were trying to pin down something which was really very difficult to pin down, because it was about impressions and images and associations, trying to get people to feel in a certain way about the product. People had mixed feelings about buying and consuming tobacco. Advertising could reassure and help them feel less ambivalent about it, and the advertising agencies cleverly recognised that. Professor Hastings would have expected ITL to employ advertising agents in the 1960s. The process of advertising had always been one of purposeful communication. Large sums of money were involved and he would have expected the process to have been done carefully and systematically.
[5.323]Professor Hastings drew attention to various statements, reported in UKHC 2000, in support of his view that the tobacco industry in general and ITL in particular had denied the health risks associated with smoking. Among these was a statement by the World Health Organization that for decades tobacco companies, including those in the United Kingdom, had "denied or minimised the overwhelming scientific evidence of the dangerous effects of tobacco." He said that the position adopted by Mr Davis in his evidence to the Committee (referred to in my account of Mr Davis's evidence at paras.[2.10] to [2.14]) confirmed "this Canute-like stance".
[5.324]Finally, on the question of a reluctance to introduce health warnings, Professor Hastings wrote in his report:
"Over the years the tobacco industry has also shown some reticence about health warnings. A British American Tobacco paper from 1974 states:
'If Government insists on warning notices on packs it is essential that the warning notice should be attributable to the Government or some other official body.'
A later BAT (1976) document states:
'If to comply with legislation warning notices have to be printed on packs, Companies must endeavour to ensure their attribution to Government or some other official body [...].'
If Imperial Tobacco were genuine in their desire for Mr McTear to know about the health consequences of smoking they would not only have refuted this stance, but also moved to put health warnings on their products and advertising as soon as the health risks were established. The Royal College of Physicians Report in 1962 would have been a suitable time, for example."
Professor Hastings said that he was not an expert in the epidemiology of smoking, but his position would be that, when extremely well-reputed bodies like the Royal College of Physicians, and indeed the Government and its American equivalent, were beginning to declare that this was beyond all doubt now established, then a responsible company would see it as part of its duty to inform its customers about the problems. He thought that a message coming from the company would have greater resonance than one coming from the Government or an official body. In reality they did nothing "until compelled to do so by primary legislation in 1971". By then it was too late for Mr McTear.
[5.325]He concluded his report as follows:
"There was undoubtedly considerable publicity about the health consequences of smoking during the 1960s, and Mr McTear must have been aware of it. However, in my opinion, its impact on his decisions about smoking would have been severely reduced by Imperial Tobacco's advertising, public denials of these health consequences and unwillingness to use health warnings until they were obliged by the legislation to do so."
Asked about the statement that Mr McTear must have been aware of the publicity, Professor Hastings said that it would surprise him if he was not aware that there was debate about this issue. His experience with the media was that they were not really interested in stories that had only one side. Debate was an important part of how they covered things. The media were covering the issue of smoking and health to a certain extent in a spontaneous way, and the Government was making ad hoc statements. But there was not what he would regard as a coherent campaign designed to move people in a certain direction until the late 1960s, when the Health Education Council and the Scottish Health Education Unit were established. This should be contrasted with a situation where tobacco advertising was very much in the form of a coherent campaign that was carefully designed to meet certain objectives and push one side of the debate, which was that smoking was acceptable, a fine and pleasant thing to do. Looking at it from Mr McTear's point of view, he would have received far more pro-tobacco advertising messages than anti-smoking media messages, particularly when account was taken of the fact that not all the messages coming from the media were anti-smoking. For most people, even now, tobacco was a small part of their lives, which were difficult and complex. They had to make challenging decisions day in and day out. The media coverage would make an impact, whether it be pro-tobacco advertising or anti-tobacco advertising or other sorts of media mention. Advertising was likely to be more successful because it was specifically designed to engage in that sort of persuasion. For many years research had been done with young people and one of the findings was that in the past young people were inclined to agree that tobacco smoking could not be that bad, otherwise the Government would not allow people to advertise it. The television advertisements for cigarettes, which were permitted until 1965, must have been quite a major influence on people. Even after 1965, other forms of tobacco continued to be advertised on television. If the media had an influence on people in terms of alerting them to the health risks of smoking, then surely it followed logically that the media used to promulgate the opposite message would also have an effect, it was as simple as that. Somebody like Mr McTear would be receiving a lot more pro-smoking messages than anti-smoking ones.
Cross-examination of Professor Gerard Hastings
[5.326]In cross-examination, Professor Hastings said that the only documents he had been given for the purposes of preparing his report were some advertisements, copies of which were attached to it. He had not seen any of the documentary productions relating to Mr McTear, the report of the commission to take Mr McTear's evidence, or the transcript of the evidence given by Mrs McTear. The statement at the conclusion of his report that Mr McTear must have been aware of the considerable publicity about the health consequences of smoking during the 1960s was not based on anything particular to Mr McTear. It was based on the obvious media coverage that would have been around at the time. He agreed that any member of the public must have been aware of the publicity that was being given to the health consequences of smoking.
[5.327]Asked to explain what social marketing was, he said that it was predicated on the idea that when commercial companies used marketing, they used a variety of techniques. They used advertising, combined with product development, distribution and price, a series of variables that they used to try to influence customers and specifically to influence consumer behaviour. Social marketing simply took that idea and said that if commercial companies could influence consumer behaviour, maybe social and health bodies could use it to influence social and health behaviour. If people's behaviour could be influenced in a positive way, then that would bring benefits. A review produced in the early 1990s in the United States came to the conclusion that over half the premature deaths there were caused by people's own behaviour. So any technology that could help to understand this better and to influence it had a potential to bring enormous benefits. Really that was all social marketing did. Part of the point was to persuade people to change their behaviour. Health campaigns of the sort run by the Scottish Health Education Unit which sought to persuade people not to smoke might be described as social marketing. The end point of social marketing was behaviour change.
[5.328]Media advocacy was a slightly different phenomenon in that it was purely focused on media activity. It was the strategic use of the mass media for advancing a social or public policy initiative. It involved using a variety of strategies to stimulate media coverage of an issue: it was focused on the media, rather than on other activities. A helpful way of thinking about media advocacy was that it was the social and public version of public relations. It was similar to what large corporations did in the commercial sector.
[5.329]Professor Hastings agreed that he had been widely quoted in the media on the subject of advertising bans. He did not regard himself as an active campaigner against the tobacco industry. He saw himself as an academic who had done research in this area and had reviewed the research of others and had come to certain conclusions. He thought that as an academic he had a duty to stand up and say what conclusions he had reached, but he did not see himself as a campaigner. People came to campaigning with a pre-set ideology, while he was saying that he had looked at the evidence and had drawn a conclusion. In his CV he stated:
"Academics exist to improve our understanding of the world and ensure that this understanding makes it a better place."
It was his view that the world would be a better place if people did not smoke tobacco. He regarded himself as an advocate for greater measures of tobacco control. He had said previously that the tobacco industry was to lung cancer what the mosquito was to malaria.
[5.330]Professor Hastings agreed that in addition to the appointments he had mentioned in his CV, he was a member of the Advisory Council of ASH, which was a campaigning body. He gave advice to ASH on his understanding of how marketing worked and the need to fully comprehend how multifaceted it was. He believed that ASH was funded through the Government. He did not know the precise origins of ASH. It was a body which engaged in advocacy and lobbying activities. He had contact with both the United Kingdom body and ASH Scotland. ASH Scotland, like the United Kingdom body, was a campaigning organisation which engaged in advertising and lobbying, it was exactly the same sort of organisation, just the Scottish version of it. He thought that it was simply the case that ASH UK, despite its name, concentrated primarily on England and Wales, and Northern Ireland, whereas ASH Scotland concentrated on Scotland. He was not absolutely sure how that worked, but in general terms ASH Scotland was a separate body and operated in that way on a day to day basis.
[5.331]In Hastings et al. 1998, of which he was one of the authors, it was stated, at p.55, under the heading "Combating tobacco marketing":
"In the UK, smoking is becoming increasingly associated with low-income and deprivation. Unskilled workers are two to three times more likely to smoke than professionals, and those who live in rented accommodation are much more likely to smoke than owner-occupiers [...]. Smoking is also strongly linked to a stressful lifestyle, with high smoking rates among the unemployed, those who are divorced or separated, and lone parents [...]."
Professor Hastings said that these were still valid statements.
[5.332]MacAskill et al. 2002, of which Professor Hastings was also one of the authors, was a report of an investigation carried out in eight Glasgow communities with the highest levels of social deprivation, over a period of three years. One of the aims of the study was to assess the level of motivation and readiness to quit of people living in these communities. Motivation was an important factor in quitting smoking. In the abstract it was stated:
"Understanding the consumer reveals that tobacco meets many needs in the struggle to cope with limited income intensified by poorly resourced local infrastructure and limited opportunities."
Professor Hastings agreed that this was one of their findings.
[5.333]At pp.21-25 the following statements were made:
"Tobacco plays an extremely important role in the lives of people in low-income communities. For many respondents in our study, the struggle to cope on a limited income, often in tandem with caring for children and other family members, was intensified by a poorly resourced local infrastructure, high levels of crime and drug use, and severely limited opportunities for recreation or respite escape from the immediate environment. Where recreation was available and affordable, it centered around drinking, drug use, and especially smoking. The latter in particular was easily accessible, relatively cheap, and, for many, their main pleasure.
Smoking offered both a respite from, and a means of coping with, this stressful and unrewarding environment. [...]
Many smokers noted how their consumption levels had risen steadily over their lifetime in response to increasing demands and worries. [...] Smoking also provided a means of coping with the frustration and demotivation of widespread unemployment. Not working had become a way of life for many, and the poor income offered by training schemes and low-paid work provided little incentive to try to move off welfare benefits. Lack of training and qualifications, combined with the stigma of living in a community whose residents were labeled as unemployable, had put many at such a disadvantage in the job market that they found it had to imagine working again. [...]
It has been suggested that people give up smoking 'for reasons connected to optimism' [...]: actual or anticipated improvements in life circumstances, health, or feelings about oneself. For many respondents in our study, there were few causes for optimism and little motivation to quit. [...] Men in particular envisaged little likelihood of a future improvement in either financial circumstances or employment, and felt little desire or confidence in their ability to change one of the few things - smoking - which helped them cope with this lack of prospects [...].
A [...] barrier to smoking cessation in low-income communities is the importance of smoking as a means of coping with stress. In our study, smoking helped respondents cope with daily anxieties and relieve the boredom of unemployment."
At p.31 the conclusion began with the statement:
"Smoking continues to be entrenched among those living in disadvantaged communities, as shown by the absence of a decline in prevalence and consumption relative to the general population. Clearly, tobacco meets a multitude of needs in these community members' lives - respite, a means of coping, and a key to social interaction and cohesion."
Professor Hastings agreed that these were the findings of the study, though he thought it important to recognise that within the paper there was discussion of the problems created by the tobacco industry's marketing activities, which presented a considerable barrier to people quitting.
[5.334]Professor Hastings was asked to consider various passages in the advertising brief for the ITL project to launch a new brand in the ultra low price sector. This brand, Richmond, was to compete with Gallahers' brand Mayfair. He agreed that the aim of the advertising was to attract smokers away from Mayfair to Richmond, by offering them a more valuable product that would give them more utility. He was shown a series of newspaper advertisements for cigarettes dating from 1964 and 1965. He agreed that he had previously written that forming associations between brands and evocative and symbolic images helped customers to differentiate between some of their products. This was part of the reason for branding.
[5.335]In his examination-in-chief, Professor Hastings had said that debate was an important part of how the media covered things. It was crucial in the news and media: if they had only one side of the story, it did not last for very long. He agreed that the media reported on events and other matters which were considered to be of interest to readers, listeners or viewers. In the 1950s and early 1960s it would be of interest to many members of the public that smoking was being linked with fatal diseases. It would be of particular interest to smokers and to people who had friends and family members who smoked, though some people would take it on board and respond to it and others might well deliberately avoid it. There was a lot of evidence that smokers really did not want to know about the health consequences of smoking, because it was so "dissonant". Awareness of a risk was a very simple way of expressing what was actually a very complex phenomenon. People often did things that involved an element of risk. People engaged in reasonable risks and indeed life without risk would be unbearable. People took risks for a variety of reasons, for example that the activity which involved the risk had some enjoyable effect. The problem emerged when people took risks that were really stacked against them. The problem with tobacco which distinguished it from all other examples was that the risks were so great. One in two long-term smokers would die as a result of that habit.
[5.336]Professor Hastings was asked about a long series of newspaper reports published in the period from 1950 to 1964. I have already referred to many of these reports in the section relating to public awareness, and I see no need to repeat the detail here. The subject matter of these reports included discussion of the conclusions reached in Doll and Hill 1950, MRC 1957, RCP 1962 and USSG 1964. Professor Hastings did not dispute that the general public would be aware, as a result of reading newspaper reports such as these, that an association had been established between cigarette smoking and lung cancer and that authoritative opinions were being expressed that the association was one of cause and effect. The newspaper reports also gave publicity to the contrary view, expressed by tobacco manufacturers and others, that a causal relationship had not been established and that further research was required. Professor Hastings said that until the early 1990s the media dealt with the issue as a debate to which there were two sides. In addition, the general public were exposed to tobacco advertising.
[5.337]A number of points were made repeatedly by Professor Hastings. He said that because the newspaper coverage presented the issue as one to which there were two sides, people reading the newspapers would not have the skills to make judgments about the risks associated with smoking, when weighed against all the other risks they encountered in their lives. It was very complex and difficult to make such decisions. In addition, it was not just a rational process. In addition to the difficulties of interpretation, individuals were exposed to all the other influences, such as advertisements for tobacco products. If a smoker felt threatened and upset by the possibility that smoking was going to cause serious illness, he would cling to any expression of doubt as a reassurance. Smokers were very uncomfortable when the health dangers of smoking were pointed out to them and they wanted to try and distance themselves from such a warning, either by ignoring it altogether or by rationalising it in some way. People did not want to take such information on board because it had very uncomfortable repercussions, particularly in relation to a habit that was so difficult to break. People did not want to know such information, so they would fend it off in all sorts of ways. There was a lot of research evidence to show that smokers were very threatened by messages of this sort and looked for get-out clauses. He agreed that readers of newspapers might be expected to have a certain degree of sophistication and to look at the source from which any particular statement came, as well as the content of the statement itself. He agreed that he had written that audiences, especially young ones, were extremely sophisticated consumers of the media. What they would also do, however, was to look for reassurance and an escape route, to help them feel a little bit easier about what was a very ambivalent consumption behaviour.
[5.338]Professor Hastings agreed that, particularly following publication of RCP 1962, the Government had taken steps to educate the public about the risks associated with smoking. He also agreed that from 1962 onwards the tobacco companies agreed not to advertise cigarettes on television before 9pm and that certain kinds of cigarette advertisements would be excluded from commercial television broadcasts, and that in 1965 cigarette advertising on television ceased. From 1968 onwards the Scottish Health Education Unit publicised the risks associated with smoking. From 1971 onwards cigarette packets bore Government health warnings, the first being "Smoking can damage your health." In 1961 an anti-smoking clinic was established in Paisley and there was publicity about it in the local press. The local Medical Officer of Health was in 1965 said to be engaged in "a fairly intensive campaign to instruct the public in the dangers of tobacco smoking". Professor Hastings agreed that doctors would to a certain extent tell their patients about the risks associated with smoking, and teachers would instruct their pupils likewise. While not disputing that any of these measures had been taken, Professor Hastings repeatedly made the point that members of the public would also be exposed to contradictory messages from the tobacco manufacturers whose promotional devices, such as sponsorship of Formula 1 motor racing, were intended to make smoking appear glamorous.
Dr Keith Kerr
[5.339]Dr Keith Kerr, BSc (Hons), MB, ChB, FRC Path, aged 47, was a Consultant Histopathologist at Aberdeen Royal Infirmary, a post he had held since 1989. His specialist area of expertise was pulmonary pathology. He acted as Consulting Pathologist to the Medical Boarding Centre (Respiratory Diseases) for Scotland and Northern Ireland. He was a member of the UK Interstitial Lung Disease Pathology Panel and a member of the International Association for the Study of Lung Cancer. He served on an international expert panel of six pathologists, with two others from Europe and three from the USA, for the ongoing trials of screening detection of early lung cancer. He had published over fifty scientific research papers, book chapters and invited review articles, and many abstracts relating to research into, and the diagnosis of lung disease, particularly lung cancer and its development. He sat on the Editorial Consensus group for the forthcoming revised World Health Organization (WHO) Classification of Lung Tumours, of which he was a co-author.
[5.340]Dr Kerr explained that his work involved the examination of cells and tissues, and making diagnoses. He would see something of the order of 500 to 700 patients' cases per month. He was actively involved in teaching at his home university and by invitation in other centres throughout the United Kingdom, and also overseas. He taught that there is a strong association between smoking tobacco and lung cancer and that there were things in tobacco smoke which caused lung cancer.
[5.341]Dr Kerr provided a report dated 28 August 2003 on his examination of slides relating to Mr McTear. There were six stained slides of cytological material including smear and cytospin preparations, and three slides, each with three sectioned levels of a bronchial biopsy specimen, stained with Haematoxylin and Eosin. He reported that the cytology preparations were of variable quality and some showed fading of the staining. In most slides there were groups of large pleomorphic malignant-looking cells with irregular large nuclei and variable amounts of cytoplasm. The bronchial biopsy sections showed several tissue fragments showing tumour and elements of bronchial mucosa. In at least two of the larger fragments there was clear evidence that the bronchial mucosa was directly invaded by the tumour. The tumour consisted of large, relatively pleomorphic malignant epithelial cells with large irregular nuclei and moderately abundant eosinophilic cytoplasm. There was a tendency to cell stratification and there were intercellular bridges. The features were those of rather poorly differentiated squamous cell carcinoma. Some of the small fragments of bronchial mucosa were lined by pseudostratified respiratory type epithelium, which showed a transition to squamous-type epithelium, which was atypical. This atypia showed sufficient cytological abnormality, architectural disarray and abnormal mitotic activity to warrant grading as moderate squamous dysplasia. The presence of dysplasia indicated changes that had taken place in a squamous epithelium. The change from respiratory type to squamous type epithelium was one of the very early changes but, thereafter, in the development of carcinoma of the lung, atypia developed within the cells in the squamous epithelium in a step-wise manner, it was believed.
[5.342]Dr Kerr interpreted his findings by saying that there was unequivocal evidence of squamous cell carcinoma in the biopsy. There was also evidence of moderate squamous dysplasia. The latter was part of the recognised spectrum of pre-invasive changes, which occurred in the bronchial mucosa during the development of carcinoma in the central bronchi. He said that he had no doubt that Mr McTear suffered from primary bronchogenic squamous cell carcinoma (squamous cell carcinoma of the bronchus).
[5.343]Dr Kerr said that he had seen thousands of biopsies like this from other patients. Squamous cell carcinoma, he said, was one of two types of lung cancer which were most strongly associated with a history of smoking tobacco. When specimens were submitted to him for examination, he might or might not be told the smoking history of the patient. If he was given any history at all, it would more often be in the unusual situation where such a specimen was sent to him in a non-smoker, simply to highlight the fact that he was being asked whether the patient had lung cancer and ought to know that the patient was a non-smoker. This sort of information was highlighted, though not very often, because it was so unusual that there would be a suspicion of lung cancer in someone who did not smoke. Specifically, with squamous cell carcinoma, 98% of cases were seen in smokers. This was based on the literature, but also his own experience: it was most unusual to see a squamous cell carcinoma of the lung in a non-smoker. He could give a figure of 98% based on his own patients. Lung cancer, he went on, was rare in non-smokers, and when it did occur, the squamous cell type was very infrequent. The pre-invasive squamous dysplasia, the precursor lesion of invasive squamous cell carcinoma, was also frequently found in the bronchi of smokers and much less so in non-smokers.
[5.344]In support of these views, Dr Kerr referred to Colby et al. 1995. At p.93 the authors wrote:
"Cigarette smoking is the major cause of lung carcinoma in the United States and around the world [...]. The lung carcinoma rate parallels smoking prevalence. There is a dose-response association between the number of cigarettes smoked and the risk of carcinoma of the lung [...].
There are some variations in the histologic subtypes among smokers and non-smokers (Table 7-4), with squamous cell carcinoma and small cell carcinoma showing the highest association with smoking. It is possible that the recent decrease in the frequency of squamous cell carcinoma is in part attributable to changing smoking habits [...]."
Table 7-4 gave figures (modified from Rohwedder and Weatherbee 1974) for five histologic subtypes of carcinoma in smokers and non-smokers. For squamous cell carcinomas, 98% were stated to have been in smokers and 2% in non-smokers. Dr Kerr said that it was from this table that he derived his figure of 98%.
[5.345]Reference was also made by Dr Kerr to Auerbach et al. 1961. He said that Oscar Auerbach conducted a series of very extensive studies in the mid to late 1950s on autopsy material, taking a very large number of tissue sections and examining by microscopy almost the entire tracheobronchial tree and the extent of abnormalities in the airway epithelium, and associated these changes with smoking habits. At p.267 the authors wrote:
"It is known that cigarette smoke contains irritants, toxic substances and agents that are carcinogenic to the skin of laboratory animals. The application of irritants to epithelial tissue usually produces hyperplasia; toxic substances can destroy cells, and carcinogenic agents produce atypical changes in cells. In this study, we found hyperplasia, destruction of cilia (or destruction of ciliated cells) and the occurrence of atypical cells all to increase greatly with the amount of cigarette smoking. We cannot escape the conclusion that a direct causal relation exists between the degree of exposure to cigarette smoke and the frequency and degree of these changes in bronchial epithelium. [...]
In our opinion the histologic evidence from this study greatly strengthens the already overwhelming body of epidemiologic evidence that cigarette smoking is a major factor in the causation of bronchogenic carcinoma."
Dr Kerr said that he agreed with this.
[5.346]He had read a number of other papers by Auerbach and colleagues which essentially repeated the findings in this paper. In Auerbach et al. 1975 a study was made of histologic type of lung cancer in relation to smoking habit, year of diagnosis, age and sites of metastasis. Of 662 autopsies, 35.2% were epidermoid (squamous cell) carcinoma. The six non-smokers of the series were all found to have had adenocarcinoma. Dr Kerr made the point, therefore, that all of the squamous cell carcinomas occurred in patients who were smokers. Dr Kerr said that the same situation prevailed in Auerbach and Garfinkel 1991. At p.1976, Table 4 showed figures for histologic type of lung cancer by smoking habits. Squamous cell carcinoma was found in no patient who had never smoked, all of the patients with squamous cell carcinoma having smoked tobacco of some form. The figure of 98% in Colby et al. 1995 was accordingly consistent with the findings of Auerbach and colleagues.
[5.347]Dr Kerr was asked about Spain et al. 1970, a paper relating to metaplasia of the bronchial epithelium. Without referring to the text, he explained that the term metaplasia referred to the change in one type of tissue to another, usually under a stimulus, where the change in tissue type was a response to irritation or injury. It was an adaptive mechanism that the human body had everywhere. The development of squamous metaplasia in the lining of the airway was a relatively common change seen in response to chronic irritation in the airway. The notion would be that squamous epithelium developed instead of the normal columnar epithelium because it was better able to resist the noxious irritant, whatever it happened to be. Squamous metaplasia developed in squamous-type epithelium. Metaplasia was a stage before dysplasia, a relatively early change in the step-wise progression towards the development of cancer. Dysplasia was the development of cancer-like changes in the cells within the metaplastic epithelium. When these were seen in the cells of a squamous metaplastic epithelium, they were referred to as squamous dysplasia, or squamous atypia, a synonymous term. If dysplasia was diagnosed, this was a pre-cancerous stage, but a recognised stage on the way to the development of cancer. Accordingly, metaplasia occurred when there was irritation in the lung. It might or might not move on to the next stage, which was dysplasia, and this was a warning sign that cancer may develop.
[5.348]Finally, Dr Kerr referred to Nasiell et al. 1987. At p.207 the authors wrote:
"There is increasing evidence that bronchogenic carcinoma, particularly squamous (epidermoid) cell cancer, is preceded by epithelial abnormalities [...] and develops through successive stages characterized by progressively more abnormal morphological and cytochemical features induced by the long lasting action of irritating agents and carcinogens on the respiratory mucosa [...]. It is of great importance to find out which alterations or at which stage the precancerous lesions are reversible, which ones are irreversible, and which ones ultimately lead to invasive cancer.
The bronchial epithelium was studied by cytological, histological, and cytochemical techniques in human and experimental dog material in order to obtain information about the problems mentioned above. [...] It was found that atypias in metaplastically altered epithelium occur which show great similarity to dysplastic/premalignant alterations of the human cervical epithelium and that these changes in the bronchi possessed similar cytochemical properties as the more or less obligatory precancerous lesions which were studied earlier in the uterine cervix [...]."
At p.217 the authors wrote:
"Consequently, it seems that a severe chronic injury of the bronchial mucosa plays a prominent part particularly in the development of squamous-undifferentiated carcinoma and probably also in adenocarcinoma, resulting in a disturbance of the morphology of bronchial epithelium in the subjects developing lung cancer."
Dr Kerr said that he referred to these passages, and to the data in Table 8.1 on p.217, but he was not asked to give further evidence about the information contained in the table.
Cross-examination of Dr Keith Kerr
[5.349]The cross-examination of Dr Kerr started with an invitation to him to demonstrate, with the aid of a model, the anatomy of the organs within the human thorax. He explained that the respiratory tract passed through the larynx and the trachea to the point where it divided at the carina into two bronchi, each of which entered the lung at the hilum. Squamous cell bronchial carcinoma often arose centrally, towards the carina. Within the lung the bronchi divided many times, eventually becoming bronchioles. The space in the thorax between the pleural sacs containing the lungs was the mediastinum, where the heart and major blood vessels, and other structures including the oesophagus, lay.
[5.350]Dr Kerr agreed that the word "cancer", in colloquial use, referred to a variety of different types of tumour. In its general sense, the tumour was any lump or swelling, but in a more technical sense it might be used to describe a neoplasm. This was an abnormal growth of tissue that had become independent of any outside stimulus. It might be benign, such as a wart, which was a benign epithelial neoplasm, or it might be malignant. A malignant neoplasm was characterised by, among other things, invasion of the surrounding tissue. A squamous cell bronchial carcinoma might invade through the bronchial wall and into the mediastinum. It could involve the pericardium, the membrane surrounding the heart, and the great vessels which passed through the mediastinum. Simply by virtue of its growth, it could impinge upon these great vessels or on the oesophagus, in a manner which could lead to their destruction. Any of these events could result in the death of the patient. Another feature of malignant neoplasm was that it might metastasise to sites removed from the primary seat of the tumour. Dr Kerr had written on the significance of lung cancer to the mediastinal lymph nodes. Primary tumours in the mediastinum were relatively rare.
[5.351]Carcinoma, he said, was a malignant neoplasm arising in the epithelium, the tissue covering the external and internal surfaces of the body. Like the rest of the body, it was made up of cells. Epithelial cells might be squamous, tuboidal or columnar. Squamous epithelium was composed in part of flattened, plate-like cells. It lined the upper respiratory tract, such as the inside of the mouth. In the lower respiratory tract, in the trachea and the bronchi, there were columnar cells which included ciliated cells. Carcinoma could arise in any part of the respiratory tract, but carcinoma of the trachea was very rare and carcinoma of the larynx was less common than bronchial carcinoma. There were many different types of carcinoma of the lung. Part of Dr Kerr's expertise was in seeking to distinguish between these types. So far as management was concerned, the important distinction was between small cell carcinoma and non-small cell carcinoma. The latter included squamous cell carcinoma, adenocarcinoma and a variety of other types of carcinoma. The WHO had classified lung tumours by histological type in a volume first published in 1967, with subsequent editions in 1981 and 1999. Dr Kerr was currently associated with this work. The classification was intended to promote the adoption of a uniform terminology to facilitate communication among cancer workers.
[5.352]Lung cancers frequently showed histological heterogeneity, by which was meant that there might be variations in appearance and differentiation from one microscopic field to another and from one histological section to another. The current edition of the WHO classification stated that almost 50% of lung carcinomas exhibited more than one of the major histological types. This fact had important implications for lung tumour classification and had to be kept in mind, especially when interpreting small biopsies. When tumours were typed on the basis of small biopsies, there was some scope for inaccuracy. Dr Kerr had been involved in the preparation of national clinical guidelines on the management of lung cancer in Scotland. According to these guidelines, there was considerable inter-observer variability in subtyping non-small cell carcinoma, especially on cytological and brochoscopically derived material. Only 10% - 15% of patients with lung cancer would ultimately have the tumour removed and the pre-operative tumour classification confirmed. Dr Kerr had participated in work which sought to promote the use of the non-small cell lung cancer category by means of using a more general type rather than a more specific type to achieve a greater degree of accuracy. He was co-author of an article published in 2000, in which it was stated that it was of concern that if 85% - 90% of patients had a diagnosis made on pre-operative specimens alone, with the likelihood of some degree of inaccuracy in tumour classification from such specimens, then epidemiological studies might be based on flawed data. He said that he wrote this, and had also written that non-small cell lung cancer was a useful and more appropriate classification to use, reflecting the view that it was sometimes better to be more accurate by being less precise in those situations where it was not possible to be more precise. He wrote that epidemiological data would be more useful if based upon more robust histological diagnosis. In another work he had written that, despite minimal changes in the WHO classification, some researchers had reported decreases in the number of squamous cell carcinomas as well as increases in the number of adenocarcinomas. He had also written that there was anecdotal evidence that in the past, and perhaps still, it was likely that where histologic typing was difficult, some pathologists might have opted for the commonest histological type, which was squamous cell carcinoma.
[5.353]In reporting on the slides relating to Mr McTear, Dr Kerr relied predominantly on the biopsy specimens because there was more information to be gained from them than from the cytology specimens. In a cytology specimen all one had were individual cells, one could not see where they were located in the bronchus or their orientation with respect to one another. He himself had written that the importance of cytological atypical cells could be difficult to determine. The point of a histopathological examination was to report on what was found in that process, which would be a large component of the job in hand. In most circumstances, it was possible to make an adequate and accurate diagnosis without any patient's history. In some situations the history was required, but he would not necessarily be given one. A biopsy specimen was in effect a small piece of the bronchus and a histological examination of this sort was possible only when a bronchial biopsy had been performed. Also, in situations where a whole tumour had been surgically removed, it was available to be examined. In such cases pre-operative diagnosis might be confirmed by looking at the whole tumour. A biopsy would not be carried out on a patient unless there was a good medical reason for it, that is to say a suspicion that the patient had a lung disease which required an invasive investigation.
[5.354]In reporting on the slides, Dr Kerr noted two phenomena, a squamous cell carcinoma and a moderate squamous dysplasia. He could not say for sure that the squamous cell carcinoma in this biopsy arose from the area of dysplasia. It was well-recognised that, when carcinoma of the lung, particularly squamous cell carcinoma, occurred, dysplasia was frequently observed in the airways surrounding the carcinoma. It was found that there was an association between the presence of carcinoma and the presence of dysplasia. He knew of no evidence to support the assertion that the dysplasia might occur in response to the carcinoma. He agreed that they might have arisen entirely independently of one another.
[5.355]Dr Kerr said he was sure that we did not know everything about the genesis and development of squamous cell lung cancer. He believed that we knew a great deal about how the tumour came about, but he would not claim that we knew everything. "How do we know what we do not know?" He himself had previously said that the origins of this common disease were not well understood and that little was known about the rate and risks of progression of squamous dysplasia to CIS (carcinoma in situ) and ultimately invasive disease. He described squamous dysplasia as a precursor lesion of invasive squamous cell carcinoma. "Lesion" was another generic term used to describe an area of abnormality. Squamous metaplasia would be described as a lesion. It was not a normal feature of the bronchus: it was an abnormality of the bronchus when squamous metaplasia occurred. It was a common occurrence during bronchial damage and chronic irritation and repair.
[5.356]Dysplasia was only one of a number of changes which might be found on the histopathological examination of a bronchial biopsy. Other changes would include hyperplasia, a thickening of the cell layer due to an increase in the number of cells, and metaplasia, a change in the epithelium, for example a finding of squamous epithelium where ciliated epithelium would be expected. Dysplasia involved a variable degree of atypia. International classification divided it into three categories: mild, moderate and severe. These changes did not show up on x-ray and most of them were not visible on a conventional bronchoscopy, so they would not normally be detected without a histopathological examination of a biopsy specimen or a resected lung. It was not possible to tell from the histopathology how any of these changes came to be there, or what would have happened to it if it had not been removed; but there was evidence to suggest that the greater the degree of atypia or dysplasia, the greater was the likelihood that the disease would progress to invasion and therefore the development of carcinoma. This evidence came from biopsies. When he used the expressions "pre-invasive" and "precursor", he was implying that there was a risk that the lesion would progress if there was no intervention, although there was no guarantee that this would be so. It was possible that all such changes were capable of regression, although it was believed that the more atypical or abnormal they became, the less likely regression was to occur. It was not known which, if any, of these lesions were obligatory for the development of squamous cell carcinoma or any other type of lesion.
[5.357]Asked whether it was the case that we did not know what proportion of the population, who exhibited no clinical symptoms and who never went on to develop lung cancer or any other condition requiring biopsy, had lesions in their lungs, Dr Kerr said that there was arguably some evidence in the papers of Auerbach and colleagues. In the autopsy studies, some patients had lung cancer, some did not, some patients were smokers and some were never-smokers, so in a sense these were studies of samples of the population at large and gave some indication of how frequent or otherwise these changes might be in the airways. A variety of the changes were found in patients who did not have lung cancer, but the changes most likely to be associated with the development of lung cancer were very rarely found in patients who were never-smokers as opposed to those who were smokers. He agreed that these were autopsy studies carried out on people who died in hospital, but said that they would be more or less typical of the population, depending on the parameter that was being examined. Auerbach worked at a veterans hospital, but Dr Kerr thought that the general population were treated at such a hospital, it was not just for ex-soldiers.
[5.358]Dr Kerr had not been familiar with Spain et al. 1970 before coming to court to give evidence. According to the abstract of that paper, in 500 apparently "healthy" adults who died suddenly and unexpectedly and who lived and worked within the environs of a large urban area noted for its air pollution, autopsy studies revealed that 50% of all adult non-smokers had metaplasia of their tracheobronchial epithelium. Metaplasia was present in 70% of male cigarette smokers. Women in each category revealed half the frequency of metaplasia present in the men. Metaplasia was present in less than 20% of men under the age of 30 years, rose to a peak of 80% at age 50 years, and gradually declined in frequency after the age of 60 years.
[5.359]The text of the paper started with the statement:
"Regenerative hyperplasia or metaplasia of the tracheobronchial epithelial lining may be caused by a variety of physical, chemical, or infectious materials."
Dr Kerr said that this was correct. He also agreed with the statement, also on p.1331, that:
"It is obviously impossible to collect adequate samples of tracheobronchial mucosa on a random selection of a healthy live population, so one must attempt to develop this information from autopsies."
The authors stated that previously, autopsy studies designed to determine the distribution of tracheobronchial metaplasia, as for example in the reports of Auerbach and colleagues, were on sick individuals who died in hospitals.
[5.360]The authors carried out a simplified study on the morphological changes in the tracheobronchial mucosa of an autopsied, apparently "healthy" population made up of individuals who died suddenly or unexpectedly from accident, suicide, homicide, or within minutes of a first acute attack of coronary heart disease. Only full-fledged metaplasia was recorded. At p.1334 they commented:
"The association of cigarette smoking with a high frequency of tracheobronchial mucosal metaplasia has been demonstrated several times in the past 15 years. Our findings now confirm this association in a different and less highly selected population. More important, however, is our observation that varying degrees of tracheobronchial metaplasia are present in a surprisingly high proportion (50%) of 'healthy' adult men who have never smoked cigarettes, cigars, or pipes. In this group the frequency is as high as 60% in those who are more than 50 years old. [...] The quality of the metaplasia changes was indistinguishable from that found in the cigarette smokers. In the nonsmokers though, it seemed to develop at a somewhat later age than it does in the cigarette smokers.
This relatively common occurrence of metaplasia in nonsmoking, apparently healthy, men who are otherwise free of pulmonary alterations cannot be explained as simply being a manifestation of the aging process, because even for those below the age of 31 years the frequency was 20%. Furthermore, there was a considerable decline in the frequency after the age of 65 years. It also can not be explained on the assumption that in a certain percentage of normal individuals there are scattered foci of metaplastic epithelium in the tracheobronchial mucosa. The curve of distribution at different age levels [...] negates this. The age distribution curve is entirely consistent with increasing time of exposure to noxious materials that might be inhaled from the external environment. [...] Because this particular population group was derived mainly from the environs of a large metropolitan area noted for its air pollution, it is tempting to incriminate the polluted air as a likely cause. However, this possibility must be regarded as speculative until such time as additional data can be developed from similar studies in other geographic areas - some of which should be free of significant air pollution."
[5.361]Dr Kerr said that the expression "full-fledged" metaplasia was not a technical term, but he inferred that it described a situation where the epithelium was easily identifiable as a squamous epithelium from its lower to its upper part. In some cases where the squamous metaplasia was in evolution, the change was not complete within the epithelium from the base to the top, and degrees of squamous change may occur in the hyperplastic zone of cells in the basal area of the respiratory epithelium. It was believed, he said, that in many cases of squamous metaplasia there was a hyperplastic change which occurred in the tracheobronchial epithelium and the squamous change took place within the hyperplastic zone. He would assume that metaplasia would be described as not full-fledged by these authors in those areas where there was squamous change within a hyperplastic zone but not a fully developed squamous epithelium from top to bottom. No one had actually observed changes going on as they occurred in the human lung, that was not possible, so experimental models had to be used; the change, apart from anything else, was believed to take a long time to develop.
[5.362]Dr Kerr said that it was possible to find dysplasia in the lungs of non-smokers. Auerbach et al. 1975 and Nasiell et al. 1987 were both studies which set out to investigate whether or not there was an association between lesions in the lung and smoking. Dr Kerr could not bring to mind any work which addressed whether or not there was an association between lesions in the lung and a family history of lung cancer. He was not aware of any similar work addressing whether or not there was an association between lesions in the lung and a history of alcohol use. Asked whether he was aware of any work which addressed whether or not there was an association between lesions in the lung and residence in an urban rather than a rural area, he said that it made a difference to his answer whether "lesions in the lung" referred to metaplasia or dysplasia. In Spain et al. 1970 the possibility of an association between urban living and metaplasia was raised speculatively, but there was no mention of dysplasia, and he knew of no work relating dysplasia to urban living. He was not aware of any work which addressed whether or not there was an association between lesions in the lung and a history of stress and depression. He agreed that the development and maintenance of the normal epithelial lining of the respiratory tract depends on an adequate supply of vitamin A, and that vitamin A deficiency might lead to abnormal cellular differentiation and proliferation. He was aware that there had been some pieces of work, with which he was not familiar, in which an association was made between the development of malignancy and vitamin A deficiency. He had no knowledge whether alcohol abuse might deplete vitamin A levels, it was not his area of expertise.
[5.363]Dr Kerr said that he was not familiar with Winternitz et al. 1920, in which there was a report of autopsies carried out on people who had died in the influenza epidemic of 1918. The authors reported, at pp.15-16:
"Sooner or later, with the subsidence of the irritating agent, repair begins in the bronchus or bronchiole. If its walls have been destroyed and the lesion has extended into the surrounding alveoli to form an abscess of greater or lesser extent, or if the necrotizing process has been superficial and confined to the epithelium in large part, the reparative process is very much the same. Mitotic figures in the fibroblasts and in the endothelial cells of the capillaries abound in the young granulations [...]. However, the granulation tissue does not have an unrestricted path of growth, for if a remnant of epithelium remains, this is stimulated to grow probably in this disease as in no other. Mitotic figures are common and the young epithelial cells stretch across the denuded submucosa or granulation [...] and extend downward into the surrounding alveoli, not only as strands, but also as solid nests of cells [...]. The bronchioles, therefore, show changes dependent upon the extent of the damage suffered by their walls. The vast majority, in all probability, will be restored; but if the wall has actually been necrotized, the bronchioles may be converted into small, saccular, bronchiectiatic cavities [...], or obliterating bronchiolitis may result from the organization of the exudate within their lumina [...]. The importance of the epithelial proliferation cannot be ignored; in many cases, it invades the surrounding lung tissue and a typical, histological picture results - an infiltrating, malignant, epithelial neoplasm [...]."
Dr Kerr said that it was correct that certain changes in the lung occurred as part of the normal process of repair, but he would not agree with the interpretation placed by these authors on their findings, indeed he probably doubted whether the pathologists found what they said they found in their autopsy studies. He said that it was possible in cases of respiratory infection, where the airway was repairing itself, that occasional atypical cells might be seen, but he thought it most unlikely that a squamous epithelium would be seen to be organised in such a way that it would be regarded and described as being a dysplastic squamous epithelium as the term was now understood and used.
[5.364]Dr Kerr was asked about Table 8.1 on p.217 of Nasiell et al. 1987, relating to the incidence of cytological changes. Among other figures, the table stated that 23% of non-smokers with chronic inflammatory lung diseases displayed atypical metaplasia. Dr Kerr agreed that atypical metaplasia would be dysplasia, as he had defined it. He said, however, that the direct comparison was difficult because the table referred to cytological changes, where cells were being described which were separated and not cohesive and related one to the other in the form of an epithelium. The description of squamous dysplasia which he made earlier was based upon the examination of the intact epithelium, where it was possible, as well as to appreciate the atypical nature of the individual cells, to appreciate the architecture and structure of the atypical epithelium and the way each cell related to the other, and also the localisation of the mitotic figures, which was also a crucial part in defining squamous dysplasia. The table accordingly required to be read subject to the qualification that it related to cytological changes. Where there were cases of atypical metaplasia in non-smokers with chronic inflammatory lung disease, that might not denote dysplasia. He could not tell, because the cells were dissociated one from the other, and the WHO definition of dysplasia, which he was applying and using, required the making of a histological examination of the tissue, not the disassociated cells.
[5.365]Dr Kerr was next asked about his evidence that, with squamous cell carcinoma, 98% of cases were seen in smokers. The reference for that was Table 7-4 in Colby et al. 1995, relating to histologic subtypes of carcinoma in smokers and non-smokers. The information in the Table was said in a footnote to have been "modified from reference 9", which was Rohwedder and Weatherbee 1974. It was pointed out to Dr Kerr, however, that this paper did not contain the information in question, and the reference should have been to reference 10, Rosenow and Carr 1979. The authors both held positions at the Mayo Clinic, Rochester, Minnesota. At p.233 they stated:
"The Mayo Lung Project of the Mayo Foundation [in Rochester, Minnesota] is conducting a controlled, prospective lung cancer screening program in males 45 years and older who smoke at least 20 cigarettes per day. The study group has a chest x-ray and pooled three-day sputum analysis every four months, and the controls are urged to have the same tests yearly."
At p.234 it was stated that Table 2 listed the prevalence of the five most common lung cancers in men and women, smokers and never-smokers "as they have presented at the Mayo Clinic". One of these cancers was epidermoid carcinoma, also called squamous cell epithelioma or squamous cell carcinoma in the text. Figures given in respect of epidermoid carcinoma in Table 2 on p.235 showed that out of a total of 992 cases, 892 were in male smokes, 7 in male never-smokers, 80 in female smokers and 13 in female never-smokers. The figures of 98% and 2% given in Colby et al. 1995 could be seen to be derived from these statistics. Dr Kerr agreed that the only passage in the text which suggested how the diagnosis was made was by exfoliative sputum cytology, at least in the males in the study group.
[5.366]Dr Kerr was asked repeatedly about the conclusions that could be drawn from the above figures without knowledge of the proportion of smokers and never-smokers in the general population. His reply, under reference to the table, was: "In patients who have squamous carcinoma of the lung, 98% of them are cigarette smokers, 2% of them are never-smokers. That is it." He said he did not agree with the assertion that in order to assess whether or not these figures had any significance, one would need to know the relative distribution of smokers and never-smokers in the population at large. Asked, however, whether he agreed that whether or not these figures were of significance depended on whether or not the patients who formed the data set were representative of the general population at large, he said: "Yes. If we are to draw an inference from these figures and apply it to the general population, then that would be the case, yes." He agreed that in order to assess this, information would be needed about the subjects of the study. He pointed out that it was not possible to tell from the text whether the smokers in the screening programme were included in the statistics. Asked whether, if these people were included within the sample, that would bias the sample towards the smokers, he said that this was not a case of bias, it was a case of the study population having many more lung-cancer-bearing patients who were smokers than it did those who were never-smokers. He said that the only response he could give was that in any study that he would be aware of, or any group of lung cancer patients that he could imagine from his experience, where histories were taken from the patients and their smoking habits were considered, a larger proportion of patients in a group who had lung cancer would be found to be smokers than would be the proportion of smokers in the general population. He thought the paper showed that squamous carcinoma in the lung was much more likely to be found in someone who had been a smoker rather than in someone who had been a non-smoker.
"That is the piece of information that I think comes from this paper, and, in my interpretation of this, the rates of smoking in the general population have nothing to do with this paper. It is quite irrelevant to the interpretation of these data."
[5.367]Dr Kerr agreed that Auerbach et al. 1975 reported on 662 autopsies of men, of whom six were non-smokers, and Auerbach and Garfinkel 1991 reported on 505 cases of lung carcinoma, the number of patients who had never smoked being ten.
[5.368]Dr Kerr was asked about his evidence that "there are things in tobacco smoke which cause lung cancer". He said he was not aware, and very much doubted, that there had been any direct studies on living human beings of any of the recognised carcinogenic agents which were in tobacco smoke. Asked then what studies formed the basis of this proposition, he said that he could not quote direct studies, but
"I am reflecting an opinion and a belief that I have over many years of reading the medical literature, of understanding and reading reports that there are a whole variety of different chemical agents within tobacco smoke, some of which are recognised in test situations using either laboratory animals or human tissue cells in culture, where those chemicals are recognised as carcinogens because they can be shown experimentally to induce tumours in laboratory animals, and also to induce changes in human cells, in tissue culture, for example; changes which we recognise as being associated with the development of the malignant process."
Asked whether it was the case that studies which sought to produce squamous cell bronchogenic carcinoma in animals by the inhalation of tobacco smoke had failed to produce such tumours, he said that he did not know the literature on the animal studies well enough to comment.
[5.369]Dr Kerr had described a theory of carcinogenesis which involved the irritation of the epithelium by some external agent. The generally accepted theory of carcinogenesis involved multiple stages and multiple changes within in a cell population before malignant behaviour eventually supervened. He agreed that ultimately carcinogenesis was a genetic process, and that in order to understand it, one would need to understand what happened at the genetic level. He agreed that bladder and cervical cancer were associated with cigarette smoking, and did not see why the irritation theory could not apply to these cancers. He said that the association with bladder and cervical cancer was less strong than with carcinoma of the lung, for example, but it was a matter of speculation that chemicals that were inhaled in tobacco smoke entered the blood stream and could therefore be delivered to those sites. He agreed that this was a very active field of scientific investigation.
Re-examination of Dr Keith Kerr
[5.370]In re-examination, Dr Kerr said that he was not wholly familiar with the details of the experiments, but he believed that studies had been done to test chemicals to see if they could induce changes in the DNA of human cells in tissue culture in the laboratory. Certain chemicals could be recognised as carcinogenic, or as mutagenic.
[5.371]Asked whether he knew what percentage of the population of the UK were smokers, Dr Kerr said that he thought the last figures he saw suggested that across the board approximately 30% of the population smoked, but he could not give a figure for the percentage of population who either were or had been smokers, his figure was for active smokers.
[5.372]In his personal experience Dr Kerr had dealt with biopsies of people with respiratory infection, and he had never found dysplasia, in the sense in which he used that term in his report, an abnormal squamous-type epithelium lining the bronchus, fulfilling the criteria laid down by the WHO. It was believed that precursor lesions carried a risk of progression, a step on the way to carcinoma. The data were very soft and difficult to interpret, but there was evidence to suggest that, as the degree of dysplasia in the cell population increased, the statistical likelihood of progression to malignancy increased over a time period of several years.
PART V: THE EXPERT EVIDENCE
(2) Expert witnesses for ITL
Professor Jeffrey Gray
[5.373]Professor Gray, aged 69, was Emeritus Professor in the Department of Psychology at the Institute of Psychiatry, University of London. He described this as a tertiary education and research establishment, generally regarded as one of the best, and perhaps the best, in the world, in the field of psychiatry.
[5.374]He qualified initially in modern languages, being awarded a BA degree at Oxford University in 1957. He obtained a second BA degree at Oxford in 1959 in psychology and philosophy, followed by a qualification in clinical psychology in 1960 and a PhD in experimental psychology in 1964 at the Institute of Psychiatry in London. He returned to Oxford in 1964 as a lecturer in psychology and in 1965 became a Fellow of University College. In 1983 he succeeded Hans Eysenck as Professor and Head of the Department of Psychology at the Institute of Psychiatry. He remained there until retiring at the age of 65 in 1999, and was thereafter Emeritus Professor.
[5.375]He said that Hans Eysenck founded the Department of Psychology at the Institute of Psychiatry in the 1950s. He was generally recognised as the most important scientist to date in the field of the experimental psychology of personality, that is, differences between different individuals in their behaviour and psychology. During his lifetime he was the most highly cited living psychologist. His most important contribution to psychology was his work in personality, in which he developed what today would be the scientific model of that field. Next in importance was his work in the field of psychological treatment, particularly the development of behaviour therapy and, subsequently cognitive behavioural therapy. He did not himself do much research in that field, but provided, in the Department of Psychology at the Institute of Psychiatry, the environment for others to work in that field, and he also did a great deal to "spread the word" that this was the way to do psychology. This was now the standard approach through the developed world. It was now accepted that, with many psychiatric disorders, the beneficial effects of these forms of psychological treatment were at least as good as the effects of drug treatment. Eysenck died in 1997.
[5.376]In addition to the foregoing posts, Professor Gray had been Visiting Professor at the Université Paris VI from 1979 to 1980, the Virginia Military Institute in Virginia in 1983 and the Collège de France, Paris in 1999. He was a Fellow at the Center for Advanced Study in the Behavioral Sciences at Stanford University from 2001 to 2002. He had served as President of the Experimental Psychology Society from 1996 to 1998, and as a member of the United Kingdom Government's Gambling Review Body in 2000-2001. He became a Fellow of the British Psychological Society in 1993. He received the Presidents' Award of that Society in 1983: he described this as a "mid-career award" given to scientists in the field of psychology for the distinction of the work they had done up until that time. He became an Honorary Member of the Experimental Psychology Society in 1999 and an Honorary Fellow of Goldsmiths College, London in 2002. He was awarded an Honorary Doctorate at Washington and Lee University, Virginia in 2000.
[5.377]He said that a most general description of his work was that it was concerned with the relationship between brain activity and behaviour. Much of it had been with animals, particularly with rats, but also mice and New World monkeys. He had been particularly interested in aspects of brain function and behaviour that related to psychiatric problems. In the first part of his career he mainly concentrated on problems to do with anxiety and its treatment. Subsequently he worked in the field of schizophrenia, again looking at "animal models", that is, behaviour in animals which bore a conceptual resemblance to the equivalent behaviour in human beings. Thereafter, at the Institute of Psychiatry, he began to work more with human subjects and patients suffering from the conditions he was interested in, such as schizophrenia. More recently, with his colleagues at the Institute, he developed methods of implanting neural stem cells into the damaged brain, in order to repair it. In parallel with that, he began to develop, with students and colleagues, methods of treating anxiety and depression by computerised versions of cognitive behavioural therapy.
[5.378]As part of Professor Gray's research he had investigated dependence on both opiates and anti-anxiety drugs, and psychological treatments for anxiety, depression and opiate dependence. He said that the effects of drugs had figured repeatedly and prominently in his areas of research. As part of his programme, he had published extensively on the effects of nicotine and smoking on both human and animal behaviour, and on nicotine's neurochemical effects on rats and on cultured nerve cells in vitro. Reference was made to a list of his publications, of which there were about 460, including seven books, and to a separate list of those of his publications which related to nicotine and smoking, of which there were about forty. He said that his most important research contributions had been concerned with the biological basis of human personality; the behavioural and brain systems that mediated anxiety and schizophrenia; and the development of neural stem cells as a means to repair the damaged brain. In preparation for giving evidence as an expert witness, he had read or re-read "between 500 and 1,000 scientific papers, nearer 1,000".
[5.379]Professor Gray said that there was a distinction between the effects of nicotine and the effects of smoking. Some of the effects produced by smoking tobacco could also be produced by the administration of nicotine, but some could not be mimicked in experiments looking at the effects of nicotine. He described smoking behaviour as "complex". It was complex both in terms of the multiplicity of chemical compounds in tobacco, of which 4,000 or so has been identified in tobacco and tobacco smoke. It was complex also in respect of the behaviour of smokers. Smokers in general reported quite a wide range of different effects of smoking and they could smoke in different circumstances and in different ways. The effects they obtained from smoking depended upon the circumstances and the ways in which they smoked. So there was no single effect of smoking, there was no single route by which smoking produced its effects and there was no single reason why an individual smoker smoked. The chemicals in tobacco and tobacco smoke contributed in a variety of ways to the satisfaction derived from the smoking habit, e.g. by influencing the taste, smell and other sensory characteristics of a cigarette. Isolating the role played by any one compound was exceptionally difficult and it was unlikely in any case that any single compound played a role in isolation from those of others. The influence that these constituents of tobacco smoke had on an individual smoker was itself modified by the type of cigarette he smoked and the way in which he smoked it. A smoker might vary the way he smoked by varying the frequency and the duration of puffing, and in doing so he altered the exact composition of the constituents of the smoke he inhaled. The environment in which the cigarette smoker was smoking and his psychological state were factors that in turn influenced the way he smoked. For example, the smoker smoked in a different manner under conditions of stress than when he was relaxed. So there was a chain in which the environmental circumstances and the psychological state altered the way in which a cigarette was smoked and that in turn altered the effects of the cigarette upon the future psychological state and behaviour of the smoker.
[5.380]The smoker would adjust his smoking behaviour according to the nicotine and also the non-nicotine (e.g. "tar") contents of a cigarette. Adjustments would be made depending on what that particular smoker was used to smoking: he would attempt typically to adjust to the level of nicotine and the level of tar that he was most familiar with. There was evidence from laboratory studies that the "tar" yield of a conventional cigarette determined the amount that was smoked independently of the effects of its nicotine yield. Thus, when nicotine yield was controlled for, smokers of lower-tar cigarettes puffed more smoke from their cigarettes than smokers of higher-tar cigarettes, i.e. they compensated for the reduced amount of tar by puffing and inhaling a greater volume of smoke. Conversely, cigarettes from which the nicotine had been removed reduced self-reported "craving" and increased ratings of smoking satisfaction and psychological reward. In the same experiment, moreover, an intravenous injection of nicotine failed to increase either satisfaction or reward.
[5.381]Reference was made to Rose et al. 2000. Professor Gray was asked to consider the text of this paper in some detail, but for present purposes it is sufficient to quote the abstract, which was in these terms:
"To dissociate the sensorimotor aspects of cigarette smoking from the pharmacologic effects of nicotine, smokers rated the subjective effects of nicotine-containing or denicotinized cigarettes, and intravenous (IV) nicotine or saline infusions. Three groups of participants (n = 20 per group) received either: (1) continuous nicotine, (2) pulsed nicotine, or (3) saline. Each group was exposed to an IV condition once while smoking a denicotinized cigarette and once while not smoking, in a 3 x 2 mixed design. A fourth group (n = 20) received saline while smoking their usual brand of cigarette. The dose and rate of nicotine administration were individualized based on previous measures of ad lib smoke intake. Denicotinized cigarette smoking significantly reduced craving and was rated significantly more satisfying and rewarding than the no-smoking conditions. IV nicotine reduced craving for cigarettes, and increased ratings of light-headedness and dizziness. However, no significant satisfaction or reward was reported after IV nicotine. The combination of IV nicotine and denicotinized cigarette smoke produced effects similar to those of smoking the usual brand of cigarette. The results suggest that sensorimotor factors are critical in mediating the immediate subjective response to smoking, and that the immediate subjective effects of nicotine administered in doses obtained from cigarette smoking are subtle. Thus, addressing smokers' needs both for the sensorimotor aspects of smoking as well as for the direct CNS [central nervous system] effects of nicotine may be critical in enhancing smoking cessation treatment outcome."
Professor Gray said that in his view this was the best controlled study to date investigating the issue of the extent to which the satisfaction and reward aspects of cigarette smoking were mediated by way of either nicotine or the rest of the events involved in smoking. The results showed clearly that, as far as the pleasure and satisfaction of smoking were concerned, the principal route did not involve nicotine, but lay somewhere else in the complex behaviour that was smoking a cigarette. The variable called "craving" was influenced by nicotine to some extent, but it was also influenced by smoking a denicotinized cigarette. So there was a joint effect of these two pathways for that variable; but for most of the positive aspects of smoking cigarettes - satisfaction and psychological reward - the critical pathway did not involve nicotine.
[5.382]Professor Gray went on to say that to add to the complexity, different smokers sought different outcomes from smoking. Individuals gave many different answers to the question why they smoked, but it was possible to organise the answers by methods of statistical analysis of the correlations between them and to reduce the overall number of answers to a small range of underlying factors. The most important of these factors were concerned with relaxation and sensory enjoyment. A second cluster of reasons was mood control: the reduction of depression, irritability and so on. Thirdly there was a set of cognitive reasons: increasing alertness, being able to perform a boring job for longer, that sort of thing. Most smokers could then be classified according to the predominance of one of those clusters of reasons in their behaviour, but most smokers would also show some degree of recognising the other reasons as well. So far example there might be a smoker who predominantly smoked under most circumstances for the pleasurable aspects of smoking, but who recognised that on some occasions he smoked in order to control his mood. Sometimes smoking was used as a means of oiling the wheels of social interaction. When smoking was more widely accepted as a respectable activity it was common to exchange cigarettes to increase social interaction. Used in this manner, smoking was essentially independent of any of the chemical constituents of tobacco. These different outcomes from smoking were not mutually exclusive. A smoker might report simultaneously, for example, that he felt more relaxed and more alert, paradoxical as this might seem at first sight. The same smoker was likely to smoke for different reasons at different times: to change his mood if he felt depressed, to increase his level of alertness if he had been drinking alcohol, and so on in many combinations. There was, however, a notable absentee from the list of effects of smoking reported by smokers: it was hardly ever reported to cause feelings of intense pleasure and euphoria ("rush") that were commonly reported after ingestion of opiates such as heroin or stimulants such as cocaine.
[5.383]Professor Gray said that while self-report was an excellent starting point from which to embark upon scientific studies, the conclusions suggested by that route required confirmation by other means. It was, however, very far from straightforward to test the behaviour and effects of smoking in the laboratory. In any scientific investigation, one wanted to eliminate anything which changed when the variable of interest was changed and which might therefore spuriously produce effects which would be attributed to the main variable. This was the problem known as "confounding". Ideally a study group and a control group would be selected at random and the variable, nicotine for example, would be applied to the study group and not to the control group, as for example by the authors of Rose et al. 2000, who applied either nicotine or saline through an intravenous line without the subjects knowing which they were receiving. There were, however, difficulties in connection with cigarette smoking. Only existing cigarette smokers could be included in a study group, as it was unacceptable to take people at random and induce some of them to start smoking; and it was known that non-smokers and smokers differed systematically so that they were not in all relevant aspects similar apart from smoking.
[5.384]Laboratory studies of the behavioural effects of smoking supplemented self-report by taking objective measurements of the effects of smoking, but, like self-report itself, they were susceptible to the potential confounds of placebo and withdrawal effects. The behavioural or psychological effects of smoking might be due, not to the inhaled smoke itself, but to the smoker's beliefs about what those effects should be, i.e. placebo effects. The observed effects might indeed be due to the inhaled smoke, but because of reversal of withdrawal symptoms rather than direct effects that would occur also in a person who had never smoked. Furthermore, any differences observed between non-smokers and smokers (whether the latter smoked or not during the experiment) might reflect, not the effects of past or present smoking, but rather pre-existing differences between people who did or did not take up smoking (smokers and non-smokers differed from one another genetically and in personality). For these reasons, he said, scientists would prefer to find some way of study the smoking habit without having people smoke at all.
[5.385]To achieve this difficult ambition scientists studied, instead, the effects of nicotine. They made a simplifying hypothesis that the effects of tobacco smoking were due to the nicotine contained in the tobacco and then they studied the effects of the nicotine. In that way, all these confounds could be eliminated. But there were problems with this approach. It would work if, and only if, it was indeed the case that all of the effects of tobacco smoking were produced by nicotine, and this was not necessarily the case. If it were to be supposed, however, that particular observed effects of nicotine (the same in non-smokers and smokers alike, and shown not to be placebo artefacts) took the same general form as those of smoking, then one could reasonably conclude both that these were likely to be real effects of smoking tobacco and that they were caused by the nicotine absorbed from tobacco smoke. Further support for this conclusion could be derived from studies with animals. If, in animals that had never before been exposed to any psychoactive compound, the administration of nicotine had effects that resembled those seen in smokers smoking tobacco, then one could again reasonably conclude that these were real effects and due to the nicotine in tobacco smoke.
[5.386]Professor Gray went on to say that a number of effects that met the criteria of having been reported by smokers as beneficial and as having been confirmed in laboratory studies with human and/or animal subjects consisted in improvements in performance and cognitive function. This was the area of psychological performance which was furthest away from emotion and closest to simple problem-solving. These effects included increased levels of arousal and alertness, improved capacity to maintain performance during long and boring tasks, improved capacity selectively to attend to task-relevant information, improved capacity to maintain concentration of attention, faster learning and enhanced "working" memory.
[5.387]There were also confirmed effects of smoking tobacco and the administration of nicotine on mood and emotion. Prominent among such negative moods was depression. However, it was controversial whether the anti-depressant effects of smoking were due to an intrinsic effect of tobacco as such, or whether they reflected a reversal of depression occurring as a withdrawal symptom in abstinent smokers. Increased depression was certainly reported by many smokers during the period immediately after they quitted smoking. It could not, however, be deduced from this sequence of events that quitting smoking led to depression as a withdrawal symptom, that is, a symptom that would not have occurred had there not been a history of smoking followed by abstinence, in the way that diarrhoea formed part of the opiate withdrawal symptom. There was good evidence that smokers differed as a group from non-smokers. Part of these differences lay in their personality and their susceptibility to mood disorder, including depression. It could be the case that smokers started out in life prior to becoming smokers with an elevated tendency to be depressed and that, when they became smokers, their smoking habit reduced their level of depression so that, when they stopped smoking, their depression returned to what, for them, would have been a normal constitutional baseline. So in that case smoking would not be alleviating depression by reversing a withdrawal symptom, but rather not smoking was unmasking a constitutionally high level of depression in the smoker. It was not possible directly, so far as Professor Gray was aware, to test that hypothesis experimentally in smokers themselves.
[5.388]The possibility of intrinsic anti-depressant action was supported by several lines of evidence. People with a history of depression were more likely to smoke than those who lacked such a history. An important twin study indicated, furthermore, that this relationship between lifetime smoking and lifetime major depression results solely from genes that predisposed to such conditions. In addition, it had been shown, in both animal studies (using behavioural models of depression) and human non-smokers treated with a transdermal nicotine patch, that nicotine reduced depression. Nicotine, then, clearly could reduce depression that was not due to smoking withdrawal; and it was likely therefore that smoking had similar effects.
[5.389]The twin study referred to above by Professor Gray was Kendler et al. 1993. In this study of personally evaluated female twins from a population-based register, average lifetime daily cigarette consumption was strongly related to lifetime prevalence and to prospectively assessed 1-year prevalence of major depression. Using the cotwin control method, the authors evaluated whether the association between smoking and lifetime major depression was causal or noncausal. While the relative risk (95% confidence interval) for ever-smoking giving a lifetime history of major depression was 1.48 (1.30 to 1.65) in the entire sample, it was 1.18 (0.88 to 1.47) and 0.98 (0.71 to 1.26) respectively in dizygotic and monozygotic twin pairs disconcordant for a history of major depression. The relative risk for a history of major depression given ever-smoking was 1.60 (1.39 to 1.83) in the entire sample, while in dizygotic and monozygotic twins discordant for smoking it was 1.29 (0.87 to 1.74) and 0.96 (0.59 to 1.42) respectively. Controlling for personal smoking history, family history of smoking predicted risk for major depression; controlling for the personal history of major depression, family history of major depression predicted smoking. The best-fitting bivariate twin model suggested that the relationship between lifetime smoking and lifetime major depression resulted solely from genes that predisposed to both conditions. These results suggested, according to the authors, that the association between smoking and major depression in women was not a causal one but arose largely from familial factors, which were probably genetic, that predisposed to both smoking and major depression.
[5.390]Professor Gray said that similar considerations applied to the greater calmness and reduced irritability commonly reported by smokers. There were the same possible confounds as previously discussed. There was much less evidence about irritability than there was about depression, but there was evidence from humans that nicotine was likely to be involved in that particular effect of tobacco, because irritability had been observed to be reduced in withdrawing smokers who were given nicotine replacement therapy. So it was likely that the effects of smoking in reducing irritability were mediated by nicotine. The question then arose whether the nicotine was working by way of alleviation of withdrawal, or as a direct effect in reducing irritability, with or without withdrawal. The evidence that it could be through an intrinsic route of action was that in animals aggressive behaviour had been reported in several studies to be reduced by injection of nicotine, so again there was a direct effect similar to that reported by smokers. So the effects reported by smokers might be real, rather than the control of a withdrawal symptom.
[5.391]The situation regarding anxiety was much less clear cut than with regard to depression. Most of the experimental work had been carried out on animals. There was a very substantial literature, but it was also very complex. There were many reports of injections of nicotine increasing behaviour in animals which was generally taken to have an important conceptual resemblance to human anxiety, but there were also many reports in which nicotine did exactly the reverse. The equivalent laboratory evidence in human was very scanty. It was a problem ethically to induce serious anxiety in the human laboratory, so there were few data to go on. The scant information about human studies was again inconsistent in the direction of the obtained effects. It was likely that both these effects were real: nicotine did indeed both increase and decrease anxiety, depending upon the nature of the environmental circumstances. On the basis of the animal literature, Professor Gray said that nicotine could have the effect of reducing anxiety by acting on some systems in the brain, while also being able to increase anxiety by acting upon others. Smoking could therefore have an anxiolytic effect, which was real rather than simply the control of a withdrawal symptom.
[5.392]As an overview, Professor Gray said that nicotine and smoking tobacco had a remarkably broad spectrum of activity in alleviating negative mood and emotion, including depression, irritability and anxiety.
[5.393]Professor Gray then explained that the functional view of smoking is that smokers smoked to obtain the broad spectrum of benefits referred to above, with some smokers smoking more for some of these effects, others smoking more for others of them, and most smokers smoking for a mixture of them. In that manner, smoking did not differ very much from most of the complicated behaviour that people engaged in. This functional view reflected his own view.
[5.394]Professor Gray next referred to what he called the "addiction" view. He said that in contrast to the complexity of smoking behaviour already noted by him, it had become almost a point of dogma to treat the continuation of tobacco smoking as entirely dependent upon one particular compound: nicotine. At its simplest (the level, indeed, at which it was most often expressed), this view was summed up in two bullet points on the back cover of RCP 2000:
| " | - Most adult smokers do not smoke out of choice but because they become addicted to nicotine [...];
- Cigarettes are highly efficient nicotine delivery devices and are as addictive as drugs such as heroin or cocaine."
|
Professor Gray said that he did not agree with the view that smokers do not smoke out of choice but because they become addicted to nicotine. He explained the "addiction" model in this way. It contained a number of key features, each of which had to be considered in turn and put together to make the entire model. The first point was that there was in the brain a reward system upon which all of the drugs that people self-administered acted, and they acted in such a manner as to become "super rewards". They activated that system to an unusual degree or in an unusual manner. According to this model, the effect of the drug on the reward system was subjectively experienced as euphoria of the kind that cocaine users reported as being a "high" or a "rush". The next point the model made was that there was a development of tolerance to the repeated use of the substance in question, meaning that the effect of the substance, in producing the euphoric state, reduced and that the user of the substance, in the effort to re-attain the initial euphoric experience, increased the dose of the substance in a process known as "dose escalation". At the same time the body in general adapted to the increasing amounts of the drug that the user was ingesting, and that adaptation served the well-known function of homeostasis. This was the process by which the body attempted always to revert to the status quo after there had been any serious shift in the balance of its activities from the equilibrium point. After tolerance had developed, there were two opposing sets of effects: the original set of direct drug effects, and the counteracting set directed at maintaining homeostasis. If the drug was not further ingested, only the counteracting set of effects remained, which were experienced as unpleasant physical withdrawal symptoms. The drug-taker now had two strong compulsions to continue taking the drug: craving for its euphoric effects and the need to avoid unpleasant withdrawal symptoms.
[5.395]Application of the "addiction" view to nicotine, Professor Gray said, given these assumptions, was accomplished as follows. First, the neurochemical signature of activation in the reward system was taken to be the release of dopamine in the nucleus accumbens of the brain. This could be readily measured in laboratory animals and there was no question that nicotine did produce that effect, in rats for example. It was also correct that the same release of dopamine was seen in animals injected with opiates such as heroin and stimulants such as cocaine. These facts were not in dispute. The interpretation placed upon those facts was that nicotine was a drug of abuse because it had those effects on the brain. Professor Gray said that he did not share this interpretation. The same effect of the release of dopamine in the nucleus accumbens could be produced in rats by an electric shock to the feet, by a tone that the animal had learned to recognise as a warning of an electric shock to the feet, or even by a tone that simply told the rat that it was going to be stimulated by a light. All of these effects had been demonstrated in his own laboratory. None of them was consistent with inferring, from dopamine release in the nucleus accumbens, that the event which had produced that dopamine release was a reward, let alone a euphoriant. So he accepted the facts about nicotine giving rise to dopamine in the nucleus accumbens, but not the inference from those facts that nicotine was producing the kind of euphoric state that the addiction model associated with those observations.
[5.396]According to the "addiction" model, the motivation to smoke tobacco and the difficulties smokers had in giving up the habit were due to the twin compulsions of craving for nicotine and avoidance of withdrawal symptoms. In Professor Gray's view, there were flaws in the model. First, there were several serious weaknesses in the "euphoria" side of the "addiction" view. Common experience, whether that of smokers themselves or those who observed smokers, gave no hint of a "rush" or "high" as described by users of cocaine or heroin. Consistent with this common-sense appraisal, in controlled studies smokers did not report euphoric responses to any significant degree to either tobacco or the intravenous administration of nicotine. This was supported by the findings of Rose et al. 2000.
[5.397]The contrary view rested upon a report that intravenous nicotine and inhaled tobacco smoke increased ratings on a "euphoria" scale on which high ratings were given also to morphine and amphetamine: Henningfield 1984. Professor Gray said that the data given in Figure 5 on p.29 of this paper, "Scores on the euphoriant scale for compulsive behaviors", had been repeatedly cited in the literature. He explained that there had previously been developed a number of self-report scales to measure various different ways in which drug users described their experiences of taking drugs. A range of compounds had been studied, as shown in Figure 4 on p.28, including morphine and benzedrine, and the point of the study was to compare the responses of such subjects to intravenous nicotine, using these scales, with the responses to the other compounds that had previously been studied. As stated on p.28:
"In these studies, volunteers are given a range of doses of the test compound and placebo under double-blind conditions. Individuals with histories of drug abuse are used as subjects because they can accurately discriminate compounds with a potential for abuse and can compare the effects of the compounds to those of abused drugs."
Professor Gray said that subjects with a history of drug abuse were not representative of the general population in two respects. First, they differed systematically from the general population in the personality characteristics which led them into taking illegal drugs on a regular basis. Secondly, it was unknown whether the taking of these other drugs would have altered the way in which they responded to a test compound, nicotine in the present case. So it was not possible to generalise these results to smokers who, for the most part, were not takers of illegal drugs. Most smokers simply smoked cigarettes and were a different population from the population of illicit drug users.
[5.398]Henningfield went on to describe how doses of the test compound and placebo were administered to volunteers who reported their responses. The responses were measured according to two scales: the Liking Scale (Single Dose Questionnaire) and the Morphine Benzedrine Group (MBG) scale of the Addiction Research Center Inventory (ARCI). Figure 5 showed responses to "nicotine, tobacco, other drugs of abuse and simulated gambling". The author stated, at p.29:
"The ARCI data are consistent with the Liking Scale data, confirming that nicotine, given by both routes of administration, was a euphoriant. When asked to identify the injections from a list of commonly used and abused drugs, subjects more frequently identified nicotine injections as cocaine."
Figure 5 set out the findings on the ARCI scale. Professor Gray said that these were the findings which had been most widely cited. He did not regard the Liking Scale as relevant to the question whether there was a euphoric response: one might like many things which did not produce euphoria. The data in Figure 5, however, were specifically concerned with a comparison between the effects of nicotine on the ARCI and those of the drugs in respect of which the scale was first formulated, morphine and benzedrine (a form of amphetamine which at that time was in common use). The argument had been used that on this scale nicotine had the same effects. Figure 5 showed nine histograms each showing two bars, one for placebo (P) and the other for the "drug" under investigation (D) or simulated gambling (SG). In all nine histograms the D or SG bar was higher than the P bar. Professor Gray said that the significance was said to be that nicotine increased scores on this scale to the same degree as that seen for morphine and amphetamine, for example, and from the way the figure was drawn that appeared to be the case. It has subsequently been pointed out by Warburton, however, that the scales on the vertical axes of each of the histograms were quite different from each other. This was standardly regarded as very poor scientific methodology and should have been pointed out by the referees of the paper at the outset; it was something that graduate students were taught at an early stage not to do. For morphine for example, the P value was below 4 and the D value nearly 10; the same for amphetamine. For nicotine, the P value was 5 and the D value just below 7. But the scales had been set so that the difference between P and D for nicotine appeared to be as large as that for amphetamine and morphine, though this was simply not the case.
[5.399]Professor Gray described Professor Warburton, who had been professor in the Department of Psychology at Reading University, as a leading researcher internationally in the field of psychopharmacology. He had recently received a lifetime award for his contribution over the entire span of his career to that field of research and was a very highly respected scientist. In Warburton 1988a at pp.31-34 there was discussion of Henningfield 1984. Warburton noted that there were remarkable differences in the scales shown in his Figure 3.1 (the same as Figure 5 in Henningfield 1984) and the results took on a different picture when plotted on the same scale, as in his Figure 3.2. If the scores for the difference between assessment of the substance and placebo were plotted it was possible to derive a ranking of euphoria, or "abuse potential" to use Henningfield's term. It could be seen that nicotine injections and smoking were low on the euphoriant scale, and had low "abuse potential" on the scale that Henningfield used for assessment. On this evidence there was not strong support for Henningfield's conclusion. From the data it seemed that nicotine was, at best, a weak euphoriant and did not act like other compounds in the maintenance of other kinds of substance self-administration, i.e. it is not like morphine in opium use.
[5.400]Warburton went on:
"In the laboratory of the Department of Psychology, University of Reading, Henningfield's work has been followed up by considering the concepts of 'euphoria' and 'pleasurable well-being' in terms of two separable experiences, pleasurable-stimulation and pleasurable-relaxation. Tests were made on 139 subjects for their recall of their experience of different substances and activities. They were asked to rate these substances and activities on a scale from zero to ten, where ten was the maximum imaginable. The sample was a set of subjects who had some experience of using a variety of different substances. In this way, ratings of the pleasurable-stimulation and pleasurable-relaxation of a set of substances and activities, including tobacco, were obtained. These ratings enabled a comparative ranking of the substances and activities on these two kinds of euphoria to be derived [...].
The most interesting comparisons were those of tobacco use with other substances and activities. Alcohol, amphetamines, amyl nitrite, cocaine, heroin, marijuana, and sex were significantly more stimulating than tobacco. Sleeping tablets and tranquillizers were significantly less stimulating than tobacco, while there were no statistically reliable differences between tobacco and caffeine or chocolate in terms of pleasurable-stimulation.
On the pleasurable-relaxation dimension, alcohol, heroin, sex, sleeping tablets, and tranquillizers were significantly more relaxing that tobacco. Amphetamine, amyl nitrite, cocaine, caffeine and glue were significantly less relaxing that tobacco, while there were no statistically reliable differences between tobacco and chocolate in terms of pleasurable-relaxation."
[5.401]Warburton accordingly disagreed with the statement in Henningfield 1984 at p.30:
"The results of these studies provide direct evidence that nicotine, in doses comparable to those delivered by cigarette smoking, is an abusable drug. That is, nicotine meets the critical criteria of being psychoactive, producing euphoriant effects, and serving as a reinforcer. These findings suggest that the role of nicotine in cigarette smoking is similar to the roles played by other drugs in the maintenance of other kinds of substance self-administration, e.g., morphine in opium use, tetrahydrocannabinol (THC) in marijuana smoking, cocaine in coca leaf use, and ethanol in alcoholic beverage consumption."
A further criticism of Henningfield's histograms, according to Professor Gray, was that there were no indications of statistical significance. There were no standard error bars, so it was not possible to state whether the modest difference in the D and P values for IV nicotine and tobacco was a statistically significant difference or not.
[5.402]Returning to the issue of self-report, Professor Gray said that smokers did, in contrast, report reduced "craving", increased smoking satisfaction and increased psychological reward when, after overnight abstention from tobacco, they smoked cigarettes from which the nicotine had been removed: Rose et al. 2000. Thus it was misleading to liken the pleasure derived from smoking cigarettes to that occasioned by cocaine or heroin; and the pleasure so derived did not depend principally upon nicotine.
[5.403]Professor Gray then turned to the question of self-administration. He said that other evidence cited in support of the notion that nicotine had directly rewarding ("reinforcing") or quasi-euphoriant effects was that animals would work (e.g. by pressing a bar) to self-administer nicotine intravenously. There were indeed many demonstrations of nicotine self-administration in animals. He said that these had been accepted rather uncritically, as was thoroughly analysed in Frenk and Dar 2000, but despite that critique he believed that the evidence was that animals would self-administer nicotine. However, the conditions under which they did so were much narrower than those in which animals self-administered heroin or cocaine. It was harder to train them to do it and once trained they did not show the extreme avidity for nicotine that in other experiments had been shown for heroin and cocaine. There were studies in which 30% of animals had kept on working to ingest the drug to the point of death and in the case of cocaine as many as 90% had done so. He had never seen a report that an animal self-injecting nicotine produced that kind of deleterious effect upon its own life or its general health.
[5.404]Professor Gray explained that Frenk and Dar 2000 came to the view that there was no good evidence that animals would self-administer nicotine. They did a very effective analysis of the great majority of experiments that had been published in this field. They demonstrated a number of potential artefacts which were not controlled for in these studies. For example, in most experiments, the possibility was not controlled for that when animals self-injected nicotine, the rate of bar-pressing went up as a consequence of the nicotine increasing activity, rather than because the animal was working in order to obtain the nicotine. Professor Gray's own view of the literature, however, was that there was evidence that animals would self-administer nicotine.
[5.405]Critically, he said, there was no reliable evidence that nicotine as such (when given by routes other than the smoking of tobacco) was liked, reported as pleasurable, or self-administered by human subjects, whether smokers or not; and some evidence, especially in non-smokers, that it was actively disliked. It was notable in this context that the various nicotine replacement therapies (such as nicotine-impregnated chewing gum, transdermal patches or nasal sprays) had only weak or no effects in aiding attempts to quit smoking, and had not themselves become a focus for drug-seeking behaviour. Abstinent smokers given nicotine replacement therapy did not normally continue to take nicotine for long periods, in sharp contrast to abstinent heroin users treated with the opiate substitute, methadone, who typically continued to take this drug for years. And, when patients were treated with nicotine for other medical conditions, such as ulcerative colitis, they did not exhibit nicotine-seeking behaviour, whether they were non-smokers or ex-smokers; nor did the ex-smokers revert to smoking as a result of this treatment.
[5.406]Professor Gray said that in the case of other drugs it was well-established that if, for example, a heroin user had not been taking heroin for a long period of time, exposure to heroin re-instated a new round of high level heroin use. Tobacco did this for smokers, but nicotine did not. When I asked him whether this kind of relapse was attributable to "addiction", Professor Gray said that the vocabulary of addiction could be used descriptively or as an attempt at causative explanation. His view was that as an attempted method of explanation the language of addiction was not helpful. It did not explain. It made sense to him to describe certain forms of behaviour as "addictive", but to describe someone as "addicted" in no way provided an explanation for his behaviour.
[5.407]Professor Gray continued by saying that, given these weaknesses in the evidence that nicotine made a major contribution to the pleasurable effects of smoking, one must consider the possibility that the appeal of cigarettes derived, at least in part, from other sources. There was little evidence that nicotine was involved in the pleasurable aspects, as distinct from the cognitive aspects and the mood-improving effects, of tobacco smoking. That raised the question to what else one might attribute the satisfaction of smoking, its pleasurable effects. Nicotine was the only individual constituent of the whole cluster of things that made up tobacco and tobacco smoking that had actually been investigated in the laboratory to any significant degree. So the rest of smoking had to be treated in a much more general manner. In doing this, one could either consider the whole of the sensorimotor aspects of smoking or the "tar", which was a conglomerate of much of the other constituents of tobacco smoke once the nicotine had been removed. One could ask questions such as whether the pleasure of smoking was in part due to the tar, or was in part due to the sensory aspects of smoking, or the motor habits involved in taking a cigarette - lighting it up and smoking it and so on - or all of those together. There was evidence that tar was involved because, when scientists altered the tar content of cigarettes, while holding the nicotine content constant, smokers chose to compensate their smoking to obtain the level of tar that they were used to in their accustomed brand of cigarette. There was other evidence from other experiments that the sensory aspects of smoking were involved, and so the pleasure probably came from a combination of those two routes.
[5.408]Professor Gray next addressed the question of tolerance. He said that the addiction model focused in particular upon the development of tolerance to the euphoric effects produced initially by a drug. Nearly all effects produced by drugs could be subject to tolerance to some degree. But in the case of the addiction model, tolerance to the euphoric effects should be such as to lead the substance user on to taking more and more of the substance. In the case of smoking, there was no euphoric effect as such, though there were pleasant effects of smoking, but no evidence that these underwent tolerance to any significant degree.
[5.409]Professor Gray went on to say that in considering the withdrawal side of the "addiction" view, two related distinctions needed to be borne in mind. First, the term "withdrawal symptom" was used both descriptively and causatively. In its descriptive use it was sufficient to observe that certain changes followed upon discontinuance of taking a substance. What smokers reported when they had recently given up smoking was correctly described as a withdrawal symptom. The term did not add to the description. Causatively however it was used with additional meaning. It implied that the observed changes were due to the absence of the discontinued substance and reflected neural and/or bodily adaptations to the substance when it was present, the withdrawal symptoms being attributable to the homeostatic counteracting process. There were further surplus meanings on top of the descriptive use when the concept of withdrawal was applied causatively. The first additional meaning was about how the withdrawal symptoms were themselves caused; the second was about what the withdrawal symptoms did to the individual who was experiencing them. It was said that the withdrawal symptoms caused the individual to take up again the habit that was being discontinued. Care needed to be taken to make the distinction, because there was no doubt that, after smoking was discontinued, smokers reported a range of changes from the state they were in when they were smoking. Professor Gray questioned the additional causative meanings thereafter. The fact that a change was observed after a drug was discontinued does not justify the inference that the change was caused by the discontinuance, still less that it was caused in just the way implied by the causative sense of withdrawal. In order to justify that inference, further evidence was needed.
[5.410]The most compelling evidence turned upon a further distinction between withdrawal symptoms, in the descriptive sense, that were or were not specific to the substance whose use had been discontinued. Normally, physiological adaptations to an ingested substance were antagonistic to the changes the substances produced directly. So the best evidence that a (descriptive) withdrawal symptom was indeed caused by drug withdrawal was that (a) it has specifically related to a change directly produced by the drug, and (b) took a direction opposite to that change. A symptom of withdrawal from heroin that clearly met this evidential criterion of causation was that of diarrhoea. Heroin, like other opiates, caused constipation to which the body adapted by homeostasis. Discontinuance of the drug unmasked the adaptation to this effect, and diarrhoea resulted. This symptom was "specific" in relation both to the discontinued drug (diarrhoea did not occur, for example, during cocaine withdrawal) and to a particular direct effect of the drug (constipation). Symptoms that did not meet these criteria were "non-specific". In general, specific symptoms were probably "withdrawal symptoms" in the full causative sense; non-specific symptoms probably were not.
[5.411]There were marked differences between the "withdrawal symptoms" described upon quitting smoking and heroin, respectively. As well as diarrhoea, symptoms of heroin withdrawal included tears from the eyes, bleeding from the nose, nausea or vomiting, sweating, fever, muscle pain, joint pain and lethargy. The symptoms described by smokers were almost entirely psychological, above all irritability, anxiety and depression, and also difficulty in concentrating, increased appetite and decreased heart rate. The two latter symptoms were probably specific, in that smoking reduced appetite and nicotine increased heart rate. Such self-reported symptoms, in the case of quitting smoking, usually peaked at about three to ten days and disappear by two to four weeks. Both "syndromes" included restlessness and disturbed sleep, but otherwise they have little in common. Quantitative comparison between two such different conditions was difficult and, to Professor Gray's knowledge, had not been attempted. From their respective descriptions, common sense would certainly judge heroin withdrawal to be much more unpleasant. This judgment was confirmed by the willingness of heroin users to undergo prolonged anaesthesia in order to get through withdrawal speedily and without actually feeling the symptoms, under a treatment in which an opiate antagonist was administered to the patient. USSG 1964 at p.352 stated that many heavy smokers might cease abruptly and, while retaining the desire to smoke, experienced no significant symptoms or signs on withdrawal; and Professor Gray said that this had been documented and had happened to people of his own acquaintance.
[5.412]As noted, he said, heroin withdrawal included a range of physiological effects, whereas quitting smokers largely reported psychological changes. The latter resembled those reported also by people who gave up cherished habits of many kinds, including those that did not depend upon any substance at all, e.g. gambling. Clinical treatments for gamblers had included measurements of those changes they reported when they gave up gambling, which were essentially identical to those reported by smokers, including increased irritability, increased anxiety, increased depression and difficulty in concentrating. One therefore needed to consider the possibility that the causal chain which led to the withdrawal symptoms in the person who quitted smoking might not involve nicotine at all, but might involve merely the habit of smoking: of carrying the cigarettes, and of smoking under certain conditions which formed an integral part of the smoker's life. In Professor Gray's view, however, the symptoms observed in a smoker who was quitting were due both to the loss of the nicotine and the loss of the habit. Some of the effects of quitting smoking could be reversed by giving nicotine, but others could not. This is "tricky territory": one had to distinguish whether the descriptively ascertained withdrawal symptoms were causative and also between the descriptive withdrawal symptoms that could be reversed by nicotine and those that could not. The psychological changes reported by quitting smokers were clearly non-specific and it could not be inferred that they were caused by the absence of tobacco or of any ingredient, including nicotine, found in tobacco. The exceptions to this generalisation were the increased appetite and the decreased heart rate observed after quitting smoking, which were both opposite in sign to the decreased appetite and increased heart rate caused directly by nicotine. However, neither increased appetite nor decreased heart rate were unpleasant, and so they could not fulfil the role putatively played by "withdrawal symptoms" in driving the quitting smoker back to smoking. With these exceptions, the behavioural and psychological changes observed in quitting smokers were more reasonably interpreted as reflecting non-specific dysphoria consequent upon disruption of a habit and loss of the pleasure or other benefits the habit provides.
[5.413]Furthermore, the addiction view of smoking focused not on withdrawal from tobacco but withdrawal from the putative addictive substance in tobacco, nicotine. If one could show changes in animals with nicotine that resembled the changes in humans with tobacco smoking, that would be good evidence that the changes in the case of tobacco smoking case reflected something to do with nicotine. At first sight, reports of a withdrawal syndrome in rats and mice that had been given nicotine offered support for the notion that the human withdrawal symptoms, after smoking tobacco had been discontinued, resulted from a withdrawal from nicotine. But the withdrawal syndrome in rodents was extremely different from the symptoms in human beings: gasping, writhing, chattering of the teeth, chewing, drooping of the eyelids, shakes, tremors and yawns in no way resembled those seen in quitting smokers, even though these were all changes that could be easily observed in human beings were they to exist. In addition, the withdrawal symptoms described in human beings who had received nicotine by way of skin patches, chewing gum or other such routes were minimal.
[5.414]If the addiction model were to apply to smoking, it would be expected that withdrawal symptoms would be a significant part of the causal chain that led the quitting smoker to resume smoking, and that in turn led to the prediction that the major time at which smokers who were quitting would resume smoking would be when withdrawal symptoms were at their strongest. This simply did not occur. In smokers who had quitted, the resumption of the habit ("relapse") did not correlate well with self-reported "craving" or withdrawal symptoms. This was borne out by evidence. Furthermore, most resumption of smoking took place well after the first few weeks of abstinence (the period when withdrawal symptoms and craving were at their greatest). Nicotine replacement therapy did reduce (as the nicotine addiction view predicted) self-reported symptoms, and did aid smokers to quit, but the improvement produced by it (relative to placebo controls) in successful quitting was modest, that is, of the order of a doubling from 10% to 20%, about the same as that produced by cognitive-behavioural counselling. Moreover, the resumption of smoking did not follow the time-course that would be expected if it were due to withdrawal severity; nor did the reduction in resumption of smoking produced by nicotine replacement therapy follow the time-course expected if it were due to alleviation of withdrawal. That is, neither the former nor the latter was especially pronounced during the period when withdrawal symptoms were greatest.
[5.415]Professor Gray said that the same point was made in RCP 2000 at p.143, where it was stated:
"NRT [nicotine replacement therapy] alleviates withdrawal discomfort. However, as has been pointed out, the severity of withdrawal is only a weak predictor of success in stopping smoking."
He disagreed, however, with a statement in the same document, at p.xiv: "The major psychological motivation to smoke is the avoidance of negative mood states caused by withdrawal of nicotine." This was because there was more than one psychological motivation to smoke, and he did not think the data warranted the selection of any one of these as "the major psychological motivation". He accepted that smoking helped the smoker to improve negative mood states. But it was not established that the smoking was leading to the "avoidance" of a negative mood state that had been caused by the withdrawal of nicotine. There was evidence of a direct intrinsic anti-depressant effect of nicotine and there was therefore no certainty that should allow the formation of such a sweeping statement. In addition, he did not agree with the statement on the same page: "Most smokers do not smoke out of choice, but because they are addicted to nicotine."
[5.416]Professor Gray's conclusions on the "addiction" view were as follows. The two central claims of the view were (1) that "cigarettes are highly efficient nicotine delivery devices" and (2) that "smokers do not smoke out of choice but because they become addicted to nicotine." He did not question the first of these claims; nicotine reached the brain in about ten seconds from a puff on a cigarette (RCP 2000, p.36). However, given the flaws in the arguments and evidence as outlined by him, he said that one could not infer that the habit of smoking was wholly or even largely based upon this fact. As to the second claim, there was at the heart of the statement a false dichotomy between two ways of viewing human behaviour. One view could be described as mechanistic: it supposed that behaviour could always be attributed to a causal chain and that therefore what an individual did at a particular moment was entirely beyond his choice. If this determinist claim was correct, then it applied, not only to the smoking of cigarettes, but to everything human beings did, because there was always a causal chain. The other view was the normal humanist view of life that we all adhered to in our everyday activities and grew up believing, namely that when we did something which it was in our power to control, we chose to do it: we chose to do anything that we were not coerced to do by some obvious means.
[5.417]Professor Gray believed the dichotomy to be false, and that it went to the heart of the issues before this court. Within the scientific investigation of human behaviour, it would now be widely accepted that the brain should be considered as an intellect set of feedback systems which attempted to control variables in a way that was good for behaviour and that was adaptive. At the highest level of the feedback systems were those that helped to obtain rewards and to avoid punishments. A reward system was concerned with maximising the benefit to the individual and minimising the costs. Such a system could be described in mechanistic terms, but there was no contradiction with the language of choice, because rational choice was precisely about choosing that which as good for us and avoiding that which was bad for us. On one understanding of the statement that smokers did not smoke out of choice but because they became addicted to nicotine, it simply meant that they smoked because they wanted nicotine and that was in fact exercising their choice. However, it was not nicotine that smokers wanted, they wanted cigarettes. So when a smoker chose to take a cigarette, it did not change any of the facts to re-describe that behaviour as the smoker was "addicted" to cigarettes. It just shifted the focus from using one of these languages of choice to another of determinism.
[5.418]A more specific reason for disputing the statement was that if it meant that it was impossible for a smoker to choose not to smoke, that was simply contradicted by the data. Millions of people who were smokers had given up smoking, in particular when the cost and benefits changed with the understanding that they were running risks to their health. In the United States some ten to twelve million people had given up smoking over a period of twelve years. So smokers could quit, they could choose to quit and, if that was true for large numbers of smokers, there was no reason to say that any individual smoker was forced to continue smoking and could not choose to give up. Reference was made in this connection to USSG 1988, in which it was stated, at p.466:
"According to the 1985 National Health Interview Survey (NHIS), there are approximately 41 million former smokers in the United States. Approximately 90 percent of former smokers report that they quit smoking without formal treatment programs or smoking cessation devices [...]."
[5.419]Professor Gray said that the claim that smokers did not smoke out of choice but because they became addicted to nicotine was sharply contradicted by the epidemiological data. What distinguished those who succeeded in quitting from those who did not was at present largely a matter of conjecture, with the exception that high socio-economic class and membership of the medical profession were strongly associated with quitting. None of the proposed behavioural or psychological predictors of quitting (such as self-reported "craving" or intensity of withdrawal symptoms, number of cigarettes smoked a day, and so on) accounted for more than a small part of the variance. The "addiction view" resolved this conundrum by stating that those who did not succeed in smoking were "addicted" and "had no choice". But this statement lacked all explanatory power. If failed even to account for the association between quitting and socio-economic class or being a doctor, as there was no reason to suppose that these variables were inversely related to vulnerability to addiction. In some, to say that a smoker was "addicted" was based upon just that observation - that a smoker had not quitted - that it purported to explain.
[5.420]Professor Gray explained that "variance" was a technical statistical term which quantified the degree to which values were spread out around their average or mean. If the addiction model of quitting smoking were correct, from supposed measurements of the degree of addiction, such as self-reported craving or withdrawal symptoms, it should be possible to predict those individuals who would find it more or less difficult to quit. To say that those variables accounted for a very small part of the variance meant that, if they were taken into account, the scatter of measurements on whether or not people quitted remained very little changed. It could not be predicted with any accuracy who was going to quit more or less easily. That being so, the normal scientific inference would be that the hypothetical model was false as it did not apply to the data.
[5.421]Professor Gray went on to say that there was an alternative, more nuanced, account of smoking behaviour, one that offered a marked contrast to the simplistic "addiction" view. This "functional" account was based upon the fact that, by smoking tobacco, people derived a variety of benefits and help in coping with everyday life. Reference was made to Warburton 1988b. In this paper, with which Professor Gray said that he agreed, the author adopted a pharmacopsychoecological approach to smoking behaviour which proposed that this behaviour could only be understood by considering the ecological context of the person. This had been discussed in previous publications. He said that smoking was adopted because it enabled the smoker to control his psychological state. At any moment this would be the outcome of both exogenous and endogenous factors, the situation and the individual. The author presented evidence to show how situations determined the individual's smoking behaviour. At p.76 he stated:
"One of the propositions of the functional model is that smoking behaviour must be interpreted within the ecological context of the person. Consequently, nicotine use is seen as a purposive, coping activity for the needs of everyday life. Smoking is maintained because it has a function and satisfies these needs. Consequently, smoking is not an irrational behaviour but the behaviour is adopted because it enables the user to effectively control their psychological state. It can be seen as a psychological resource that the person uses [...].
As a smoker may have more than one motive, nicotine use may have different functions in different situations. However, smoking behaviour can be the outcome of not only the characteristics of the situation, but the personality of the individual. Personality characteristics will determine the way in which the person interacts with situations. Consequently, differences in smoking behaviour will be the result of the interaction of the individual with the situation, the person and their ecology."
[5.422]Professor Gray commented further on RCP 2000. He said that the conclusions in this report, and other such reports, formed part of an attempt to change behaviour, part of a health action, and as such, in interpreting the conclusions from a scientific point of view, one must always bear that context in mind. So he would not necessarily take the conclusions in the report as simply straightforward accounts of scientific evidence or conclusions. In addressing oneself to a scientific question the data that carried most weight were those in the primary experimental or empirical reports: the so-called archival data. So one would go, wherever possible, to those primary reports. One might then, or in advance of that, rely upon reviews of a particular field, in order to see what the general conclusions were, but also as a means of orientating oneself to the primary reports. One would not normally start with a book so far removed from the primary data as was RCP 2000.
[5.423]Warburton 1988b mentioned the importance of personality in smoking behaviour. There had been investigation into whether smokers tended to have personality characteristics which differed from those of non-smokers. Professor Gray elaborated on this. He referred to the general theory of personality, which in turn was based upon particular methods of data-gathering and data analysis. If many individual observations on large groups of individuals were collected and it was then considered whether, if individuals were ranked on one of these observations, this would predict how they would rank on other measures, and the overall set of correlations so obtained was reduced in order to obtain the simplest description of the underlying dimensions of variation, all of the research agreed that there was a dimension of introversion/extraversion so that individuals might be more or less socially withdrawn (introverted) or socially outgoing and ready to engage with others (extraverted). There was also universal agreement that there was a dimension of neuroticism. At one end of that scale, people were anxious, depressed, moody, irritable and so on, and at the other end they were calm and phlegmatic and did not have many mood changes. Then there was what Professor Gray called "the P dimension". "P" stood for "psychoticism" or "psychopathy". The simplest description was that "P" stood for high tendencies to engage in antisocial behaviour at the high end of the scale, or tendencies towards psychotic behaviour. If these three broad axes of variation were imagined as a three-dimensional space, all individuals fitted somewhere within it. If smokers were randomly drawn from the entire population, they would have average scores on each of these dimensions, with scatter similar to the rest of the population. In fact however smokers tended to be somewhat extraverted, somewhat neurotic and somewhat high on the P scale. Their positions on these scales were not necessarily immutable over the years, because they were themselves a response to social circumstances. This was because, as described by Warburton 1988b, smoking was not an immutable fixed effect of personality but was an interaction between the personality and the situational and cultural effects prevalent at the time. Spielberger and Jacobs 1982 found that smokers had significantly higher scores than non-smokers on the Eysenck Personality Questionnaire (EPQ) extraversion, neuroticism and psychoticism scales. Previous studies had led to the conclusion that smokers were more extraverted and had more antisocial tendencies than non-smokers, and the evidence was reasonably convincing that smokers were also more impulsive. Professor Gray said that introversion- extraversion, neuroticism and psychoticism were features which had a genetic base, and were determined by genetic factors to an extent of 30 to 50% of the variance, depending on the particular studies.
[5.424]On the question "Who smokes?", Professor Gray said that the incidence of smoking in the United Kingdom population had varied considerably over time. However, at any one time, smokers were not a random sample of the population, but rather had distinctive characteristics of their own, which were of several kinds: genetic, family environment, personality and social environment. Chronologically speaking, the first factor to come into play consisted in the inheritance of a genetic predisposition that favoured smoking. This term ran the risk of misinterpretation. It did not imply lack of choice. Nobody in the field of the genetics of human behaviour and psychology believed that a single gene determined irrevocably that someone would have a certain characteristic, but so-called genetic determinism had become sufficiently widespread, as a "straw man" set up by its opponents, that it was necessary to state the matter clearly. A "predisposition" was just that: a tendency which, other things being equal, made it more likely that the predisposed event (in this case, smoking cigarettes) would come to pass. Other things, of course, were rarely if ever equal; and the final outcome, in respect of this and all other behaviour, reflected an interaction, usually highly complex, between a variety of different factors that predisposed towards or against it. The genetic influences on smoking behaviour were in part mediated by the smoker's personality.
[5.425]Predisposing influences from the early environment worked in the same general manner as genetic predisposition, that is to say, they increased or decreased the probability that the individual would be a smoker. A particularly important role was played by the family environment: children whose parents smoked were more likely to smoke themselves. Interpretation of this correlation, however, was not straightforward. It might arise because: (i) parents passed on to their children genes that predisposed to smoking; (ii) children modelled their smoking behaviour on that of their parents; (iii) both parents and children were influenced by factors in the general environment in which the family was situated (e.g. within a culture in which smoking was prevalent); or (iv) a combination of these causal pathways. However, statistical genetic research had developed powerful methods for distinguishing them.
[5.426]It was usually impossible to establish all the actual factors involved (e.g. specific genes, or specific features of the family or general environment) or how they interacted with one another. What was possible, however, was to calculate the relative contributions of genetic factors and environmental factors. These relative contributions were described in statistical terms as the proportions of variation, technically "variance", in the relevant behavioural trait for which they accounted.
[5.427]It had been estimated, from studies of the similarities in smoking behaviour between identical and fraternal twins, that the genetic route accounted for about half the variance in taking up smoking. A further 30% of the variance was accounted for by shared family environment. Putting these two factors together, then, the family background accounted for about 4/5ths of the variance in taking up smoking, by way jointly of shared genes and shared early environment. Genes played an even greater role in the continuation of smoking than in taking it up, accounting for as much as 70% of the variance, with the influence of shared family environment falling to zero. Reference was made to True et al. 1997. In this paper the authors estimated the magnitude of genetic and shared environmental contributions to risk of initiation and maintenance of smoking. Genetic models were fitted to data from male monozygotic and dizygotic twin pairs. The best fitting model allowed for both genetic and shared environmental effects on smoking initiation, accounting for 50% and 30% of the variance in risk, but allowed for only genetic effects, accounting for 70% of the variance in risk, on persistence in smoking among those who had become regular smokers. They stated that this finding of a major genetic influence on smoking persistence confirmed similar results from twin studies in Scandinavia and Australia. The results yielded by these studies were consistent with the conclusion that there was an important genetic contribution to the risk in men of becoming long-term smokers, with heritability estimates ranging from 47% to 74%.
[5.428]A fourth factor relevant to the question "Who smokes?" was, Professor Gray said, social environment. Aspects of social interaction relevant to smoking behaviour included peer pressure, social rituals of sharing and exchange, the social setting and the self-image that the individual sought to project. There was considerable interaction between an individual's personality and these social factors. For example, an extravert would seek out social gatherings. Under conditions where social gatherings involved a large amount of tobacco smoking, and where rituals of exchange in sharing formed part of what went on at them, then an extravert was both more likely to encounter them and to be influenced by them. The level of an individual's score on neuroticism scales taken relatively early in life predicted the subsequent diagnosis of a range of psychiatric conditions, most notably anxiety and depression. Smoking had an antidepressant effect and might have an anxiolytic effect. Against that background the association between neuroticism and smoking could be explained by reference to the functional model of smoking. A person who was high in the dimension of neuroticism was likely frequently to experience moments of anxiety, depression and also irritability, general loss of calm and feelings of tension. Such a person, upon smoking a cigarette, was likely to discover that these moods were reversed rather rapidly. So an individual would discover that smoking a cigarette was a useful way of making himself feel better.
[5.429]Warburton 1988b found that an individual, by smoking, was able to reduce negative emotional feelings occurring during times of stress and to increase concentration. In an experimental vigilance session, individuals who had high degrees of extraversion and neuroticism improved their performance after smoking. At p.74 the author stated:
"It can be argued that the improved performance after smoking was a consequence of the tranquillising effects of nicotine, which reduced situational anxiety."
Professor Gray said that this provided an excellent example of the manner in which there was a constant interaction between the individual's personality, the demands that a situation placed on the individual, and the effects of smoking.
[5.430]At pp.74-75 Warburton wrote:
"Coping strategies can deal directly with the environmental challenge or indirectly to reduce its impact on the organism temporarily. Smoking can have both of these effects. In a challenging work situation, nicotine can enhance performance and experience of this enhanced efficiency will reduce an individual's anticipatory concerns about their behavioural competence [...]. When there is an uncontrollable life event, the nicotine can calm the person and improve mood generally. In both cases, the impact of the stressor on the person is reduced. In this regard, it is interesting to compare nicotine with alcohol, which is often used to calm and improve mood. The action of alcohol is to escape from stressors, while nicotine enables the person to confront them."
Professor Gray said that the different outcomes from smoking were not mutually exclusive. A smoker might report simultaneously, for example, that he felt more relaxed and more alert, paradoxical as this may seem at first sight. The same smoker was likely to smoke for different reasons at different times: principally to change his mood if he felt depressed, but principally to increase his level of alertness if he had been taking alcohol, and so on in many combinations. A person with a high P score, who was inclined to be aggressive, might find smoking useful because it could calm him down. This again fitted with the functional model. He also said that the reason why individuals who had quitted smoking might return to it well after the disappearance of any withdrawal symptoms could be explained by reference to the functional model. Returning smokers often cited periods of stress, depression and negative mood changes as the background for the resumption of smoking.
[5.431]Professor Gray was asked to consider averments in the pleadings for Mrs McTear that after commencing smoking, Mr McTear quickly became addicted to cigarettes, that in about 1971 he attempted unsuccessfully to give up smoking and thereafter attempted on numerous occasions to give up smoking but, due to his addiction, he was unable to do so. In order to comment on these averments, he had read the transcripts of the evidence given by Mr McTear on commission and by Mrs McTear at the proof, and records relating to Mr McTear's medical history, employment history and criminal record. He said that during the period when Mr McTear smoked, smokers were relatively high on extraversion, low on neuroticism and high on the P dimension. There was not a complete picture of Mr McTear's personality, but his early history demonstrated the kind of active social life one would expect from a relatively extraverted young man. This picture was strengthened by his Army records, which stated that "he has no interest other than in his own personal experience", a typical extravert characteristic. A high level of neuroticism was suggested by the diagnosis he was given in later life of suffering from an anxiety state. Also suggestive of high neuroticism was his need to drink alcohol to "increase his confidence" (Dr Lind's letter 23 October 1990). Evidence of antisocial behaviour suggestive of an elevated P score could be found at several points in his records, particularly his Army records. His frequent and poorly motivated changes of employment were testimony to the accuracy of his Commanding Officer's judgment that he appeared not to know where he was going in life, and were again consistent with a high P score. Criminal offences were especially associated with high P scores. At later ages, it was impossible to exclude his excessive drinking as a factor in the high rate of offending throughout much of his life. Excessive drinking was, however, unlikely to have been responsible for all of the offences committed by him, even in the form of acute intoxication. Furthermore, excessive drinking was itself associated with high P scores.
[5.432]Among the functional effects of smoking, the ones that figured more prominently in Mr McTear's testimony were concerned with mood control. He said that he liked, enjoyed or even loved smoking. He described the use of smoking to control negative moods. As previously stated by Professor Gray, smoking tobacco might alleviate depression, not because it had a direct antidepressant effect, but rather because, for a habitual smoker, deprivation of smoking had a depressant effect. This type of explanation perhaps applied to Mr McTear's descriptions of the use of smoking to control mood. He emphasised the period when he had temporarily given up smoking and in consequence could have been especially depressed and irritable. It was impossible to determine in Mr McTear's individual case whether the depression he experienced when he temporarily gave up smoking reflected a withdrawal symptom or the return to a natural relatively depressed baseline mood which smoking elevated. In an individual case, it was impossible to make a determination whether symptoms such as those described by Mr McTear when he tried to give up smoking reflected a return to a natural relatively depressed baseline mood, which smoking might have elevated, or withdrawal symptoms, or the effect of other factors such as alcohol, or indeed a combination of some or all of these factors.
[5.433]In Professor Gray's opinion there was nothing which prevented Mr McTear from giving up smoking at an earlier time than when he in fact decided to do so about a year before he died. The decision whether to continue or to cease smoking was made by the individual smoker from time to time in the light of all of the costs and benefits. Mr McTear did stop smoking when his balance sheet changed with the discovery that he had a diagnosis of cancer. The only change was in his state of knowledge about his medical condition. Had he formed a similar opinion earlier on, that would have increased the costs relative to the benefits of smoking and he could have stopped smoking at any earlier time. In general, he said, people did what they were motivated to do. Motivation depended upon the perceived costs and benefits of action that one could choose to perform or avoid. It was easy to understand, within such a motivational framework, that Mr McTear's discovery that he had cancer should alter his perception of the costs and benefits attached to smoking so that he at once quitted the habit. Common-sense would describe such a change as one in the willingness to give up smoking, not in the ability to do so.
[5.434]Professor Gray referred to a paper of which he was one of the authors, Gray et al. 1994. In that paper it was acknowledged that part of the authors' research programme had been supported by the UK Medical Research Council, the Wellcome Trust (a private charity providing similar support on a somewhat larger scale), RJ Reynolds Tobacco Company, the Council for Tobacco Research, BAT (British American Tobacco) and Schering AG Berlin (a pharmaceutical company). The first time Professor Gray received funding from the tobacco industry was in the mid-1970s. There was a shortage of funding from the Medical Research Council. He was interested in the functions of the cholinergic system in relation to Alzheimer's disease and, because of the role of nicotine in acting upon the brain as though it were that same system, the tobacco industry seemed to be a possible source of funding. So he obtained funding from RJ Reynolds Tobacco Company. It was very common for scientists to seek and receive funding for research from relevant sectors of industry. At that time it was not unusual for scientists to receive funding from the tobacco industry. No tobacco company had ever prevented him from publishing his research. It had, however, become unusual in the UK for medical or scientific research to be funded by the tobacco industry and indeed had latterly become impossible because universities and hospitals, in which this type of research was conducted, had formulated a policy not to accept funding from the tobacco industry. Both the Medical Research Council and the Wellcome Trust had adopted policies under which they declared that they would not fund research for either a scientist or his institution if he accepted funding from any part of the tobacco industry. In order to accept funding from these bodies, the acceptance of support from the tobacco industry was precluded.
Cross-examination of Professor Jeffrey Gray
[5.435]In cross-examination, Professor Gray was asked about his conclusion on the question why Alfred Mr McTear smoked. In his report he wrote:
"[He] smoked for a variety of reasons, to obtain a variety of different benefits, and to cope in a variety of ways with the problems and stresses of everyday life. In this respect, he behaved just like the majority of other people in his time and place, especially those from similar social groups, in similar social settings and with a similar family background."
He agreed with the suggestion that Mr McTear was much like the average person who smoked.
[5.436]Asked about funding he had received from the tobacco industry, Professor Gray said that this was for only the minority of his research, dealing with nicotine. The greatest part, and possibly all, of the articles he had written about nicotine were funded in part by the tobacco industry. Asked about his remuneration in connection with the present case, he said that he was being paid for his time spent as being an expert witness. He was paid by the hour and the total would "reach five figures".
[5.437]Shown cigarette packets with the legend "Smoking kills", he said that this was not his field of expertise. He was not medically trained. He had a personal view, but not a view as an expert. His personal view was that smoking had been established as a strong risk factor for a number of diseases. This did not mean that smoking killed. Ask about the statement in UKWP 1988, in the preface by the Prime Minister, that in Britain today more than 120,000 were going to die over the next year from illnesses directly related to smoking, he said it was not his field of expertise, he did not know. As an individual, he believed that smoking carried risk. Asked whether it would be extremely irresponsible for a Prime Minister to put out a message like this in a White Paper unless there was extremely strong evidence to back it up, he said he did not know, his understanding was that he had been called in this case as an expert witness. He was not as an expert entitled to any view on the degree of responsibility that fell upon the shoulders of the Prime Minister when he made a particular statement, though as a citizen of the United Kingdom he believed that our Prime Minister normally weighed carefully his words and the reasons for writing them, at least he hoped that that was the case. This was not a matter on which he had any expert opinion.
[5.438]Asked about the statement in the White Paper at para.1.8 that smoking was addictive, he said that he accepted a use of the word "addictive" in which it was descriptive of certain types of behaviour. Used descriptively, it was not unreasonable to talk of smoking in that way. But to say that smoking was "addictive" provided no explanation for the fact that people engaged for large parts of their lives in smoking behaviour. He would accept the statement that smoking was addictive if it implied that it was a former of behaviour in which people engaged frequently and repetitively over long periods of their lives. The definitions in DSM-IV were mutually contradictory as between addiction in general and addiction to nicotine in particular to the point that it was not possible to say it was one thing or the other. So Professor Gray would not agree that it was possible clearly to refer to nicotine as addictive, or to smoking as addictive behaviour, with reference to those sets of definitions. The critical causative sense of addiction, with which he did not agree, was that it caused smoking and smoking continuation. He could agree with a statement that nicotine could be seen as addictive, if what is meant by this was that it was capable of creating some of the dependence and withdrawal symptoms that were described in DSM-IV and ICD-10, so long as it was taken descriptively but not causatively. In common parlance the word "addictive" was typically used in response to the descriptive characteristics of a form of behaviour, but at the same time to give the misleading impression that one had understood the nature of the mechanisms that gave rise to that behaviour. It was ambiguously used in common parlance. Some smokers had a strong urge to smoke because of the multiplicity of effects that they found beneficial in smoking a cigarette, as previously described. Professor Gray knew many people who had stopped being smokers and in general they had told him that giving up smoking was somewhat unpleasant but not too difficult.
[5.439]Professor Gray did not agree that the statistics demonstrated that not a large proportion of smokers managed to give up. One of the "key points" in RCP 2000 at p.xiv stated that only about 2% of smokers succeeded in giving up in any year. Professor Gray said he thought that that number was probably correct, because if accumulated over twenty years it would correlate with the forty million or so US smokers who gave up smoking over that period. He saw no reason to dispute the further statement that 50% of young adult smokers would still be smoking when they were 60. He said that to know why 50% gave up by the age of 60 and 50% did not, would mean that there would be some way of predicting in advance who would quit smoking and who would not. None of the purported individual level predictors of quitting or failing to quit were able to predict to more than a very slight degree. The variables that were predictive were to do with social class. The reasonable inference that he would make from those figures was that a greater understanding of behaviour and the reasons for it and the particular costs and benefits attached to it was most important in accounting for quitting or failure to quit. The only solid predictor was socio-economic class, and beyond that it was a matter of inference. The statement in RCP 2000 that over two-thirds of smokers said they would like to quit and about one-third tried to quit in any year, but only 2% succeeded, meant, he said, that 6% of smokers who tried to quit succeeded in quitting in one year. This was rather low in relation to a large number of published clinical trials in which the number who tried to quit and who stayed quit was typically 10% without any additional help, rising to 20% with additional help. So in his view the statement in RCP 2000 rather strongly understated the percentage of smokers who succeeded in quitting and it did so in order to convey a particular kind of health message.
[5.440]There had been less substantial investigation of what happened over repeated attempts to quit. The evidence to date was that the chances that a particular individual would succeed in quitting on any individual attempt remained constant over a series of attempts; so that if there was a 10% chance of quitting on each of these occasions unaided, by the tenth attempt it became 100%. It was not possible to say, in respect of those who had not quitted by the age of 60, how many had tried unsuccessfully to quit. He had no reason to disagree with the statement that about two-thirds of smokers said they would like to quit and about one-third tried to quit. As for the reasons, the data tended to come from studies in which a fairly large cohort of smokers were asked rather simple questions and it was unlikely that any further probe could have been undertaken to establish how much they would like to quit, their reasons for wishing to do so and so on. The present state of the scientific art was that measurement of the behaviour of individual smokers prior to a quit attempt was a very poor predictor of which individuals would succeed. So he could not say why it was that on a particular occasion one smoker succeeded in quitting while another did not. The reasons were most likely, he thought, to reside in the smoker's individual circumstances and his perception and evaluation of those individual circumstances at the time he made each quit attempt. If the quitting were quitting from nicotine use, rather than smoking, then there was no problem whatsoever: the quitting rates from nicotine delivered by any other mode were essentially 100% immediately. Smokers smoked cigarettes, as he had previously explained, for a variety of reasons.
[5.441]Professor Gray was asked about a paper entitled "Motives and incentives in cigarette smoking" by William L Dunn, Jr of the Philip Morris Research Center, Richmond, Virginia. The paper was described in the text as a "presentation". It related to a conference on the Caribbean island of St Martin in 1972, attended by twenty five scientists, described as "pharmacologists, sociologists, anthropologists and a preponderance of psychologists". It was not clear from the text to whom the presentation was made. Mr McEachran told me that he thought it was "an internal report", but this did not explain who were the audience to whom it was addressed. At all events, especially because I only allowed it to be lodged on the morning of the day on which Professor Gray was cross-examined, he had not had an opportunity of considering it previously. Professor Gray agreed with a statement in the paper that the primary incentive to cigarette smoking was the immediate salutary effect of inhaled smoke upon bodily function. He said that his view was that there was something about the interaction between nicotine, on the one hand, and the rest of what was in tobacco, on the other, which underlay its great popularity. The paper contained criticisms of Eysenck's theory of personality as part of his explanation of smoking. Professor Gray said he agreed with the comment that it was absolutely impossible for the concentration of level of nicotine required to induce neural depression to be attained by means of smoke inhalation. He did not agree with the statement that to postulate both activating and sedating effects was to defy the documented universality of the activating, physiological effect of smoke inhalation. Under reference to Warburton 1988a, Professor Gray said that all of the effects that he had been talking about in relation to nicotine were produced by way of its action on the brain. Warburton had shown experimentally that the more extraverted the subject was, the more he would wish to do something to reverse the decline in alertness towards the end of a boring task, and one way of achieving this was the nicotine which produced the desired change in the level of arousal.
[5.442]Professor Gray was asked about passages in MacAskill et al. 2002. The authors stated that in Scotland there was in 1988 a marked social class gradient in respect of smoking between AB groups and DE groups, 13% of the former and 49% of the latter being smokers. He would expect Mr McTear to fit into Group D, "partly skilled/unskilled". He would not dispute that tobacco played an extremely important role in the lives of people in low-income communities, and that for many smoking was their main pleasure. He accepted that smoking offered both a respite from and a means of coping with a stressful and unrewarding environment. He had no reason to dispute that studies had shown that disadvantage was inversely associated with cessation success: the more disadvantaged, the less likely a person was to succeed in quitting smoking. He agreed that this would be a factor to take account of in the case of Mr McTear. Another factor, he agreed, would living in a poor neighbourhood and being a member of a disadvantaged community with limited exposure to non-smoker or ex-smoker "role models". He accepted that a barrier to smoking cessation in low income communities was the importance of smoking as a means of coping with stress. He also agreed that fair points were that smokers in such communities had low confidence regarding cessation and an unsupportive environment for it. But the evidence, to which he had previously referred, was that the family environment contributed to the initiation of smoking but not, apart from the genetic route, to the persistence of smoking once commenced. He did not, however, disagree with what was said in the document about barriers to quitting.
[5.443]Professor Gray was asked about various passages in USSG 1988 to the effect that nicotine had addicting properties. He agreed that he was "out on a limb" by comparison with many distinguished scientists and doctors. He did agree that nicotine was a psychoactive drug with actions that reinforced the use of tobacco. He would agree with the use of the word "addicting" descriptively, but not if it was intended to be explanatory of the activity of smoking cigarettes. A similar description could be applied to gambling. A report such as this was essentially part of a strategy aimed at changing people's behaviour and was supplying messages concerning health and the measures that people could take. So it was a mixture of propaganda and the scientific evidence upon which it was based, but with the interpretations and the language used to describe those data biased towards the interests of the message that the report was conveying. With regard to the scientific standard of proof it was a biased report.
[5.444]His attention was drawn to a passage in the introduction, on p.5:
"This Report was developed by the Office on Smoking and Health, Center for Health Promotion and Education, Centers for Disease Control, Public Health Service of the US Department of Health and Human Services [...].
The scientific content of this Report reflects the contributions of more than 50 scientists representing a wide variety of relevant disciplines. These experts, known for their understanding of and work in specific content areas, prepared manuscripts for incorporation into this Report. The Office on Smoking and Health and its consultants edited and consolidated the individual manuscripts into appropriate chapters. These draft chapters were subjected to an extensive outside peer review [...] whereby each chapter was reviewed by up to 11 experts. Based on the comments of these reviewers, the chapters were revised and the entire volume was assembled. This revised addition of the Report was resubjected to review by 20 distinguished scientists inside and outside the Federal Government, both in this country and abroad. Parallel to this review, the entire Report was also submitted for review to 12 institutes and agencies within the US Public Health Service. The comments from the senior scientific reviewers and the agencies were used to prepare the final volume of this Report."
Professor Gray agreed that this was an appropriate way to go about making a report on a matter like this, but his understanding was that the actual writing of the report was done by the Office on Smoking and Health and its consultants, it was they who edited and consolidated the individual manuscripts into appropriate chapters. He could vouch for the efficiency with which the scientific information of the time was gathered together in the chapters, but the final messages which had been quoted to him from the introductory material, as distinct from the individual scientific chapters, were put together as part of a health message by civil servants in the Office on Smoking and Health. Summaries, such as the one in this report from which Mr McEachran had quoted, mainly contained the views of those who had a particular health message that they wished to be heard.
[5.445]Professor Gray said that prior to this report the scientific literature was not concerned with the question whether one word or another - "habitual" or "addictive" - should be applied to one form of drug use or another. The report substituted a previous classification which separated heroin and alcohol on the one hand from smoking and other activities on the other, but the change was not based upon new scientific evidence of any kind. It was based upon a health message decision that it would be better to include them all as "addicting" drugs. The clinical community had preferred to use the expression "dependence" rather than "addiction", but the report prepared to define drug dependence and drug addiction as the same thing. None of these changes rested upon scientific or medical knowledge. In his view, the reason why smokers found it difficult to give up was partially habit-based, partially nicotine-based and partially the seeking of the positive aspects of smoking, such as taste and
enjoyment, which were not mediated by nicotine and were not simply the habit, but the consequences of the habit; the sensory characteristics. He did not agree that most smokers did not smoke out of choice but because they were addicted to nicotine. This might be the conclusion of USSG 1988, but it did not alter his own assessment of the evidence. He did not form his opinions on the basis of the authority of public health organisations.
[5.446]RCP 2000 stated at p.100:
"On current evidence, we can conclude that cigarettes are properly categorised among the most addicting substances as this form of nicotine delivery maximises the addictive effects of the drug. The fact that nicotine is of low abuse potential in controlled dosage form such as the transdermal nicotine patch or nicotine gum supports the conclusion that the form of delivery is an important determinant of its addiction potential."
Professor Gray said that he did not agree with this because exactly the same evidence supported the conclusion that nicotine was not an addicting substance; if it was, the change of the form of delivery would not have such an important effect. The final conclusion in this passage was a good example of the way in which the conclusions had to fit both the scientific evidence in such a report but also the health message that was being conveyed.
Re-examination of Professor Jeffrey Gray
[5.447]In re-examination Professor Gray pointed out that Warburton had been involved in the preparation of USSG 1988. In Warburton 1988b he referred to criticisms he had published of the conclusions of the editors of the report. Professor Gray said that the view he had reached on his reading of the evidence was not dissimilar, as regarded the addiction model, to that of Professor Warburton. Frenk and Dar 2000 expressed views with which he also agreed about the inappropriateness of describing nicotine as addicting.
Dr Deryk James
[5.448]Dr James, aged 40, had been senior lecturer in Forensic Pathology at the University of Wales College of Medicine since 1977. He was Honorary Consultant in Forensic Pathology to Cardiff and Vale NHS Trust, also since 1997. In the latter post his responsibilities were to run the hospital consent autopsy service, in association with other pathologists, to teach the postgraduate pathology trainees and carry out other teaching duties, and to liaise with other clinicians on matters relating to mortality and post mortem examination of their patients. He was a Home Office registered pathologist since 1994. In that post he performed autopsies on behalf of the coroner and, in dealing with suspicious deaths, in conjunction with the coroner and the police. He held the degrees of MB, ChB, the Diploma in Medical Jurisprudence of the Society of Apothecaries (in forensic pathology) and he was a member of the Royal College of Pathologists. He sat on the Forensic Sub-Committee of the Specialist Advisory Committee in Histopathology of the Royal College of Pathologists. He was an examiner and the specialty training advisor in forensic pathology of that college.
[5.449]Dr James's interests included death certification and the investigation of death. He had written a number of papers about this and had recently given evidence to the Smith Inquiry (the Shipman Inquiry), to the Review of Death Certification and to the Review on Death Certification and Coroners (the Luce Report). The last mentioned of these was a fundamental review of the coroner system in England and Wales, also encompassing matters relating to death certification. He gave evidence on death certification, on cremation certificates, on the function of the coroner system and the role of the pathologist and of the medical advisor within it. The Review of Death Certification was a departmental review within the Home Office. He submitted to the Shipman Inquiry a document based on his previous documents to the Luce Inquiry and also relating to other matters more particularly addressed by the Shipman Inquiry. He was then asked for further input and took part in a series of seminars chaired by Dame Janet Smith in 2003.
[5.450]Dr James was one of the signatories of a letter published in the British Medical Journal on 3 October 1992, James et al. 1992. The letter started:
"The reasoning behind the decision that doctors can now put smoking as a cause of death on death certificates without the death having to be reported to a coroner is obscure."
Later in the letter the authors wrote:
"That smoking is associated with several potentially fatal diseases is not in dispute; the difficulty lies in applying an epidemiological and statistical association to individual cases. How is a doctor to determine that smoking is of sufficient causal importance to be separated out from other possible risk factors in those diseases - particularly coronary artery atherosclerosis - regarded as multifactorial in aetiology? Even those diseases with the highest smoking related mortality ratios - lung cancer and chronic obstructive pulmonary disease - can occur in non-smokers. [...] Faced with the spectre of possible future litigation, will doctors feel sufficiently confident in their knowledge of the complexities of epidemiological association to specify smoking as the underlying cause of death?"
Dr James said that he remained of this view. His interest was in being sure that death certificates were fit for use. In the letter he and his co-authors stated that the accuracy of clinical death certification, without validation by necropsy, was known to be suspect. He said that this was a widely held view. There were many papers in the international medical literature which showed that doctors seemed to find accurate formulation of causes of death difficult. It seemed inevitable that doctors would differ over the precise role that smoking might have had in individual cases.
[5.451]Publication of the letter led to Dr James's being approached by solicitors for ITL. He was asked by them to report whether the increase in recorded lung cancer incidence between 1900 and 1950 was real. He reported:
"My opinion is that it cannot be known to what extent the reported rise in incidence was real or artefactual as a result of the changes in medicine and society discussed below.
This opinion has been formed from an extensive review of the scientific literature, my specialist knowledge of death certification, cause of death and autopsy pathology, and my knowledge of the history of medicine."
[5.452]Dr James went on to say that there was a reported rise in lung cancer incidence between 1900 and 1950. Reference was made to MRC 1957 in which, under the sub-heading "The increase in lung cancer" the Medical Research Council stated:
"In its annual report for 1948-50 the Council drew attention to the very great increase that had taken place in the death rate from lung cancer over the previous 25 years. Since that time, the death rate has continued to rise, and in 1955 it reached more than double that recorded only 10 years earlier (388 deaths per million of the population in 1955 compared with 188 in 1945). Among males, the disease is now responsible for approximately 1 in 18 of all deaths. Although the death rate for females is still comparatively low, it also has shown a considerable increase in recent years and the disease is now responsible for 1 in 103 of all female deaths.
Three comments may be made on these figures. In the first place, the trend over the last few years indicates that the incidence has not yet reached its peak. Secondly, the figures are not to be explained as a mere reflection of the introduction and increasing use of improved methods of diagnosis, but must be accepted as representing, in the main, a real rise in the incidence of the disease to an extent which has occurred with no other form of cancer. Thirdly, only a small part of the rise can be attributed to the larger number of older persons now living in the population; in the last ten years the lung cancer death rates among both men and women have risen at all ages from early middle life onwards."
Dr James said that his investigation was concerned with the question whether the rise in lung cancer incidence over the years 1900 to 1950 was real or apparent.
[5.453]In RCP 1962, at p.12, it was stated:
"23.During the past 45 years lung cancer has changed from an infrequent to a major cause of death in many countries. This increase has been most serious in men and women in late middle age, when family and professional responsibilities are at their height. [...] While death rates from lung cancer have been increasing, those from other forms of cancer, and other respiratory diseases have been declining or, like bronchitis, remaining stationary.
24.The experience of chest physicians and surgeons in the past 30 years leaves no doubt in their minds that there has been a very large and real increase in incidence of lung cancer, though some pathologists consider that the disease used to be more common than mortality figures suggest and that much of the increase may be due to improved accuracy of diagnosis on death certificates."
Reference was made to Table II on p.14, which showed average annual numbers of death from various causes during five-year periods from 1916 to 1959 in men and women aged 45 to 64 in England and Wales. Dr James said that the information in the Table had come from death certificates.
[5.454]At the end of the passage quoted above from RCP 1962 there was a reference to Willis 1961, the author of which was a tumour pathologist. In the article he asked the question whether carcinoma of the lung was increasing in frequency, and reviewed lung cancer records before 1900, from 1901 to 1930 and from 1931 to 1960. Although Dr James was taken through much of the text, I propose only to quote from the "Concluding comments on the incidence of carcinoma of the lung" on p.436:
"From the foregoing outline the following main points emerge. In the later decades of last century, pathological records show that bronchial carcinoma was not a rare disease, although it was rarely identified as such by pathologists and was almost unknown to clinicians. In the first three decades of the present century, pathologists became increasingly aware of the characters of bronchial cancers, and the common 'oat-cell' tumours were for the first time clearly recognised as carcinomas and not sarcomas. The fourfold increase in the number of lung-cancer death certificates which took place during this period is readily attributable to these advances in pathological knowledge. The last three decades have witnessed many further advances, not only in pathological knowledge, but also in the establishment of special chest clinics and thoracic surgery units with special diagnostic facilities and techniques - radiology, bronchoscopy and cytological and biopsy studies; and, even more important, clinicians as well as pathologists have become lung-cancer-conscious instead of lung-cancer-ignorant, as most of them were in the earlier period. Under these circumstances it was inevitable that increasing numbers of this clinically misleading and elusive disease should have been detected and correctly identified; and this progressive improvement in diagnosis certainly accounts for a large part of the greatly increased numbers of lung-cancer deaths registered during recent years. Whether or not improved diagnosis accounts for the whole of this increase we shall probably never know, for it is impossible to assess retrospectively just what proportion of clinical and pathological misdiagnoses were made at any given past time, and even now this proportion is still substantial, in spite of our greatly improved diagnostic armamentarium and our awareness of the disease."
Dr James concurred with the content and the conclusions of Willis 1961.
[5.455]Dr James said that the reported rise in lung cancer incidence between 1900 and 1950 was based largely on death certificates and autopsy results; it was supported by doctors' subjective impressions of lung cancer frequency. It could not be known what part of this supposed rise was real because of changes in: the age distribution of the population; the ability to diagnose; the ability to treat; medical knowledge and practice; the role of hospitals; the availability and character of medical care; death certification practice; and medical statistics generally. There was a perception in the early 1950s that lung cancer was rare in 1900 but was common by 1950. Of the evidence that was cited to support this perception, he said that he would address: clinical diagnosis having risen many-fold; autopsy diagnosis having risen many-fold; deaths attributed to lung cancer on death certificates having risen many-fold; and similar findings having been reported world-wide.
[5.456]Dr James said that there was an impression amongst doctors in the late 19th century and early 20th century that lung cancer was a rare disease, but that careful reviews of 19th century literature did not confirm this view and demonstrated that those 19th century physicians familiar with lung cancer were convinced that it was a much more common disease frequently missed. He referred to a series of papers. In Boyd 1886 the author expressed the view that the existence of thoracic cancer was frequently overlooked. In Adler 1912 the author expressed the view that misdiagnosis did occur, with what he believed to be lung cancer being diagnosed as tuberculosis; and that whilst many clinicians might believe lung cancer to be rare, he disagreed. Reference was then made to Weller 1929, in which the author stated, at p.482:
"As is true of all cancer statistics, those dealing with primary carcinoma of the lungs and bronchi are of value only to the extent that the material units have been critically selected. The authenticity of the individual case is the crucial test. Obviously, only those reputed examples of primary carcinoma of the lung are of value on which a complete autopsy has been done. Certainly, too, there must be microscopic verification of each case, if results are to be fully accepted. Routine microscopic examination reveals many errors in the conclusions of even the most experienced gross pathologists."
Finally, in Onuigbo 1971 the author discussed diagnostic difficulties, the influence of preconceived notions, post mortem diagnosis and confusion with tuberculosis among other topics as having a bearing on the recognition by 19th century practitioners that lung cancer was being under-diagnosed. Reference was also made to Horsfall 1966a, which Dr James said was relevant to the extent that it indicated that in the United States the effective treatment of infectious diseases had been such as to help explain why so many more people went on to survive into late middle-age, the age at which cancer was more likely to appear.
[5.457]Dr James said that at the turn of the 20th century lung cancer was widely regarded as being a secondary cancer - having spread from a primary cancer in another organ - rather than originating in the lungs themselves. This was a view disseminated by Rudolf Virchow, a 19th century doctor regarded then as one of the leading lights of medicine and now as the father of modern pathology. Reference was made to Adler 1912 and to Rigdon and Kirchoff 1952. In the latter paper the authors referred to a number of factors which in their view pointed to there being insufficient evidence to prove that the reported increase in lung cancer over the previous fifty years was either apparent or actual. The factors mentioned by them included the questionable authenticity of many death certificates, improved methods in diagnosis, a progressive increase in the number of individuals reaching the age at which cancer might develop and the recognition as primary epithelial tumours of what had previously been classified as metastatic sarcomita.
[5.458]Dr James went on to say that the age distribution of the general population was changing markedly; the group most at risk of lung cancer - those over fifty years old - tripled in number between 1851 and 1921. Without a change in age-specific lung cancer rates, a physician in 1920 would be expected to see three times as many cases, compared with his counterpart in 1850, thus getting a subjective, though false, impression of a real increase. The frequency of diagnosis of any disease depended in part on the availability of medical care. Between 1900 and 1950 the number of people per doctor fell from 1,400 to 900 in England and Wales. This was a phenomenon widely linked with an increase in the diagnosis of cancer in general and lung cancer in particular: Rigdon and Kirchoff 1952 discussed this in relation to various states in the United States. Smithers 1953 said that much of the recorded rise in England and Wales could be attributed for by changes in age distribution and improvement in diagnostic techniques:
"What the clinician so readily attributes to his diagnostic skill the research worker is apt to believe may well be due to the action of a specific carcinogen. Both need to take particular notice of the way their natural bias is apt to lead them and to remember their responsibility to an anxious and ill-informed public when they publish their views on serious problems of fatal disease."
Dr James added that the population receiving medical care was also changing; men received more frequent medical care, probably partly as a result of the National Insurance Acts from 1914 giving benefit to those in work and the Workmen's Compensation Acts from 1918 requiring certain workers to have medical examinations.
[5.459]He went on to say that the discovery of diseases, their frequency and the attribution of death to them were dependent upon hospitalisation, because it had always been through the hospital system that advances in knowledge, practice and provision of facilities were made and disseminated in the literature, and hospitals were where autopsies were performed. From 1900 to 1950 there was considerable development of hospitals with a steady increase in admissions throughout that period and a change in the "type" of patient. In 1900 hospitals had not yet shaken off their role as "refuges for the sick poor" which selected their patients very differently from the "centres of specialised diagnosis and treatment" which they were to become by 1950. Not only would hospitalised patients in 1900 reflect the profile of diseases prevalent in lower socio-economic classes, but also the low life expectancy in these classes would further distort lung cancer incidence, since lung cancer's peak incidence was in later life.
[5.460]Lung cancer, he continued, was extremely difficult to diagnose in life in the absence of modern diagnostic techniques, or at death in the absence of an autopsy. It was in the hospitals that new diagnostic techniques became available and awareness of lung cancer first increased. It was also in the hospitals that autopsies could be performed. Since access to medical care was restricted by limited availability, the number of admissions to hospital was an important determinant of the frequency of diagnosis of lung cancer. During the period from 1900 to 1950 the nature of hospitals and the number of patients being treated in them changed considerably. For example, between 1894 and 1928 the number of admissions to sixteen British teaching hospitals went up by a factor of 2.5; this reflected the increase in the accessibility of medical care. Moreover the proportion of men to women was about 2 to 1 which would favour an unequal distribution of lung cancer diagnosis between the sexes, exaggerated by the 25% lower female mortality (since there would be a relatively greater proportion of autopsies in men).
[5.461]The ability to diagnose and treat lung cancer was extremely limited as of 1900 but had increased massively by 1950. As of 1900 doctors had only the basic skills of history taking, inspection, palpation, auscultation and percussion. There were no x-rays, no bronchoscopy and bronchography, no effective sputum cytology or biopsy, no exploratory thoracotomy and little medical specialisation. There was little awareness of lung cancer, partly because it was widely held to be rare. There was no effective treatment beyond palliation with morphine and therefore doctors had no incentive to diagnose it. By 1950, radiology had become a speciality in its own right during the 1930s and chest x-ray was a simple, effective and available test to discriminate between different chest diseases and a reliable means of diagnosing lung cancer. It was used in mass screening programmes to detect tuberculosis and this facilitated lung cancer diagnosis. Simple chest x-rays were supplemented during the 1930s with lipiodol bronchography which outlined obstruction of the airways by tumour. Bronchoscopy had been well validated but little used by 1930 but its use then took off, very rapidly supplemented by the use of biopsy for precise diagnosis. Sputum cytology using the Papanicolaou method was introduced in the 1940s and was an effective and simple means of diagnosis. Sputum examination was also used for tuberculosis; the failure to detect tubercle bacilli in a case of chest disease was an indication for further investigation. By 1925 there were only about eighty-five case reports of exploratory thoracotomy in the literature but, when directed by radiology and coupled with histological examination of biopsies, it was such a successful means of diagnosis that during the 1930s it became a commonly used procedure. The development of antibiotics in the 1930s, and the resulting improved cure rates for pneumonia, allowed the detection of underlying diseases (a frequent presentation of lung cancer was pneumonia caused by obstruction of an airway). In previous times the patient might have died of pneumonia without the realisation that he or she had an underlying lung cancer. Histopathology had become a speciality and considerable advances were made in tissue diagnosis with repercussions for biopsy and autopsy diagnosis. More accurate and useful classifications for disease were produced; for example, tumours of the mediastinum previously described as sarcomas were recognised as lung cancers. Treatment options for lung cancer prior to 1930 were virtually non-existent. There had been the occasional attempt at lobectomy or pneumonectomy from about 1908 but these were unsuccessful until Sauerbruch performed a lobectomy in 1926, and Graham a pneumonectomy in 1933, by which time radiation was being used with some success for palliation. The realisation by the mid-1930s that cure was possible convinced doctors of a need to diagnose the disease and the unsuitability of the majority of cases for surgical treatment due to their advanced disease led to calls for earlier diagnosis. The availability of a treatment only for early disease encouraged clinicians to rule out lung cancer as a possible diagnosis. This was facilitated by the use of mass radiography (primarily as a means of diagnosing tuberculosis but having a "spin-off" of lung cancer diagnosis).
[5.462]The propositions contained in the previous paragraph were vouched by references in the course of Dr James's evidence. Reference was made to Rosenblatt 1969, in which the author discussed the effect of improved diagnostic techniques in hospitals in the United States in the diagnosis of lung cancer. He related improvements in diagnosis to the progressive decline in the rate of increase of the disease, and at p.32 stated:
"It is impossible to reconcile a declining rate of increase in lung cancer mortality with the epidemic concept. The deceleration of the rate of increase implies that there has been a relatively fixed prevalence of the disease in the population and that expansion of diagnostic facilities has resulted in the recognition of a greater number of cases each year, leaving proportionately fewer cases undiagnosed. The trend toward progressive decline of the rate of increase is crystal clear and will ultimately produce a standardization of the age-adjusted death rate of lung cancer. Inasmuch as lung cancer is a disease of older individuals, the total number of cases may continue to rise because of the increasing longevity among all groups of the population."
[5.463]Dr James went on to say that the effects of these changes individually and collectively were not measured (and, probably, were not measurable) at the times they occurred and could not be assessed with any accuracy in retrospect. It was possible, however, to match the approximate time at which these changes had practical effect (not necessarily when they were first developed or introduced) to the recorded increase in lung cancer. He referred to a graph in Steiner 1953. In this, a comparison was made between the annual number of deaths attributed to lung cancer in males in England and Wales during the period from 1900 to 1950 and the methods available for the diagnosis of lung cancer during life in that period. The methods in question were history and physical examination, which Dr James said were all that was available in about 1900, followed by introduction of the examination of pleural fluid and the biopsy of occasional distant metastases between 1905 and 1910. Between 1920 and 1930 the use of x-rays became more general, and during that period aspiration biopsy was introduced, followed by bronchoscopic biopsy in about 1930. In about 1935 lobectomy and pneumonectomy were introduced, followed by cytological examination of sputum and bronchial washings in about 1940 and exploratory thoracotomy in about 1945. Dr James said that this graph showed that the changes which would be expected to result in a greater number of diagnoses of lung cancer occurred in conjunction with the steepest parts of the incidence curve, thereby presenting a satisfactory explanation for the increase in recorded incidence without the need for a "real" change in incidence having happened. He said that he broadly agreed with Steiner's model.
[5.464]In support of the foregoing views, Dr James referred to various papers. In Johnson et al. 1949 the authors had reviewed the records of 384 patients operated upon by one of them, and stated:
"Our experience with thoracic disease in recent years has convinced us that exploratory thoracotomy carried out as a diagnostic measure is a valuable and important procedure that is not appreciated generally but which can contribute greatly to improvement in results of treatment of pulmonary disease."
In Barnard 1926 the author demonstrated the advantages of the use of microscopic among other techniques in support of his view that tumours then usually called "oat-celled sarcomata" of the mediastinum were primarily carcinomas of the lung.
[5.465]Dr James said that it was not only the improvement in diagnosis that affected mortality statistics and thereby the incidence of deaths attributed to lung cancer. There were changes in collection of mortality data involving improved completion of the medical certificate of cause of death and improved coding of the cause of death. A clinical diagnosis was thus more effectively and reliably translated into an accurate mortality statistic. Four revisions of the International Classification of Disease up to 1950 had progressively refined the classification of lung cancer, and medical statistics had developed as a speciality with increasingly detailed data being provided by the Registrar-General's reports. Death certificates and the quality of diagnoses in general showed improvements in precision through the late 19th century and the first half of the 20th century. The precise degree to which improved death certificate diagnosis altered disease incidences between 1900 and 1950 was difficult to determine, but it was instructive to note that in a study of autopsies carried out in a Japanese city between 1961 and 1987 improvement in the death certificate diagnoses of various cancers was not only still ongoing but was responsible for 60% of the recorded rise in incidence of those cancers.
[5.466]It had been recognised since the 19th century that lung cancer might be missed because physicians misdiagnosed it as one of the other, far more common, respiratory diseases. In the view of Adler 1912, lung cancer was common and a doctor might come across it any day in his practice but, for the symptoms of lung cancer, tuberculosis was a comfortable and satisfactory diagnosis. Even in 1950 there were nearly 90,000 people a year in England and Wales dying with respiratory symptoms, many times more than those who were dying of lung cancer. It was well-recognised that the symptoms of lung cancer were non-specific and commonly present in other more frequently diagnosed diseases; this was an explanation for why nearly all lung cancer diagnosed prior to the First World War was diagnosed in the post mortem room. In various studies looking at autopsy-diagnosed lung cancer it was discovered that between 20% and 36% had been misdiagnosed in life as tuberculosis, 15% as syphilis, 18% as pneumonia and 23% as cancer of another organ.
[5.467]In support of these views reference was made to the following papers. Wells 1923 concluded that the necropsy statistics under discussion "show convincingly that we have at the present time no reliable statistics relative to the frequency of cancer as a cause of death." Anonymous 1950 stated:
"One of the first questions likely to be asked in any discussion of the aetiology of cancer of the lung is whether there has been any real increase in the disease since, say, the beginning of this [the 20th] century. The answer is that we do not know, because there are no figures either here or in any other country on which the actual death-rate from intrathoracic cancer of forty years ago can be compared with that of today."
[5.468]Gilliam 1955 discussed the trends of mortality attributed to carcinoma of the lung in the United States between 1914 and 1950 and the possible effects of the faulty certification of deaths to other respiratory diseases, particularly tuberculosis. The author said that there was abundant evidence attesting to the erroneous diagnosis of lung cancer as tuberculosis. In addition, use of antibiotics in recent years had permitted the survival until correct diagnosis of an unknown number of patients who formerly would have died of pneumonia or some other respiratory cause before discovery of the underlying cancer of the lung. From published data there was no ready way to estimate directly the frequency with which this might have occurred and thus no way to determine precisely how well the recorded mortality measured the magnitude of the true increase. Looking at tuberculosis on its own, Gilliam noted that a 10% error in diagnosis in 1914 decreasing to a 2% error in 1950 would account for a reduction in the apparent increase in lung cancer from 26.4-fold to 2.2-fold in white men and from 6.7-fold to 0.8-fold in white women. Furthermore, if 2% of cases diagnosed as respiratory diseases other than lung cancer between 1914 and 1950 were, in fact, really cases of lung cancer, then the apparent increase in lung cancer incidence, between those dates, in white men, would be reduced from 26.4-fold to 4.5-fold and a 6.7-fold increase in white women would be reduced to 1.3-fold.
[5.469]It was, Dr James said, in that context, particularly interesting that Auerbach 1949 described a series of fifty lung cancer autopsies derived from a tuberculosis hospital having been mistakenly diagnosed. During the time that these lung cancer cases were being accrued, more than 2,000 tuberculosis autopsies were performed, indicating an error rate in 1948 (when sanatoria and specialised means of diagnosis were commonly available) of approximately 2.5%. Tuberculosis was not the only disease with which lung cancer might have been confused; the list of other possible diseases was long, encompassing many acute and chronic respiratory disorders together with malignancies of other sites. The low level of histological confirmation of diagnosis (38%) or autopsy (11%) in 3,280 cases of lung cancer in 1945 and 1946 discussed in one study indicated a potential for such misdiagnoses to cause a significant distortion of the figures. Since these figures related to a time when the major improvements in diagnosis had occurred, it suggested that earlier in the century the misdiagnosis rate might have been considerably higher.
[5.470]Examination of series of autopsies might be used as an alternative way of looking at the changing incidence of a disease and might also be used to act as a means of checking death certificate data. A problem with such series was that they represented a highly selected population - people who had consulted a doctor, been admitted to hospital, died in hospital, and been selected for autopsy. Where series had been done in a single location and where the autopsy rate was high, some of this bias was cancelled out. Bonser 1929 could find no increase in the proportion of lung cancer cases to all cancer cases in the period from 1891 to 1927 in Leeds with an autopsy rate of 83.6%. Passey and Holmes 1935 found no evidence of an increase in lung cancer (when corrected for an increase in hospital admissions) in twelve out of sixteen teaching hospitals in the United Kingdom between 1894 and 1923 and in eight out of sixteen up to 1928. In these two studies the absolute numbers had increased, and this accounted for the subjective impression amongst physicians and pathologists of a real increase in incidence. Jaffe 1934, in large series from Vienna (1915-18) and Chicago (1927-33) was unable to demonstrate any change in incidence of lung cancer (expressed as a percentage of all cancer), there being 11.47% in the first series and 10.73% in the second. Steiner 1953 reviewed the work of others and could find no evidence that the incidence at autopsy of lung cancer was out of proportion to other cancers and concluded that it was not possible to tell if any real increase had occurred. Smithers 1953 stated:
"Even to-day, however, the accuracy of the diagnosis of bronchial carcinoma in the country as a whole and the reliability of death certification from this cause must still be under grave suspicion."
[5.471]Dr James said that autopsy series might also be used to assess the accuracy of clinical diagnosis (from which, for the most part, death certificate data were based). Those series in which such a comparison of clinical diagnosis with autopsy diagnosis was possible indicated a false negative rate (i.e., clinical diagnosis = not lung cancer; autopsy diagnosis = lung cancer) of 97% in 1904, 91% in 1923 and 42% in 1948. The average figure for the period 1930 to 1950 would be about 30%. During the later part of the period from 1900 to 1950 this false negative rate would have been off-set to a large extent by the false positive rate (i.e. clinical diagnosis = lung cancer; autopsy diagnosis = other than lung cancer) but around 1900 there was no evidence of false positives (it was not a diagnosis often made). It should be apparent that if, in 1900 to 1920, only 3% to 9% of cases from lung cancer were attributed to lung cancer on a death certificate, compared with well in excess of 70% between 1930 and 1950, the validity of the trend was seriously questioned. (References were made to Smithers 1953, Wells 1923 and Willis 1948, among other papers, in support of the foregoing figures.)
[5.472]Dr James concluded that the death certificate data constituting the reported rise in lung cancer incidence between 1900 and 1950 were not reliable. Widespread, detailed knowledge and awareness of lung cancer developed hand-in-hand with effective and widespread means of diagnosis and treatment options. The times at which these developments became significant in lung cancer diagnosis (as opposed to their introduction) were strongly associated with the steepest part of the graph and a reduction in the autopsy-derived false negative rate (indicating better diagnosis and fewer missed cases). The earlier part of the graph, less associated with diagnostic change, rose only slowly (and equally, male and female), at a time when the false negative rate was extremely high, suggesting massive under-diagnosis.
[5.473]Dr James added that many scientists and major journals were cautious about drawing conclusions from the incidence data presented by 1950. Most of the data described by him were available to them and most of the problems in differentiating a real increase from an apparent increase had been identified. Many found no reason to suppose that the increase was real. Reference was made to Anonymous 1942 and Anonymous 1950. Fried 1948 concluded at p.12:
"The author is of the opinion that the more frequent occurrence of this disease [cancer, particularly cancer of the lung] today as compared with the past, can be explained on the basis of the following factors: (1) Progress in medicine in the past five decades resulting in improved methods of diagnosis; (2) Progress in public health resulting in increased longevity (more people reach the 'cancer age'); (3) Vastly developed means of hospitalization; (4) Rise in the social and economic levels leading to more people seeking medical advice; (5) Increased attention to the disease. The increase, therefore, is in all likelihood more apparent than real."
Willis 1948 expressed the opinion that it was not possible either to affirm or deny that there had been a real increase of carcinoma of the lung. Auerbach 1949 said:
"A review of the literature makes it appear that much of the increase in bronchial carcinoma is apparent. How much is real will probably never been known."
Dr James stated:
"In conclusion it is my opinion that it cannot be determined how much of the apparent rise in lung cancer mortality between 1900 and 1950 was real because of changes in population; in diagnosis and treatment; in medical knowledge and practice; in the role of hospitals; in the availability of medical care and in death certification and general statistical methods."
[5.474]Referring to RCP 1962, para.24, in which it was stated that the experience of chest physicians and surgeons in the previous thirty years left no doubt in the authors' minds that there had been a very large and real increase in the incidence of lung cancer, Dr James said that in his review of the literature he had found no pathologist who did not consider that the disease used to be more common than mortality figures suggested, and that it was not difficult to see why cancer of the lung should have become so much more frequently diagnosed. Lung cancer was a peculiar disease and was idiosyncratic amongst other cancers in terms of its discovery, presentation, diagnosis and treatment and its impression upon physicians and surgeons.
Cross-examination of Dr Deryk James
[5.475]In cross-examination Dr James said that he was an occasional smoker. His only contact with ITL had been through lawyers acting on their behalf. He understood that his remit was to look at what measures there were of the incidence of lung cancer at the beginning of the period from 1900 to 1950 and through that period, in order to see if it could be known what the incidence really was and, therefore, whether there was a rise of any degree. One of the problems was to put a figure on how much, if any, the rise was.
[5.476]Asked about the statement "Smoking kills" on modern cigarette packets, he accepted the message for what it was, a public health warning, but not that smoking directly killed, because it was neither necessary nor sufficient to kill someone. For that reason he said that smoking did not cause lung cancer. It depended in part on the interpretation of the word "cause".
[5.477]Dr James agreed that there were many scientists and doctors who considered that during the period in question there had been a real rise in rates of lung cancer. There were statements to that effect in some of the papers referred to by him in his evidence-in-chief, for example Passey and Holmes 1935, Smithers 1953, Rosenblatt 1969 and Auerbach 1949. When asked "so there was a lot of material, a lot of doctors and a lot of scientists saying that the increase was real?", he answered in the affirmative.
[5.478]Mr McEachran asked Dr James about RCP 1962, which contained statistics showing a "massive increase" in lung cancer in men during the period in question, by contrast with a much smaller increase in other cancers. Dr James said that in 1950 the reporting of lung cancer was not as good as it was now, but much more to be relied upon than in 1900. He regarded the figures for 1946 to 1950 as still being an underestimate, but probably not a significant one. The figures for the next decade were reasonably accurate in the sense that when "cancer of the lung" was written on a death certificate, that was likely to be a correct diagnosis. But other cases might have been missed. Figures given in RCP 1971 for lung cancer deaths in the 1960s were likely to be reasonably accurate, probably within perhaps 20% or 30%, judging by the overall accuracy of death certificates in that period, but Dr James had not considered the period after 1950 in detail. The figures given in RCP 2000 for the incidence of lung cancer in the 1990s were likely to be reasonably accurate. Asked about the statement in IARC 1986 p.203 that about 94% of deaths attributed to lung cancer were confirmed by hospital diagnosis in a study based on the Third National Cancer Survey in the USA, Dr James said that lung cancer was a diagnosis that was made virtually always in hospital and always had been, so this was a completely unsurprising statement and did not really mean anything about the accuracy of diagnosis.
[5.479]Dr James was asked to comment on Figure 4.1 at p.49 of RCP 1971. This was a graph showing death rates from lung cancer, other forms of cancer, tuberculosis of the lung and bronchitis in men aged 45 to 64 from 1916 to 1965. He commented that this was the same as Figure 7 in RCP 1962, p.15, with the addition of years after 1959 and a line for "all cancer". He said that if there had been an "all cancer" line in the earlier graph, it would have been flat apart from a slight rise at the end, occurring around 1950. He regarded the whole statistics as flawed and he looked at RCP 1962 with distrust, because it was talking about rises in lung cancer incidence of up to about fifty-fold. That made him immediately think that people like Bonser, who were doing autopsy series from around 1900 at an autopsy rate of 80% to 90%, so that they were very representative samples from one place, were finding 1% of autopsies were lung cancer and about 8% of all cancer was lung cancer. If this had gone up fifty-fold, they should have been reporting every other autopsy as lung cancer and a massive proportion of cancer as lung cancer, and this clearly had not happened. So something was very wrong, and this graph showed what it was. This was that as lung cancer appeared to increase, diagnoses of other forms of cancer were decreasing, because there were misdiagnoses which were being corrected. By 1950 to 1960 the correct diagnoses were "kicking in" and the graph was then altering. But that occurred very much later than many people in the 1950s were saying. Lung cancer was a disease that was poorly understood in the 19th century and by 1968 to 1970 was very common. There were an enormous number of changes in society and in medicine between those dates, so working out when the real increase started was immensely difficult. The graph in RCP 1971 showed strong support for the view that the increase did not really start until about 1950, but the data were poor, especially the earlier data, and we were never really going to know. There might have been real increases prior to 1950. The fact that there had been increases since 1950 did not demonstrate that there had been increases prior to that.
Professor Jeffrey Idle
[5.480]Professor Idle, aged 53, was Professor in Medicine and Molecular Biology at the Institute for Cancer Research and Molecular Biology, Medical Technical Research Centre, Norwegian University of Science and Technology, Trondheim. He had held that post since 1995. He was awarded the degree of BSc in applied chemistry in 1972 and the degree of BSc with First Class Honours in Medicinal Chemistry in 1973. He was awarded a PhD in biochemistry at St Mary's Hospital Medical School, University of London, in 1976. He was a Chartered Chemist and became a Fellow of the Royal Society of Chemistry in 1987. He was a Chartered Biologist and became a Fellow of the Institute of Biology in 1999. He became a European Chemist in 2000, meaning that his qualifications as a chemist in the United Kingdom were recognised by the European Union. He became a European Professional Biologist in 2000 also, his qualifications in biology in the United Kingdom thereby being recognised across the European Union.
[5.481]Professor Idle was Lecturer in Biochemistry in 1976, Lecturer in Biochemical Pharmacology from 1976 to 1983, Wellcome Trust Senior Lecturer from 1983 to 1985 and Reader in Pharmacogenetics from 1985 to 1988, all at St Mary's Hospital Medical School. He was Professor of Pharmacogenetics from 1988 to 1995, Chairman of the Department of Pharmacological Sciences from 1992 to 1995 and Head of the School of Clinical Medical Sciences, Faculty of Medicine, all at the University of Newcastle.
[5.482]He was a Visiting Scientist with Curtis C Harris at the Laboratory of Human Carcinogenesis, National Institutes of Health (NIH) and National Cancer Institute (NCI), USA, in 1982. He described carcinogenesis as the process by which a normal cell becomes a cancer cell, in lay terms, but more correctly as the process by which an epithelial cell becomes a carcinoma. He was World Health Organization (WHO) Special Adviser and WHO Committee Chairman (genetic predisposition to toxic effects of chemicals) in 1989. He said that the remit of this Committee was to read, discuss and digest a large amount of data over the period of about one week, as a group, and to produce a report for the WHO, which went out to all Member Governments on the United Nations on the subject in question. He was a member of the Cancer Research Advancement Board of the Irish Cancer Society from 1986 to 1991 and from 1995 to 1996. He said that this was the grant-giving arm of a charity, the Irish Cancer Society, and its role was to consider grant applications from universities around Ireland and to make recommendations for the award of grant funding. He was a member of the Scientific Advisory Board of The Council for Tobacco Research - USA, Inc., New York from 1986 to 1991. He said that the function of this Board was to consider grant applications from scientists and to score them on the basis of their scientific merit and their relevance to smoking and health, and to make recommendations regarding funding. The scoring system was identical to that used by studies sections of the NIH in the USA. When he joined the Board it was Chaired by Leon Jacobson who had been the Dean of Medicine and Professor of Medicine at the University of Chicago and was a Member of the National Academy of Sciences, USA, which was roughly equivalent to the Royal Society in the United Kingdom. Several other members of the Board were members of the National Academy of Sciences; they were all eminent scientists and/or eminent academics. They were drawn from all over the United States, plus one from Canada.
[5.483]Professor Idle was Founding Editor and Editor-in-Chief of Pharmacogenetics from 1991 to 1998. He said that this journal published original scientific articles and some review articles and occasionally correspondence on the subject of pharmacogenetics, mainly human pharmacogenetics, and all the issues that surrounded the role of genes and the response of individuals to chemicals and drugs. He was on the editorial boards of two other journals. He was Consultant in Medical Genetics and Head of Department at the Regional Teaching Hospital, Trondheim from 1996 to 1998. He was Visiting Professor at the University of Bern, Switzerland, with effect from 1 January 2003. He was Consultant in Metabolism, Laboratory of Metabolism, NCI, NIH from 2002. Additional society memberships were of the British Pharmacological Society, the American Association for the Advancement of Science, the American Society for Pharmacology and Experimental Therapeutics, the American Society for Biochemistry and Molecular Biology and the American Chemical Society. His CV listed numerous refereed papers, book chapters and review articles, communications, abstracts, letters and editorials.
[5.484]Professor Idle was asked by ITL's solicitors to give an opinion based upon his own area of scientific expertise in answer to the following five questions:
"(1)In your opinion was it 'almost universally accepted by scientists' in 1964 [as averred on behalf of Mrs McTear] that cigarette smoking can cause lung cancer?
(2)In your opinion had cigarette smoking been established as a cause of lung cancer as at 1964?
(3)In your opinion had cigarette smoking been established as a cause of lung cancer as at 1971?
(4)In your opinion had cigarette smoking been established as a cause of lung cancer as at September 2003?
(5)In your opinion did cigarette smoking cause Mr McTear's lung cancer?"
He said that his report was structured into a number of time periods: the period up to 1964, the period from 1965 to 1971 and the period from 1972 until the completion of the report in September 2003. In constructing the report he had reviewed the scientific evidence involving the various theories of the causation of cancer in general, and of lung cancer in particular; the toxicological experiments that comprised the administration to experimental animals of cigarette smoke or its derived condensates; and the chemistry of cigarette smoke and its derived condensates. He took a chronological and historical perspective of the published laboratory data that he judged to be of relevance to answering the above questions. He reviewed approximately 1,600 original scientific articles, books, reports and scientific communications. On and off, this took about six years. He concluded by answering the first four questions in the negative and, in response to the fifth question, stated that it could not be determined whether or not cigarette smoking caused Mr McTear's lung cancer.
[5.485]In Doll 1997H Sir Richard Doll said at pp.25-26:
"In the three subsequent decades [i.e. subsequent to the 1950s], cigarette smoking has been found to be positively associated with nearly 50 diseases or causes of death and to be negatively associated with eight or nine. In a few instances the associations are due to confounding with other factors, but the great majority arise because tobacco smoke is a contributory cause. Pace Berkson, this is not surprising; not only because of the complexity of tobacco smoke, but also because many of the diseases are different clinical manifestations of common processes, such as DNA damage, vascular occlusion, and damage to small airways."
Professor Idle said that the complexity of tobacco smoke was something he had investigated in the course of researching for his report, as was DNA damage, which indeed he dealt with in his normal academic working life.
[5.486]RCP 2000, Table 1.2, p.17, gave figures for deaths from disease estimated to be caused by smoking in the United Kingdom in 1997. Diseases caused in part by smoking were said to include cancer at seven specified sites and also in unspecified sites, and myeloid leukaemia. Among other diseases were ischaemic heart disease, cerebrovascular disease, aortic aneurysm, myocardial degeneration and atherosclerosis, in the category of circulatory diseases; and ulcer of the stomach or duodenum, in the category of digestive diseases. Professor Idle said that in preparing his report he had given some thought to the biological plausibility of cigarette smoking being responsible for some of this range of diseases.
[5.487]In Berkson 1959, the author stated at p.445:
"For myself, I find it quite incredible that smoking should cause all these diseases. It appears to me that some other explanation must be formulated for the multiple statistical associations found with so wide a variety of categories of disease. And if we are not crassly to violate the principle of Occam's razor, we should not attribute to each separate association a radically different explanation.
One explanation is that the associations have a constitutional basis. This hypothesis has been formulated - and rejected - by Doll and Hill in the following terms:
'... it has been suggested that constitutional and psychological factors might have such an effect.... that persons of a certain "make up" are peculiarly liable to lung cancer and to smoke. We know of no published evidence to this effect.'"
To the quotation from Doll and Hill Berkson added a footnote, also at p.445:
"Cancer is a biologic, not a statistical, problem. Statistics can soundly play an ancillary role in its elucidation. But if biologists permit statisticians to become the arbiters of biologic questions, scientific disaster is inevitable."
(The expression "Occam's razor" is defined in the Oxford English Dictionary as: "The leading principle of the nominalism of William of Occam, that for purposes of explanation things not known to exist should not, unless it is absolutely necessary, be postulated as existing; usually called the Law of Parsimony".) Professor Idle said that during the course of his researches he had read work that indicated that "persons of a certain make up" were "peculiarly liable to lung cancer". Berkson's view was strong and in some respects surprising, because Berkson himself was a very senior statistician. Here he was at least being even-handed, rather than protecting his own constituency. The content was absolutely right: statistics often pointed the way but, as a laboratory scientist, Professor Idle would, he said, stick absolutely to the view that it was necessary to carry out, with the scientific method, scientific experiments in order to demonstrate proof.
[5.488]In USSG 1964 at p.20, under the subheading "Criteria of the epidemiologic method", the authors of the report stated:
"Clinical, pathological and experimental evidence was thoroughly considered and often served to suggest an hypothesis or confirm or contradict other findings. When coupled with the other data, results from the epidemiologic studies can provide the basis upon which judgments of causality may be made.
In carrying out studies through the use of the epidemiologic method, many factors, variables, and results of investigations must be considered to determine first whether an association actually exists between an attribute or agent and a disease. Judgment on this point is based upon indirect and direct measures of the suggested association. If it be shown that an association exists, then the question is asked: 'Does the association have a causal significance?'
Statistical methods cannot establish proof of a causal relationship in an association. The causal significance of an association is a matter of judgment which goes beyond any statement of statistical probability."
Professor Idle said, under reference to this passage, that epidemiological studies could point the way, other data could be brought into the equation and, taking all of that together, a judgment could be made. The scientific method entailed, first of all, making an observation and then constructing a hypothesis or series of hypotheses that might explain it. A hypothesis might and should be used to predict other phenomena that would occur out there in the world or in a laboratory, and should also be able to predict a quantitative outcome in a particular experiment. So it should have a qualitative component and, if appropriate, also a quantitative process. Then the process was set in train to carry out experiments to test if the hypothesis was correct or not. It was usually necessary to run through a fair number of iterations of the third and fourth points until everything fitted into place, until all observations fitted the final hypothesis. So the hypothesis was something which had to be continually modified until all the observations could be explained by it.
[5.489]This led to the creation ultimately, over a period of time, and in collaboration with other scientists, of a model for the world and how it operated. In carrying out experiments the object was both to establish that the hypothesis was correct and to establish that it was wrong. The final hypothesis must explain all the positives and the negatives. He agreed that "statistical methods cannot establish proof of a causal relationship in an association".
[5.490]Reference was next made to Hill 1966. Professor Idle described the author, Professor Bradford Hill, as a very eminent statistician. He was asked to comment on passages in Chapter XXIV, entitled "Statistical evidence and inference". At p.302 Hill wrote:
"The aim of this book has been to make clear in non-mathematical terms some of the techniques that the statistician employs in presenting and in interpreting figures. Much attention has been paid to two basic problems:-
(1)The 'significance,' or reliability in the narrow sense, of a difference which has been observed between two sets of figures - be those figures averages, measures of variability, proportions or distributions over a series of groups.
(2)The inferences that can be drawn from a difference which we are satisfied is not likely to be due to chance."
Professor Idle said that this passage set out a two-stage process: first, to establish whether there was statistical significance in an association; and, secondly, to determine the nature of the relationship.
[5.491]After discussing means of determining whether an observation was statistically significant, Hill wrote, at p.306:
"Faced then with a clear and significant association between some form of sickness and some feature of the environment, what ought we specifically to consider in drawing conclusions about the nature of the relationship - association or causation?"
He then went on to discuss the strength of association, consistency, specificity, the relationship in time, the biological gradient, biological plausibility, coherence of the evidence, the experiment and reasoning by analogy. At pp.313 to 314 he wrote:
"This interpretation of statistical data turns, it should be seen, not so much on technical methods of analysis but on the application of common sense to figures and on elementary rules of logic. The common errors [...] are not due to an absence of knowledge of specialised statistical methods or of mathematical training, but usually to the tendency of workers to accept figures at their face value without considering closely the various factors influencing them - without asking themselves at every turn 'what is at the back of these figures? what factors may be responsible for this value? in what possible way could these differences have arisen?' That is constantly the crux of the matter. Group A is compared with Group B and a difference in some characteristic is observed. It is known that Group A differed from Group B in one particular way - e.g. in treatment. It is therefore concluded too readily that the difference observed is the result of the treatment. To reject that conclusion in the absence of a full discussion of the data is not merely an example of armchair criticism or of the unbounded scepticism of the statistician. Where, as in all statistical work, our results may be due to more than one influence, there can be no excuse for ignoring that fact. And it has been said with truth that the more anxious we are to prove that a difference between groups is the result of some particular action we have taken or observed, the more exhaustive should be our search for an alternative and equally reasonable explanation of how that difference has arisen."
Professor Idle said that he agreed with this passage. It was still as valid today as it was when Professor Bradford Hill wrote. It was a tremendous problem for scientists to avoid becoming slaves of numbers without any logical interpretation. The discussion in the passage about Group A and Group B was equally applicable where the difference was in exposure. The conclusion of the passage quoted was a very important aspect of the scientific method.
[5.492]Professor Idle then turned to the biology of cancer. He said that it was quintessentially a biological entity. It was a general term for more than 100 malignant diseases that were characterised by uncontrolled, abnormal growth of cells and the spread of these cells locally and through the bloodstream and lymphatic system to other parts of the body, by a process known as metastasis. The understanding today of what was this biological entity, in its nature, in its behaviour, and in its ferocity, rested upon a mountain of both related and unrelated observations collected across the decades, in a wide range of disciplines, together with a broad range of clinical specialities such as oncology, surgery, radiotherapy, internal medicine, paediatrics, endocrinology, haematology, pathology and numerous others. These different disciplines were very disparate, both intellectually and in many respects geographically, but in almost every academic environment in a university or hospital there was a group working on cancer of some type or other, and they came together through the scientific literature and through scientific conferences, which were tremendously important in bringing minds together.
[5.493]The term "lung cancer", he said, also represented a group of diseases, those malignancies found in the lung. They can be either primary lung cancers, those originating in lung tissues, or secondary lung cancers, those resulting from metastasis of a tumour originating in a different organ, such as the colon. Primary lung cancers were sub-divided upon the basis of both their characteristics and their cellular origins. The principal lung cancer types were squamous cell carcinoma, adnocarcinoma (both currently grouped together as "non-small cell lung cancer") and small cell carcinoma. There were other more minor categories. A small cell carcinoma was so called because the cell had shrunk and almost all of it was made up of the nucleus. Among the minor categories was benign adenoma, which grew out of glandular tissues, but without the characteristics of a malignant tumour; it would stop growing by itself and often regress and disappear, and it did not metastasise. Benign adenomas frequently arose in experimental animals, yet rarely, if ever, in humans.
[5.494]One could not understand lung cancer without first comprehending cancer as a biological phenomenon. Any consideration of the biology of lung cancer must, therefore, be built on a foundation of cancer biology in general.
[5.495]In the period prior to 1965 there were a number of competing theories regarding the origins of cancer. These theories included the ideas that cancer arose after chronic irritation, or from embryonic tissue, from a filterable invisible virus, from macroparasites, from perturbations in cellular metabolism, from ionising radiation, or from chemicals in the environment. Each of these theories was offered as an explanation of cancer and the scientific literature of the day was replete with references to "the mechanism" of cancer causation. The competition between these theories was quite vigorous at times.
[5.496]According to the scientific method, progress from hypothesis to substantiation should be made through a series of rigorously controlled and reproducible experiments at the laboratory bench. In an effort to determine whether or not one or more of the competing theories of cancer causation could evolve to a position of pre-eminence, carefully planned and executed studies had needed to be undertaken in experimental animals. But the scientific method had not always been rigorously applied, he said. In the 19th century, the use of animals in a laboratory setting had become commonplace. For example, Louis Pasteur employed sheep, cattle, guinea pigs and rabbits.
[5.497]The idea that cancer was caused by chronic irritation, articulated by Virchow in the mid 19th century, dominated thinking for over half a century. By the end of 1964 irritation was still seen to play a role in carcinogenesis. Professor Idle made it clear that throughout his report and his evidence, the terms "carcinogen", "carcinogenic" and "carcinogenesis" were used exclusively in the context of appearance of carcinomas in experimental animals. Carcinomas were malignant new growths arising in epithelia, those layers of cells that cover the internal and external surfaces of the body, including the lining of vessels and other small cavities.
[5.498]Professor Idle next mentioned the virus theory. He said that the first clues that a virus could be an infectious cause of cancer came from the influenza epidemic of 1918. Winternitz et al. 1920 drew attention to the proliferative changes in the lung that resembled those of malignant neoplasms in survivors of this epidemic based on post mortem examinations of a large number of cases of influenza. They reported that in many cases the epithelial proliferation invaded the surrounding lung tissue and a typical, histological picture resulted of an infiltrating, malignant, epithelial neoplasm. They observed in abundance, in the injured bronchiolar lining, mitotic figures, a term used to describe chromosomes that were visible under a microscope when a cell was dividing and thus an indication of cell division.
[5.499]Viral carcinogenesis had been extensively studied in animals. Under the leadership of Dr Clarence Cook Little, staff at the Jackson Laboratories in Maine, USA, demonstrated that a virus was the cause of the high incidence of mammary tumours in a breed of mice and its transmission from mother to daughter in the mouse. Rabson and colleagues successfully produced "epidermoid carcinoma" (squamous cell carcinoma) in Syrian golden hamsters after inoculation with polyoma virus. Viruses were discovered that could cause malignancies in many other species, although these were largely of haematopoietic (e.g. lymphomas) or connective tissue (e.g. sarcomas) origin, rather than arising from epithelial tissues. In 1964, Kotin reported the results of work on a strain of mice that had been administered a combination of influenza virus and city smog extract in the form of ozonised gasoline aerosols. The only group of mice to develop squamous cell carcinomas of the lung were those exposed to both the virus and the smog. By the end of 1964, influenza virus was suspected as a cause of lung cancer in humans and, in combination with smog, had produced squamous cell carcinomas in the mouse lung. Additionally, a number of other viruses had been shown to cause cancer in experimental animals.
[5.500]During the period from 1965 to 1971, the fields of chemical and viral carcinogenesis were beginning to cover less. Workers were beginning to recognise that there might be some common threads in the mechanisms by which viruses and chemicals might cause cancer. Reference was made to various experiments. In one, addition of extracts of city smog to cultures of hamster or rat cells infected with leukaemia virus caused malignant transformation of the cells. In another experiment, mice were treated with the synthetic chemical carcinogen 20-methylcholanthrene. Cells of the resultant tumours displayed properties very similar to certain cancer-causing viruses and it was postulated that the chemical interacted with some endogenous virus present in every mouse cell. This foreshadowed the later discovery of the oncogenes. Horsfall 1966b stated that several thousands of viruses were then known and several hundreds of them could infect human beings. At p.181 Horsfall concluded:
"[T]he cancers of animals do not seem to be different in any significant way from those of human beings. They are of the same types and may occur in the same sites. In some animal species they develop with frequencies similar to those seen in human beings. The cancers of animals are, frequently, attributable to viruses. Indeed, it appears that, in those instances in which the primary incitant of naturally occurring animal cancers has been demonstrated, it has turned out to be a virus.
The number of cancer-inducing viruses and the number of species affected by them are sufficiently large to suggest that, unless one takes a rather forced point of view and insists that cancers of human beings are unique, it would be difficult to defend the idea that viruses do not have anything to do with some human cancers."
Professor Idle said that the views expressed in this passage were still current.
[5.501]Whilst other authors wrote in general terms about how viruses could cause cancer, Dulbecco, writing in 1967, envisaged specific mechanisms which required the interaction of viral genes with host DNA (he subsequently shared a Nobel Prize for these insights). In 1970 independent pivotal discoveries were made of an enzyme within certain tumour virus particles which became known as "reverse transcriptase", which could make DNA copies of viral RNA genes. Prior to these reports it was thought that RNA could only be synthesised from DNA, and not vice versa. This discovery suggested a mechanism by which certain RNA viruses could cause cancer.
[5.502]During this period, researchers were also examining the possible role of viruses specifically in connection with lung cancer. Leuchtenberger and colleagues reported in 1965 that they had found that a strain of influenza virus transformed cells from mouse kidney and bronchus and yielded transplantable tumours. Professor Idle said that one of the hallmarks of a malignant tumour was that it could be transplanted from one animal into another of the same strain and that it would grow and continue to grow there, so the fact that the tumours were transplantable suggested that they were malignant. Mohr and colleagues reported in 1969 that they had isolated a transforming virus-like particle from human alveolar cell carcinoma, suggesting that it was a causative agent. Professor Idle said that the history of viruses as causes of human cancer rested to a particular extent on the detection and then isolation of virus particles in human tumours, which had now been done on a number of different occasions. The isolated particles were grown up in a host cell in the laboratory and these were used to re-infect animals. It was first necessary to see them, and they were usually discovered under the electron microscope in a tumour cell. Staemmler and colleagues reported in 1970 that, using a small amount of a strain of influenza virus, they were able to produce tumours in very high numbers in the bronchi and the alveoli of mice. The tumours appearing early were mostly of the squamous cell type whereas the later ones predominantly showed the features of adenocarcinoma, though often transition to the squamous cell type was observed. By the end of 1971, therefore, the evidence suggested that viruses could cause human cancer and that respiratory virus infection might be a cause of human lung cancer.
[5.503]Defendi and Jensen reported in 1967 what Professor Idle called an interesting reaction between radiation and viruses. They irradiated three different viruses and were able to destroy their infectivity, without nullifying their tumorigenicity (their ability to cause tumours, whether benign or malignant, to form). One of the viruses was unable to cause cancer itself in the animal model but after irradiation with ultraviolet light it was, and the assumption therefore was that a change had occurred in the genetic material of the virus - possibly mutation - that led to its carcinogenic properties. Thus, he said, it was possible that radiation, chemicals and viruses might interact in causing cancer. In a review article, Miller and Miller, writing in 1968, stated in summary that no carcinogenic mechanism, be it incited by radiation, virus, or a chemical, was understood at that time in molecular terms. Professor Idle described this statement of the position as at 1968 as being "both accurate and ex cathedra". Gelboin and Bates, writing in 1966, were convinced that cancer was the result of modification of key genes by carcinogens. This view was shared by Huebner and colleagues, writing in 1971, who envisaged chemical carcinogens and viruses sharing a common mechanism by working through the genes of the host organism to cause cancer. Huebner was a laboratory chief at the NCI in the USA.
[5.504]In the early 1970s, researchers reported the discovery of viral proteins in cells from chickens and mice that had not been infected by a virus. These chickens and mice were kept in sterile conditions in a laboratory animal facility and in addition it was by then possible to look at their tissues and detect the presence of virus. It was very surprising to workers at the time, Professor Idle said, that proteins could be found which originated from a virus when the virus was making more viruses in large numbers before it burst out of the cell. These were found in the cells of mice and chickens which had not been infected with viruses, so they must therefore come from the hosts' own genetic information. It led to a theory that animal cells contained genes related to viral genes, which became known as "virogenes". The first of these genes were discovered in various animal species by Varmus and Bishop in 1976; they became known as "proto-oncogenes". Professor Idle said that proto-oncogenes were genes present in all cells of all animals that play a role in "housekeeping". They were involved in the normal growth of cells and in maintaining the nature of a cell, a process known as "differentiation", so making sure that a liver cell, for example, stayed like a liver cell and the next time it divided it did not go into bone. These processes were all regulated by housekeeping genes, of which the proto-oncogenes formed one group. He described the name as "unfortunate", because of the suggestion of a link with cancer, but said that they were so named because of the way they were discovered in association with cancer.
[5.505]This discovery, that the animal genome contained endogenous genes that closely resembled viral genes that could cause tumours in animals, led to the "oncogene theory" of cancer. This involved the idea that cancer originated from these genes, already within the cells, that had normal cellular functions, but somehow the gene became activated and did things that it did not normally do in a normal cell. This formed part - maybe even a early part - of the process that set a cell on a pathway to becoming a malignant or cancer cell. The pathways below oncogene activity were very complex and involved a number of different signalling molecules and other proteins that set different reactions in train; but, in general, they upset the process by which a cell recognised where it was in what was called a "cell cycle". The cell went through a cycle when it grew; at a certain point it divided into two, and at another point, for example, it rested in a "resting phase". The cell needed to have sensors to know where it was in the cell cycle at any time so that it could switch on and off different genes because, when a cell was dividing, it needed to do different things from when it was resting. Oncogenes seemed to play a role in the recognition of where a cell was in its cycle and also in maintaining the differentiated integrity of the cell. The proto-oncogene might then be thought of as having lost its housekeeping function and as becoming a sort of rogue, allowing the cell to get out of control so far as growth and differentiation were concerned.
[5.506]The oncogene discovery propelled cancer research into the fields of virology and genetics. In 1972, there was beginning to emerge evidence that viral particles could be detected in certain human tumours. Very rapidly the question became not whether viruses could cause human cancer, but what proportion of cancers did viruses cause. The NCI continued to receive large appropriations from the United States Congress for its Special Virus Cancer Program, which was designed to develop a vaccination programme against cancer, on the proposition that cancer could be eliminated in the way that many infectious diseases, such as polio, had been eradicated. The use of viruses to study the process of carcinogenesis was very attractive because, unlike the host, the virus contained within a very small number of genes all the information necessary to cause cancer. The Program was later disbanded because it required special containment facilities, very special operating procedures and buildings. Also the nature of the Program had changed; many virologists who worked in it still held senior positions in direct research in the fields of viruses and cancer, but not in an attempt to produce a vaccine.
[5.507]Estimates of the proportion of human cancers induced by viruses ranged from 10% to 25%. Anonymous 1986 stated, at p.1431: "[A] reasonable estimate suggests that at least 25% of all human cancer worldwide is likely to be virus-induced." Specifically, Professor Idle stated, with respect to lung cancer, two human viruses and a number of animal viruses had been proposed as aetiological agents: first, the T-cell leukaemia virus, HTLV-1, which was endemic in certain regions, was found to be associated with small cell lung cancer in Japan; secondly, several studies had reported a high incidence of lung cancer in HIV-positive patients; and, thirdly, human papillomavirus (HPV) had been suggested to contribute to the pathogenesis of human lung cancer based upon the finding of statistically significantly elevated HPV in the blood of 47.7% of 149 lung cancer patients, compared with 12.6% of 174 non-cancer controls in a study conducted in Taiwan: Chiou et al. 2003.
[5.508]The situation today, Professor Idle said, was that viruses were believed to play a role in the aetiology of a broad range of human cancers, including lung cancer. The molecular genetic techniques available today to detect the presence of viruses in human and animal tissues had been developed only over the past decade or so. There were also vastly improved laboratory methods for the study of virus life cycles and this work continued in the hope of finding viral particles in more types of tumour and thus aiding an understanding of the role of viruses in human cancer.
[5.509]Professor Idle then turned to the macroparasite theory. He said that Fibiger reported in 1913 the occurrence of carcinoma in the stomach and oesophagus of rats that had fed on cockroaches infected with a parasitic worm, and was subsequently awarded a Nobel Prize for the claim that he had discovered that this worm could cause the cancers he observed. His work was, however, discredited by investigators within a decade, the consensus being that the gastric cancer he reported was due to vitamin deficiency. Nevertheless, by the end of 1964, the macroparasite theory was still being considered as a possible cause of some human cancers, for example in certain types of bladder cancer, particularly in Third World countries.
[5.510]Next mentioned was the chemical theory. In the period from approximately 1870 to 1930, coal and the products manufactured from it evolved into the mainstay of the chemical industry and provided many of the familiar household products of the day. The production of oils and tars from coal and shale, involving pyrolysis and distillation, produced new chemicals, such as the simple aromatics, which could be used in the manufacture of synthetic dyestuffs and pharmaceuticals. Whereas combustion involved a rapid chemical reaction between substances that was usually accompanied by a generation of heat and light in the form of flame, and in most cases oxygen comprised one of the reactants, pyrolysis was the destruction of organic materials by heat in the absence of oxygen. Pyrolysis of an organic material would yield destructive products, typically comprising a mixture of tars, oils and gases. Distillation was used to separate volatile oils, such as paraffin oil, from non-volatile residues, such as tars. Professor Idle explained, with the aid of a sketch, that the compounds referred to as "aromatic" were formed of six carbon atoms usually, but not always, joined in a ring, each with one hydrogen atom attached.
[5.511]The bulk production of oils and tars was associated with sporadic cases of skin cancer in workers exposed to these products. Workers exposed to paraffin oil developed skin tumours in areas of their bodies that normally came into contact with it. Reports such as this stimulated the scientific community of the time to ask the question whether chemicals could cause cancer, about which there was some scepticism. This question was addressed, in the first half of the 20th century, largely by one individual, Dr Kennaway, and his research group, working in London. In 1918 Yamagiwa and Ichikawa produced experimental cancer on the rabbit ear using a chemical mixture, specifically coal tar. This was the beginning of a period when coal tar was painted onto the skin of animals in an attempt to reproduce an occupational disease in humans. The purpose of the experiments was to produce an animal model upon which substances could be tested to see what was in the coal tar, with the hope of being able possibly to modify the process and remove the substance.
[5.512]Professor Idle said that it was important to appreciate the differences between skin tumours and skin cancer. A tumour was an abnormal mass of tissue, resulting from excessive cell division, that served no physiological purpose. A benign tumour simply stopped growing. A skin cancer was a malignant tumour which did not stop growing, had unregulated cell growth, invaded the surrounding tissues, metastasised to distant organs and, without any other intervention, would kill the animal or individual. Certain of the studies discussed in his report, particularly the earlier studies, referred only to "tumours", without specifying that they were largely benign growths which resolved after the treatment ceased. Later papers reported the incidence of both papillomas and epitheliomas (squamous cell carcinomas of the skin), the latter reportedly resulting from malignant transformation of the former. This was simply observational science. The appearance of papillomas on the skin of a rabbit ear or the back of a mouse, most of which disappeared, followed by the appearance of squamous cell carcinomas, led to the assumption that one followed the other. But this was not substantiated by any particular experiments and remained in the realm of hypothesis.
[5.513]Leitch, writing in 1922, reported that he painted the skin of mice, rats, guinea pigs and rabbits with different fractions of shale oil distillate; only mice ever developed malignant tumours. After conducting his animal studies in London, where he was the director of the Cancer Hospital Research Institute, he concluded, despite the observation of very few tumours, that in relation to human exposure to paraffin oil "we are dealing with an actual, in contradistinction from a predisposing, cause of cancer." Professor Idle said that he thought that this was one of the earliest observations in toxicology of a qualitative species difference in response to a challenge.
[5.514]An important figure at this time was Kennaway, also working at the Cancer Hospital Research Institute in London. His aim, as stated by him in 1924, was to identify "the cancer-producing substance in coal tar". His interest was in the development of methods that used mouse skin as a bioassay which would help in his search for this. Prior to this, the only discrete chemical that was thought to cause cancer in humans was arsenic. Kennaway pursued various fractions and individual chemical components of coal tar and realised rather quickly that this was not going to lead him to the answer. Professor Idle explained that coal tar was a material that could be sub-fractionated not only by the physical process of distillation but by extraction with various solvents. These fractions were then tested on animals. In a series of experiments Kennaway attempted to mimic coal tar. He pyrolysed substances at high temperatures under a stream of hydrogen gas to yield pyrolysis products with a simpler composition than that of coal tar. Starting with the simple hydrocarbon isoprene, a tar which he called "isoprene tar" was collected from the pyrolysis apparatus. Studies in which Kennaway painted this substance on the backs of mice led him to conclude that the coal tar carcinogen must be a hydrocarbon, since isoprene comprised only carbon and hydrogen, and was probably aromatic (the molecules being composed of closed rings) rather than aliphatic (the molecules being in open chains), like isoprene itself. Reference was made to a figure in Professor Idle's report showing the effect of high temperatures on simple aliphatic molecules to produce complex aromatic compounds. Kennaway then repeated this high temperature pyrolysis under a stream of hydrogen gas with a variety of other organic substrates, including other simple chemicals, one of which was human skin. All of these yielded fractions which he tested for carcinogenicity on mouse skin. Pyrolysis of human skin yielded a tar which was found to be carcinogenic when painted on mouse skin. Kennaway, writing in 1925, was perhaps the first to realise that the temperature at which substances were pyrolysed critically altered the biological properties of the resultant products. He found that products were not carcinogenic if the pyrolysis was at either too low or too high a temperature.
[5.515]One of Kennaway's collaborators was Dr Izrael Hieger who used ultra-violet spectroscopy to shine a beam of ultra-violet light through solutions of hydrocarbons and diffract the resulting fluorescent emissions into spectral bands, recording these on glass photographic plates. Kennaway was able to track down the carcinogenic constituents of his tars because, fortuitously, the carcinogenic fractions had a characteristic fluorescence spectrum. Schroeter in 1920 had shown, in an experiment in which the hydrocarbon tetralin was treated with aluminium chloride, that a fraction was produced, which became eponymous with him. When tested by Kennaway, this was found to be a mouse skin carcinogen. It was also found to produce a strong blue-violet fluorescence with three characteristic bands on the photographic plate, which became known as the "Schroeter bands". The Kennaway laboratory then embarked on a series of experiments that were based on the premise that when a compound displayed a particular pattern of Schroeter bands, that compound would be a mouse skin carcinogen.
[5.516]Together with Hieger, Kennaway screened by ultra-violet spectroscopy the large number of pure polycyclic aromatic hydrocarbons that had been prepared from the distillation of coal tar and from the pyrolysis of organic materials. Having identified the compound with the best match to the Schroeter bands, Kennaway then sought to modify its structure chemically to find an even better match to the Schroeter bands, and this resulted in the de novo chemical synthesis and subsequent testing on mouse skin of a number of compounds. One of these, 1,2,7,8-dibenzanthracene was reported to be carcinogenic to mouse skin and thus became the first synthetic chemical reported to be a carcinogen. Kennaway was also able to identify a large number of polycyclic aromatic hydrocarbons as being non-carcinogenic to mouse skin.
[5.517]The discovery of the first synthetic chemical carcinogen occurred because the researchers had correlated the particular physico-chemical characteristic (the Schroeter bands) of a chemical with carcinogenicity on mouse skin. They still had the problem of finding what it was in coal tar that caused carcinogenicity in the mouse. Kennaway's laboratory continued screening a large number of synthetically produced polycyclic aromatic hydrocarbons. They were able to find that some were carcinogenic, others were mildly carcinogenic and the majority were non-carcinogenic. They started to put together some ideas of how the structure of the compounds might dictate their biological activity, but, at the end of the day, this could not go on forever and they had to stop. Kennaway and his colleagues therefore returned to their original 1924 aim of identifying the carcinogenic agent in coal tar itself. Starting with two tons of coal pitch, they isolated crystals of a highly carcinogenic substance with the exact Schroeter bands which, by comparison with authentic chemically-synthesised material, turned out to be 1,2-benzpyrene (now referred to as benzo[a]pyrene, B[a]P). (Professor Idle explained that benzpyrene existed in two distinct chemical forms, benzo[a]pyrene (known then as 1,2-benzpyrene) and benzo[e]pyrene (known then as 3,4-benzpyrene). Only benzo[a]pyrene was carcinogenic on mouse skin. It was, he said, a point of great confusion that at some point in history the numbering system was changed and 1,2-benzpyrene became 3,4-benzpyrene and vice versa. Thus, today, the carcinogenic benzo[a]pyrene was also known by the trivial name of 3,4-benzpyrene. The biological properties of this chemical, first reported as a constituent of a carcinogenic mixture (coal tar) in 1933, were still being investigated. Benzo[a]pyrene seemed to occupy a special place in the minds of scientists in the field of experimental carcinogenesis. This featured also in research into smoking and lung cancer: reference was made to RCP 1962, in which it was stated, at p.10, para.19, that some sixteen different substances capable of initiating cancer in experimental animals had hitherto been identified in tobacco smoke; among the references were papers relating to the presence of benzpyrene and other polycyclic hyrocarbons in cigarette smoke.
[5.518]Work continued to focus on benzo[a]pyrene in the 1930s and 1940s and a vast number of other polycyclic aromatic hydrocarbons were synthesised in the laboratory. Many of these were tested in Kennaway's laboratory on mouse skin and subsequently in other bioassays, primarily to understand the relationship between chemical structure and carcinogenesis. There was an underlying belief that chemicals that could produce cancer must have some common motifs in their chemical structure: it was not the belief then that chemicals randomly could produce cancer. So they were trying to understand what in the chemical structure might be the determining motif in the carcinogenesis process. The testing of single agents on mouse skin continued until the early 1940s. In the course of these experiments, it was reported that different strains of mice were differentially sensitive to the skin painting protocol. Professor Idle said that when different strains of mice demonstrated different biological properties, it was almost invariably due to genetic differences between the strains. This was, in his view, all part and parcel of evolutionary differences.
[5.519]By the end of 1964, it had been established that chemicals could be carcinogenic to mice and rabbits and thus might cause cancer in humans. The chemical theory of carcinogenesis prompted considerable research and this continued in subsequent years. It had been proposed, in the period prior to 1965, that when a polycyclic aromatic hydrocarbon, such as benzo[a]pyrene, was painted on to mouse skin it was converted to a metabolite that exerted the carcinogenic effect of the benzo[a]pyrene. The role of metabolism in chemical carcinogenesis became the subject of enquiry in the subsequent period. Professor Idle said that it was the subject of a very vigorous debate at that time. Metabolism was the process of modification of the chemical structure of things within the body, both endogenous and exogenous compounds. There were those that proposed that the carcinogenic activity of a substance like benzo[a]pyrene resided in a metabolite produced from it, although this was not a universal view at the time. Boyland was a professor at what was then known as the Chester Beatty Research Institute in London, previously the Laboratory of the Cancer Research Hospital; this was the premier cancer research establishment in the United Kingdom at that time. Boyland, who was a biochemist, developed the idea that polycyclic aromatic hydrocarbons required conversion to an epoxide in order to exert their carcinogenic effects. That view was considered as risible at the time; people really did not believe it at all. Epoxides were reactive metabolites. Reactive metabolites of chemical carcinogens were formed in a reaction between the chemical and the host organism. Reactive metabolites possessed the property of being able to react chemically and spontaneously with other molecules, particularly the macromolecules of the cell, such as proteins, RNA and DNA (deoxyribonucleic acid).
[5.520]Polarisation in the debate was largely between the Chester Beatty Institute and the McArdle Laboratories in Wisconsin, where the view of James and Elizabeth Miller at that time was that polycyclic aromatic hydrocarbons were per se carcinogenic, requiring no metabolism to exert their effects. The McArdle Laboratories were the first cancer research institute in the United States to be built on a university campus and grew into a very formidable and important research institute; it had several Nobel Prizes. Miller and Miller were amongst the first individuals to study chemical carcinogenesis and were very highly regarded scientists. Conney was a PhD student studying with the Millers at the time of a report in 1957. Working with rats, he reported that if they were pre-treated with benzo[a]pyrene, their livers were mashed and a fraction was made from them that contained an enzyme which he called "benzpyrene hydroxylase", the benzpyrene hydroxylase activity of animals so treated was much higher than in untreated animals, and he deduced that benzo[a]pyrene could induce the metabolism of itself and other related chemicals. By the end of 1964, the role of metabolism in carcinogenesis had become an active area of research.
[5.521]Professor Idle went on to discuss the debate that took place between proponents of the "protein loss theory of carcinogenesis" at the McArdle Memorial Laboratory and the "DNA theory" of carcinogenesis at the Chester Beatty Research Institute. The protein loss theory was based upon an observation in bacteria that the gene which coded for an enzyme known as lactate dehydrogenase (which converted lactate acid to pyruvic acid), was regulated by a protein in the cell. A relationship was discovered between the cell and the DNA: as described by Professor Idle, there were "on/off switches" that were regulated by proteins. At the McArdle Laboratory the theory was that, if there was a key protein that regulated something in the genetic regulatory apparatus of the cell and a chemical damaged the protein in some way, then that altered the way in which the whole cell apparatus was regulated, hence the protein loss hypothesis of carcinogenesis. The DNA theory was somewhat similar, except that it omitted the protein intermediary. Under this theory, there would be an effect of the chemical directly at the genetic level on the gene, disrupting the information process and causing the cell not to operate properly and perhaps go too fast or get out of control. At that time this theory was rudimentary. There was considerable tension between the two theories that lasted up to the end of 1964, and beyond.
[5.522]In Boyland 1952 the author, working at the Chester Beatty Research Institute, advanced the theory that carcinogens interacted with nucleic acids. At p.81 he stated:
"Although some carcinogenic compounds may produce their specific effects by enzyme inhibition, the hypothesis that the results are due to the more direct action on chromosome nucleic acid seems more likely in some cases. Because the carcinogens produce specific damage to chromosomes and chromosomes contain desoxyribosenucleic acid, it is tempting to assume that the carcinogens act by producing abnormalities in the nucleoprotein."
Researchers at the McArdle Memorial Laboratory continued to insist that carcinogenesis did not result from an interaction of carcinogens with DNA, but rather with proteins. Aware of this debate, Brookes and Lawley, from the Chester Beatty Research Institute, published evidence in 1964 that polycyclic aromatic hydrocarbons bound to DNA in mouse skin and suggested that non-carcinogenic polycyclic aromatic hydrocarbons did not bind, whilst carcinogenic ones did. Thus the two phenomena, binding to DNA and carcinogenesis, were reported to be related. They also suggested that the polycyclic aromatic hydrocarbons must first undergo metabolism to enable this binding. They concluded, however, that the results obtained in their work at that time did not give a conclusive indication of the nature of the significant cellular receptors of chemical carcinogens. Professor Idle commented that this dispute, between two of the foremost cancer research institutes in the world, indicated that there was no consensus amongst cancer researchers about the cellular target of chemical carcinogens.
[5.523]In the same period, Nordling published in 1953 what he called a new theory on the cancer-inducing mechanism, that cancer arose in cells by mutation. A mutation is a permanent change in the genetic information in the DNA of a cell, which may be passed on to progeny cells. Nordling proposed a multi-step process in carcinogenesis involving serial mutations. Burdette, writing in 1955, in an extensive review of the role of mutations in carcinogenesis, concluded that evidence for the existence of cancer susceptibility genes was compelling and extensive. He proposed that there was no justification for a general correlation between mutagenesis and carcinogenesis. Whereas Nordling had seen carcinogenesis as depending upon mutagenesis, Burdette concluded that a carcinoma could arise without the intervention of changes in the DNA sequence. He also tended to dismiss somatic mutation, a permanent mutation that occurred in a cell that could be passed on to progeny. Brues, in agreement with Nordling, dismissed the idea of a single mutation leading to cancer, and stated that there was a threshold below which neither chemicals nor radiation caused cancer. The single discovery that most radically altered the understanding of how living systems worked was the description of the structure and function of the DNA double helix by Watson and Crick in 1953. This showed the molecular structure of DNA and its genetic implications, and was a breakthrough which was to have a profound and long-term effect upon cancer research.
[5.524]As at the end of 1964, there was an unresolved debate between the "DNA" and the "protein" proponents. There was also an ongoing discussion in the scientific literature of the role that might, or might not, be played by genetic mutation in cancer.
[5.525]Turning to the topic of chemical structure and metabolism during the period from 1965 to 1971, Professor Idle said that considerable progress was to be made in this period in answering the questions concerning the chemical structure of carcinogens in relation to their biological properties and, in particular, whether or not a carcinogen was active per se, or required conversion to some reactive intermediate by the host's own endogenous metabolic processes. Miller and Miller, writing in 1965, noted that their present knowledge of the metabolism of chemical carcinogens, like that of their structures, was of no great predictive value in evaluating the possible carcinogenic hazards of a new chemical structure. They had not been able to understand how the structure of a particular polycyclic aromatic hydrocarbon might predict the biological outcome. Then they had gone on to look at some of the metabolites of polycyclic aromatic hydrocarbons and they still were unable to predict the outcome. They also were of the view that the polycyclic aromatic hydrocarbons were carcinogenic per se and did not require metabolic activation, but that the nitrosamines did require the intervention of host metabolism to generate carcinogenic molecules. Nitrosamines, Professor Idle said, were a ubiquitous group of chemicals that were formed very readily from substances known as "secondary amines" and their reaction with either the oxides of nitrogen in the atmosphere or nitrate and nitrite, which were two inorganic ions.
[5.526]Meanwhile, a contrary idea had developed that the polycyclic aromatic hydrocarbons did require metabolic activation and that this probably occurred in the form of metabolites known as epoxides. This had originally been suggested in Boyland 1950, but there was no experimental evidence for such an effect. The Millers had tested polycyclic aromatic hydrocarbons and found that they were no more nor less carcinogenic than some of the synthetic epoxides that had been made. Other scientists now entered the arena who made theoretical calculations and synthesised other chemicals. They carried out additional experiments which led further towards the idea that epoxides required to be made to render these molecules carcinogenic. Pullman and Pullman, working in Paris, identified part of the polycyclic structure as the motif which caused cancer, and coined the expression "K region epoxides". Miller and Miller tested a number of K region epoxides on mouse skin and found them to be non-carcinogenic, thus reinforcing their earlier view that polycyclic aromatic hydrocarbons were carcinogenic per se. Other researchers tested other K region epoxides and found them to have very low carcinogenicity or to be only weakly carcinogenic.
[5.527]Professor Idle said that despite these results Dipple and colleagues in 1968 offered the important and insightful conclusion that the distinction between carcinogens and non-carcinogens would most likely be a consequence of the chemical structure of the reactive intermediate rather than of the structure of the parent compound. They produced experimental data from the testing of a series of polycyclic aromatic hydrocarbons to support this contention. In the same year Miller and Miller modified their earlier view regarding the metabolism of polycyclic aromatic hydrocarbons, stating that an examination of the literature suggested strongly that most, if not all, chemical carcinogens either were, or were converted in vivo to, reactive electrophilic derivatives which combined with nucleophilic groups in crucial tissue components, such as nucleic acids and proteins. A chemical entity was said to be "nucleophilic" when it attacked other molecules through the parts of their chemical structures which were low in electron density. Nucleophiles, in general, had areas of their molecules which were abundant in electrons. In turn, nucleophiles were attacked by electrophiles, which is what Miller and Miller believed all chemical carcinogens to be. Thus the Millers now agreed with Boyland 1950 that the polycyclic aromatic hydrocarbons required to be metabolised before they became carcinogenic.
[5.528]The epoxide metabolites proposed by Boyland 1950 for polycyclic aromatic hydrocarbons were electrophiles, but the existence of epoxides as biological metabolites was merely theoretical until a report in 1968 that their occurrence had been observed for the first time. It was reported in 1969 that benzo[a]pyrene required metabolism by enzymes known as microsomal hydroxylases before binding to DNA, and in 1970 evidence was provided that the K region epoxides were probably the metabolites that bound to DNA and protein. In 1971 it was reported that an epoxide was formed when another polycyclic aromatic hydrocarbon underwent metabolism, and there was a further report that several K region epoxides of polycyclic aromatic hydrocarbons were able to transform rodent cells in culture to a malignant phenotype, and that epoxides were indeed the metabolites of polycyclic aromatic hydrocarbons. Magee and Barnes, writing in 1967, stated that nitrosamines were mutagenic by virtue of their metabolism by an unknown process by host enzymes. Professor Idle said that it was unusual to find exactly the same enzyme in two different species, such as a rat and a mouse, so the process of metabolism of any compound by enzymes was likely to vary from species to species, though it would not be known whether this was so until experiments were carried out.
[5.529]At this time, another important discovery was made by Nebert and Gelboin at the NCI. They discovered that different mouse strains responded to the induction response in different ways. If an animal was pre-treated with a polycyclic aromatic hydrocarbon like benzo[a]pyrene, the enzyme that metabolised this and related compounds reached a higher level in the tissues of the animal. Nebert and Gelboin found that there were strains of mice that were poorly induced by polycyclics and strains that were readily induced by them; they bred these animals and showed that this was a genetic characteristic and varied from strain to strain, due to a gene. The question that then emerged was whether or not there existed in the human population a similar genetic variation in the induction of polycyclic aromatic hydrocarbon metabolism. This question was to be addressed in the next time period and still occupied researchers today. Professor Idle said that there was little doubt that homo sapiens was the most variant of all the mammalian species, with tremendous variation in most biological processes. These were covered, unseen variations in metabolic pathways. This had been learnt through the field of pharmacogenetics. There were tremendous intersubject and interethnic variations in metabolic processes in the human species. Metabolic processes might vary between the genders: many enzymes were regulated by hormones, including sex hormones, so there might be a process which was at a very high level in females and at a very low level in males.
[5.530]Taken together, he said, all these observations pointed to a role for endogenous metabolic activation in the carcinogenicity and mutagenicity of two classes of chemical carcinogens, polycyclic aromatic hydrocarbons and nitrosamines. It appeared that the structure of the metabolite, rather than the original chemical, was what determined its carcinogenicity. For example, in the case of benzo[a]pyrene, it was not the benzo[a]pyrene molecule itself which was carcinogenic, but rather the product or products of its metabolism within the tissues that were. Having considered, until this time, that metabolism was a process that removed toxic foreign molecules from the body, scientists were now faced with a paradigm shift, whereby metabolism could contribute materially to the carcinogenic process. Professor Idle thought that this did not surprise people working in the field of drug metabolism as much as it did people in other branches of medicine who were not familiar with this field.
[5.531]By the end of 1971, it was known that some but not all carcinogens needed to be metabolised to exert their carcinogenic effects. The occurrence of genetic factors that might control this metabolism was beginning to be explored. This exploration continued throughout the subsequent period.
[5.532]A continuing question during the period from 1965 to 1971 concerned the molecular mechanism of attack of a chemical carcinogen or its reactive metabolite on cellular constituents: did the carcinogen strike at protein molecules or DNA molecules? Miller and Miller stated in 1965 that the cellular and molecular mechanisms were not known for any carcinogen and, while there had been reports of interactions with DNA and RNA (the molecules of cell information transfer) there were really no correlations with carcinogenesis. Pitot and Heidelberger had advanced in 1963 a novel theory involving protein-carcinogen interactions. Brookes, writing in 1966, cast some doubts on this "protein-deletion theory", but stated that in the past when several rival theories had each received strong support, the truth had ultimately been shown to embrace all points of view, and asked whether it was possible that this might be so for the obviously complex process of carcinogenesis. Horsfall came out in favour of the DNA theory in 1966. Prehn, writing in 1964, used his "clonal selection hypothesis" to support the protein-deletion theory. Professor Idle said that this was unlike any other theory of cancer that had gone before. Prehn stated that, within a population of normal cells, there were some that were already programmed and destined to become cancer cells. He saw chemicals as killing off the least fit cells, in a Darwinian sense, and that the fittest, pre-programmed cells would then be selected for and grow into malignant clones. He distinguished between an instructional process, where an outside signal instructed a cell to become a tumour cell, and a non-instructional one, where the cell was simply selected for. In 1967 Goshman and Heidelberger said that the question whether DNA, RNA or protein was the primary cellular receptor of chemical carcinogens remained unanswered; it was evidence that, although binding of carcinogens to DNA might be necessary for carcinogenesis, the appearance of tumours depended upon a series of cellular events which had not yet been elucidated.
[5.533]By this stage, Professor Idle said, the debate about the activation of carcinogens had been settled. The DNA/protein target debate was still continuing and evolving, and he thought that in many ways it converged during this period. In 1969 Brookes and Heidelberger generated further experimental evidence for the interaction between polycyclic aromatic hydrocarbons and DNA, but were unable to characterise the interaction. Miller wrote in 1970 that neither the DNA nor the protein-deletion hypothesis, nor any other hypothesis, had yet received unequivocal experimental support in any incidence with any carcinogenic agent. Professor Idle said that this was consistent with his reading of the literature of that period. In the context of the search for the cause of causes of lung cancer, it was clear to him at least that scientists were struggling to define and agree upon a mechanism by which cancer, as a phenomenon, could occur. There was little attention to individual cancers such as lung cancer. The big question was what cancer was and how it occurred. This was the time when he entered into the drug metabolism field and he remembered these issues. In 1971 Huberman and colleagues provided in vitro evidence for DNA as the molecular target for chemical carcinogens. They concluded that there was a good correlation between chemical reactivity, mutagenicity, and binding to DNA in the test tube and in cells. Their work established a better correlation between metabolic activation of hydrocarbons and mutagenic activity than was previously reported, but did not establish a critical association between the processes of mutagenesis and carcinogenesis. Professor Idle said that this was an accurate reflection of the state of the art as at 1971. In relation to nitrosamines, Magee and Barnes discussed in 1967 the competing DNA and protein-deletion hypotheses. They favoured the former because of the proven interactions between nitrosamines and the DNA molecule, but were forced to conclude that there was no experimental proof that reaction with these macromolecules rather than other cellular components was related to carcinogenesis. Other researchers in 1968 attributed tumorigenesis to enzyme inhibition; Professor Idle described this as a novel theory unrelated to the aforementioned principal theories of chemical carcinogenesis, but without support from other investigators.
[5.534]He said that by the end of 1971, there still existed a lively debate as to whether the critical site of action in the cell was protein or DNA or something else. At a cellular or molecular level, the mechanism of action of chemical carcinogens remained unknown. The period from 1972 to date had seen the coalescence of a number of diverse threads of evidence into the current paradigm of chemical carcinogenesis. Nowak and colleagues, writing in 2002, said that the concept that tumours developed through the accumulation of genetic alternations of oncogenes and tumour suppressor genes was now widely accepted as a fundamental principle of cancer biology. Professor Idle explained that tumour suppressor genes were originally called "anti-oncogenes", because they appeared to serve the opposite purpose to that of oncogenes. They were also involved in the housekeeping functions that regulated how cells grew and divided and sometimes how they died, but they provided a "hub", through which a whole series of pathways was triggered. Where a tumour suppressor gene was removed from the circuit, then a number of different processes failed: DNA repair, repair of modifications to DNA, the ability of the cell to enter into the process known as apoptosis and various other integral processes concerning the well-being of the cell. Apoptosis was one of the great discoveries of the last two or three decades. Cells were always thought to die by damage from the outside, undergoing a certain transformation during death that could be seen under the microscope, a process called necrosis. It was then observed that cells died, not just by necrosis, but by what was now called apoptosis. A signal was sent from the nucleus of the cell, usually to itself but also to other cells, saying that it was time to die. The cell shrank and a dissolution took place, enabling its materials to be used by other cells. Interference with either an oncogene or a tumour suppressor gene affected the division, differentiation and death of a cell.
[5.535]DNA repair was possibly the most important housekeeping function of any cell, because damage occurred to DNA all the time. The simple use of oxygen for respiration by all organisms created very reactive intermediates which damaged DNA. DNA itself was an unstable molecule: it could hydrolyse, reacting with water to break some of its bonds. So DNA became modified in the normal everyday process of all life, and these modifications had to be repaired. If they were not, then the gene contained erroneous information that could be passed on to another generation in the case of a bacterium, for example, or that could alter the functioning of the liver cells of a human. There were 130 discrete DNA repair enzymes that had been described in humans. Each of them repaired a different type of modification of the DNA structure, and some of them backed up the effects of others. There were tens of thousands of modifications to DNA in every single cell of the human body every day. These had to be repaired if the cell was to function normally and throughout a normal life span of an animal or an individual. There were tens of thousands of DNA repair events every day in a mammalian cell. The processes of misuse of oxygen molecules, known as "oxidative stress", and of hydrolysis gave rise to at least 60,000 discrete events requiring a similar number of repair events per cell per day.
[5.536]Professor Idle said he thought that the view of Nowak and colleagues was partly correct. What the evidence showed clearly was that tumour suppressor genes and oncogenes became modified through genetic alteration, leading to an increased speed of division of cells and certain other characteristics. He did not agree that it was a fundamental principle of cancer biology, if the authors meant that this led to cancer. It certainly was part of some of the early transformations that might occur on a pathway that might or might not lead to cancer, bearing in mind that cells had the ability to kill themselves off by apoptosis and the immune system could also remove them. Other factors had been recognised as relevant in carcinogenesis. Professor Idle thought that viruses clearly could play a part. Radiation was sometimes described as the classical carcinogen, by damaging DNA randomly. Oxidative stress and many other factors had been identified.
[5.537]Professor Idle said that the tumour suppressor gene which was of the greatest interest and which had been the most extensively studied over the past twenty years was p53 (the protein coded for by this gene having a molecular weight of 53,000). The p53 gene served as a hub to contribute to the control of apoptosis, DNA repair, the cell cycle and differentiation pathways: many of the housekeeping and important functions of a cell. Robles and colleagues, writing in 2002, stated that since the discovery of this gene an overwhelming volume of literature had accumulated supporting its role as a central regulatory node in the protein network that mediated cellular responses to endogenous and exogenous stresses. Disabling this pathway through mutation or silencing of its components led to self transformation and was thought to contribute to tumorigenesis.
[5.538]Professor Idle said that the assorted elements of the chemical theory carcinogenesis as it involved oncogenes and tumour suppressor genes could be itemised as follows: (i) certain chemical carcinogens entered into cells and participated in metabolic processes carried out by the enzymes within the tissues that converted them into chemically reactive metabolites; (ii) chemically reactive metabolites remained in the tissues chemically bonded to DNA, in a process known as "covalent binding", and survived the processes of DNA repair, becoming "persistent DNA adducts" that were considered to be detrimental to the processes of transcription and replication within the cell; (iii) persistent DNA adducts were then seen to cause DNA mutations; and (iv) if these mutations happened to occur by chance in oncogenes or tumour suppressor genes, these led to perturbations of cell function and ultimately to cancer. Overall, he said, these jigsaw pieces were seen as forming a picture of chemical carcinogenesis. Whilst some of the component pieces of the current paradigm were uncontroversial, others might or might not turn out to be valid. There were points of the theory that were worthy of careful consideration.
[5.539]First, it was generally accepted that certain chemicals could be converted by the tissues into both inactive water-soluble metabolites, in a process known as "detoxication", and short-lived chemically reactive metabolites, in a process known as "activation". Some of the reactive metabolites of polycyclic aromatic hydrocarbons had half lives of a second or so, so that the longest lived ones probably had lives of the order of one minute. What often distinguished a toxic from a non-toxic compound was the balance between detoxication and activation. Most, but by no means all, chemical carcinogens formed reactive metabolites that themselves were often further metabolised to relative inert and excretable metabolites. Boyland 1950 first proposed that the chemically inert benzo[a]pyrene was metabolised, within the mouse skin upon which it had been painted, to a more chemically reactive epoxide derivative. The metabolic activation of chemicals was currently accepted as the first step in chemical carcinogenesis and there existed ample evidence that it occurred. This evidence was found from the administration of chemicals either to living animals or to cells derived from living animals and sometimes from humans in vitro.
[5.540]Secondly, it was also generally accepted that reactive metabolites of chemicals could bind to nuclear DNA. The current paradigm focused on this, in contradistinction to the "protein loss" theory. However, these reactive metabolites also bound to other cellular macromolecules, including proteins, RNA, and mitochondrial DNA. Mitochondria were organelles that occurred in almost all cells and which generated almost all the energy in a cell. They were small discrete cellular structures responsible for energy production and cellular respiration. The mitochondrial DNA differed from nuclear DNA in that all of it was used to code for RNA molecules that were used in the making of proteins, whereas in nuclear DNA about 90% was not currently thought to have any function. Thus, any disruption or mutation of mitochondrial DNA sequences would be likely to have effects upon the physiology of the cell. In addition, nuclear DNA had multiple processes by which damage could be repaired, whereas mitochondrial DNA had a limited repair system. It has been reported that polycyclic aromatic hydrocarbons, among other substances, bound to mitochondrial DNA very much more avidly than to nuclear DNA in experimental animals. Professor Idle said that the current paradigm of chemical carcinogenesis did not take account of the binding of chemically-reactive carcinogen metabolites to mitochondrial DNA. It was highly focused on nuclear DNA and particular on oncogenes and tumour suppressor genes and very surprisingly had failed to focus on the interesting observations with mitochondrial DNA, given its special characteristics and that while there might only be handful of genes in each of the mitochondria, there were often many thousands of mitochondria per cell, so the amount of DNA present in a cell in the mitochondria was quite considerable and in addition it was not repaired when there were modifications to the sequence. So in his opinion this was a major oversight.
[5.541]Thirdly, the formation of persistent DNA adducts could result in the death of the cell. Fourthly, almost all insights into the relationship between adduct formation and mutagenesis derived from studies using bacteria, rather than investigations in mammals. Fifthly, the finding of mutations in the proto-oncogenes and the tumour suppressor genes had generated particular interest in recent years. The obvious interpretation of this observation was that the upsetting of the role of these housekeeping genes could lead to carcinogenesis. The current theory of chemical carcinogenesis was built upon the mutation and activation of proto-oncogenes and the mutation and inactivation of tumour suppressor genes. The tumour suppressor gene of greatest current interest was p53, which Lane, one of its co-discoverers, has named "the guardian of the genome". The observed response of p53 to cellular imbalance had been to switch on DNA repair, and when repair has been incomplete and had not solved the problem, it then told the cell to die by apoptosis. Thus, the effect of mutated and thus activated oncogenes would be neutralised by the switching on of the p53 gene, the resulting synthesis of the p53 protein and the subsequent benefits to the cell. If, however, p53 was also mutated, then what has been called "the oncogenic stress pathway" was seen as running unchecked, with the consequence of unregulated cell growth ultimately leading to cancer. The aforementioned chain of events, involving the mutation and activation of oncogenes and the mutation and inactivation of tumour suppressor genes, had so far been established only in colorectal cancer.
[5.542]Under reference to a figure in his report, Professor Idle said that it had been reported that the p53 gene contained mutations in most types of human cancer, ranging from a frequency of between 13% and 14% in prostate carcinoma, up to more than 70% in small cell lung cancer. The frequency in non-small cell lung cancer, which included mainly adenocarcinoma and squamous cell lung cancer, with a frequency of about 40%, placed this group in the middle of the range, so it was no different from other tumours essentially. Professor Idle said that it was noteworthy that, while 40% of non-small cell lung cancer tumours were reported to have had p53 mutations, 60% did not. The data were drawn from an international database held in France and associated with IARC; they came from a relatively small sample of the population. The observation that certain proto-oncogenes and tumour suppressor genes were mutated in various human tumours had become a major focus of the current paradigm of chemical carcinogenesis.
[5.543]Sixthly, activated ras oncogenes were thought to occur on average in about 30% of human cancers, most notably pancreatic and colon carcinomas. Proto-oncogenes were always counterparts of viral genes, ras was the cellular counterpart in mammalian cells for a virus known as the rat sarcoma virus. Even in experimental animals where tumours had been induced by the administration of large doses of carcinogens, a mutated and thus activated ras and a mutated and thus inactivated p53 were usually not found together, never mind in the same cell. This was inconsistent with this plank of the current paradigm that dictated that these mutations should occur together in the same cell. Some workers had commented that pathways independent of ras activation and p53 inactivation were involved in the experimental tumours they had produced. These findings had led researchers to propose that not just any kind of p53 mutation is associated with cancer formation; rather, mutations in certain regions of the gene were required.
[5.544]Genes contained the information necessary for coding for a protein that had some cellular function, whether it be architectural or metabolic. They were always thousands of bases long and were divided into exons, units that coded for part of the protein, separated by usually larger regions of introns, which were thought to be just "garbage" in biochemical terms, nonsense information. So a gene was a very long piece of DNA with some useful and some non-useful sequences in it. Mutations could occur anywhere at any single base along the many thousands of bases in a line, and researchers had proposed that mutations in certain positions on that gene were the key thing, not just mutations anywhere within the gene. Genetics was a very new subject and was moving very rapidly. New genes had been discovered to be hidden inside what was thought to be "garbage", and there were still many secrets to be discovered. Over 90% of human DNA had a function that could not be ascribed to anything, and in the case of only a small fraction of the 30,000 genes that had emerged in the human genome project was their function known.
[5.545]It might be seen therefore, Professor Idle said, that not all of the four consecutive elements of the current model of chemical carcinogenesis had been demonstrated to occur for human cancers, including lung cancer. The first element, that chemicals were activated through metabolism, had been the best studied and was generally accepted. The second element, the formation of persistent DNA adducts, had certainly been well-studied in experimental animals and adducts had been detected in various human tissues. That this might follow from the first element was uncontroversial. However, the third element, which required that a particular DNA adduct led to a specific DNA mutation, had not been demonstrated in relation to any human cancer, most of the experiments having been performed in bacteria. Finally, the fourth element of the current paradigm, that mutations in certain proto-oncogenes and tumour suppressor genes, as they were found in some human cancers, were the cause of these cancers, had also not been demonstrated. The only exception to this statement was the understanding of the serial genetic steps that led to certain forms of human colorectal carcinoma. Mutations in oncogene and tumour suppressor genes might explain how cells could be stimulated by chemicals to grow faster, but that did not explain the features of invasion and metastasis. In Professor Idle's opinion, the pathways that led to cancer required considerably more research before a robust paradigm could emerge.
[5.546]Professor Idle then turned to the radiation theory. Muller was awarded the Nobel Prize in 1946 for his discovery that x-rays could cause inheritable genetic damage in fruit flies. Gates and Warren, writing in 1961, commented that "epidermoid carcinoma" (squamous cell carcinoma) of the lung had been produced in rats and mice, using alpha-radiation, beta-radiation and gamma-radiation emitting radioisotopes, as early as 1938. They concluded that the increase in the particulate and gaseous radioactivity in the atmosphere in the previous decade, and the expanding industrial uses of artificial radioisotopes, had made it desirable to define more explicitly the potential dangers of these new additions to the environment. Professor Idle said that by the end of 1964 there existed concern that environmental radiation might be a cause of human cancer, including lung cancer.
[5.547]In the period from 1965 to 1971, the question was being asked whether or not x-rays and other types of radiation could, by breaking chemical bonds, generate cancer. There was an understanding of the amount of energy required to break different kinds of chemical bond. Ionising radiation, for example gamma-radiation or x-rays, possessed enough energy to break chemical bonds in the irradiated material, in contrast to visible or infra-red radiation, which were of lower energy. In 1966 De Villiers and Gross reported success in producing squamous cell carcinoma of the lung in hamsters using x-rays. They stated that under these circumstances, the reproducible initiation of squamous cell carcinomas by external radiation, a total incidence of 12% among deaths occurring within twenty post-irradiation weeks, in the lungs of hamsters, was unique and highly significant. Professor Idle said that these were among the first observations of researchers producing squamous cell carcinoma in animals with radiation. He was almost certain that what was occurring was that in the period from the 1930s until the 1960s, radiation was a topic of public concern. It was then a new science, and the ability to work with radioisotopes in the laboratory was new. Then it was radiation, today it was genetics. Trends came and went, and he thought activity in this area had died out to some extent and had been replaced by other activities.
[5.548]The next theory discussed by Professor Idle was that of personality, emotion and stress. He said that this might be the most long-lived of the all the theories. There was still an interest today in the role of the mind in medicine: psychosomatic medicine was an important area of activity and very important in cancer treatment. All the oncologists he knew had always said to him that people's belief that they would recover and survive was an important component. The idea had originated with the Ancient Greeks. Among more recent writers, Sir James Paget, the famous surgical pathologist, wrote in 1870 that it could hardly be doubted that mental depression was a weighty addition to the other influences that favoured the development of the cancerous constitution. The first laboratory investigations of stress were by Selye who, in 1936, described experiments in which rats, when suddenly confronted with a critical situation, developed a stereotyped syndrome characterised by enlargement and hyperactivity of the adrenal glands, atrophy of the thymus gland, lymph nodes, spleen and liver, and the appearance of gastrointestinal ulcers. Critical situations that could precipitate this syndrome were cold, infection, trauma, excessive muscular exercise, and intoxications with sub-lethal doses of drugs and chemicals. He termed this syndrome the "general alarm reaction"; in 1956 he referred to this response to stress as the "general adaptation syndrome". An example of a similar process in humans, Professor Idle said, was the general recognition that gastric ulcers could be caused by stressors. Selye was the President of the International Institute of Stress until his death in 1982 and became the leading figure researching the effects of stress on the endocrine and immune systems and its predisposition to disease. LeShan, writing in 1959, was one of the first to point to personal loss as a cause of cancer in humans, when he wrote that the most consistently reported, relevant psychological factor had been the loss of a major emotional relationship prior to the first-noted symptoms of the neoplasm.
[5.549]In the early 1960s Dr David Kissen in Glasgow began a detailed clinical psychological study of individuals diagnosed with lung cancer, which he reported in Kissen 1963a and Kissen 1963b. Professor Idle said that he himself was neither a psychologist nor a psychiatrist, and his knowledge was a general one and came from the reading of Kissen's papers and other papers in this field, but what he took from Kissen's papers were the conclusions that lung cancer patients had a lower rate of "childhood behaviour disorders", a finding "in keeping with the hypothesis that lung-cancer patients have a diminished outlet for emotional discharge", and that statistically significantly more lung cancer patients than controls stated that they tended to repress emotional problems.
[5.550]Professor Idle said that in the period prior to 1965, there had been a long historical interest in psychological factors as they might predispose to cancer. As Sir William Osler said in 1906, it was much more important to know what sort of a patient had a disease, than what sort of disease the patient had. Before 1965, studies had commenced on psychological factors in both childhood and adulthood that might lead to lung cancer. These psychological and emotional factors became the foundation in the next time period for the discussion of the role of stress in cancer causation. Green reported in 1996 a study of patients newly diagnosed with leukaemia or lymphoma and concluded that to the extent that psychological factors might prove to be relevant to the pathogenesis of leukaemias and lymphomas, it was a matter of the individual's running out of psychological resources. Kissen continued his studies in Glasgow until his death in 1968, by which time he was recognised by his peers as the leading authority on psychosomatic factors leading to lung cancer. In a study reported in 1967 of male lung cancer patients and non-cancer control patients he found that the lung cancer patients reported significantly more adverse life situations, such as the death of a parent, an unhappy home (mainly due to drunkenness), and a higher incidence of problems with interpersonal relationships, work upsets, financial difficulties, sexual difficulties and a miscellaneous group of adverse life situations that included trouble with the police and a police record. He concluded that long-standing adult difficulties of more than ten years' duration appeared to have a greater influence on the genesis of lung cancer than those of shorter duration.
[5.551]In Kissen and Rao 1969, Kissen's previous work was summarised. It was stated that lung cancer patients had diminished outlets for emotional discharge compared with non-cancer patients. Among the empirical evidence supporting this was the finding that lung cancer patients had a lower mean score on the neuroticism scale of the Short Maudsley Personality Inventory than did non-cancer patients. This was taken to indicate a lesser ability to discharge emotion and was independent of smoking habits. Significant differences between the same lung cancer patients and the controls were later found in the reported incidence of certain environmental and social factors such as adverse events in childhood and adulthood. In this paper, the results of an investigation of certain markers of the endocrine system in lung cancer patients were reported. As described by Professor Idle, they were interested in having objective measurements of stress. One such measurement would be the activity of the adrenal cortex to produce and release a hormone, cortisol, the metabolites of which could be measured in the urine of patients. The authors said that the endocrine system was the obvious choice since it was well known that it was influenced by emotional factors through the hypothalamus, the hypophysis (the pituitary gland) and the autonomic nervous system. The authors predicted that the patterns of urinary steroids would fluctuate in response to the stress experienced by patients during the first days of admission to hospital. They reported that the urinary steroid levels showed markedly different patterns in a group of lung cancer patients compared with a group of controls and they stated, at p.476:
"The results of the present study showed that lung-cancer patients have some abnormalities in adrenal function, compared with control patients, and these abnormalities are related to certain psychological measures that are characteristic of lung-cancer patients."
The authors recognised, however, that urinary steroid levels in lung cancer patients could have been a result of the disease.
[5.552]Rao refined this work, and in 1970 reported on the ratio of two corticosteroid metabolites in the urine, which was approximately half the value in a group of inoperable lung cancer patients compared with groups of healthy controls and hospital controls. The ratio was also reported to be unchanged two weeks after resection of the lung cancer for lung cancer patients undergoing surgery, suggesting that the presence of the tumour was not the cause of the abnormal ratio. This assertion was further confirmed by Rao in 1971, with the additional interpretation of the data that steroid excretion after removal of tumours would include the response to the physical and emotional stress after surgery. Rao's work therefore suggested that lung cancer patients had an altered endocrine system response to both hospitalisation and, when resection was possible, to the surgery itself.
[5.553]Professor Idle said that the overall work of Kissen and Rao during that period showed that both childhood-acquired and adult-acquired psychological factors modified the emotional structure of certain individuals in such a way as to leave them with a poor outlet for emotional discharge, which might be related to the role of corticosteroids, whose release by the adrenal glands was normally associated with stress. The link with lung cancer might be through the immune system, which was impaired after corticosteroid release. Research of this nature continued into the next time period.
[5.554]In the period from 1965 to the end of 1971, therefore, clinical psychologists had taken an increased interest in aspects of an individual's personality and emotional make-up that might be linked to cancer development. One theme that was beginning to emerge, and was developed thereafter, was that internally generated "stress" might lead to perturbations of immune function and consequent cancer.
[5.555]In addition to a continuing effort by psychologists in the period from 1972 onwards to discover and define the personality and emotional factors that might lead to cancer, there started to emerge a large body of work on the relationship between neurological and immunological functioning. A particular focus of this work was to understand the mechanisms by which internal and external stresses might modify immune function and thus lead to cancer. Pointing to the problem of the ignorance of different scientific and medical disciplines of each others' work, Holden wrote in 1978 that potential research had been greatly impeded by the lack of communication between, for example, biochemists and psychologists. There were independent reports in 1979 of findings in humans that pointed to a relationship between stress and the immune system, in relation to cancer causation. Psychologists also began to turn to animal models of stress to investigate these relationships.
[5.556]Professor Idle explained that the immune system provided a very important defence against external and internal foreign agents, not only viruses and bacteria and so on, but also newly developing cancer cells. These could be destroyed by an antibody produced by an immune cell, if the body recognised the cancer cell as foreign, as it sometimes did, or by cytotoxic T cells and natural killer (NK) cells. Visintainer and colleagues described in 1982 the effects of electric foot shock, comparing rats that were able to avoid the shock with rats that were not, on the rejection of transplanted tumour cells: the latter were only half as likely to reject the tumour and twice as likely to die as rats receiving escapable shock or no shock. The authors offered a mechanistic explanation that when an animal was exposed to a stressor, the arousal released adrenocorticotrophic hormone and adrenocortical activation occurred, which in turn caused immunosuppression. The more aroused the animal, the greater the immunosuppression. Subjects receiving inescapable stress might experience greater arousal, as indicated by emotional responses and physiological changes, than subjects receiving escapable stress.
[5.557]Glaser and colleagues reported in 1986 that stress, in the form of examinations in medical students, depressed the amount of interferons produced by white blood cells and also decreased the activity of NK cells, both by a large margin. In their earlier work they suggested that stress might contribute directly to carcinogenesis by impairing DNA repair processes. They concluded that longer-term stress-related alterations in cellular immunity might carry an increased risk for immunodeficiency disorders and malignant and infectious disease. A study in 1989 stated that NK cell activity was significantly reduced in a group of depressed patients, melancholic subtype, compared to sex- and age-matched controls. Another study, in 1990, stated that both major depressive disorder and the presence of threatening life events in control subjects were independently associated with a 50% reduction of NK cytotoxicity. A decrease in natural cytotoxicity was significantly associated with depressive symptoms but not with age, alcohol consumption, or tobacco smoking. Rosch, writing in 1995, said that many brain transmitters that could influence malignant growth also participated in the humoral response to stress, including melatonin, serotonin, dopamine, and the endorphins, and that lower immune defences clearly predisposed to the development of malignancy. Professor Idle explained that the humoral response meant that where stress was experienced a number of different substances were released which passed round the body from one place to another, including the hormones mentioned above, and local hormones. Most recently, Fortes and colleagues reported in 2003 on a study of depression in residents of a home for the elderly over a period of four years. They determined the numbers of various immune cell types in the blood of the subjects, who had also been evaluated on a depression rating scale, and reported that the results suggested an adverse effect of depressive symptoms on immune response. They suggested that immune cell killing of target cells might be impaired, placing these individuals at risk of various diseases.
[5.558]Professor Idle concluded by stating that there was now a burgeoning body of work that had linked personality, emotional problems and stress to the occurrence of cancer and, moreover, it was believed that these factors operated through the immune system. One of the many proposed mechanisms was that cancer might arise when personality, emotion and stress influenced the immune system by reducing number and function of NK cells, together with the neuromodulators, such as interferons, that regulated their activity.
[5.559]Professor Idle next turned to endogenous factors and the theories relating to them. He said that during the period up to 1965, the question arose as to whether cancer was caused by something inside, rather than outside, the body. In 1933, Cook first proposed that aberrant metabolism of an endogenous steroid might explain spontaneous tumours in animals. Cook and his group had previously heated an endogenous steroid known as deoxycholic acid under pyrolysis conditions. He wondered whether the body could carry out some metabolic reactions that would generate a carcinogenic or pro-carcinogenic material from an endogenous steroid. Cramer, a researcher at the Imperial Cancer Research Fund Laboratories in London, wrote in 1934 that the failure to account for the apparently arbitrary selection of victims of cancer was to be found in the fact that until then comparisons had been made taking into account only extrinsic factors and neglecting altogether the complicating influence of the intrinsic factor of susceptibility. He was of the view that the total burden of cancer in different populations was essentially the same, but that endogenous factors determined the organ distribution of the disease. By the end of 1964, therefore, it was appreciated that endogenous factors played a role in cancer and this became a fertile area of future research.
[5.560]In the next period, Coombs and Croft investigated in 1969 how a group of polycyclic aromatic hydrocarbons, the cyclopenta[a]phenanthrenes, might be manufactured within the body itself. Building upon the original ideas of Cook, they proposed that these chemicals could be produced within the body from bile acids, like deoxycholic acid, and they wrote extensively on the chemistry and biochemistry of this process. But Professor Idle had been unable to find literature that showed the end of this line of research, and in particular whether or not this group of carcinogens was produced within the body itself. Separately, Magee and Barnes, the leading researchers in nitrosamine carcinogenesis, questioned whether the bacteria living in the gut might synthesise nitrosamines under certain conditions.
[5.561]This led Professor Idle to introduce the additional topic of host factors. He said that it had long been known that endogenous factors could play a role in cancer. Of particular importance were genetic factors that were associated with disease outcomes in individuals, including cancer. Genetic differences could influence the individual's response to exposure to the ubiquitous chemicals that were found in foodstuffs, pharmaceuticals, cosmetic products and drinking water, for example. These genetic differences were manifested as genetic polymorphisms. Genetic polymorphism was the existence in the same location of two or more forms of a characteristic, where the form of lowest incidence was greater than 1%. Different blood groups, eye colours or skin colours were all characteristics which were almost invariably genetically determined, and each formed a part of a polymorphism, or multiple types of a particular characteristic. Human characteristics such as height and blood pressure were the product of a large number of genes (and their environmental interactions) and were thus not subject to polymorphism.
[5.562]Asked further about genetic polymorphism, Professor Idle explained that the 30,000 genes in the human genome contained sequence variations between different individuals, so that there were literally thousands and thousands, perhaps millions, of genetic differences in the human genome between different individuals. This was not recognised twenty or thirty years ago, but certainly was today, as the result of the human genome project. So, at almost any genetic locus, there existed multiple alleles, alternative forms of the gene, in the population. These included not only such matters as the colour of eyes, hair or skin, or blood groups, but all the biochemical characteristics that made up our cells: the enzymes, the structural proteins, even lipids and carbohydrates, were there by virtue of genetic characteristics. No two persons, with the exception of identical twins, were genetically identical.
[5.563]In 1968, Nebert and Gelboin at the NCI reported that the activity of an enzyme, which they renamed aryl hydrocarbon hydroxylase (AHH), could be induced by the treatment of rodent cells in culture with a polycyclic aromatic hydrocarbon such as benz[a]anthracene. They reported that different strains of mice had different degrees of induction of AHH. This work represented the first study on the genetics of the cytochrome P450 (CYP) system. Professor Idle explained that cytochrome P450s were a family of enzymes that occurred in all animals and plants that had so far been studied, including humans. These enzymes carried out the metabolic oxidation of virtually every foreign chemical that entered the body, including many nutrients, and were extremely important in the body's defence against small molecules. P450, in adding oxygen, generally rendered the molecule more water-soluble, or created a handle on the molecule, to which the body added a water-soluble substance, such as a sugar molecule. Several things were therefore produced overall, in one or two phases: the pharmacological or toxicological activity of the material was reduced, its water solubility was increased and its ability to be excreted from the body was increased. So generally, but not always, water-soluble, excretable metabolites are produced. The levels of the enzyme could be increased by an external stimulus by a factor of between two- and ten-fold, depending on the circumstances. The experiments had been carried out almost exclusively on laboratory rodents. The increase in the amount of the enzyme in general had the effect of increasing the rate and extent of metabolism of chemicals that were substrates for that enzyme. It appeared to be AHH that metabolically activated polycyclic aromatic hydrocarbons, such as benzo[a]pyrene, to reactive, carcinogenic metabolites, and it was observed that the polycyclic aromatic hydrocarbons themselves could induce AHH and thus their own metabolic activation.
[5.564]The report by Nebert and Gelboin that there were mouse strains for which AHH was inducible and others for which it was not led to the hypothesis that chemical carcinogenesis might be genetically controlled and gave rise to the proposition that different people might react differently to chemical carcinogens. The first report of human studies of this paradigm came from Kellermann, Shaw and colleagues, who concluded that susceptibility to bronchiogenic carcinoma was associated with the higher levels of inducible AHH activity. But over the subsequent two decades, no other research group was able to duplicate these findings and their work was discredited.
[5.565]Professor Idle said that there was broad agreement that what first energised the field of what might now be called cancer pharmacogenetics was the discovery by his own group of the so-called debrisoquine 4-hydroxylation polymorphism and its subsequent application to lung cancer. They were interested in the early to mid-1970s at St Mary's Hospital Medical School in London in the reasons why some patients responded to the drug debrisoquine, which was a new antihypertensive agent, and some patients did not. They could see clearly that this might be a metabolic phenomenon and they worked in an environment of drug metabolism. They set about doing a study in medical students and some members of staff in which debrisoquine was given to every subject and measurements were made of the amount of debrisoquine and its principal metabolite, the pharmacologically-inactive 4-hydroxy-debrisoquine. They made a ratio of the debrisoquine divided by 4-hydroxy-debrisoquine and expressed this in a histogram of the population. They found that 3% had very high values of this ratio, while the rest all had low values. They proposed then that these were two different phenotypes which they called "extensive" and "poor" metabolisers. They then carried out family studies on the individuals with the high values to see if there was a clustering of other poor metabolisers in their families and were able to demonstrate that the character known as "poor metabolism" was inherited, and inherited in a recessive fashion.
[5.566]Their research developed in many directions, one of which was to carry out a study in lung cancer using the technology that they had developed for typing people as either extensive or poor metabolisers. A study was carried out on lung cancer patients at the Whittington Hospital in London, where there was a large and active chest clinic, and on controls who were matched for age, gender and smoking history. They carried out the debrisoquine hydroxylation test on the subjects and measured their debrisoquine metabolism in the laboratory. They found that the lung cancer patients differed from the controls in two major respects. First, the cancer group comprised many fewer subjects who were poor metabolisers than did the control group; this suggested that poor metabolisers, who made up almost one-tenth of the United Kingdom population, were at considerably reduced risk of lung cancer. Secondly, as shown on a histogram to which Professor Idle made reference, the metabolic ratio values were shifted to the left in the cancer group, suggesting that the persons with the lowest values of metabolic ratio (fastest metabolism) were at the highest risk of the disease. Professor Idle's group did not at that time include an epidemiologist, so the terminology of epidemiology was not used by them. Their early investigations had now been repeated and refined by them and many others in numerous populations and patient groups. Other groups had not, however, always found the same result and some had reported no difference between lung cancer patients and controls. The position today was that there was still a debate as to what role this enzyme might play in lung cancer, it was quite uncertain.
[5.567]Many other host factors had since been identified, he said, some of which were derived from enzymes thought to be involved in chemical carcinogen activation and detoxication and others which were related to DNA repair enzymes. For example, there were now known to be a number of P450 enzymes that displayed genetic polymorphism and these were beginning to be evaluated as factors in human cancer, including lung cancer. Debrisoquine hydroxylase, know called CYP2D6, was one of a large family of enzymes, among which were other enzymes of which humans and animals were either extensive metabolisers or poor metabolisers. Investigators were thus provided with far more tools for their studies. Moreover, other groups of non-P450 enzymes that metabolised chemicals foreign to the body had been reported to be polymorphic. Professor Idle said that as science delved deeper into the genetics of these enzyme systems it was becoming apparent that most persons differed from each other in their complement of chemical metabolising enzymes. Additionally, other genetic polymorphisms related to DNA repair enzymes, oncogenes and tumour suppressor genes were starting to emerge. The various aspects of the field of molecular epidemiology of cancer were now very active, involving hundreds of research groups. Approximately 300 genes were thought to be involved in the cancer process, so it was not surprising, he said, that workers looked for differences at these gene loci in cancer patients in an attempt to understand who was at greatest risk of the disease. There was now an enormous compendium of data from such studies. Some of the research had been directed at uncovering associations between certain polymorphisms and lung cancer, but no gene had yet been discovered that explained why certain persons developed lung cancer whilst others did not.
[5.568]The next topic was the stages of cancer development. Professor Idle said that Berenblum was the first to report, in 1941, that certain irritants, notably croton oil, turpentine and xylene, augmented the carcinogenicity of benzo[a]pyrene on mouse skin. Later, Friedewald and Rous, writing in 1944, coined the terms "initiation" and "promotion" of skin carcinogenesis to explain the co-carcinogenic action of benzo[a]pyrene and chloroform, respectively. Professor Idle explained that co-carcinogenesis occurred when two substances acted together, often in a multiplicative rather than an additive manner, to increase the incidence of experimental tumours. In those days there was little understanding of the molecular mechanisms and the theories were based on good observation. It was observed that if polycyclic aromatic hydrocarbons, specifically benzo[a]pyrene and 20-methylcholanthrene, were applied to a rabbit ear, for example, and some cells were initiated to become cancer cells, the subsequent application of chloroform appeared to promote the appearance of cancer in these cells. These polycyclic aromatic hydrocarbons were labelled as initiators and described as "calling forth" the skin tumours. Solvents and irritants were labelled as promoters, in that they hastened the formation of the skin tumours on rabbit ears after the application of the initiator, but were not carcinogenic when applied in isolation. Some chemicals were believed to possess the qualities of both tumour initiators and promoters and were thus known as "complete carcinogens", meaning that they could be carcinogenic alone, without the intervention of any other agent. Hieger reported in 1962 that croton oil, formerly thought only to be a promoter, produced sarcoma in a certain strain of mice, which suggested that croton oil might have been misclassified as a tumour promoter. This demonstrated that it was not always easy to distinguish between an initiator, a promoter and a complete carcinogen. Boutwell, after carrying out a large number of detailed experiments with turpentine on mice, concluded in 1964 that carcinogenesis might be separated into three stages, involving initiation, conversion and propagation. Conversion was seen by him as the change of an initiated cell which appeared to be normal into a malignant-appearing cell, which then went on to form a tumour through the process of propagation.
[5.569]Based on observations of the results of skin painting in laboratory animals, by the end of 1964 the two-stage theory of carcinogenesis, that is initiation and promotion, had been broadly accepted. Professor Idle added that the only two-stage animal models were mouse skin, bladder and thyroid, and rat liver. Nevertheless, the model was erroneously referred to when discussing other tumour types in other organs. There was, he said, no established two-stage lung cancer model and today very few researchers accepted a two-stage model. Today, in general, researchers would speak of a multi-stage model. The vast majority of experiments, in the model itself, as used today, were on mouse skin. Even with mouse skin, researchers would speak of there being multiple stages, not just simply two or perhaps three.
[5.570]In the subsequent period, although the two-stage model had only been shown to operate in skin cancer in experimental animals, Wynder and Hoffmann proposed in 1967 a three-stage mechanism for human lung cancer comprising a disruption of cilia-mucus defence, followed by initiation and promotion. This theory was pursued by these authors in subsequent papers. Professor Idle said that certainly in the 1970s and 1980s there was a growing recognition that there must be more than two or three stages involved in the carcinogenic process and experiments were producing data consistent with these developing ideas.
[5.571]The next concept which Professor Idle introduced was that of anticarcinogens. The expression "anticarcinogenic" was coined by Berenblum in 1931 to relate to a phenomenon first reported by him in 1929. He found that the production of "warts" (papillomas) on the skin of mice by coal tar could be almost completely prevented by the addition of a small proportion of mustard gas to the tar. This was a surprise, because both of these substances were known to be carcinogenic. He later demonstrated that a number of other skin irritants had marked anticarcinogenic actions with respect to coal tar. Lacassagne and others reported in 1945 that weakly carcinogenic polycyclic aromatic hydrocarbons could inhibit the effects of highly carcinogenic polycyclic aromatic hydrocarbons on mouse skin. Falk and others reported in 1964 that non-carcinogenic polycyclic aromatic hydrocarbons and crude mixtures containing a spectrum of polycyclic aromatic hydrocarbons could inhibit the appearance of sarcomas in mice injected with the polycyclic aromatic hydrocarbons benzo[a]pyrene and dibenz[a,h]anthracene. Accordingly, as at the end of 1964, Professor Idle said, it was known that experiments with chemicals in isolation could not predict their biological activity when they occurred in combination with other chemicals. Reference was made to Falk et al. 1964. At p.178 the authors summarised their findings in these terms:
"The activity of carcinogenic hydrocarbons can be inhibited by closely related pure compounds or by crude mixtures including a spectrum of polycyclic aromatic hydrocarbons when both carcinogen and anticarcinogen are administered simultaneously. Though the effect is maximum when the agents are administered simultaneously, inhibition can also be observed when the anticarcinogen is administered several days before or after the administration of the carcinogen."
The authors said that in the absence of an understanding of the mechanism of carcinogenesis on the intracellular level, any explanation of inhibition would be compounding a theory upon a theory.
[5.572]On the topic of genetic differences, Professor Idle said that the period from 1965 to 1971 witnessed the emergence of a belief that genes, either alone or in concert with other factors, could cause human cancer. In addition, this period saw the development of the field of pharmacogenetics, in which it was recognised that genetic differences could have effects upon the metabolism of chemical carcinogens. Heston in 1965 discussed the role of genes in the origin of all tumours. He was particularly convinced that the so-called "spontaneous tumours" in animals were due to genetics. Gelboin and Bates, writing in 1966, were convinced that cancer was the result of modification of key genes by carcinogens. This view was shared by Huebner and colleagues, writing in 1971, who envisaged chemical carcinogens and viruses sharing a common mechanism by working through the genes of the host organism to cause cancer. This opened the way for consideration of gene-environment interactions in cancer causation. Koller, writing in 1967, was convinced of the central role played by genetics in carcinogenesis. Lynch wrote in 1968 that although the organism interacted with the environment, the critical point was that the genotypic endowment of the host might determine resistance as well as susceptibility to cancer; the aetiology and pathogenesis of cancer in man were, he wrote, extremely complex and for the most part remained an enigma. Keith and Brown in 1970 analysed the differences in cancer incidences between monozygotic (identical) and dizygotic (non-identical) twins and remarked that environmental factors appeared to be more important than genetic factors, but the data were not available to make a clear judgment. Lynch and Krush, in relation to colon cancer, remarked in 1971 on the importance of acquiring family histories from cancer patients. It had not previously been common practice to take family histories from such patients, and this limited the understanding of the role of genetics in cancer. During this period, Knudson published in 1971 one of the most important papers on cancer genetics. He analysed familial retinoblastoma, a childhood cancer of the eye known to have a dominant inheritance (meaning that all affected persons had at least one affected parent) and calculated that the genesis of the tumour required two mutations, one inherited and the other occurring in the early years of life. This theory led some cancer researchers to the view that cancer did not require a number of mutational events as other researchers had earlier claimed.
[5.573]In this period, research aimed at investigating the influence of genetics on lung cancer was in its infancy. Severi had observed in 1965 that the appearance of lung tumours in mice was under the influence of at least 10 known genes. In the same year, Hueper studied the role of genetics in resistance to benzo[a]pyrene in mice, but his results were equivocal. Burch commented in 1964 on the report by Tokuhata in the same year that lung cancer deaths among non-smoking first-degree relatives of lung cancer cases were four times greater than in the non-smoking first-degree relatives of controls without lung cancer. Burch recognised that the proportion of lung cancer cases in the population that arose due to a "specific predisposition" could not be accurately estimated, but he nevertheless used an estimate of 50%, which allowed him to calculate that the frequency in the population of any particular allele predisposing to lung cancer was likely to be appreciably less than 3%. (An allele was any one of two or more different genes that occupied the same position (locus) on a chromosome, such as the alleles which determined eye colour.) So, by the end of 1971, Professor Idle said, researchers were exploring the possible role of genetics in human cancer, including lung cancer.
[5.574]Professor Idle summarised his research into the period prior to 1965 by saying that there were competing theories regarding the origins of cancer. Among these theories were those concerned with the possible roles of chronic irritation, viruses, macroparasites, chemicals, radiation, personality, emotion and stress, embryonic tissue and cellular metabolism in cancer causation. It was also postulated that endogenous factors played a role, albeit undefined, in cancer causation. It was in this period that it was first proposed that carcinogenesis occurred in two, or possibly three, distinct stages. There was also considerable debate concerning the cellular target of chemical carcinogens, either protein or DNA. Such a debate was only made possible by the discovery of the structure and function of DNA by Watson and Crick in 1953. Finally, chemicals were identified that had anticarcinogenic properties. In 1964, scientists who were struggling to identify the causes of cancer were also seeking to define the mechanisms involved in cancer formation. Boutwell, who was a senior investigator at the McArdle Memorial Laboratory, wrote in Boutwell 1964, at p.207:
"The problem of cancer has received more intensive research effort than any other single medical problem, yet the essential facts needed for understanding and controlling the disease continue to elude us."
At p.211 he wrote:
"The ultimate comprehension of the problem of cancer is dependent upon elucidating the chemical processes responsible for the biological phenomenon known as cancer. However, the voluminous efforts of the biochemists have not been successful, partially because the biological descriptions are still incomplete."
[5.575]Professor Idle said that in his opinion, as at the end of 1964, none of the competing theories of cancer causation had gained general acceptance. The cause or causes of cancer were unknown and there was little understanding of the mechanisms whereby cancer in general, and lung cancer in particular, developed. During the period from 1965 to the end of 1971, competing theories of cancer causation continued to evolve, and new theories emerged. Substantial research was devoted to investigating how viruses might cause human cancer. Progress was made in understanding the metabolism of chemicals. The possible role of radiation as a cause of cancer continued to be explored. Researchers continued to investigate whether or not the body itself might produce cancer-causing chemicals. Continued research was carried out into the roles of personality, emotion and stress in cancer causation. Wynder and Hoffmann, building on the two-stage model of carcinogenesis, proposed a three-stage model of human lung cancer. Debate continued on the nature of the cellular target for chemical carcinogens. Finally, researchers started to consider the role of genes in cancer susceptibility.
[5.576]During this period, there emerged no single hypothesis as to how cancer was caused. Horsfall, a virologist and Director of the Sloan-Kettering Institute, one of the premier cancer research establishments in the United States, wrote in 1966 that the necessary and sufficient causes of cancer were still unknown and that their elucidation was the pressing priority for cancer research. There were those who said that knowledge of the nature of cancer had not advanced in 25 years. Indeed, in 1967, Magee and Barnes, the world experts on nitrosamine mutagenesis and carcinogenesis, were still proceeding on the historical hypothesis that cancer followed a mutation in a somatic cell. As with cancer in general, during the period 1965 to 1971 there was no single hypothesis as to how lung cancer was caused. The importance of the biological approach to cancer research was underscored by Roe, who was a pathologist working in London, associated with the Chester Beatty Research Institute and its attendant hospitals. In Roe 1966 he stated, at p.101:
"The epidemiologist can only find associations, he cannot approach very close to proving cause-and-effect relationships. He has no control over many possible relevant factors in the environment of the populations he studies. The experimentalist, on the other hand, can control many more factors in the environment of his test animals. He can come much closer to proving that exposure to a particular agent causes a particular effect. Secondly, the experimentalist is in a position to investigate the mechanism by which the effect is brought about."
Professor Idle added that he did not believe that at the present date the necessary and sufficient causes of cancer, referred to by Horsfall in 1966, were yet known.
[5.577]In summary, Professor Idle said, in the period up to 1972, there were competing theories regarding the origins of cancer. These included viruses, chemicals, radiation, endogenous factors, and personality, emotion and stress. The nature of a chemical carcinogen in structural terms was not understood, but it was accepted that chemical carcinogens needed to be metabolised to exert their effects. The proposition that such metabolism was under genetic control was being investigated, and this research would continue into the next period. Similarly, the molecular target for such carcinogens had also not been agreed, and there was continuing debate whether this target was protein or DNA. The role of genetics in cancer was beginning to be appreciated. In his opinion, as at the end of 1971, none of the competing theories of cancer causation had gained general acceptance. The causes of cancer were unknown and there was little understanding of the mechanisms whereby cancer in general, and lung cancer in particular, developed.
[5.578]Throughout the period 1972 up to the present, Professor Idle went on to say, a number of competing theories had been proposed regarding causation of cancer, including lung cancer. The scientific views that had been advanced during this period involved viruses, failure of host immunity, personality, emotion and stress, failure of DNA repair, host genetics, chemical carcinogenesis, mutations in oncogenes and tumour suppressor genes, oxidative stress, epigenetics and aneuploidy. It could be seen from this list that some of the theories that were being explored in the earlier periods continued to be explored in this period while some had been discarded, and other theories had emerged during the most recent period.
[5.579]He said that this period had witnessed an explosion of scientific activity and publications on the subject of the biology of cancer. Both basic and clinical scientists from fields as diverse as chemistry, biochemistry, physiology, haematology, immunology, bacteriology, virology, endocrinology, cell biology, molecular biology, pharmacology, toxicology, genetics, oncology, therapeutics, radiology, internal medicine, surgery, psychology and psychiatry had come together under the single umbrella that was cancer research today. Additionally, we had witnessed in the recent past the creation of new subject areas both in research and in undergraduate curricula, which provided both a focus and a framework for the evolving concepts of biology that could be utilised to tackle the as yet unsolved questions of cancer causation. Such new subject headings included the hybrid disciplines of pharmacogenetics, genomics, proteomics, metabonomics, biochemical and molecular epidemiology, molecular virology and molecular toxicology. Professor Idle explained that genomics was a subject that dealt with the genome, using information derived from the human genome project of genetic sequencing. Proteomics was the second stage after genomics and was a subject which dealt with variation and behaviour in protein molecules and what that told us. Metabonomics was the study of the complete complement of small molecules and their flux within a cell. Epidemiology underwent a transformation some years ago with the recognition that it would be useful to make objective measurements, rather than simply use the instrument of questionnaire. Biochemical markers were measured, for example in blood or urine, and this formed the field of biochemical epidemiology, for example in a case-control study. Molecular epidemiology used molecular markers in the same setting, particularly genetic factors measured in case-control or cohort-type studies. This re-ordering of the landscape and constituencies of biological research and teaching had become necessary with the realisation that questions regarding the nature of cancer had produced yet more complex questions that defied investigation, within the confines of a single traditional subject area. The multidisciplinary and often multicentre approach to cancer research today was a testament to the increasing complexity of the question of cancer causation.
[5.580]Since 1953 research centred around DNA had steadily increased and, by today, dominated much of the activity in cancer research. Professor Idle explained that DNA was the molecule that passed to the next generation the information of how to build and operate a new organism. It was found in the nucleus, the cell body that contained the chromosomes, and, to a lesser extent, the mitochondria, the small intracellular bodies responsible for energy production and cellular respiration, of living cells. DNA comprised four "bases": two purines, adenine (A) and guanine (G); and two pyrimidines, thymine (T) and cytidine (C). The bases were joined in a chain by a "sugar-phosphate backbone", a polymeric thread of sugars and phosphates which were joined together, with the bases attached to them. When two strands of the single-stranded DNA polymer coiled together to form double-stranded DNA, known as the "double helix", the structure was held together by obligatory pairings between G and C, and between A and T. In this way, the second strand was a mirror image of the primary strand, containing within it all the information the cell needed to synthesise a new primary strand. The copying, from the secondary strand, of every A into T, every T into A, every G into C and every C into G, produced an identical copy of the original primary DNA strand sequence. The primary and secondary strands were known as "complementary" DNA strands. When a cell divided, the primary strand was used as a template to make a complementary copy, and the secondary strand was also used to make a complementary copy, the two newly synthesised strands re-combining to form a second double helix, to be used by the daughter cell. Professor Idle referred to a figure illustrating this process, part of the primary strand having the sequence TAGCTACG, and part of the secondary strand having the sequence ATCGATGC. When the primary strand was copied, by a process called "replication", into a complementary strand, its sequence would be the same as for the original secondary strand, and when the original secondary strand was replicated, the resulting complementary strand would have the same sequence as the original primary strand. Thus, the two new single strands of DNA were able to pair into a double helix, having replicated the complete genome of the organism, and so providing the genetic basis for mitosis, or cell division.
[5.581]The scientific era since 1972 had also witnessed a number of discoveries in the development of revolutionary laboratory techniques that had radically altered the way in which cancer research could be pursued today. One of the most important techniques that emerged in the mid-1980s was the polymerase chain reaction (PCR). PCR enabled tiny amounts of DNA to be detected by amplification of particular sequences of interest, so that an individual might be identified from the DNA contained in a single cell. The discovery of the proto-oncogenes and the tumour suppressor genes prompted new lines of research on cancer mechanisms. More than anything, the observation of single mutations in these genes led scientists to hypothesise that the carcinogenic process was a set of clearly discernible cellular events, each of which could be defined in molecular terms. It had not, however, been possible to reduce cancer to a linear set of simple genetic alterations.
[5.582]In 1982, Weinberg made the landmark discovery of the first mutated and activated oncogene in a human tumour. In the following three decades, research demonstrated that there were approximately 300 genes which might be involved in human cancer. About half of these were oncogenes and tumour suppressor genes. The other half coded for substances known as cytokines, growth factors and their receptors, which were also involved in the regulation of cell growth. Professor Idle said that cytokines were another group of messenger molecule which passed from one cell to another, often within the immune system. Despite these major advances in knowledge, however, human cancer, as a clinical entity, still evaded scientific definition and understanding. Twenty years after his discovery of the first activated oncogene in a human cancer, Weinberg wrote in 2002:
"For those who believe in the simplification and rationalization of the cancer process, the actual course of research on the molecular basis of cancer has been largely disappointing. Rather than revealing a small number of genetic and biochemical determinants operating within cancer cells, molecular analyses of human cancers have revealed a bewilderingly complex array of such factors."
[5.583]One of the new theories in the period after 1972 was the failure of host immunity theory. Professor Idle explained that the body's key defence system was the immune system. This was composed of many different cell types that collectively protected the body from bacterial, parasitic, fungal and viral infections and from the growth of tumour cells. The immune response was based upon the paradigm of self and nonself, i.e. that there was an immune response to anything recognised as foreign or nonself. Thus, invading organisms and tumour cells were recognised through their foreign proteins ("antigens"), and part of the body's response to antigens was to synthesise "antibodies" that neutralised them. This was the principle, for example, of vaccination, which introduced a specific antigen into the body to stimulate the production of a specific antibody.
[5.584]The Australian immunologist and subsequent Nobel Laureate, Sir Frank Macfarlane Burnet, evolved the principal theory in this field. Stated simply, in his hypothesis of immunological surveillance, clones of malignant cells were thought to arise at regular intervals in all individuals; but such cells hardly ever survived because they were rejected as allografts (foreign), unless some unspecified defect in the immune response permitted these spontaneously arising clones of malignant cells to be tolerated. This theory was favoured in the early 1970s but, as Laroye wrote in Laroye 1974 at p.1099:
"All arguments about immunological surveillance tend to postulate that neoplastic cells acquire tumour-associated antigens which subsequently can become susceptible to immunological attack. This does not seem to be true in all instances: many tumours, indeed, especially those induced by chemical carcinogens, seem to be devoid of any significant tumour antigenicity."
Professor Idle said that this observation was based upon studying these types of cells in vitro and by transplant experiments into animals, and the recognition that tumours, particularly those caused by chemicals, could sometimes give themselves an "immune privilege" around themselves. Epidemiologists concluded that there was some evidence that failing immunosurveillance might be related to skin cancer and adenocarcinomas of the stomach and lung.
[5.585]One of the strong arguments in favour of the immune surveillance theory of cancer, he said, was the mounting incidence of cancer with increasing age, an approximate doubling every five years after the age of 25, and the parallel decline in immune competence with increasing age. Added to the age factor of the observations in the immune deficiency syndromes, whereby mortality rates for cancer in immune deficiency patients exceeded by 100 times the expected rates, there were inherited immune deficiency syndromes in addition to the acquired immune deficiency syndrome (AIDS). There were those who had observed a lower death rate from cancer in persons who were given BCG vaccination against tuberculosis at birth. Reference was made in this regard to Rosenthal 1984, in which it was reported that in various studies it had been found that BCG vaccination at birth lowered the mortality from leukaemia and, in the author's studies, to all forms of cancer followed over a period of twenty years. The author proposed that the mechanism of cancer mortality reduction in those vaccinated with BCG at birth was at least in part due to the detection and destruction of embryonic cells or components thereof. He wrote that in the embryo thousand of errors were made in the development, most of which were corrected before birth but thousands of which remained. These foetal remnants acted as foreign bodies to the host and were removed by the lymphoreticulo-endothelial system, which could be markedly stimulated by BCG, which thus helped appreciably in removing foreign cells from the body. It had been proposed in another paper that BCG vaccination enhanced the tumour cell killing efficiency of two types of white blood cell, macrophages and lymphocytes. Kripke 1988 stated that the immune surveillance theory, once highly controversial, had survived over three decades and had been modified as our understanding of the immune system developed. Nevertheless, there were those who did not accept that "immune senescence" contributed to this increased risk of cancer with increasing age.
[5.586]Professor Idle said that during the 1990s, there was still much discussion of the immune surveillance theory of cancer. The theory was restated in simple terms by Chowdhury and others in 1991, with the concluding statement that the survival and growth of the tumour cells depended crucially on how the tumours evaded the immune surveillance mechanism of the host and escaped the killer cells as well as the antibodies.
[5.587]The development of understanding of the immune system had led to the awareness that three immune cell types were involved in the control of neoplasia. First, the NK cell was a type of white blood cell that attacked tumour cells by binding to them and releasing lethal chemicals. NK cells were thought to play a key role in cancer prevention by killing abnormal cells before they multiplied and grew. Secondly, the macrophage was a phagocytic cell that played an important role in killing tumour cells and releasing substances that stimulated other cells of the immune system. Phagocytic cells engulfed foreign particles, such as bacteria, and destroyed them using bursts of reactive oxygen species. Thirdly, the tumour-infiltrating T cell (or cytotoxic T cell) was a type of white blood cell that could recognise and destroy abnormal cells, such as tumour cells and virus-infected cells. All three immune cell types had been observed in vitro, using human cells. Immune response to a foreign organism or to a tumour cell, therefore, was an integrated response involving multiple cell types. It had been reported that cancer patients may have a deficiency in their T cell responsiveness and that injection into the skin of lung cancer patients with bacterial or chemical antigens demonstrated a clear immune impairment. Reference was made to Gorski et al. 1994.
[5.588]There were those, nevertheless, who rejected the immune surveillance theory of cancer, which had been premised on the concept that the body's immune system erroneously recognised a tumour as "self" and thus did not attack and destroy it, allowing the tumour to "sneak through" immune surveillance. Fuchs and Matzinger, writing in 1996, argued for rejection of the self/nonself paradigm. They proposed that this paradigm provided a satisfactory explanation in the context of infectious disease originating from foreign organisms. However, they postulated that the default response of the immune system to new antigens, including those produced by a tumour, was to ignore them, in the absence of a secondary "danger signal", arising from tissue damage or distress. This, they explained, was why the administration of the BCG tuberculosis vaccine, which supplied the "danger signal", seemed to be an effective therapy for certain tumours. As if to demonstrate the lack of a scientific consensus on this topic, Kavanagh and Carbone catalogued in 1996 all the possible defects in immune surveillance that could permit a tumour, including specifically a lung tumour, to "sneak through".
[5.589]Meanwhile, new mechanistic theories of how certain types of tumour cells, including lung carcinoma cells in culture, could become antigenic were continuing to be advanced. The elevated incidence of lung cancer in HIV-positive patients and the fact that AIDS patients could have a 3.8-fold elevated risk of lung cancer compared with persons without AIDS merely added weight to the immune surveillance theory. It appeared that lung tumours could utilise a variety of mechanisms to evade immune detection. It had also been argued that an individual's human lymphocyte antigen (HLA) type, known commonly as "tissue type", might predispose that individual to cancer. The HLA type could be thought of as the white cell equivalent of ABO blood groups, except that there were many more HLA types than ABO blood types, running into the thousands. People with certain HLA types appeared to be "cancer prone", further suggesting a role for the immune system in the development of cancer. Furthermore, it had been proposed by O'Connell and colleagues, writing in 1999, that tumours could generate an environment of "immune privilege", through a process called the "Fas counterattack". Fas was a receptor present on cells of the immune system. In the ordinary process of the work of the immune system, the Fas receptor interacted with the "Fas-ligand", which had been produced by either that cell itself or some other immune cell. The Fas-ligand signalled to the cell that it was time to die, the process of apoptosis. The immune system, therefore, having mobilised immune cells to fight an infection or neoplasia, terminated this assault when these cells were no longer required. Certain tumours themselves had the capacity to produce the Fas-ligand, which engaged and destroyed immune cells, thus creating an environment of immune privilege for the tumour cell.
[5.590]Several factors are known to impair the functioning of the immune system and, in so doing, might place the individual at greater risk of cancer. The immune system had been shown to be impaired by the presence of various diseases, including common diseases such as the common cold and mononucleosis. Many drugs could lower the immune defences, and some were indeed frankly immunosuppressant. Experiments in animals, together with clinical observations, demonstrated that immunosuppression occurred as a result of malnutrition, and that nutrition was a critical determinant of immunocompetence and risk of both illness and death. Another important factor was stress. Overall, the relationship between tumours and the immune system had been described elegantly, in Professor Idle's view, by Pettit et al. 2000, at p.1903:
"In summary, the process of immune selection may be considered to occur in three non-discrete phases [...]. During the first phase, initiation, proliferation and diversification of tumour occurs against a background of immune ignorance. The second phase is entered when an anti-tumour immune response is activated. Consequent immune selection pressure allows a process of microevolution to lead to the gradual acquisition of adaptations that permit immune evasion. The third phase of immune escape is reached when tumour cells acquire sufficient adaptations to allow proliferation unchecked by immunological control."
Professor Idle said that the situation today was that much of Burnet's original concepts, having been ignored for some time in the past, were now again part of mainstream immunological thinking. Thus, there were many cancer immunologists who held fast to the concept that tumours might develop means to evade detection and that this was an essential component of the process of human cancer. It still remained to be determined to what extent stress might impair the immune system and contribute to lung cancer.
[5.591]Professor Idle next discussed the failure of host DNA repair theory. He said that many types of chemicals modified the structure and sequence of cellular DNA and its functions. The repair of DNA modifications corrected most of these changes. The chemicals that modified DNA were both endogenous and exogenous and the DNA sequence changes they caused were normally repaired by DNA repair enzymes. Changes of sequence might involve a piece of a chromosome moving to another place in the chromosome, or even to a different chromosome, in a process known as "translocation", or the substitution of one base for another, a process known as "point mutation". Most DNA repair occurred during cell division. The apparatus recognised that the strands did not agree, and the mismatches were repaired and the correct sequence produced. DNA repair enzymes were really good at removing bases that had been modified in their chemical structure and replacing them quickly with new ones, a process which happened tens of thousands of times in each cell every day. This was a tremendously important process which happened constantly to maintain the fidelity of DNA division and cell division. Endogenous DNA modification occurred continuously, not only through the effects of oxidative stress on DNA, but due to spontaneous hydrolysis of the DNA molecules, a phenomenon that occurs in the order of 10,000 events per cell per day (Rouse and Jackson, writing in 2002). It had now been hypothesised that cancer arose when a modified cell by-passed the system that detected when the cell's DNA was modified and signalled this to the DNA repair enzymes. How these checkpoints normally relayed information to the correct DNA repair system was unknown, and Rouse and Jackson had concluded that the question of how lesion-specific repair factors were initially directed to DNA lesions also represented a major challenge for future research.
[5.592]As a major defence against modification of DNA, processes of DNA repair were present in all organisms that had been examined, including bacteria, yeast, fruit flies, fish, amphibians, rodents and humans. A viable cell needed to be able to detect DNA modifications and signal this to the DNA repaired apparatus. Different enzymes repair different types of DNA modification; a total of 130 discrete enzymes had been shown to participate in human DNA repair. Among these were, first, the synthesis of aberrant proteins arising from the modification of DNA that might be toxic to the cell: the potentially deleterious effects of such DNA modifications could be seen when they were inherited, such as in genetic diseases, for example cystic fibrosis. A second consequence might be the persistence of the DNA modification which, if it occurred in a germ cell (a cell specialising in the production of ova or sperm), would be passed on to subsequent generations. This could possibly give rise to a teratological outcome, the formation of a foetus with some gross abnormality. Thirdly, there might be errors in the process of replication involved in the course of mitosis, which errors would be passed onto the daughter cell and subsequent generations. Fourthly, chromosomal rearrangement might be triggered that scrambled the cell's genetic information, a process that was associated with cancer. Fifthly, there might be apoptosis.
[5.593]Abnormalities in the processes of DNA repair had been associated with both cancer and ageing. One of the commonest cancers in the western world was colorectal carcinoma, 5% to 8% of which comprised an inherited sub-group known as hereditary non-polyposis colon cancer (HNPCC). This was exclusively a disease of deficient repair of a specific type of DNA modification that occurred during replication of the DNA molecule. The most deleterious type of DNA modification to the cell was the double-strand break that could be caused by radiation and by certain chemicals. A double-strand break was damage to the double helix of DNA such that both strands had been severed, thus breaking the continuity of the genetic sequence. In inherited disorders of DNA repair, such as ataxia telangiectasia, patients had an increased incidence of cancer. The commonest cancer in persons of European origin was skin cancer, which had been associated with exposure to UVB radiation from sunlight. Persons with the inherited disease xeroderma pigmentosum, who had a deficiency in a type of DNA repair mechanism, were extremely sensitive to both sunlight and strong artificial light with a UVB component. They readily developed squamous cell carcinomas of the skin in areas, such as the head and neck, which were exposed to the light.
[5.594]The role of DNA repair enzymes in the cell's defence against carcinogenesis was complex and not fully understood. For some time it had been possible in the laboratory to make a so-called "gene knock-out mouse", using embryonic stem cells from which genes had been deleted (a technique that had not yet proved possible with any other species). This enabled direct observations to be made of the exact function of each gene. A knock-out mouse lacking the xeroderma pigmentosum group A gene (XPA) had been made; these animals were deficient in a specific type of DNA repair mechanism. Irradiation of these mice and control mice with UVB showed the importance of DNA repair in the genesis of skin tumours. Additionally, these studies showed that the development of skin tumours in these DNA repair-deficient mice also required an element of immunosuppression that was caused by the UVB radiation. Thus, skin cancers in xeroderma pigmentosum patients might arise due to a perturbation of two distinct defence mechanisms, DNA repair and immune surveillance.
[5.595]A further DNA repair system, called XRCC1, might play a role in squamous cell lung cancer. It was reported by Park and colleagues in 2002 that an inherited deficiency in XRCC1 was associated with squamous cell carcinoma of the lung. Other studies had also shown associations between deficiencies in DNA repair and lung cancer. Attenuated DNA repair in combination with urban air pollution had been proposed as the source of DNA modifications.
[5.596]Professor Idle concluded this passage by saying that deficiencies in DNA repair had been recognised as playing an important role in a number of human cancers and might play a role in lung cancer. Investigation of DNA repair was one of the fastest growing fields in cancer research. In fact, in a paper published in September 2003, Paz-Elizur and others reported that there was 18% lower activity of the DNA repair enzyme OGG (which repaired DNA modifications caused by oxidative stress) in a group of patients with non-small cell lung cancer as compared with a group of non-cancer control subjects. This represented a substantial impairment of DNA repair defences against oxidative stress.
[5.597]Oxidative stress occurred in a cell when there existed an excess of chemically-reactive by-products of oxygen metabolism. These were molecules known as "reactive oxygen species" (ROS), "oxygen free radicals", "free radicals" or, simply, "radicals". ROS were clusters of atoms, one of which contained an unpaired electron in its outermost shell of electrons, known as a radical or free radical. This was an extremely unstable molecular configuration, and radicals quickly reacted with other molecules or radicals to achieve the stable configuration of electrons in their outermost shell. If not removed by the cell's antioxidant system, ROS were thought to lead to a range of detrimental cellular events. The studies which had been carried out had been in vitro, almost always involving individual cells in culture. There were problems of extrapolation from these types of system when talking about tissue damage, organ damage, or damage to an animal or human. There were various theories and hypotheses about the meaning of the detrimental events that could be seen when a cell was exposed to an excess of ROS. Professor Idle referred to a figure which illustrated that approximately 95% of the oxygen breathed by humans was utilised in the normal processes of metabolism and converted into water. However, the residual part of the oxygen passed down an alternative pathway, the formation of ROS, such as hydrogen peroxide and the hydroxyl radical.
[5.598]ROS had been seen to play a role in the cellular changes associated with both ageing and cancer. The molecular target of ROS was DNA. The principal modification brought about by ROS was to add an oxygen atom into the normal guanine (G) in DNA, thereby creating 8-hyroxyguanine (8-HG) adducts. This was a very small modification and hard to detect. If these modifications were not repaired by the enzyme OGG, then they caused a change in the base sequence of the DNA from a G to a T. This was a mutation known as a "G ý T transversion", which was commonly found in the p53 and K-ras oncogenes of lung and renal tumours. This type of mutation could be provoked by ROS in the p53 gene and bore clear similarities to the type of mutation caused in vitro by the benzo[a]pyrene metabolite BPDE. Thus, the normal physiological processes that utilised oxygen, such as respiration, could lead to the generation of ROS and produce DNA modifications that resembled those that had been observed when cells were incubated with such mutagens as BPDE.
[5.599]In addition to the ROS mentioned by him, Professor Idle said that there were a number of other endogenously-formed free radicals that were capable of modifying DNA. The essential characteristic of free radicals was that they involved themselves like a set of "chemical domino effects"; there were chain reactions triggered by one chemical and the electron was then passed from one chemical to another, so it was not surprising that other chemicals became involved. For example, the result might be nitrogen-containing free radicals, such as nitric oxide, and lipids (fats) which were converted to lipid hydroperoxides; and even sulphate, which was an endogenous material, produced a sulphate radical.
[5.600]The foregoing, he said, showed that there might be a connection between cancer and the endogenous processes that produced oxidative stress and DNA modification and repair. Some authors believed that there was sufficient evidence to establish that oxidative stress furnished a comprehensive and unifying theory of human cancer. In this regard, exogenous chemicals and their metabolites were perceived as being able to generate ROS and this process was proposed by these authors to underlie the cancer-causing potential of a broad range of agents, including radiation, quinones, polycyclic aromatic hydrocarbons, phenols, aromatic amines, N-nitroso compounds and alkylating agents. However, the views expressed by Kovacic and Jacintho in 2001 required comprehensive investigation and substantiation. It was, however, pretty well established in radiotherapy that radiation generated oxygen free radicals in the environment of a tumour which killed the tumour, and the relationship between radiation and oxidative stress had been appreciated for a considerable time.
[5.601]The generation within each cell of large numbers of highly chemically reactive oxygen radicals, by processes that were an obligatory consequence of the use of oxygen, placed an oxidative stress upon the cell. The ROS were capable of interfering with cellular structure and function. Failure by the cell to prevent or to repair such impairments could have profound consequences for the cell, including the triggering of pathways that might lead to cancer. In Professor Idle's judgment, whether or not oxidative stress played a role in human lung cancer was not established, though work continued on this question.
[5.602]Professor Idle's next topic was epigenetics. This term was coined by the eminent biologist CH Waddington, who was Professor of Genetics at the University of Edinburgh. He did not believe that genetics, embryology and evolution were separate sciences, and attempted to understand the link between the genotype and the phenotype of an organism. A phenotype was a genetically-determined characteristic of an individual, such as eye colour or blood group. The genotype was the genetic information held in those genes that coded for the phenotype, so that the latter was a manifestation of the former. Epigenetics was the study of the processes by which the genotype gave rise to the phenotype, how the phenotype was manifested from the genetic information in the cell.
[5.603]The human genome was now known to encompass about 30,000 genes that made up just a small part of the 3 billion base pairs that comprised human DNA. In any given cell type, for example a sensory nerve cell in the skin, only a tiny fraction of the 30,000 genes was transcribed into RNA and then protein. When a gene was expressed in a particular tissue, it was copied into an RNA molecule that carried all the genetic information. This then found its way into the cell itself and interacted with part of the cell known as "ribosomes", which were small, spherical structures attached to an inner membrane of the cell. Ribosomes were the places where proteins were made; the genetic information in the form of RNA sat on the ribosome and the ribosome read each of three base pairs, forming triplets known as codons. A protein was made up of amino acids. There are twenty different amino acids, so a huge number of possible different proteins could be made. Each amino acid was coded for in this process by a codon. The codons were contained one after another, like a series of words, in the RNA molecule. This molecule attached itself inside the cell on top of a ribosome and the ribosome read each of the codons. By this process, known as "translation", the RNA molecule added different amino acids to produce a chain which would be the primary protein. In this way, the protein was specified in order to perform a particular function.
[5.604]The vast majority of genes were silenced by epigenetic mechanisms which were only just beginning to be understood; they were kept in a quiescent form so that they were not expressed into RNA and ultimately into protein. What made a sensory neuron different from a liver cell, and indeed different from a neuron in the brain, was the pattern of gene transcription which translated inherited genotypes into functional phenotypes. The state that underlay this distinction between different cell types in the body, often in close proximity to each other, such as an epidermal cell and a keratinocyte in the skin, was often referred to as "differentiation". Processes that controlled how genes were "switched on and off" and caused one tissue to differ outwardly and functionally from another were described as epigenetic processes. Epigenetic processes, whilst inherited, were not represented in the coding sequence of the DNA.
[5.605]The field of epigenetics was centred principally around two biochemical processes, methylation of DNA by the addition of a methyl group, and acetylation of proteins called histones by the addition of an acetyl group. Professor Idle explained that it so happened that within a sequence of DNA there were areas within certain genes, or close to certain genes, that were very rich in GC sequences. It seemed that the purpose of these was to control the epigenetic nature of the gene, to act as a "switch". The body seemed to have an ability to add a methyl group to the C bases. When an area of the gene rich in CG sequences, or an area close to the gene rich in these sequences, was methylated, then the gene could not be expressed. So when the apparatus for transcription into RNA reached this part, it skipped over it, it was not able to make an RNA copy and, therefore, a protein from that gene. Acetylation of histones was a grosser, larger process. The double helix was tightly coiled. Histones sat on top of the DNA sequence and helped it pack into a tight ball inside the nucleus. These proteins would prevent the transcription of an area of DNA that sat underneath them. In order for a gene to be copied into RNA, the histone had to move out of the way. When this underwent acetylation, the histone broke free from the DNA and lifted up, opening a "trap door" in the chromosome, enabling the apparatus to make an RNA copy and a protein. When the histones were deacetylated, the DNA could return to its tightly coiled state that inhibited gene transcription. The acetylation-deacetylation process was a continuous and reversible one that formed part of the circuitry within which genes were transcribed.
[5.606]It had recently been proposed by Urnov, writing in 2002, that dietary insufficiencies could affect the epigenetic methylation pathways in the nucleus, leading to genome misregulation. Epigenetic changes were frequently observed in cancer. Certain key genes were often "switched off" in tumours, permitting cell cycle checkpoints to be by-passed that would normally, when triggered, lead to apoptosis and the death of the tumour cell. For example, aberrant DNA methylation and histone deacetylation were associated with the silencing of the enzyme known as death-associated protein kinase (DAPK), which brought about apoptosis in response to various signals in colorectal and gastric cancers.
[5.607]With respect to lung cancer, rates of DNA methylation had been measured in readily accessible cells, those from the buccal mucosa, the mucous membrane lining the inside of the cheek. Using assays that measured the rate of incorporation of methyl groups into C bases in nuclear DNA, and the detection of the methylated product in situ, researchers had reported in 2002 that changes in global methylation in buccal mucosal cells might reflect changes in tissues at high risk of developing lung cancer. These authors also reported on studies where human squamous cell carcinoma of the lung was associated with a deficiency within the tumour of two vitamins, folate and B12, together with reduced DNA methylation. In contrast, an excess of vitamin C was found in squamous cell carcinoma of the lung and larynx compared with adjacent uninvolved tissue. This phenomenon appeared to be associated with increased methylation of DNA. Professor Idle said that these studies suggested that diet acted upon epigenetic mechanisms that might lead to lung cancer.
[5.608]An epigenetic mechanism that had been proposed to lead to lung cancer was that of "tumour acquired promoter hypermethylation". The DNA sequence that controlled the transcription of a gene was known as the promoter (to be distinguished from the expression "tumour promoter"), and when CpG sequences in the promoter were hypermethylated, the gene was silenced, i.e. not transcribed in that tissue. It had been found recently that "tumour acquired promoter hypermethylation" was a phenomenon that occurred in the promoter region of many tumour suppressor genes in, for example, non-small cell lung cancers. The promoter regions in nine separate tumour suppressor genes had been reported to be hypermethylated in non-small cell lung cancer relative to unaffected tissue from the other lung. The theory was that the hypermethylation silenced the tumour suppressor genes and was thus part of the multistage mechanism of lung cancer. But these very recent findings had yet to be confirmed and the interpretation of them was still preliminary.
[5.609]In summary, Professor Idle said, changes to the regulation of the genome that were not genetic (i.e. not involving mutations), rather than those that were epigenetic, might be involved in the genesis of cancers, including lung cancer. There was some evidence that DNA hypermethylation, the process that silenced gene expression, might be influenced by cellular vitamins and, by association, diet.
[5.610]Professor Idle next turned to aneuploidy, genome instability and the "mutator phenotype". He explained that aneuploidy was the state of having the wrong number of chromosomes in the cells, either too many or too few. The complement of chromosomes in a cell was known as the karyotype. A normal cell had twenty-three pairs of chromosomes. In certain situations, a cell might have an abnormal karyotype, which was always associated with a disease process. When the karyotype was grossly abnormal, due to the addition or deletion of chromosomes, the situation was referred to aneuploidy and the cell was known as "aneuploid". Professor Idle referred to a figure in his report showing a normal karyotype and an abnormal karyotype from a cancer cell, including both missing and extra chromosomes that might result from fusions between pieces of different chromosomes. He said that there existed very little agreement among scientists as to how cancer cells acquired such a large number of genetic and epigenetic abnormalities. At what stage in the development of cancer, whether early in the mechanistic process or later, the cell became aneuploid, was unclear.
[5.611]According to Duesberg and co-workers, reported in Li et al. 2000, gene mutation was an insufficient explanation of the cause of cancer, except when the mutation was so gross as to be characterised as aneuploid. In other words, simple mutations, even within a large number of genes such as tumour suppressor genes or oncogenes, were not sufficient to cause malignancy. Cancer, according to these authors, must be viewed at the level of the chromosome not the gene. They stated in the abstract at p.3236:
"The aneuploidy hypothesis predicts the long latent periods [of cancer] and the clonality [of tumours] on the basis of the following two-stage mechanism: stage one, a carcinogen (or mutant gene) generates aneuploidy; stage two, aneuploidy destabilises the karyotype and thus initiates an autocatalytic karyotype evolution generating pre-neoplastic and eventually neoplastic karyotypes. Because the odds are very low that an abnormal karyotype will surpass the viability of a normal diploid cell, the evolution of a neoplastic cell species is slow and thus clonal, which is comparable to conventional evolution of new species."
Professor Idle explained that clones were organisms or cells that were genetically identical by descent, meaning that the progeny all had the identical genetic make-up of the parents. A diploid cell was one in which all chromosomes, except sex chromosomes, were two in number and were structurally identical with those of the species from which the culture was derived.
[5.612]The 26 July 2002 issue of the premier scientific journal Science was dedicated to genome instability. One author wrote:
"Cancer cells are chock-full of mutations and chromosomal abnormalities, but researchers can't agree on when and how they come into play. Inside a cancer cell is a veritable gallery of horrors: inactivated genes, extra or missing chromosomes, and a host of other genetic abnormalities, large and small."
Professor Idle said that the origin of the aneuploidy that was proposed to generate genomic instability as a forerunner of cancer was not known. Given that aneuploidy required the complete loss of at least one chromosome or the addition of one new one, the genetic change must be quite drastic.
[5.613]Somewhat in parallel to the aneuploidy theory of cancer of Duesberg and co-workers was the "mutator phenotype" theory championed by Loeb and colleagues. This theory started with the premise that tumours, once detected either experimentally or clinically, contained far too many mutations (tens of thousands, in some cases) to have occurred by normal processes of mutation, and postulated that, early in its life, the tumour required a so-called mutator phenotype. This characteristic of the cell permitted multiple random unrepaired mutations to occur during development of the tumour. Loeb and colleagues had proposed that it was oxidative stress that drove the mutator phenotype and thus genomic instability, so much so that they had proposed (in 2001) the use of antioxidants to reduce DNA modifications by ROS and delay the progress of cancer.
[5.614]In summary, Duesberg's group had made a strong case that aneuploidy could be the only explanation for carcinogenesis as it was understood today, and it was certainly the case that tumour cells isolated ex vivo or developed in cell culture always had an abnormal karyotype and were aneuploid. These views were not universally shared, especially by Weinberg's group, who pointed to a small number of defined mutations, as few as three, as the first step of carcinogenesis, or by Loeb and other proponents of the mutator phenotype theory. Nevertheless, whether it was a small number of mutations or a much larger number due to a mutator phenotype and genomic instability, or even gross karyotypic changes such as aneuploidy, that "kick-started" the process of cancer, these theories were the subject of an active and current debate amongst some of the most senior figures in cancer research.
[5.615]Professor Idle summarised the competing theories of cancer causation as follows. He said that there had been competing theories advanced by senior scientists and that each theory was credible. Nevertheless, there remained little agreement today as to how cancer arose. As with any area of scientific endeavour, this represented the normal process of proposition, counter-proposition and wider scientific debate, that might ultimately lead to a consensus view, or, through the discovery of new facts, to yet further proposition and debate. The cancer question was one of the most complex that medical science had yet faced. An enormous store of cellular and molecular data had been accumulated, the exact meaning of much of which was still unclear to the cancer research community. Mortality from cancer today was largely equivalent to what it was fifty years ago (though there had been variations in the occurrence of cancer at different sites). As he had previously stated, most of the understanding about the mechanisms by which lung cancer arose was built on the knowledge base of cancer in general. In this section of his evidence, he had focused on theories of cancer causation that in his judgment could be the most relevant to lung cancer. These included viruses, chemicals, failure of host defence mechanisms and various processes that operated at the level of genes and chromosomes. Additionally, there was now a major effort to understand how the nervous and immune systems might be inter-related and mediate the effects of personality, emotion and stress in the cause of cancer. However, in his view, for the reasons given, none of these provided an adequate basis for explaining how or why lung cancer arose.
[5.616]The next main section of Professor Idle's report and evidence related to laboratory investigations with tobacco derivatives and public health reports up to the end of 1964. He said that, as previously described by him, in the period up to the end of 1964 cancer researchers were concerned with the big questions of what cancer was and by what mechanisms it arose. In this same time period, a statistical association between lung cancer in males and heavy cigarette smoking was reported. A number of researchers began laboratory work on tobacco derivatives on the view that, if this association was causal, it ought to be possible to identify and remove the constituent or constituents of tobacco smoke responsible for causing lung cancer. This concept had evolved from the work, previously discussed, on shale oil and coal tar.
[5.617]Professor Idle next discussed condensate and derivatives of tobacco. He said that it was pertinent to consider the differences between cigarette smoke, total particulate matter, tobacco smoke condensate and tobacco "tar", terms that appeared in the literature of the period prior to 1964. Cigarette smoke was a dynamic mixture consisting of a fine aerosol of coated particles, known as the particulate phase, and a gas phase, also referred to as the "vapour phase". Many tobacco smoke constituents existed in both phases in a dynamic equilibrium between the two. The total particulate matter (TPM) was the material that could be trapped by passing the cigarette smoke through a Cambridge glass fibre filter. Gas phase was that material which escaped such filtration. If the cigarette smoke was passed through a series of glass vessels chilled to a very cold temperature, such as -60oc, then there condensed out a material known as "tobacco smoke condensate", which was sometime referred to, perhaps erroneously, as "tobacco tar". The "tar" yield referred to on a packet of cigarettes was the TPM captured on a Cambridge filter minus the water and nicotine content. It was not really an entity, it was a number. It was different from tobacco smoke condensate. It was the result of an experiment and then a calculation. A smoker was never exposed to tobacco smoke condensate because this material was created in a laboratory by cold-trapping cigarette smoke. In addition, a number of the studies involved the separation of tobacco smoke condensate into various fractions for biological testing. Extraction of the tobacco smoke condensate with various solvents and other fractionation processes led to the production of three main fractions, the acidic, the basic and the neutral fractions. Benzo[a]pyrene and the other polycyclic aromatic hydrocarbons were found in the neutral fraction.
[5.618]Against the background of previous studies, Wynder and others reported in 1953 a study in which tobacco smoke condensate was painted on the skin of mice. Their experimental method, as described by Professor Idle, was first to produce tobacco smoke condensate using a smoking machine, to take a solution of that material in a solvent and to paint it with a brush onto the backs of mice in places from which the hair had been clipped, repeating this a number of times per week for many weeks. The experiments used a particular strain of mice. Some additional animals were painted with a solution of 20-methylcholanthrene. All of these developed skin carcinomas in less than five months, thus demonstrating that this strain were particularly sensitive to skin carcinogens. The test animals were divided into two groups. One group was treated with tobacco smoke condensate in the solvent acetone. A second, smaller group, were treated with acetone alone to act as a control group. The treatment continued, with some important variations, three times a week for up to twenty-four months. The experimenters found that they were able to increase the concentration of the condensate in the acetone from one part in three eventually to equal parts. The problem was that when the experimenters started to paint the material on at a very high concentration, some of the animals died, so they gradually increased the amount over a period of time. Professor Idle commented that, when they had observed the appearance of papillomas on the animals' skin, they specifically painted only the papillomas once the animals "became weakened by old age or disease", rather than painting the whole shaved area uniformly. The authors reported data from eighty-one mice (from an original group of 112) that had been painted with the tobacco smoke condensate. The reported incidence of skin carcinomas in these animals was 44.4% and of papillomas was 59%. The reported incidence of carcinomas was dramatic in light of the results obtained by previous researchers, who had reported either no incidence or a very low percentage of incidence. The report by Wynder and others generated wide publicity and considerable scientific debate and controversy. The results were never replicated by them or by any other researchers. There were hundreds of studies carried out on skin painting of mice with tobacco smoke condensate, some of them by Wynder and his colleagues, but the same result was never achieved. Professor Idle said that he thought that the consensus view was probably that the material used by Wynder was somehow contaminated by having decomposed or not been stored correctly.
[5.619]Passey and others reported in 1954 that, in an attempt to replicate the results of Wynder and colleagues in 1954, they observed no tumours, and that the results of their experiments at most suggested that any carcinogenic properties possessed by the tars used were very attenuated. Kosak in 1954 catalogued the known and putative constituents of tobacco smoke, listing 43 known chemicals. Cooper and colleagues reported in 1954 that they had made new findings, namely the presence of small amounts of acenaphthylene and benzo[a]pyrene in tobacco smoke condensate. The same investigators, in a further report, identified the presence of various polycyclic aromatic hydrocarbons in condensed smoke from "cigarettes" made entirely of cigarette paper. Hamer and Woodhouse prefaced a study in 1956 with the statement that since the evidence that cigarette tars were carcinogenetic had come from only one group in one country, it seemed desirable that the results of other workers should be presented as soon as possible so that the position could be better evaluated. These British workers did not obtain skin tumours in either rabbits or mice that had been painted with tobacco smoke condensate obtained from a smoking machine. In addition, the tobacco smoke condensate did not initiate tumours in mice that were subsequently painted with the tumour promoter croton oil. In mice previously painted with benzo[a]pyrene, a tumour initiator, some tumours were reported, suggesting a possible tumour promoting effect of the tobacco smoke condensate. The authors discussed the possible reasons for the discrepancy between their findings and those of Wynder and colleagues, noting that the latter prepared a tobacco smoke condensate using cigarettes that were smoked at temperatures up to 960oC, in contrast with their own condensates which were prepared using cigarettes that were smoked at a temperature up to only 780oC which, they stated, was comparable to smoking cigarettes by mouth.
[5.620]Roe and co-workers, who had turned their attention to the study of initiation and promotion, concluded that since the effect of cigarette smoke condensate could be increased by the addition of initiators but not of promoters, the relative weakness of the carcinogenic action of cigarette smoke condensate was due to the paucity of initiators. Professor Idle said that in this period workers were expressing the view that cigarette smoke condensate did act weakly as a carcinogen. Roe et al. 1959 stated at p.631:
"Man, whether a smoker or not, is exposed to substances of proved tumour-initiating power in the polluted atmosphere, and in the products of some industrial processes and in some kinds of food. The correlation between smoking habits and lung tumour incidence may well be determined not primarily by the carcinogenic effect of tobacco smoke, but by its predominantly tumour-promoting action on the bronchial epithelium."
[5.621]Professor Idle summarised the laboratory studies involving skin painting in the period up to 1964 as follows. Prior to the publication in 1950 of the first reports of an association between lung cancer and cigarette smoking, there was relatively little laboratory research on cigarette smoke. But what research existed indicated that tobacco smoke condensate was weakly carcinogenic to mouse and rabbit skin. Following the 1950 reports, Wynder's laboratory began conducting studies in which tobacco smoke condensate was painted on the backs of mice. The 1953 report provoked considerable controversy among other scientists. Other laboratories reported that the findings of Wynder and colleagues could not be replicated. Moreover, Wynder's laboratory itself was never able to duplicate their original findings. In a number of subsequent publications, Wynder and his colleagues made clear their view that the purpose of their laboratory research was to identify the constituent or constituents of cigarette smoke that might account for the epidemiological association between lung cancer and cigarette smoking, thereby permitting its removal. They stressed that the mouse skin painting studies were not designed to prove that smoking caused lung cancer. In Wynder et al. 1957b, the authors wrote:
"As we have repeatedly stated, the primary proof that smoking is a cause of cancer in man must be based not upon animal experimentation but upon human epidemiological, pathological, and clinical studies. However, if animal data confirm the carcinogenic activity of a substance suspected to be carcinogenic to man, the evidence that this substance is active in man is strengthened.
The basic purpose of animal experimentation is to define the mechanism of carcinogenesis and to identify the specific carcinogens responsible for this activity."
[5.622]Professor Idle then turned to what he called "tobacco smoke condensate versus fresh whole cigarette smoke". He explained that cigarette smoke freshly produced by a cigarette was a highly changing and dynamic mixture of two phases: a fine aerosol coated with a liquid film and a gas or vapour phase, and that substances moved in and out of the liquid coating of particles and the vapour phase constantly. It was a dynamic, forever-changing chemical mixture, whereas the tobacco smoke condensate was a viscous liquid that had been collected at cold temperatures. He said that it was well established by 1965 that chemical changes rapidly occurred in the smoke after its formation in the burning zone of the cigarette and that these changes continued to occur in the collected tobacco smoke condensate. The sudden cooling of the smoke in the traps also allowed the formation of new chemical entities that were either not present in the smoke hitherto, or were present at a very low level. Cold-trapping permitted the gaseous and highly volatile constituents of the smoke to escape; these constituents comprising the great majority of the mass of the cigarette smoke. Thus, the four principal components of cigarette smoke by weight - nitrogen, oxygen, carbon dioxide and carbon monoxide - were not condensed in the cold-traps. Likewise, the other gases, such as nitrogen oxides and volatile components of the smoke, which were legion, were not condensed in the cold-traps. In summary, in his opinion, fresh whole cigarette smoke and tobacco smoke condensate differed in both their nature and chemical composition. This told us that we must extrapolate with great care from mouse skin painting experiments, using cigarette smoke condensate, to the effect of cigarette smoke on the lung.
[5.623]Professor Idle next turned to the question of the amount of cigarettes needed to produce condensate versus human smoking. He said that it was common practice in the mouse skin painting studies prior to 1965 for a mouse weighing 25-35g to be painted with an amount of tobacco smoke condensate that had been derived from at least one cigarette, and sometimes as many as five, that had been smoked on a smoking machine. Laboratory mice were not exposed to a dose of tobacco smoke condensate comparable to the number of cigarettes smoked by a typical cigarette smoker. It could be calculated from reports of the Wynder group that the number of cigarette equivalents received by a mouse in skin painting with tobacco smoke condensate per month equated to a human dose of 6,400 cigarettes per month, or over ten packs of cigarettes per day. On this basis, it could be calculated that mice were not exposed to a dose of tobacco smoke condensate equivalent to the number of cigarettes smoked by a cigarette smoker per day. In summary, in Professor Idle's judgment, the amount of tobacco smoke condensate applied to mouse skin each day was derived from a number of cigarettes far in excess of the number of cigarettes smoked by any human smoker in one day.
[5.624]The next comparison made by Professor Idle was that of mouse skin epidermal tissue versus respiratory epithelium. He said that the mouse skin, like most mammalian skin, was comprised of epithelial tissues, organised in layers. Within these layers were specialised tissues, such as various types of gland, hair follicles and so on. When the outer layers were damaged, they came off, and new layers rose up, hardened and became the outside surface. In the lung, while the tissue was epithelium, it was structurally very different. The cells were not arranged in flat layers, they were arranged in columns known as "columnar epithelium". On the top of each column, at least in the tracheobronchus, were little cilia, which wafted the mucus blanket up from the lung to the level of the larynx. Between these columns were goblet cells that produced the mucus. The epithelial cells of the skin arranged in layers, sometimes described as a "squamous" or "pavement" morphology. Thus, the epithelia of the skin were and the tracheobronchus were architecturally different and they served distinctly different functions for the host.
[5.625]There were further dissimilarities. The skin was keratinised, meaning that it had a hardened surface. The columnar epithelial cells in the lung were not hardened. Their purpose was not like that of the skin, which was to keep out the outside world, but to provide a structure on which the mucus could be produced, taken up and moved along to remove any particles or dead cells from down in the lung, up and to the level of the throat, where it could be swallowed or expectorated. Since the mucus was primarily an aqueous solvent, it would also trap water-soluble chemicals, aerosols and particular aggregates, expelling them by the same process. In a cigarette smoker, a proportion of the tobacco smoke constituents, therefore, was absorbed in the mouth and by the mucus of the tracheobronchial tree. In addition the lung was home to a type of white cell known as the pulmonary or alveolar macrophage, which was able to engulf and digest particles or micro-organisms. Like certain of the cells of the lung itself, these macrophages also were rich in enzymes that could metabolise and detoxicate chemicals. In summary, in Professor Idle's judgment, the results of experiments on mouse skin could not be carried over to respiratory epithelium.
[5.626]The next comparison was that of mouse versus man. He said that there were many differences at biochemical, anatomical, pathological and physiological level between mouse and man. Whilst we might share over 90% genetic similarity, nevertheless there were differences, both obvious and less obvious. It was an archaic point of view, no longer accepted, in toxicology to think of a mouse as simply a small human. Green, who was Chairman of the Department of Pathology at Yale University School of Medicine, testifying in 1957 before a sub-committee of the Committee on Government Operations in the United States House of Representatives, said that Wynder's experiments demonstrated that tobacco tar extracted by a special technique induced cancer on the skin of one strain of mice, and nothing more. Different results had been achieved with different strains of mice. The occurrence of such high differential susceptibility among most strains would suggest the existence of an even more pronounced difference between species, and an extrapolation of the findings to man would be absurd. There was no surety that a substance capable of inducing cancer in mouse skin would also induce cancer in mouse lung, to say nothing of human lung. Professor Idle said that he agreed with this conclusion.
[5.627]Professor Idle next considered the interaction of constituents of tobacco smoke. He said that in the period up to 1965, a number of studies were conducted in an effort to identify a constituent or constituents of tobacco smoke that might account for lung cancer in human smokers. Despite these efforts, no such constituent was identified. The studies showed that tobacco smoke condensate was active as a complex mixture in the mouse skin painting model and no binary combination of individual initiators and promoters was likely to explain this activity. Thus, by 1965, mouse skin painting studies had not identified any constituent or group of constituents, as they existed in tobacco smoke, that accounted for lung cancer in cigarette smokers.
[5.628]The next topic was inhalation. By 1965, researchers had begun to conduct studies in which laboratory animals were exposed to whole cigarette smoke by inhalation. The objectives of this research were to determine whether or not evidence could be produced that cigarette smoke could cause lung cancer in animals, and thereby investigate a possible relationship between human lung cancer and cigarette smoking. Thus, Stewart and Herrold, the first of whom was a prominent researcher at the NCI, stated in Stewart and Herrold 1962 that were it possible regularly to induce pulmonary cancers in laboratory animals by exposure to inhalation of cigarette smoke, this would constitute good evidence that cigarette smoking could cause cancer of the lung in man. Professor Idle said that this was in contrast to the objectives of mouse skin painting, which had been mainly to identify a constituent or constituents of tobacco smoke that might account for the occurrence of lung cancer in cigarette smokers with a view to removing it or them. So the purpose of inhalation experiments with laboratory animals was to induce lung cancer. Nevertheless, Hinshaw and Garland 1963 stated that despite literally hundreds of careful and prolonged experiments designed to produce lung cancer by exposure of mice or rats to prolonged breathing of cigarette smoke, no bronchogenic carcinomas had been produced. Professor Idle said that prior to 1965, none of the studies that exposed laboratory animals to cigarette smoke by inhalation reported a statistically significant increase in squamous cell carcinoma of the lung.
[5.629]The next topic was ciliastasis. Professor Idle said that certain investigators turned their attention to the gas phase of cigarette smoke, in contrast to the particulate phase which had been focused upon in relation to polycyclic aromatic hydrocarbons, such as benzo[a]pyrene. Hilding, writing in 1956, cited an article in the New York Times in 1955 that stated that Yemeni Jews never developed lung cancer despite smoking "a good deal of strong tobacco but passed the smoke through water in a special type of pipe." This author investigated the extent to which cigarette smoke, on entering the mouth, might be retained by the wetted surfaces of the mouth. Employing the tracheas and lungs of freshly slaughtered cows, he demonstrated that smoke components were deposited on the "mucous blanket" as a "visible scum of tar" and, at a high enough concentration, this was capable of causing the ciliary action (which persisted after death) to cease. He extended these experiments, using India ink as a marker of mucus flow, in a subsequent paper.
[5.630]Interest in the gas phase of tobacco smoke continued to grow in the late 1950s, particularly with respect to the ciliastatic properties of tobacco smoke constituents. Falk and others reported in 1959 on a study of tobacco smoke constituents in an effort to determine which of them might possess ciliastatic properties using the ciliated trachea of rats and rabbits and the ciliated epithelium of the frog oesophagus. They reported that cigarette smoke had ciliastatic properties and that nicotine elicited the greatest ciliastatic effect. They also determined that polluted atmospheric air (smog) had ciliastatic properties. Kensler and Battista reported in 1963 that several constituents of the gas phase of cigarette smoke, specifically hydrogen cyanide, formaldehyde, acrolein, ammonia and nitrogen dioxide, were ciliastats in experiments performed on the rabbit trachea. Wynder and others investigated in 1963 whether or not various constituents of tobacco smoke condensate were ciliastats, using the gill lamellae of the fresh-water mussel as their model. They reported that the phenols were the most active ciliastats.
[5.631]Thus, Professor Idle concluded, prior to 1965, three groups of researchers, and possibly more, had reported that individual constituents of cigarette smoke and tobacco smoke condensate had ciliastatic properties using various animal models. In his judgment, by 1965, it was unclear whether or not ciliastasis played a role in human lung cancer.
[5.632]In the period from 1965 to the end of 1971 the action of phenols as ciliastats began to attract the attention of investigators. A number of researchers investigated whether or not constituents of cigarette smoke had the ability to slow, or even halt, the movement of the cilia found in the tracheobronchus. It was thought that the ciliastats in cigarette smoke were found in the gas phase and particular attention was paid to certain groups of constituents, the phenols, the aldehydes and the acids. Wynder and Hoffmann, writing in 1967, were definitive in their view about the role of ciliastasis in lung cancer. They stated that the impairment of ciliary function and mucus transport in the respiratory system was clearly a phase preceding the manifestation of metaplasia in the bronchial epithelium. Wynder and his colleagues continued to perform experiments designed to measure the effect of constituents of tobacco smoke condensate or gas phase on the ciliary activity of the gills of clams and other molluscs. However, Professor Idle pointed out, this animal system was very different from the human tracheobronchus. In addition, the physiological function of the clam gill cilia was to extract oxygen from the water, in stark contrast to that of the mammalian tracheobronchial cilia, which was to move foreign matter up the ciliary escalator to the throat. Wynder and colleagues, writing in 1965, justified their use of the mollusc gill assay on the basis of its "simplicity, ease of operation and reproducibility".
[5.633]Other researchers preferred to use other animals. One group used mammalian trachea, from sheep, rabbit or rat, to conduct their studies. Battista and colleagues reported in 1967 that cigarette smoke applied to the larynx of the whole (live) chicken had little or no effect on ciliary action, but did result in a greater than four-fold increase in mucus secretion. Dalhamn from the Karolinska Institute in Stockholm, one of the leading researchers on ciliastasis, in a criticism of the methodologies employed to investigate it, wrote in 1970 that vertebrates, possibly mammals, were preferable to inferior species; this was in the context of a critique of using shellfish gills as a model to test ciliastasis. He also proposed other criteria for the investigation of ciliastasis, such as the preferential use of in vivo experiments, direct measurement of ciliary activity rather than indirect measurement on mucus, and the use of high-speed cameras for filming the cilia in in vivo experiments. Not many of the reported investigations met these stringent criteria.
[5.634]Pavia and others reported in 1970 on an investigation of ciliastasis using human volunteers, both non-smokers and smokers. The volunteers inhaled polystyrene pellets labelled with a radioactive isotope, and it was reported that they did not exhibit impaired tracheobronchial clearance (an in vivo measurement of ciliary function). The authors concluded that although the study had shown that the cilia were apparently functioning normally in spite of a lifetime of smoking, it was possible that temporary stasis occurred in the cilia after a smoke, with complete recovery between smokes and overnight. Camner and others reported in 1971 that the speed of mucociliary transport in a group of smokers was significantly higher during intensive cigarette smoking than when they were not smoking and that on the average tracheobronchial clearance diminished in the same persons when they had abstained from smoking for one week, although the decrease was not significant; accordingly, ciliastasis did not seem likely to occur in connection with ordinary smoking. Professor Idle commented that this remarkable finding suggested that smoking actually increased ciliary activity, rather than diminishing it, as had been claimed by others. Das and colleagues reported in 1970 that diluted cigarette smoke also stimulated ciliary activity in frog oesophagus.
[5.635]Professor Idle concluded that by the end of 1971 a number of volatile phenols, aldehydes and acids were reported to have ciliatoxic properties in the mollusc gill, but the relevance of these studies to humans was questioned. Direct investigation of ciliary activity in smokers versus non-smokers and in smokers in relation to patterns of smoking was unable to detect any ciliatoxic activity of cigarette smoking. The belief that ciliastasis brought about by smoking was part of a mechanism of human lung cancer had been virtually eliminated. To his knowledge this had never been resurrected.
[5.636]Professor Idle was next asked to comment on passages in various public health reports. In RCP 1962 it was stated at p.26, para.37:
"Skin cancer can be produced in mice by applications of tar condensed from tobacco smoke but the results obtained by various investigators have not been uniform and exposure of animals to tobacco smoke in inhaled air has failed to produce lung cancers."
Professor Idle said that these statements were accurate. The paragraph continued:
"Moreover the amount of cancer-producing substances in the smoke itself does not seem likely to be sufficient to account for the large number of cases of cancer associated with the habit."
Professor Idle said that he thought that the Royal College of Physicians were recognising at that point that workers had not been able to identify any substance or substances in the smoke in sufficient quantity to explain the statistical association between cigarette smoking and lung cancer. RCP 1962 stated at p.26, para.39:
"In addition to the known carcinogens which have been detected in tobacco smoke others as yet undetected may be present; possibly two or more in combination may reinforce each other in producing cancer. It is possible that tobacco smoke may contain substances which act in conjunction with substances generally present in the air we breathe to produce cancer, although neither substances might do so alone. Indeed the action of tobacco might be simply to produce chronic irritation which, as in other tissues, may increase liability of the lung to cancer. There is a wide field for further investigation here, but no ground for refuting the evidence from human experience."
Professor Idle commented that this passage contained speculation, unvouched by experimental evidence, and he agreed that there was scope for further investigation. In RCP 1962, at p.S5 of the summary, among the facts mentioned which might be considered to conflict with the conclusion that smoking was a cause of lung cancer was the fact that no animal had yet been given lung cancer by exposure to cigarette smoke. Professor Idle agreed that this statement was correct.
[5.637]Turning to USSG 1964, Professor Idle repeated that he agreed with the statement, at p.20, that:
"Statistical methods cannot establish proof of a causal relationship in an association. The causal significance of an association is a matter of judgment which goes beyond any statement of statistical probability."
[5.638]At p.33 of the report it was stated:
"Seven polycyclic hydrocarbon compounds isolated from cigarette smoke have been established to be carcinogenic in laboratory animals. The results of a number of assays for carcinogenicity of tobacco smoke tars present a puzzling anomaly: the total tar from cigarettes has many times the carcinogenic potency of benzo(a)pyrene present in the tar. The other carcinogens known to be present in tobacco smoke are, with the exception of dibenzo(a,i)pyrene, much less potent that benzo(a)pyrene and they are present in smaller amounts."
Professor Idle said that these statements accorded with his own view.
[5.639]In the same passage of the report, it was suggested that this discrepancy might possibly be due to the presence of cocarcinogens in tobacco smoke, and/or damage to mucus production and ciliary transport mechanism. Professor Idle referred to his previous evidence about the latter hypothesis. As to the former, he was asked to comment on a passage at p.58:
"The results of a number of such assays [of tobacco smoke tars for carcinogenicity by skin-painting] present a puzzling anomaly: the total tar from cigarettes has about 40 times the carcinogenic potency of the benzo(a)pyrene present in the tar."
This, he said, quantified the anomaly.
[5.640]At p.146 of the report it was stated:
"The amount of known carcinogens in cigarette smoke is too small to account for their carcinogenic activity. Promoting agents have also been found in tobacco smoke but the biological action of mixtures of the known carcinogens and promoters over a long period of time is not understood."
At p.59 the report stated: "Assessment of all conceivable synergistic effects presents a gigantic problem for exploration." Professor Idle said that this problem had never been solved.
[5.641]At p.167 of the report it was stated:
"The lungs of mice, rats, hamsters, and primates have been found to be susceptible to the induction of bronchogenic carcinoma by the administration of polycyclic aromatic hydrocarbons, certain metals, radioactive substances, and oncogenic viruses. The histopathologic characteristics of the tumors produced are similar to those observed in man and are frequently of the squamous variety."
Professor Idle said that this meant simply that it was possible to induce squamous cell carcinoma of the lung in the animals mentioned.
[5.642]At p.165 the report stated: "The production of bronchogenic carcinomas has not been reported by any investigator exposing experimental animals to tobacco smoke." Professor Idle said that his research in the literature led to the same result.
[5.643]Professor Idle concluded that as at the end of 1964, none of the competing theories had been established as the cause of human cancer. None of these theories provided an adequate basis for explaining how lung cancer arose. Some researchers conducted studies in which tobacco smoke condensate was painted on the backs of laboratory mice. The methodologies used in these studies were not standardised and, in addition, other variables contributed to the widely divergent incidence of mouse skin cancer reported in these studies. These studies did not result in the identification of a constituent or group of constituents that explained the occurrence of lung cancer in cigarette smokers. None of the studies in which laboratory animals were exposed to whole cigarette smoke by inhalation reported a statistically significant increase in squamous cell carcinoma of the lung in the exposed animals.
[5.644]By the end of 1964, three public health authorities had concluded that cigarette smoking was a cause of lung cancer. These judgments were based almost entirely upon an interpretation of epidemiological reports. These conclusions were not, however, based on a consideration of lung cancer as a biological phenomenon. For the reasons thus far given by him, he did not agree with these conclusions. In his opinion it was not "almost universally accepted by scientists" (as averred on behalf of Mrs McTear) in 1964 that cigarette smoking could cause lung cancer. Moreover, in his opinion, cigarette smoking had not been established as a cause of lung cancer as at the end of 1964. This opinion was expressed on the basis of the literature which he had considered.
[5.645]In the period up to the end of 1971, research continued on the factors thought to cause cancer and on the competing theories of cancer causation. Laboratory research on tobacco derivatives also continued in this period. This research involved both mouse skin painting and inhalation studies. Much of this effort continued to be directed towards the identification of constituents of tobacco smoke that might be responsible for lung cancer in smokers. The principal investigators included Day and colleagues at the Tobacco Research Council Laboratories in Harrogate. By 1965, it had been recognised that a number of the variables in the mouse skin painting studies might account for the disparate results obtained. These included the type of tobacco used to produce the tobacco smoke condensate, the preparation and storage of the tobacco smoke condensate, the method and schedule of application of the tobacco smoke condensate to the mouse skin, the strain of mouse used in the studies, and the criteria used to determine the biological end points of the studies. If an investigator were to determine whether a skin tumour had been produced on a mouse, then it was necessary to distinguish between benign skin tumours and various types of malignant skin tumour, whether a tumour appeared malignant under the microscope, behaved in a malignant manner in the mouse, had invaded underlying tissues and probably that it had metastasised to other organs. During this period, researchers at the Harrogate Laboratories investigated and standardised many of these variables. In their papers they stated clearly that there were difficulties that they recognised in comparing studies between different laboratories for these reasons, and so they set about an attempt to standardise as many of them as possible.
[5.646]The principal study was by Day, writing in 1967, who calculated that 8,000 mice would be required to perform a study that could distinguish between a tumour rate of 20% and a tumour rate of 30% with 98% confidence: this was a very much larger number than had been used in any previous study, for example those of Wynder. Day attempted to standardise a number of the experimental variables: females of a strain of mouse that were resistant to nicotine toxicity were used; large group sizes were used; a measured amount of condensate was applied, using an automatic pipette; the study continued until each animal died or became sick, rather than finishing at an arbitrary time point; the diagnosis of skin cancer was made by an animal pathologist who could make a diagnosis of an invasive skin cancer by ascertaining whether the skin was attached to underlying muscle by the tumour; and complete autopsies, including the histopathology of all major organs, were performed on all mice, including those without skin tumours. The autopsies constituted an important difference between this study and the other published skin painting studies in this period, because Day was able to report on the probable cause of death for each test animal. The author reported an overall incidence of 3% of malignant tumours in the painted area (in control groups as well as tested animals). This was the eleventh most common pathological finding at the time of death in these animals. He also reported on a dose-response relationship. In a further paper, published in 1968, Davies and Day commented on the divergent findings between Day's results, and those of Wynder and others, published in 1953. They observed that the differences were possibly due to the type of tobacco smoke condensate used and the method of application of the condensate.
[5.647]In this period, Professor Idle said, the results of the mouse skin painting studies were offered by some as evidence that cigarette smoking was a cause of human lung cancer. Thus, Dr Thomas Carlile, Chairman of the Committee on Tobacco and Cancer of the American Cancer Society and past President of the American Cancer Society, in testimony at the 1965 United States House of Representatives Hearings on Cigarette Labeling and Advertising, identified one of the points that the American Cancer Society had considered in reaching its decision that cigarette smoking was a major cause of the increase in lung cancer to be the fact that cancer had been produced repeatedly by the application of tar condensed from cigarette smoke to the skin of experimental animals. Leading medical scientists, however, disagreed with the view that the mouse skin painting data were relevant to human lung cancer. For example, Dr Harry S N Greene, Chairman of Pathology, Yale University School of Medicine, testified at the same hearings that it was true that cancer had been produced in the skin of mice by long-continued painting with tobacco condensates. It should be emphasised, however, he said, that cancer had also been produced in mice by a variety of common innocuous substances such as salt, sugar, egg white, and cellophane. Dr R H Rigdon, Professor of Pathology at the University of Texas at Galveston School of Medicine, also testifying at these hearings, stated that the fact that tobacco tars would produce a tumour on the skin of a specific strain of mouse did not, in his opinion, lead to the conclusion that cigarette smoke would produce cancer in the lungs of man. He said that as he continued his work in the field of experimental carcinogenesis, he found puzzling variations in the response observed from one species of animal to another with respect to the development of cancer, so data concerning cancer in animals should not be considered proof of a similar effect in man.
[5.648]Dr Clarence Cook Little gave evidence at the 1969 United States House of Representatives Hearings on Cigarette Labeling and Advertising: Little 1969. At that time he was Scientific Director of The Council for Tobacco Research - USA. He had been Director and thereafter Director Emeritus of the Jackson Laboratory for Research in Genetics and Cancer, and Managing Director of the American Society for the Control of Cancer (subsequently the American Cancer Society). He served two terms as President of the American Association for Cancer Research. He had been actively interested in cancer research as a biologist for more than 60 years. In the course of his evidence he said, at p.1106:
"When this [the painting of animal skin with tobacco smoke condensate] is done the painting is followed in some cases by abnormal growth of the skin and, in some of these cases, later by skin cancer. In this respect the condensate of tobacco smoke joins more than 500 other substances, many of which are known to be entirely harmless to man, in producing a more or less standardized effect on mouse skin. There is nothing unusual or peculiarly characteristic about the reaction of these animals to smoke condensate. However, an important fact which has been overlooked or ignored is that the relative cancer-producing effects of condensates of cigarette smoke, of pipe tobacco smoke and of cigar smoke do not follow the same order of activity or coincide with the recorded degrees of statistical association between cancer and these three types of smoking exposure in man. This discrepancy is basic. It shows that if we accept the statistics as a basis for a working hypothesis we must also admit that skin painting with condensates of tobacco smoke is not a significant or valid method of testing the relative cancer-forming potentials of such smoke required by the working hypothesis [that smoking causes lung cancer]. In other words, the employment of a different agent (condensate instead of smoke) on a different target organ (skin instead of lung) and on a different animal (mouse instead of man) is not a firm basis on which to develop a broad and comprehensive research program to determine the quantitative effects of smoke on man."
Professor Idle said that this passage reflected his own views.
[5.649]He concluded that by the end of 1971, it was recognised that continued screening of tobacco smoke condensate in the mouse skin bioassay in an effort to identify a constituent that might be responsible for the occurrence of lung cancer in cigarette smokers was unlikely to produce a result. Therefore, the testing of tobacco smoke condensate in the mouse skin model came to a close in the period immediately following 1971. In his opinion, the reported results of the various experiments in which tobacco smoke condensate was painted on the skin of mice could not answer the question of whether or not cigarette smoking caused human lung cancer. He said that the position in this regard remained the same now as it was then.
[5.650]Professor Idle's attention was next directed to IARC 1986. At pp.135-136, in discussion of the administration of tobacco smoke condensates, reference was made to the 1952 paper of Wynder and others. At p.136 it was stated:
"Animal studies conducted prior to 1964 provided an important measure of support for the epidemiological demonstration that cigarette smoke is an important human carcinogen."
Professor Idle said that he did not agree with this view, for the reasons already given by him. This statement, in IARC 1986, was at variance with Wynder's statements about the purpose of his studies, which was to identify constituents that might be carcinogenic and to remove them, rather than to prove a causal connection between cigarette smoking and lung cancer. For the reasons he had given, studies in which tobacco smoke condensate was painted on to mouse skin were not designed to answer, and could not answer, the question of whether or not cigarette smoking was the cause of human lung cancer. Thus, in the period 1965 to the end of 1971, there was an increased focus on experiments that exposed experimental animals to whole cigarette smoke by inhalation. This was seen, at the time, as a model which more closely resembled human smoking than the mouse skin painting model.
[5.651]Professor Idle then turned to experimental animal inhalation models. He said that there were four principal animal models that were used in the inhalation studies, the mouse, the rat, the hamster and the dog. It should be appreciated at the outset that the objective of these studies was to produce squamous cell carcinoma of the lung in animals exposed to whole cigarette smoke by inhalation.
[5.652]First, there were studies in mice, the methodology and results of which were summarised in his report. He was asked simply to state the conclusion, that in none of them was squamous cell carcinoma of the lung induced.
[5.653]Among studies in rats, Alexandrov and Raitchev reported in 1965 on the passive exposure of 107 rats to cigarette smoke for two years. They reported that six out of 107 developed adenomas and two out of 107 developed adenocarcinomas, both in the lung. They also reported that none of 113 controls developed lung tumours. Laskin and others reported in 1970 on a study in which rats were exposed to the irritant gas sulphur dioxide mixed with the polycyclic aromatic hydrocarbon benzo[a]pyrene. Some rats developed squamous cell lung tumours, and this established that the rat was a species susceptible to develop squamous cell lung carcinomas.
[5.654]Investigators at the Research Institute of the German Tobacco Industry were engaged in an undertaking to establish if hamsters might be a suitable model for cigarette smoke inhalation. Dontenwill reviewed this work in 1970. No lung tumours were reported. Progressive epithelial changes were found in larynx which Dontenwill described as "precancerous". Professor Idle said that what was observed was not therefore cancer.
[5.655]Auerbach and others, and Hammond and others, both reported in 1970 on a study of eighty-six male beagle dogs trained to smoke cigarettes through a tracheostoma. Before being asked to comment on these studies, Professor Idle gave evidence that in the period 1965 to the end of 1971, a number of studies were conducted in which mice, rats, hamsters and dogs were exposed to cigarette smoke by inhalation. In the studies with mice, rats and hamsters, no squamous cell carcinomas of the lung were reported. Only the study by Auerbach and Hammond reported the development of "invasive squamous cell carcinoma of microscopic size" in two dogs.
[5.656]In RCP 1971, p.37, para.3.4, it was stated:
"In many experiments animals have been made to inhale cigarette smoke for various periods. The efficiency of the filtration by the noses of animals used is such that a large proportion of the smoke is removed before it reaches their lungs [...]. Until recently there was only one report of an inhalation experiment with mice in which lung cancer had been induced and this was of a different type from human lung cancer [...]. Production of typical cancer of the larynx in hamsters by exposure to cigarette smoke has now been reported [a reference to a paper by Dontenwill and others then in press]. Furthermore, two out of twenty-four dogs taught to inhale cigarette smoke directly into the lungs by means of tubes inserted into their windpipes have now developed lung cancer, similar to the human disease, after two and a half years of smoking seven unfiltered cigarettes daily. Ten developed other types of lung cancer. Dogs which had smoked the same number of filtered cigarettes during the same period did not develop cancer though some showed precancerous changes."
[5.657]The information in the latter part of this paragraph was derived from a report by Auerbach and Hammond in 1970 entitled "Smoking gives dogs invasive lung cancer". Professor Idle said that the study of Auerbach and Hammond attracted much contemporaneous attention and was highly controversial. For example, Sterling wrote in 1971 that it appeared from the description of the experiment that the lungs of the dogs were infused daily with unfiltered air drawn directly into the lungs through holes in the trachea and so by-passing the usual protective mechanisms which kept out or removed dust, bacteria and other impurities. It was well known, he wrote, that many changes in lung tissue, including true metastatic cancers, could be observed as a consequence of introducing dust and impurities into the lungs of animals. Professor Idle added a number of comments of his own. First, the control animals were very small in number, and they were not true controls, inasmuch as they had at some time been exposed to cigarette smoke, being dogs which had been taught to smoke earlier and had been tracheostomised. The eighty-six dogs had been divided into four exposure groups and one control group of eight dogs. In a normal laboratory experiment the number of controls was at least equal to the number of test animals, and in many studies the number of controls was double that of exposed subjects. The small number of controls used by Auerbach and Hammond did not provide a basis for saying that what was observed was greater than would be expected from the control observations. There was, he said, an adage well known amongst laboratory investigators that an experiment was only as good as its controls, and he regarded this as axiomatic. If the controls had been taught to smoke earlier, then they had been exposed to cigarette smoke. Secondly, there were doubts about the interpretation of the reported results. The authors reported that twelve out of seventy-four dogs that had smoked non-filter cigarettes developed locally invasive bronchiolo-alveolar carcinomas. They also reported that two out of eight control dogs developed non-invasive bronchiolo-alveolar carcinomas. Furthermore, they reported that two out of twelve dogs with bronchiolo-alveolar carcinomas also developed "invasive squamous cell carcinomas of microscopic size". Professor Idle said that bronchiolo-alveolar carcinomas were rare in humans and, as stated by the authors, the bronchiolo-alveolar tumours found in their smoking dogs differed in several respects from bronchiolo-alveolar tumours found in man. These tumours also occurred in 25% of control dogs. Moreover, he said, the relevance to human lung cancer of the finding of "invasive squamous cell carcinomas of microscopic size" in the lungs of two dogs was unclear. Such microscopic lesions were not invasive and metastasising squamous cell cancers. They do not therefore fulfil many of the criteria for lung cancer per se.
[5.658]In Professor Idle's judgment, in the period prior to 1972, no animal exposed to fresh whole cigarette smoke developed squamous cell carcinoma of the lung. He then turned to consider the research into the constituents of cigarette smoke in the period from 1965 to 1971. Researchers continued, during this period, with an effort to identify a constituent of cigarette smoke that might be responsible for human lung cancer, so that it might be removed. Several constituents and groups of constituents were the focus of this endeavour.
[5.659]Many tobacco smoke constituents existed in both a particulate phase and a gas phase, in a dynamic equilibrium between the two. The total particulate matter was the material that could be trapped by passing the cigarette smoke through a Cambridge glass fibre filter. Gas phase was that material which escaped such filtration. By the end of 1971, approximately 1,000 constituents of tobacco smoke condensate had been identified. Fewer than 100 constituents of the gas phase had been identified by this time.
[5.660]Before discussing the biological properties of the constituents of tobacco smoke, and in particular their potential as a cause of human lung cancer, it was necessary to define the occurrence of such constituents. By 1971, little laboratory work, either chemical or biological, had been carried out with the total particulate phase. In almost every case, the experiments were performed with tobacco smoke condensate, which was used as a surrogate for tobacco smoke. Tobacco smoke was seen as sufficiently chemically complex that the scientific literature of the day was replete with phrases such as "thousands of compounds", which gave tobacco science an air of mystery. According to Wynder and Hoffmann, writing in 1967, the total mainstream smoke from a cigarette amounted to about 500mg, more than 85% of which was comprised of the atmospheric gases nitrogen, oxygen and carbon dioxide. The total particulate matter comprised only about 8% by weight. The gas phase, excluding the common and inert atmospheric gases, comprised about 1% of the smoke by weight. Thus, the chemical constituents of the particulate phase and gas phase combined, that had generated toxicological interest, comprised less than 10% by weight of the cigarette smoke.
[5.661]By the end of 1971, polycyclic aromatic hydrocarbons were among the most studied group of constituents in tobacco smoke condensate. Benzo[a]pyrene continued to be the focus of research interest. Professor Idle said that it was pertinent, in analysing whether or not the total polycyclic aromatic hydrocarbons, as they are found in tobacco smoke, might cause lung cancer, to ask to what extent their presence explained the observed carcinogenicity of tobacco smoke condensate on mouse skin. He divided this into two questions: first, whether there was enough present to explain the carcinogenicity of tobacco smoke condensate; and, secondly, to what extent might interactions with other constituents in the mixture influence the mouse skin carcinogenicity of the polycyclic aromatic hydrocarbons. As he had already explained, compounds acting in combination might either act as co-carcinogens or as anticarcinogens. As to the first of these questions, benzo[a]pyrene could be calculated to possess approximately 80% of the mouse skin carcinogenicity of the polycyclic aromatic hydrocarbon group of constituents and thus it might be used as a surrogate for the group of carcinogenic polycyclic aromatic hydrocarbons as a whole. Earlier studies had led to the conclusion that benzo[a]pyrene could not account for more than 2.5% of the carcinogenic activity of tobacco smoke condensate on mouse skin. The total polycyclic aromatic hydrocarbon fraction was therefore unlikely to contribute more than 3% of the total activity of the tobacco smoke condensate. Professor Idle agreed with the conclusions of Wynder and Hoffmann in 1967 and Van Duuren in 1968 that the polycyclic aromatic hydrocarbons did not exist in sufficient quantity in cigarette smoke to explain the carcinogenicity of tobacco smoke condensate on mouse skin. As to the second question, various studies, including that of Wynder and Hoffmann in 1967, had shown that the mouse skin carcinogenicity of benzo[a]pyrene, and indeed other carcinogenic polycyclic aromatic hydrocarbons, could be diminished by the presence, in the tobacco smoke condensate, of other members of this constituent group and indeed by other chemically-unrelated constituents. In addressing this question, the effect of interactions that might enhance the carcinogenicity of benzo[a]pyrene must also be considered. By the end of 1971, tumour promoters, particularly the phenols, that could enhance the mouse skin carcinogenicity of benzo[a]pyrene, had been identified in cigarette smoke, but in this period the interaction of polycyclic aromatic hydrocarbons and phenols was not understood. Accordingly, by the end of 1971, the polycyclic aromatic hydrocarbons, as they existed in cigarette smoke, had not been shown to be a cause of lung cancer in cigarette smokers.
[5.662]Having already considered phenols, aldehydes and acids in the context of his discussion of ciliastasis, Professor Idle next briefly mentioned the isotope polonium-210, which was present in the atmosphere, the soil and certain plants, including tobacco. Despite an initial difference of views, by 1971, he said, there was general agreement that polonium-210, as it existed in tobacco smoke, was not a cause of lung cancer in smokers. Another group of compounds that were being discussed in this period as a possible cause of lung cancer in smokers were the nitrosamines. By the end of 1971, most commentators were sceptical that nitrosamines actually occurred in tobacco smoke, believing that it was more likely that they were being formed as artefacts during the condensation process. The formation of nitrosamines from amines and nitrogen oxides took place in an exothermic reaction, in which heat was given out, so the cooling process in the traps in which tobacco tar condensate was formed provided an appropriate environment for the formation of nitrosamines, since the heat of the reaction was taken away in the cooling process.
[5.663]Among other constituents which were considered during this period were selenium in cigarette paper, pesticides and nickel. In each of these cases, the constituents were researched, often by only one laboratory, and then discounted as potential causes of human lung cancer. By 1971, there was general agreement that these other constituents, as they existed in tobacco smoke, were not a cause of lung cancer in smokers.
[5.664]By the end of 1971, Professor Idle said, no constituent or constituents had been identified in cigarette smoke that accounted for lung cancer in cigarette smokers. Dr William Lijinsky of the Oak Ridge National Laboratories in the United States gave evidence in the course of hearings before a subcommittee of the United States House of Representatives Committee on Government Operations in 1971 that "in spite of twenty years' work on tobacco smoking we cannot identify or nobody has been able to identify a carcinogen to explain the incidence of lung cancer in man."
[5.665]Professor Idle's conclusions were that, as at the end of 1971, none of the competing theories had been established as the cause of human cancer. None of these theories provided an adequate basis for explaining how lung cancer arose. In this period, researchers continued to paint tobacco smoke condensate on the backs of mice. Skin painting protocols were improved and standardised by the Harrogate Laboratories. None of the skin painting studies, or any other investigation, resulted in the identification of a constituent that explained the appearance of lung cancer in cigarette smokers. By the end of 1971, a number of researchers conducted studies in which several species of laboratory animals were exposed to whole cigarette smoke by inhalation in an attempt to determine if cigarette smoke could cause lung cancer in these species, and thereby provide data concerning a possible relationship between human lung cancer and cigarette smoking. These studies were not able to produce squamous cell carcinoma of the lung in the exposed animals. In his opinion, cigarette smoking had not been established as a cause of lung cancer as at the end of 1971.
[5.666]Professor Idle next discussed laboratory investigations with tobacco derivatives from 1972 to the present. He said that some researchers continued to focus their investigations on the small group of tobacco smoke constituents that had been reported to be carcinogenic in the prior periods. Others took the view that a complex mixture such as cigarette smoke must be evaluated in its entirety, due to the myriad interactions that might occur when an organism was exposed to that complex mixture.
[5.667]In this period, a number of human cancers that had been associated with specific chemical exposures were successfully modelled in experimental animals. By this he meant that experimental animals exposed to those chemicals developed the same tumour type in the same organ as that observed in humans exposed to these chemicals. Exposures and diseases in which this had been demonstrated included: asbestos and pulmonary mesothelioma; vinyl chloride monomer and liver angiosarcoma; bis-chloromethyl ether and small cell lung cancer; aflatoxin B1 and hepatocellular carcinoma; and β-naphthylamine and bladder cancer. Additionally, it had been stated in USSG 1964 that experimental animals had been reported to develop squamous cell carcinoma of the lung following the inhalation of a number of carcinogens, including several dusts, metals and radioactive materials. Several of the studies in this time period reported that cigarette smoke reached the lung during inhalation experiments in the mouse, the hamster and the dog, using a technique called "nose-only exposure" and the addition of tracer materials to experimental cigarettes. In view of these reports, a number of researchers conducted experiments in which animals were exposed to whole cigarette smoke, in the period after 1971.
[5.668]The most substantial study of cigarette smoke inhalation in animals was that funded under contract by The Council for Tobacco Research - USA, Inc, performed in mice by the contract toxicology laboratory, Microbiological Associates of Bethesda, Maryland. This company's laboratory was located close to the NIH, and it was their principal contractor. More than 10,000 hybrid mice, containing several strain backgrounds, were exposed to the smoke from over 800,000 cigarettes. In one experiment, a total of 2053 female mice were exposed (nose only) to fresh whole cigarette smoke, together with 1014 sham-exposed mice and 449 shelf controls. It was reported that the results of this study suggested that unfiltered experimental reference cigarette smoke had weak carcinogenic activity in mouse lung tissue. No bronchogenic squamous cell carcinomas were observed in any of these animals. Alveolar adenocarcinomas, as well as other alveologenic lesions, were observed in smoke-exposed animals, and the incidence was higher in the smoke-exposed animals than in the sham-exposed animals. The difference in incidence of these alveolar adenocarcinomas and other alveologenic lesions, however, never reached a statistical level of significance. In addition, 20-methylcholanthrene was administered to mice as a positive control and produced squamous cell carcinoma of the lung. Daily smoke administration was reported not to alter the incidence or distribution of the 20-methylcholanthrene lesions. Moreover, benzo[a]pyrene was administered intratracheally to a further 320 (smoke-exposed), 260 (sham-exposed) and 130 (shelf controls) mice. Daily smoke exposure for 110 weeks was reported not to alter the incidence or the latency of benzo[a]pyrene-induced lung tumours. In his foreword to the final report, CTR 1984, Dr Sheldon C Sommers, Scientific Director of The Council for Tobacco Research - USA, Inc, wrote:
"The results observed included these: none of the smoke-exposed animals developed pulmonary squamous cell carcinoma; mice pretreated with a pure carcinogen did not have significantly increased lung cancers after prolonged smoke exposure; and the overall numbers of pulmonary neoplasms identified were not statistically significantly different in the smoke-exposed mice, compared to the sham smoke-exposed or shelf control mice."
[5.669]Witschi and colleagues reported in 1997 that in a study carried out by them the incidence of pulmonary adenoma/adenocarcinoma was not statistically significantly different between two exposed groups of mice.
[5.670]Among studies in rats, Davis and colleagues, working at the Harrogate Laboratories, reported in 1975 that neither squamous cell carcinomas nor any other types of lung tumour were reported to occur in any of the groups of rats exposed to tobacco smoke condensate and the gas phase of cigarette smoke in various combinations. In another study, also reported in 1975, of 406 rats that had been exposed to cigarette smoke, four reportedly developed squamous cell lung tumours, only one of which was described as a squamous cell carcinoma. The authors reported that the incidence of squamous cell carcinoma in the exposed and control groups was not statistically significantly different. They also reported that the effects of a single administration of benzo[a]pyrene, followed by smoke exposure, were in general similar to those of smoke exposure only. Kendrick and colleagues reported in 1976 on an experiment in which 160 rats were exposed to the smoke of seven to ten cigarettes per day. Sham exposed and shelf controls were also used. No lung tumours were reported in any group.
[5.671]Dalbey et al. 1980 reported on an experiment in which eighty female rats were exposed to the smoke from seven cigarettes per day, five days per week, for the lifetime of the animals. Seven of the smoke exposed rats were reported to have developed eight lung tumours, including adenoma (5/80), alveologenic carcinoma (2/80) and squamous cell carcinoma (1/80). One of the thirty sham-exposed control animals, but none of the sixty-three untreated controls, was also reported to develop a lung tumour, alveologenic carcinoma. The authors stated that the occurrence of one squamous cell carcinoma of the lung in eighty rats was not statistically significant. However, Professor Idle commented, they combined the total number of lung tumours with two nasal tumours observed in the exposed animals and reported this total to be statistically significantly greater than the tumours observed in the combined control groups. They did not discuss the observation reported by them that tumours in the pituitary gland, uterus and ovaries, together with the lymphoid system, occurred statistically significantly more frequently in untreated and sham-exposed groups than in the smoke-exposed group.
[5.672]Wehner and colleagues reported in 1981 on the results of a study in which groups of eighty female rats were exposed to the smoke from eight cigarettes, seven days per week, up to twenty-four months. Sham-exposed and untreated controls were also employed. A single squamous cell lung carcinoma (reported by the authors as a "lung epidermoid carcinoma") was reported to have developed in a group exposed to low-tar, medium-nicotine cigarette smoke. Heckman and Dalbey reported in 1982 on the results of a study in which female rats were exposed to cigarette smoke. No tumours of any kind were reported to develop in any rat, even with the greatest dose and duration of smoke exposure. Heckman and Lehman reported in 1985 on a study in which female rats were exposed to the same dose of cigarette smoke as in the preceding study. No lung tumours were reported in any rat.
[5.673]Turning to studies in hamsters, Professor Idle mentioned first a report by Dontenwill and others in 1973 on a study in which large numbers of hamsters were actively exposed (nose only) to the smoke of various cigarette types. The authors reported that the incidence of "early invasive carcinoma" in the larynx, which did not invade the underlying cartilage, was greater in the smoke-exposed animals than in the controls. No statistical evaluation of these data was reported. In a study by Wehner and others, reported in 1974, on the exposure of hamsters to cigarette smoke for the lifetime of the animal, with a similar number of sham-exposed controls, neither lung nor laryngeal tumours were reported to develop in the smoke-exposed animals. Bernfeld and others reported in 1974 on a study in which hamsters were actively exposed (nose only) to cigarette smoke. No lung tumours were reported in the exposed groups of either of the strains that were used. The authors reported the appearance of "microinvasive" carcinomas in the larynges of the exposed hamsters. In another study by Dontenwill and others, involving the active exposure (nose only) of a large number of hamsters to cigarette smoke for various types of cigarettes, no lung carcinomas were reported in any animal. Bernfeld and others reported in 1979 on the results of another study carried out by them, in which no carcinomas of the lung were reported. Professor Idle commented that in all the aforementioned hamster smoke inhalation studies, the expected end point was bronchogenic squamous cell carcinoma. Such tumours were not found. However these studies did report various incidences of laryngeal carcinoma in the experimental animals. This had been attributed to the unusual anatomy of the hamster airways by Dontenwill and others, writing in 1973. They wrote that since the flow characteristics of air in the upper regions of the respiratory tract were different in the golden hamster and in man, the highest deposition of smoke particles per surface unit occurred in the region of the larynx. The concentration there was approximately 300 times that in the lungs and bronchi.
[5.674]Hecht and others reported in 1983 on a different kind of study carried out on hamsters, to examine the effects of cigarette smoke inhalation on the carcinogenicity of subcutaneously injected NNK, a tobacco-specific nitrosamine known in 1983 to be carcinogenic in hamsters to the nasal mucosa, trachea and lung. Hamsters were given an injection of increasing doses of NNK, and in addition identically sized groups were either sham-smoked or exposed to the diluted smoke from thirty cigarettes, twice daily for seventy-two weeks. It was reported that eight out of fifty-nine hamsters developed adenomas and adenocarcinomas of the lung after NNK administration alone, and that when animals that had been injected with NNK were also exposed to cigarette smoke inhalation, eighteen out of fifty-nine developed adenomas and adenocarcinomas of the lung. No statistical evaluation of these data was reported, and in addition no squamous cell carcinomas of the lung were reported.
[5.675]Among studies in dogs, an unpublished industrial report from Hazleton Laboratories America, Inc in 1971, cited by Coggins in a review article in 2001, described a study in which 240 male beagles were exposed to cigarette smoke by tracheostomy for 108 weeks (the same procedure as that used by Auerbach and Hammond). There were no reports of neoplasia.
[5.676]Professor Idle then offered a critique of the inhalation studies. He said that the negative results for squamous cell carcinoma obtained in the cigarette smoke inhalation studies in laboratory animals should be viewed alongside similar investigations of other inhaled substances. As expected by the researchers, the inhalation of certain dusts, metals and radioactive materials by mice, rats, hamsters and dogs elicited squamous cell carcinoma of the lung. These laboratory studies were prompted by the occurrence of squamous cell lung cancers in humans exposed in the work place to dusts, metals and radioactive materials.
[5.677]The largest and best design smoke inhalation study was that performed by Microbiological Associates, reported in CTR 1984. In this study, no squamous cell carcinomas were reported to develop in mice exposed to fresh whole cigarette smoke. Positive controls demonstrated that the mice used in the study were capable of developing squamous cell carcinoma of the lung when exposed to the carcinogen 20-methylcholanthrene. Inhalation studies, such as the Microbiological Associates study, demonstrated that the inhaled cigarette smoke alone did not cause squamous cell lung carcinoma in laboratory animals. However, the question as to whether or not inhaled cigarette smoke might be acting as a tumour promoter had also been tested in the laboratory. When known chemical lung carcinogens, such as 20-methylcholanthrene, benzo[a]pyrene or NNK, were first administered to animals, followed by long-term inhalation exposure to cigarette smoke, the carginogenicity of the chemical lung carcinogens was not enhanced. It was unlikely, therefore, that cigarette smoke was acting as a promoter of tumour initiating chemicals.
[5.678]Certain workers reported the development of laryngeal lesions, including laryngeal carcinomas, in hamsters that had been exposed to cigarette smoke inhalation through the nose. Hamsters were obligatory nose-breathing animals. Particulate matter from the cigarette smoke aerosol was deposited at high concentration on to the tiny surface area of the larynx due to the peculiar hamster physiognomy. Because the observations were made in the larynx, the hamster studies did not tell us anything about the origins of lung cancer. In Professor Idle's opinion, there was no good explanation as to why Syrian golden hamsters developed laryngeal carcinoma, but not lung cancer, after the inhalation of cigarette smoke, except that it was a species-specific phenomenon and highly strain-dependent.
[5.679]Critique of the controversial study reported by Auerbach and Hammond in 1970 continued into the current period. For example, Hoffmann and Wynder commented in 1976 that the forced exposure of dogs to cigarette smoke by means of a tracheostomy led to hyperplastic and metaplastic changes in the bronchi. The observed carcinomas in situ needed reconfirmation. Professor Idle said that the claims by Auerbach and his colleagues had since been dismissed in IARC 1986. Their expert working group, comprising Doll, Peto, Hoffmann, Wynder and others noted that Auerbach and his colleagues had failed to include measures of exposure to cigarette smoke, had included an inappropriately small number of control dogs, and had failed to mentioned focal inflammatory lesions or to give any information about the upper respiratory tract or other organs. They also described the authors' interpretation that the photomicrographs represented neoplasia as "not entirely convincing".
[5.680]Professor Idle said that the foregoing passage of his evidence demonstrated that laboratory animals exposed to whole cigarette smoke by inhalation did not develop squamous cell carcinoma of the lung.
[5.681]The next topic was short-term mutagenicity testing. Professor Idle was told that Dr Kerr had given evidence that "there are things in tobacco smoke which cause lung cancer", a view based on, inter alia, reports that chemicals in tobacco smoke had induced changes in human cells, in tissue culture for example, recognised as being associated with the development of the malignant process. Professor Idle said that he recognised that this was a process that occurred. Ames proposed in 1974 that carcinogens caused cancer by somatic mutation. He also suggested that a test system (which became known universally as "the Ames test"), that utilised frameshift mutagenesis in bacteria, be employed to detect carcinogens. For the first time, it appeared that the carcinogenic property of a chemical could be tested for in a rapid, simple and inexpensive laboratory assay that did not require recourse to long-term studies in large numbers of animals. The proposal was an attractive one and was enthusiastically, if somewhat uncritically, received by the cancer research community. Other short term mutagenicity tests followed. These were sometimes referred to as tests for genotoxicity and they were sub-divided into tests that employed sub-mammalian systems (other than the Ames test) or cultured mammalian cells, and utilised end points such as chromosomal abnormalities in mammalian cells, DNA damage and repair, and cell transformation or altered growth properties, all of which were conducted in vitro.
[5.682]Since the mid-1960s, Ames had been working on the genetics of the bacterium Salmonella typhimurium, with particular emphasis on the "histidine operon", a genetic element in the bacterial chromosome that regulated the bacterial synthesis of the essential amino acid histidine. Organisms required twenty separate amino acids for the synthesis of proteins, such as enzymes; some of these were synthesised endogenously, while others were obtained only from the diet. Humans could not, but bacteria could, synthesise histidine. By introducing mutations into the histidine operon, Ames developed bacteria that required exogenous histidine for growth. He then discovered that certain chemicals could reverse these mutations, and thus permit the bacteria to synthesise histidine again. This could be observed by the growth of colonies of bacteria on histidine-free nutrient in a dish. This rekindling of the ability of the bacteria to grow in the absence of exogenous histidine was the basis of the Ames test of mutagenicity of chemicals. Ames went on to liken the mutagenicity observed in his in vitro test to in vivo carcinogenicity, when he advocated his test to the cancer research community.
[5.683]Further genetic engineering of the bacteria took place. Ames developed new strains of bacteria lacking the usual impermeable coat and thus permitting large mutagenic molecules to enter the bacterium. These molecules introduced a new mutation into the bacterial genome at a particular site and switched on the bacterial apparatus that synthesised histidine. Next, the removal of a key DNA repair enzyme prevented the bacterium from repairing this new mutation. In combination, these two manipulations to the basic tests amplified the response of the bacteria and thus their sensitivity to mutagenic molecules. Finally, since almost all carcinogens required metabolic activation by an enzyme system which was lacking in the bacteria, Ames made a further refinement by adding fractions of rat or human liver homogenates to the culture. The test was now complete. Liver enzymes activated the added chemical, reactive metabolites entered the quiescent bacterium and switched the histidine synthesis control system to an active state, thereby permitting the bacterium to synthesise histidine, and to grow and divide, producing a visible colony. The more colonies, the more mutagenic the chemical and, according to Ames, writing in 1974, the more carcinogenic the chemical. This was a simple and quick test, and it was not long before a plethora of chemicals were tested in this assay and declared as mutagens with potential carcinogenic activity. These included polycyclic aromatic hydrocarbon epoxides, aromatic amines, aflatoxin and benzo[a]pyrene.
[5.684]Meanwhile the process of testing chemicals on rodents, particularly in the National Toxicology Program (NTP) in the United States, continued. Data were accumulated over a considerable period on chemicals that were carcinogenic or not in rodents, according to NTP criteria, and at the same time the same chemicals, in general terms, were being tested in the Ames test. Comparison of the two sets of results showed that there were chemicals that were carcinogenic in rodents but not mutagenic in the Ames test and, more importantly, that there were a considerable number of chemicals and groups of chemicals that were mutagenic in the Ames test, but for which no carcinogenicity could be demonstrated in laboratory rodents.
[5.685]Professor Idle said that to see the bigger picture of the impact of the Ames test on the investigation of human lung cancer in cigarette smokers, it was pertinent to examine the recent literature in this area. Ames had proposed at the outset, in 1974, that his assay could be used to determine the mutagenicity of human urine concentrates. A small number of papers subsequently reported that smokers voided a urine that was more mutagenic in the Ames test than that of non-smokers. In order to understand the origin of these bacterial mutagens in smokers' urine, Doolittle and colleagues studied the phenomenon in rats. High-dose intraperitoneal injections of cigarette smoke condensate in rats produced a urine that was two to three times more mutagenic than background. However, when rats were exposed to cigarette smoke, by nose-only inhalation, for one hour per day up to ninety days, no mutagenicity could be detected in the urine. Thus, direct investigation in rats of the effects of cigarette smoke and its derivatives cast doubt on the interpretation of bacterial mutagenicity of smokers' versus non-smokers' urine. Professor Idle said that in the absence of more detailed research into this subject it was not possible to draw any firm conclusion regarding the relevance of the Ames test to the occurrence of lung cancer in cigarette smokers.
[5.686]His conclusions regarding short-term mutagenicity testing were that bacterial mutagenicity as measured by the Ames test for a series of chemicals did not correlate with in vivo carcinogenicity in experimental animals. Mutagens were not necessarily carcinogens and carcinogens were not necessarily mutagens. Bartsch and Tomatis stated in 1983 that long-term animal tests were still the only ones capable of providing evidence of the carcinogenic effect of a chemical. In relation to short-term mutagenicity tests, they concluded that the conflicting results of experimental data published so far with regard to a possible quantitative correlation between the potency of a chemical carcinogen in animals and its activity in short-term mutagenicity tests did not yet sufficiently establish such a relationship for all classes of carcinogens to allow its general use for the confident prediction of carcinogen potency of new compounds. Professor Idle said that whatever the Ames test might demonstrate regarding the mutagenicity in bacteria of extracts of urine from animals and humans exposed to cigarette smoke, the fact remained that animals exposed to whole cigarette smoke did not develop squamous cell carcinoma of the lung. In his opinion, whilst tobacco smoke condensate was mutagenic in the Ames test, the mutagen itself had not been identified, and the Ames test was, in any event, merely a first screen for mutagenicity. Whether a mutagen was a carcinogen required investigation in long-term rodent carcinogenicity studies.
[5.687]Professor Idle then went on to consider research in the period 1973 to the present date into the individual chemical constituents of cigarette smoke with a view to understanding which constituent or group of constituents might cause lung cancer in cigarette smokers. Having reviewed various areas of research in this period, he concluded that as at September 2003, no constituent or constituents had been identified in cigarette smoke that accounted for lung cancer in cigarette smokers. As stated by Peto and Doll in 1985, thirty years of laboratory research had yet to identify reliably the important carcinogenic factors in cigarette smoke. In his judgment, nothing had appeared in the scientific literature since 1985 that would alter this conclusion.
[5.688]Professor Idle then discussed the challenges in analysing complex mixtures. After referring to chemical and biological interactions and ambiguous carcinogens, he summarised the position by saying that the problems in evaluating the toxicology of cigarette smoke from a component-based point of view (bottom-up) were also shared by other complex mixtures that had been studied, including air pollution, groundwater pollution and diesel exhaust. The dilemma existed on many levels. First, there were at least 4,000 chemical entities in cigarette smoke. Little was known about the propensity of these constituents to react chemically together both within and without the body to produce novel and undetected chemical entities. There had been very little attempt to elucidate new chemical entities in cigarette smoke for many years, but it had been suggested that there might be hundreds, and perhaps even thousands, of polycyclic aromatic hydrocarbons in coal tar, and scientists had stopped looking for them. Secondly, little was known of the myriad spontaneous chemical reactions that might occur in vivo between different constituents of tobacco smoke, between smoke constituents and endogenous molecules. Moreover, the biological ramifications of such chemical reactions were unknown, but might include the slowing or enhancement of biological processes, both by inhibition and induction of enzyme systems. We did know, however, that the entire encyclopaedia of organic molecules was represented within cigarette smoke and that spontaneous chemical reactions must therefore occur. In view of the foregoing, analysis of cigarette smoke that was predicated on an evaluation of the individual components of this complex mixture was not achievable.
[5.689]By at least the 1980s, there was an awareness of the problems inherent in the evaluation of complex mixtures using a component-based approach. These problems arose from attempts to model the toxic responses, particularly carcinogenesis, of a mixture based upon knowledge about the toxicity of its component parts. In the United States, this awareness culminated with the National Institute of Environmental Health Sciences asking the National Academies' National Research Council to evaluate the toxicity testing of mixtures and to make recommendations for improving that testing. A committee which was formed to consider methods for the in vitro toxicity testing of complex mixtures under the auspices of the Board on Environmental Studies and Toxicology of the National Research Council's Commission on Life Sciences concluded in 1988 that a new approach to toxicological testing of mixtures was needed. They observed that people were seldom exposed to single chemicals. Most substances to which they were exposed, whether naturally or artificially produced, were mixtures of chemicals. Mixtures that were of particular concern included chemicals generated in fire, hazardous wastes, pesticides, drinking water, fuels, and fuel combustion products. They wrote that testing complex mixtures presented a formidable scientific problem. The key to attacking this problem lay in the analysis and planning of the strategy or experimental approach. The extent and nature of testing should be guided closely by recognition of what was known and what needed to be learnt. If the question being posed was related to the effects of a mixture, the strategies invoked involved toxicity testing of the mixture itself. Professor Idle said that he agreed with this. In essence, the Committee's recommendations were that the mixture should be tested under circumstances that reflected human real life exposures and then, if consistent positive results had been obtained, the bioassay could be used to track down which constituent or group of constituents might be responsible for the activity of the mixture.
[5.690]The Committee stated that bioassay-directed fractionation, which was not used for single agents, was the most useful strategy for studying mixtures. Professor Idle said that experiments had shown that, when groups of unrelated chemicals with unrelated targets of toxicity were administered to rodents simultaneously (i.e. as a mixture) at doses equal to their subsequent NOAELs (no-observed-adverse-effect levels), no toxic effects were observed; each chemical acted independently, not additively or synergistically. The same was true for chemicals with the same target but with different mechanisms of action. Studies in which similar chemicals with similar mechanisms of action and similar targets were administered simultaneously indicated that antagonism, not additivity or synergism, was the usual outcome, thereby reducing the overall effect. Antagonism was the inhibition by one chemical of the biological properties of another.
[5.691]With respect to cigarette smoke, with 4,000 chemical components, the "factorial design" would call for 24000-1 individual binary interaction experiments. This number might also be expressed as 1.32 x 101204. To perform the binary interaction experiments at two doses of each component, which was the recommended procedure, the number of experiments required rose to 1.55 x 101908. Professor Idle said that clearly this was neither feasible nor desirable. A rigorous, bottom-up, component-based, toxicological analysis of tobacco smoke was impossible.
[5.692]However, what was not only feasible, but had already been accomplished, was a "top-down", mixture-oriented evaluation of cigarette smoke. To date, inhalation studies with fresh whole cigarette smoke conducted in mice, rats, hamsters and dogs had not produced squamous cell carcinoma of the lung. Because the mixture itself did not produce squamous cell lung carcinoma in the test animals, the testing of fractions of the smoke was not indicated by the top-down protocol proposed in Feron et al. 1998. In short, the end point of the toxicological testing of cigarette smoke, with respect to squamous cell carcinoma of the lung, had been reached and no further investigations of this type were indicated. Laboratory studies on individual constituents of cigarette smoke, while they had undoubtedly revealed much about the various properties of those individual constituents, did not, he said, inform us about the biological properties of the complex mixture. These studies did not take into account the chemical and biological interactions, and their consequences, which he had considered.
[5.693]According to Feron et al. 1998, to perform a top-down analysis the mixture should be available in its entirety for toxicity testing, adequate doses needed to be applied that were not acutely toxic, and the analysis should not require extrapolation from low to high doses, because the interactions between chemicals might be dose-dependent. Professor Idle referred to a figure derived from Feron et al. 1998. According to the path shown in this figure, where complex chemical mixtures were readily available for testing in their entirety, testing in their entirety was indicated, and if no adverse effects were found in adequate and relevant studies, the research should stop, as the data should be useful for risk assessment. Even if one constituent or group of constituents of a complex mixture, such as cigarette smoke, induced changes in cells in tissue culture, one could not properly conclude that the complex mixture would induce similar changes, because the biological and chemical interactions between individual constituents were not the same as they were in the complex mixture.
[5.694]In explaining his conclusions as at September 2003, Professor Idle said that it was his judgment that cigarette smoking had not been established as a cause of human lung cancer. Indeed, as explained by him, the cause of cancer was unknown. Moreover, the mechanisms by which lung cancer developed were not known. Researchers had not produced squamous cell lung carcinoma in laboratory animals by inhalation exposure to cigarette smoke. No constituent or group of constituents, as they existed in the complex mixture which was cigarette smoke, had been shown to be a cause of lung cancer in smokers. In view of this, it could not be determined whether or not smoking caused Mr McTear's lung cancer.
[5.695]Professor Idle said that he did not always hold the view that cigarette smoking had not been established as a cause of human lung cancer. He entered into the field of lung cancer as a young researcher from pharmacology, a background of pharmacogenetics, and he adopted the received wisdom of the day that smoking causes lung cancer. More than twenty years of association with studies and becoming familiar with the literature caused him to look at the subject in a serious way, and then to understand that there were so many components missing that he could not see where, in the history of the subject, it had been scientifically established by experiment using the scientific method. So his view had altered within the last ten years.
[5.696]Professor Idle said that he had studied the question of what risk might be occasioned by environmental tobacco smoke. In 1995 and 1996 he was a member of a European working group which was set up to evaluate whether or not there was evidence that passive smoking could be a cause of lung cancer. The study was funded by the tobacco manufacturers Philip Morris, British American Tobacco and Rothmans, but the committee had formed its own independent judgment. Overall the committee concluded that it had not been established that environmental tobacco smoke exposure (passive smoking) could be a cause of lung cancer, and there was no reason to suppose that it did. All the contrary views of which Professor Idle was aware were based upon a study of the Environmental Protection Agency in the United States, who categorised passive smoking as a lung carcinogen. As he understood it, the conclusions of the report had been nullified because of false methodology in reaching conclusions, but the consequences of it remained unchanged. Professor Idle's committee had reviewed all the relevant scientific literature before reaching its conclusion.
[5.697]Professor Idle was asked to comment on Table 1.2 at p.17 of RCP 2000 (reproduced in UKHC 2000 at p.xv). The Table was headed "Estimated number and percentage of deaths attributable to smoking by cause, UK 1997". Professor Idle said that he believed that these estimates were made on the basis of epidemiological studies, but he did not know the methodology by which particular estimates were based on such studies. He could only speculate about the use of the word "attributable", but believed that it came from odds ratios, so-called relative risks. He did not know the methodology by which odds ratios could yield the figures given in the table. A number of diseases were listed under the heading "Diseases caused in part by smoking" (the word "smoking" is omitted in UKHC 2000). From a biological point of view, Professor Idle said that he did not understand how one could attribute diseases caused in part by smoking.
Cross-examination of Professor Jeffrey Idle
[5.698]In cross-examination Professor Idle said that he was not a smoker. He had first been approached in 1997 by a firm of New York lawyers, acting for ITL, who asked him to review literature in relation to lung cancer. He had not been asked to give advice to the Board of ITL. He had given an oral presentation at a seminar at which Board members were present, in about 2001. The presentation took about one hour. He might have provided those present with a copy of his PowerPoint presentation. It was a general presentation on lung cancer. His view when he gave it was the same as when giving evidence. He had been approached by a scientist from a law firm in London, representing Philip Morris, to chair the committee on environmental tobacco smoke and lung cancer. He did not know whether it would have been known that he was someone who did not subscribe to the generally held view that tobacco smoking caused lung cancer. Each member of the committee billed his consultancy fees separately, for time and travelling expenses.
[5.699]When Professor Idle moved from the University of Newcastle to the University of Trondheim, he received a bridging grant of about $30,000 from January 1996 to help him to move from one place to another and start up research in a new place. The funding continued for one or two years. He did not know whether other people at the University of Trondheim received research funding from the tobacco industry. He believed that the Council for Tobacco Research in New York was funded by the American tobacco industry. He was a member of the Scientific Advisory Board from 1986 to 1991.
[5.700]Having first been approached in connection with the present case he reviewed scientific literature and prepared a briefing document for the lawyers regarding the scientific literature that he had read and analysed. This was sent to New York. He did not know whether it was made available to the Board of ITL. This was in 1998. He continued to work with the New York lawyers on another period of literature in 1999 and produced another report. He thought the intention was for it to be used to brief counsel in the present case on the scientific issues. He thought that he was aware that it was a case involving Mrs McTear and ITL from the outset of his involvement, in late 1997 or early 1998. It would not be fair to describe him as an advisor to ITL: he had never met anybody from ITL. He was not giving advice, but was reading the literature and producing a scientific analysis of it as a scientist. He had once previously given a deposition in a case brought against manufacturers of smokeless tobacco (chewing tobacco and snuff).
[5.701]He went on leave of absence from the University of Trondheim in about September 1998. He retained a portion of his salary from there and had supported himself by carrying out consulting work. He had not been funded by ITL. He had been paid for the time spent on preparing the report. He agreed that he had been paid a "six-figure sum". He was provided with a copy of the pleadings in the present case. He had not made any special study of Mr McTear's medical records. He was not made aware of ITL's position prior to writing his report. He thought he did know their position in relation to the question of smoking and lung cancer: he understood that they believed that it had not been established that smoking caused lung cancer, at least that was what he had read in the press.
[5.702]Professor Idle was asked questions about the evidence given by Mr Davis to the House of Commons Health Committee on 13 January 2000, as recorded in UKHC 2000, pp.238ff. He was not aware of this publication, or of the words chosen by Mr Davis to state the position of ITL. He said that he was aware that ITL believed that smoking had not been shown to be the cause of lung cancer and other diseases, but he did not know that ITL did not deny that smoking was such a cause. He was not told that by any of the lawyers. He was not aware that ITL had never challenged, or sought to challenge, the public health message, or indeed to challenge the figures, as stated by Mr Davis. He had come to give evidence not knowing the position of ITL in this detail. Asked by me whether it would have made any difference to his approach if he had known, he said it would not; he was a scientist interested in what scientific experimentation produced and what one took from the laboratory.
[5.703]Professor Idle said that his area of scientific expertise, in relation to the present case, was his scientific investigation for more than twenty years of risk factors in lung cancer specifically, and the genetics of lung cancer. His general background and training were as a chemist and biologist. His conclusions were reached against that background and his research into lung cancer over an extended period of time. Counsel said that it was not challenged on his side that, as stated by Professor Idle, the mechanisms by which lung cancer developed were not known. The professor said that this came from his biology and chemistry background. Another statement that was not challenged was that researchers had not produced lung cancer in laboratory animals. This came from Professor Idle's review of the literature. Again, it was not challenged that no constituent or group of constituents, as they existed in the complex mixture which was cigarette smoke, had been shown to be a cause of lung cancer in smokers. Professor Idle said that this came from his review of the literature and his own background in carcinogenesis, chemistry and biology. His judgment that cigarette smoking had not been established as a cause of human lung cancer came from his general training in these areas, and his reading of an extensive literature. He was not an epidemiologist.
[5.704]Apart from the above-mentioned references in his evidence, he had not considered the epidemiology. He did not refer to more up-to-date material with respect to the epidemiology of lung cancer because he was not a epidemiologist, he had to leave that to others. Asked whether there was not a great deal of evidence which established cigarette smoking as a cause of lung cancer, he said no, he believed that there was evidence which had established an association, if counsel was referring to epidemiology. There were over 4,000 constituents in tobacco smoke, and there might be many more. Asked whether these constituents, whether singly or in combination, were a perfectly plausible mechanism for the causation of lung cancer, he said that this was so, if applied individually in animals. Experiments in animals formed part of the judgment.
[5.705]Professor Idle agreed that there was a general view in science and the medical profession, about the relationship between smoking and lung cancer, that smoking was a cause of lung cancer. Shown statements on cigarette packets that "Smoking kills", he said that he did not know if smoking killed or not. Asked about a packet bearing the statement "Smoking causes fatal lung cancer", he said that this had not been established. His position was that he did not know: it might, but it had not yet been established. He did not know why these warnings appeared on cigarette packets. He was not aware of Directive 2001/37/EC of the European Parliament and of the Council of 5 June 2001 on the approximation of the laws, regulations and administrative provisions of the Member States concerning the manufacture, presentation and sale of tobacco products. He agreed that in adopting this Directive, which included that each unit packet of tobacco products must carry a general warning, one of which was that "Smoking kills", and an additional warning, one of which was that "Smoking causes fatal lung cancer", the Parliament and the Council must have been satisfied of these matters.
[5.706]Asked what was the teaching in the medical schools about lung cancer and its likely causes, Professor Idle said that in none of the medical schools in which he had worked had he been involved in that part of the curriculum, so he did not know. He would accept that in the medical schools of the United Kingdom the current teaching was that cigarette smoking caused lung cancer. He had not read the Oxford Textbook of Medicine, but would accept counsel's statement (without seeing the text) that it was suggested in this book that cigarette smoking was a cause of lung cancer. Asked about the statement in UKWP 1998 that smoking killed, he said he did not know if smoking killed or not. He did not agree that this had been known for years. He did agree that the epidemiological evidence linking smoking with lung cancer had been known for years. As for the position of other tobacco companies in the UK with respect to cigarette smoking and lung cancer, he said that he was aware of the position of Philip Morris and British American Tobacco, but did not know about the others. So far as these two were concerned, he thought they had stated that there was evidence that supported the contention that smoking caused lung cancer, so they went further than he did. He did not know if he was "out on a limb", or was one of a very small minority who held this view.
[5.707]Professor Idle did not believe that epidemiology could ever uncover a cause in the case of medical conditions found in association with environmental exposure. In the case of asbestos and mesothelioma there was an animal model that replicated the disease seen in the exposed humans in the workplace. He thought that the association was made on the basis of epidemiology, but cause and effect required various other criteria to be met. Epidemiology on its own could never be sufficient. He was aware of the writings of Sir Richard Doll. His stature in the medical and scientific community was high, because he showed the association between lung cancer and smoking a very long time ago. He did not refer to any of Sir Richard's material in his paper because it was epidemiology, and it was not helpful to him in his analysis. He was looking at experimental carcinogenesis, the laboratory-based studies, not the statistical studies. Asked about Sir Richard's evidence that MRC 1957 effectively settled the issue as far as England was concerned, he said that he did not accept that statement because epidemiology on its own could not demonstrate the cause of lung cancer and it was not generally accepted in the scientific community that it did. Many scientists were unhappy with the extrapolation from association to cause. He had not dealt in his report with the epidemiological evidence, but had dealt with the statements derived from it. He was looking to see whether there were chemical and biological data which would add to the epidemiology. There was a whole period of science, for example, when viruses were seen as principal candidates of much of human cancer, and these were dealt with in his report. There were various statements from people saying that epidemiology on its own could never lead to cause and effect.
[5.708]Professor Idle explained that the Medical Research Council (MRC) was a body that co-ordinated the funding of medical research in the United Kingdom, a body made up of doctors, scientists and administrators. They had a number of ad hoc committees which looked at grant applications and were populated by scientists and medical doctors from around British universities, many of them professors. Their views on medical matters and with respect to grant funding were respected. Counsel asked Professor Idle about various passages in MRC 1957. On p.1524, conclusions were set out, one of which was in these terms:
"4.Evidence from many investigations in different countries indicates that a major part of the increase [in the death rate from lung cancer] is associated with tobacco smoking, particularly in the form of cigarettes. In the opinion of the Council, the most reasonable interpretation of this evidence is that the relationship is one of direct cause and effect."
The witness agreed that this statement was being put out in 1957 as an interpretation of the epidemiology. He could not say whether in concluding that there was a relationship of "direct cause and effect" the MRC represented the majority of scientific opinion at that time.
[5.709]In the paragraph preceding the conclusions, the MRC stated:
"In scientific work, as in the practical affairs of everyday life, conclusions have often to be founded on the most reasonable and probable explanation of the observed facts, and so far no adequate explanation for the large increase in the incidence of lung cancer has been advanced save that cigarette smoking is indeed the principal factor in the causation of the disease. The epidemiological evidence is now extensive and very detailed, and it follows a classical pattern upon which many advances in preventive medicine have been made in the past. It is clearly impossible to add to the evidence by means of an experiment in man. The Council are, however, supporting a substantial amount of laboratory research which may throw more light on the mechanism by which tobacco smoke and other suspected causative factors exert their effect, and which may thus eventually add to the degree of proof already attained as a result of studies of human populations. It must be emphasized, however, that negative results from work with animals cannot invalidate conclusions drawn from observations on man."
Professor Idle agreed that it was impossible to add to the evidence by means of an experiment in man, and that laboratory research continued after 1957. He regarded the last sentence of the paragraph quoted above as a statement of the opinion of the MRC. He thought it was possible that animal experiments could overturn interpretations of a statistical nature.
[5.710]In the summary of RCP 1962, at p.S3, it was stated:
"There has been a great increase in deaths from [cancer of the lung] in many countries during the past 45 years. [...] Many comparisons have been made in different countries between the smoking habits of patients with lung cancer and those of patients of the same age and sex with other diseases. All have shown that more lung cancer patients are smokers, and more of them heavy smokers than are the controls. The association between smoking and lung cancer has been confirmed by prospective studies [...]. All these studies have shown that death rates from lung cancer increase steeply with increasing consumption of cigarettes. Heavy cigarette smokes may have thirty times the death rate of non-smokers."
Asked about this passage, Professor Idle said that he was aware that there had been epidemiological studies. Prospective studies were one of the methods used by epidemiologists. He did not quarrel with this. It was one of the available methods of looking at associations. He was aware of the statistics about the death rates of heavy smokes and non-smokers. He said it had not been established scientifically that smoking caused lung cancer.
[5.711]In the main report, in the section on smoking and cancer of the lung, the following conclusion was stated at p.27, para.41:
"The strong statistical association between smoking, especially of cigarettes, and lung cancer is most simply explained on a causal basis. This is supported by compatible, though not conclusive, laboratory and pathological evidence namely (a) the presence of several substances known to be capable of producing cancer in tobacco smoke; (b) the production of cancer of the skin in animals by repeated application of tobacco tar; and (c) the finding, in the bronchial epithelium of smokers, of microscopic changes of the kind which may precede the development of cancer. The conclusion that smoking is an important cause of lung cancer implies that if the habit ceased, the death rate from lung cancer would eventually fall [...]."
Professor Idle said that he accepted that several substances known to be capable of producing cancer were present in tobacco smoke, and that there had been some episodes of production of cancer on the skin of animals by repeated application of tobacco tar. He was not familiar with the literature relating to the finding in the bronchial epithelium of smokers of microscopic changes of the kind which might precede the development of cancer. He said that the RCP was a group that represented the profession of medicine in the United Kingdom and he agreed that when they put out a report like this, they were putting their name behind it. He also agreed that the RCP was "an extremely prestigious professional body".
[5.712]Counsel next invited Professor Idle's comments on passages in USSG 1964. At p.iii the Surgeon General's Advisory Committee on Smoking and Health were listed. Professor Idle said that he had attended a presentation given by one of them, Dr Farber, who was talking about diet and cancer in rats. At p.x, in the foreword, the Surgeon General stated that he had appointed a Committee, drawn from all the pertinent scientific disciplines, to review and evaluate both the new and older data and, if possible, to reach some definitive conclusions on the relationship between smoking and health in general. Professor Idle agreed that it was appropriate to proceed in this manner. At pp.ix ff the assistance of a number of individuals was acknowledged. Professor Idle said that he was aware, in broad terms, of "the depths to which this Committee went in looking at the available literature and seeking the assistance of people outside", and that it was extensive.
[5.713]Counsel next asked Professor Idle about passages in IARC 1986. At pp.9-10 the members of the IARC working group on the Evaluation of the Carcinogenic Risk of Chemicals to Humans: Tobacco Smoking were listed. Of these members, Professor Idle said that he knew of DM De Marini who worked on bacterial mutagenesis at the Institute of Environmental Health Sciences and was regarded as an expert. HJ Evans of the MRC Clinical and Population Cytogenetics Unit at the Western General Hospital, Edinburgh, was, he said, an expert and leader in the field of human genetics. T Hirayama, of the Epidemiology Division of the National Cancer Center Research Institute in Tokyo, Japan, was a leader in the field of epidemiology, perhaps one of the more prominent in Japan; Professor Idle had been at a meeting with him. He knew of D Hoffmann, of the Naylor Dana Institute for Disease Prevention, American Health Foundation, Valhalla, New York, as a specialist in chemical carcinogenesis, specifically tobacco and cancer issues. MAH Russell, Reader in Addiction, Institute of Psychiatry, The Maudsley Hospital, London: Professor Idle believed that he was a leading man in his field. M Sorsa, Institute of Occupational Health, Helsinki, Finland: a specialist in occupational health and occupational carcinogenesis, well-thought of in her field. P Vineis, Unit of Cancer Epidemiology, Istituto di Anatomia Patologica, Turin, Italy: an epidemiologist with some interest in pharmacogenetic epidemiology, considered to be one of the top epidemiologists in Italy. NJ Wald, Department of Environmental and Preventive Medicine, The Medical College of St Bartholomew's Hospital, London: a leading epidemiologist in the United Kingdom. EL Wynder, President, American Health Foundation, New York: a specialist in tobacco and health and the author of papers referred to in the evidence. Professor Idle was also asked to indicate in passing that he recognised the names of the Chairman of the working group, Sir Richard Doll, and another member, Sir Richard Peto.
[5.714]At p.16 it was stated: "The IARC Monographs are recognized as an authoritative source of information on the carcinogenicity of environmental and other chemicals." Professor Idle said that he agreed with this, and that he thought the whole series of monographs was a wonderful source of tabulated information, of a pulling together of data, a very useful encyclopaedic source. He consulted the published volumes from time to time.
[5.715]Counsel read out the passage from pp.16-17 quoted in Professor Friend's evidence at para.[5.37]. Professor Idle said that this was one way for such a body to proceed. He was next asked to look at the list of references at pp.315-375. He agreed this was "quite a lot of material to review" and that this would be an appropriate thing to do. He said he did not know whether the findings of this body had ever been challenged.
[5.716]In the chapter relating to biological data relevant to the evaluation of carcinogenic risk to humans, it was stated in the summary at pp.194-195, under the heading "Carcinogenicity Studies in Animals":
"Considerable effort has been devoted to developing experimental animal systems to study the carcinogenicity of cigarette smoke. Useful models have been developed for testing both whole smoke, by inhalation, and smoke condensate, by topical application.
Studies involving inhalation of smoke are hampered by difficulties in reproducing the exposure of humans. Technical problems occur in the generation of smoke and its delivery to animals; moreover, the respiratory systems of animals and humans differ. Rodents are obligatory nose breathers, and the structure of their nasal turbinates is more complex than that of humans. Unlike humans, experimental animals smoke involuntarily with shallow, hesitant breathing patterns. Other difficulties are caused by the toxicity of nicotine and carbon monoxide. Despite these problems, however, informative data have been obtained concerning the carcinogenicity of whole smoke and its gaseous phase.
In some experiments in mice, exposure to whole cigarette smoke results in the induction of lung tumours. In one study involving long-term exposure of rats to cigarette smoke, tumours of the respiratory tract were induced. In hamsters, various experiments demonstrated reproducibly the induction of laryngeal carcinomas. [...]"
Professor Idle said he agreed that the respiratory systems of certain species of animals and of humans differed, that rodents were obligatory nose breathers and that the structure of their nasal turbinates was more complex than that of humans. He did not know that experimental animals smoked involuntarily, with shallow, hesitant breathing patterns. It was correct that other difficulties were caused by the toxicity of nicotine and carbon monoxide. He agreed that in some experiments in mice, exposure to whole cigarette smoke resulted in the induction of lung tumours, and said that he was aware of one study involving long term exposure of rats to cigarette smoking, in which tumours of the respiratory tract were induced. He said that certain strains of hamster developed laryngeal carcinomas.
[5.717]At the end of this part of the summary, at p.195, this statement appeared: "Cigarette smoke contains many chemicals known to be carcinogenic to experimental animals and/or humans [...]." When this was put to Professor Idle, he said that the first half of the statement was correct: there were chemicals that were carcinogenic to experimental animals, but could not be evaluated in humans. Obviously one could not do an experiment administering chemicals to humans. Carcinogenicity was demonstrated by producing tumours in an animal, including the human, and if you could not do the experiment in humans, then your definition was restricted to experimental animals.
[5.718]In the chapter setting out the Working Party's conclusions and valuations, at p.309 under the heading "Conclusions" and the subheading "(b) Carcinogenicity in animals" the following paragraph appeared, which Mr McEachran put to Professor Idle:
"Cigarette smoke has been tested for carcinogenicity in experimental animals by inhalation and by topical application of condensate and in other ways. Exposure of hamsters and rats to whole smoke results in the induction of malignant respiratory-tract tumours. Cigarette smoke condensate induces skin cancers in mice and rabbits after application to the skin, and lung cancers in rats after intrapulmonary injection. Cigarette smoke contains many chemicals known to produce cancer in animals and/or humans."
Professor Idle said that he agreed with this paragraph, except for the concluding statement about humans, for the reasons already given by him. In the same part of this chapter, under the subheading "(f) Cancer in humans", the following passage appeared, which again was read to Professor Idle:
"Lung cancer is believed to be the most important cause of death from cancer in the world, with estimated total deaths in excess of one million annually. The major cause of the disease is tobacco smoking, primarily of cigarettes. Risk of lung cancer is particularly dependent on duration of smoking; therefore, the earlier the age at initiation of smoking, the greater the individual risk."
Professor Idle said that he did not agree with this. He did not doubt the association, but his problem was that the cause had not been demonstrated experimentally. He did not know whether the association was more clearly demonstrated, the earlier the age at initiation of smoking. He said he was not competent to give an expert opinion on epidemiology.
[5.719]In the evaluations, on p.314, it was stated:
"The occurrence of malignant tumours of the respiratory tract and of the upper digestive tract is causally related to the smoking of different forms of tobacco (cigarettes, cigars, pipes, bidis [small, hand-rolled, Indian cigarettes])."
Professor Idle agreed that this group of scientists and doctors had concluded that the occurrence of lung cancer was causally related to smoking. He said that it was a public health report destined for member governments of the United Nations. It was prepared by scientists of high standing in their particular fields. He did not know whether it was the case that this conclusion had never been challenged.
[5.720]In the chapter relating to epidemiological studies of cancer in humans, the section relating to cancer of the lung and the sub-section relating to factors affecting risk, under the subheading "Duration of smoking" the following statement appeared, at p.206:
"One of the key features of the relationship between cigarette smoking and lung cancer is the relevance of duration of regular cigarette smoking to lung cancer onset rates. For example, using a statistical model fitted to data from the British male doctors study, Doll and Peto (1978) estimated that the excess annual incidence rates of lung cancer after about 45, 30 and 15 years of cigarette smoking were in the approximate ratio 100:20:1 to each other [...]."
Professor Idle said that this ratio showed an association which was greater for 45 year exposure, less for 30 and less for 15, in the ratio of 100:20:1. He did not agree that if it was a very long period of smoking that increased the risk of lung cancer, then that sort of length of time could not be reproduced in animal experiments. He said that the data of Doll and Peto showed, so far as he understood them, that smoking for somewhere around half a human lifetime - 45 years - produced these figures. So, in animal experiments, the investigators sought to put the animals on a lifetime exposure. He accepted that the lifetime of animals was very short in terms of a human lifetime. He agreed that experimental animals did not live as long as humans did. The life expectancy of mice and rats was four or five years at most.
[5.721]In the same chapter, at pp.199-203, there was a summary of cohort (prospective) studies on smoking and cancer. Professor Idle said that he was aware of the existence of some of them. Mr McEachran put in figures of the numbers of subjects involved in some of these studies: in the American Cancer Society Nine-State Study, reported by Hammond and Horn in 1958, about 188,000 men were involved; in the Canadian Study, reported by Best and others in 1961 and Lossing and others in 1966, 92,000 war veterans; in the British Doctors Study, reported by Doll and Hill in 1964, Doll and Peto in 1976 and Doll and others in 1980, 3,440 male and 6,194 female British doctors who had responded to a questionnaire were followed up; and in the American Cancer Society 25-State Study, reported by Hammond in 1966 and Hammond and Seidman in 1980, more than 1 million subjects were enrolled. Professor Idle agreed that these were large groups of people. He did not agree that it would be fair to describe these studies as "the same sort of thing as laboratory studies done on animals". Counsel put to him that these were much larger populations being looked at in a prospective way and asked whether one was not going to get extremely accurate information from this. Professor Idle said this was not so, because the investigators usually did not meet any of the subjects. They trained people such as relatives or friends to fill in questionnaires and the data were all collected in an office somewhere and that was when the epidemiologists started, when they got the data to analyse; whereas, in the laboratory, the investigator was very close to what was going on and could investigate material by scientific method, which was not so for epidemiology, as he understood it. He had read that there were problems; he believed "confounding" was a problem in epidemiological studies, "but I am not competent to comment further on that."
[5.722]Returning to USSG 1964, counsel read out the first paragraph of chapter 1 on p.5, which was in these terms:
"Realizing that for the convenience of all types of serious readers it would be desirable to simplify language, condense chapters and bring opinions to the forefront, the Committee offers Part I as such a presentation. This Part includes: (a) an introduction comprising, among other items, a chronology especially pertinent to the subject of this study and to the establishment and activities of the Committee, (b) a short account of how the study was conducted, (c) the chief criteria used in making judgments, and (d) a brief overview of the entire Report."
Counsel next drew attention to p.6, where it was stated that since 1939 there had been twenty-nine retrospective studies of lung cancer, and on the same page the statement:
"During the decade 1950-1960, at various dates, statements based upon the accumulated evidence were issued by a number of organizations. These included the British Medical Research Council: the cancer societies of Denmark, Norway, Sweden, Finland, and the Netherlands: the American Cancer Society: the American Heart Association: the Joint Tuberculosis Council of Great Britain: and the Canadian National Department of Health and Welfare. The consensus, publicly declared, was that smoking is an important health hazard, particularly with respect to lung cancer [...]."
Professor Idle said that he was aware of these matters, as stated in the report.
[5.723]At pp.6-7 the report stated:
"The US Public Health Service first became officially engaged in an appraisal of the available data on smoking and health in June, 1956, when, under the instigation of the Surgeon General, a Scientific Study Group on the subject was established jointly by the National Cancer Institute, the National Heart Institute, the American Cancer Society, and the American Heart Association. After appraising 16 independent studies carried on in five countries over a period of 18 years, this group concluded that there is a causal relationship between excessive smoking of cigarettes and lung cancer."
Professor Idle said that he was not aware of this study group. Asked whether this would not impinge on his view that it was not established in the scientific community by 1957 that smoking was a cause of lung cancer, he said that he did not dispute the associations or the health warnings. He believed that it had not been scientifically established, then or now. He agreed that some bodies had concluded by 1957 that smoking caused lung cancer. Asked whether there were not a substantial number of bodies who had looked at a very large body of scientific evidence "to back this up", he said that there were scientific opinions such as these, and the literature also contained opposing opinions that questioned the interpretation of the associations.
[5.724]Asked by me about the reasons for his reluctance to accept the conclusions of the epidemiologists, Professor Idle said that his problem lay, for example, in a statement in IARC 1986, that this was "the simplest interpretation of these data". For him, unfortunately, not everything was that simple in medicine and in science. He agreed that the interpretation of the data, that there was causation, was plausible and might be right, but it also might not be right. For him the scientific method dictated that certain other types of experiment and hypothesis must be formed and answered. The epidemiology, in other words, was a pointer: it pointed towards the laboratory and said "Look, here is the hypothesis, now go and test it". "It does not matter for me how much epidemiology you have, it is still just a pointer to scientific investigation. That is my difficulty." Even if an absolute association were found, where all subjects who were exposed to a particular substance contracted a particular condition, he would describe that as a very strong indication that required relatively little experimental confirmation, and would be confirmed very rapidly by laboratory experiment. He said:
"It is only because of the nature of epidemiology, that one is dealing with statistics and how the numbers are collected by questionnaire and so on. There is obviously scope for error within the methodology, unlike an experiment with enzymes, animal cells or whatever, where the experimenter has it under very carefully controlled conditions, with control investigations to ensure that what he or she sees is real. I think one must always be adopting the Popperian view to try to disprove one's own hypothesis, and I find epidemiology is often - not always, but often - lacking in that approach: that you get a result and then it is interpreted 'in the simplest way possible', for example, to quote the IARC report, rather than to go to the laboratory and see if it is real or not. I am sorry for a complicated answer [.......], but this is a complex subject."
[5.725]Counsel returned to p.7 of USSG 1964:
"Impressed by the report of the Study Committee and by other new evidence, [the Surgeon General] issued a statement on July 12, 1957, reviewing the matter and declaring that: 'The Public Health Service feels the weight of the evidence is increasingly pointing in one direction: that excessive smoking is one of the causative factors in lung cancer.'"
Counsel then drew attention to a passage relating to the establishment of the Surgeon General's Advisory Committee on Smoking and Health in 1962. Professor Idle agreed that it was appropriate to form an advisory committee composed of "outstanding experts who would assess available knowledge in this area [smoking vs. health] and make appropriate recommendations". At p.8 the report referred to a meeting held in July 1962 between the Surgeon General and representatives of various organisations, including the American Cancer Society, the American College of Chest Physicians, the American Heart Association, the American Medical Association and the Tobacco Institute, Inc. The participants in this meeting compiled a list of scientists and physicians working in the fields of biology and medicine, and during the next month this was screened by the representatives of organisations present at the meeting in July. "Any organization could veto any of the names on the list, no reasons being required." Professor Idle said he agreed that this was an appropriate way in which to proceed, but he was not able to confirm that the Tobacco Institute Inc. represented the tobacco industry in the US, so that the tobacco industry were able to exercise a veto.
[5.726]The Committee was eventually composed of ten members and a chairman. Counsel asked Professor Idle about these: he had already indicated knowledge of Dr Emanuel Farber, and he recognised also the name of Dr Louis F Fieser, Professor of Organic Chemistry at Harvard University, who was appointed for his interests and competence in the field of carcinogenic hydrocarbons. Professor Idle had studied his book as an undergraduate, and said that he was a leader in his field. He agreed that there were "a variety of fairly outstanding people on this committee, on the face of it".
[5.727]Counsel next referred to a paragraph in chapter 2, p.13, relating to the conduct of the study, in which it was stated:
"With an enormous amount of assistance from 155 consultants, from members and associates of the supporting staff, and from several organizations and institutions, the Committee feels that a document of adequate scope, integrity, and individuality has been produced."
Professor Idle agreed that on the face of it the preparation of the report was a "huge operation". He also agreed that, as stated on p.14, it was appropriate for the Committee to take steps to review the relevant literature.
[5.728]Counsel drew attention to passages in chapter 3, entitled "Criteria for judgment". It was stated at p.19 that the Committee made decisions or judgments at three levels:
"I.Judgment as to the validity of a publication or report. Entering into the making of this judgment were such elements as estimates of the competence and training of the investigator, the degree of freedom from bias, design and scope of the investigation, adequacy of facilities and resources, adequacy of controls.
II.Judgment as to the validity of the interpretations placed by investigators upon their observations and data, and as to the logic and justification of their conclusions.
III.Judgments necessary for the formulation of conclusions within the Committee."
Professor Idle agreed that the making of such judgments was appropriate.
[5.729]In a passage discussing "Criteria of the epidemiologic method", on p.20, the Committee stated:
"Statistical methods cannot establish proof of a causal relationship in an association. The causal significance of an association is a matter of judgment which goes beyond any statement of statistical probability. To judge or evaluate the causal significance of the association between the attribute or agent and the disease, or effect upon health, a number of criteria must be utilized, no one of which is an all-sufficient basis for judgment."
These criteria included the consistency, the strength, the specificity, the temporal relationship and the coherence of the association. Professor Idle noted that these criteria were applied to the epidemiology.
[5.730]Counsel asked Professor Idle to note the discussion of "causality" on pp.20 and 21, including the statement at p.21:
"The word cause is the one in general usage in connection with matters considered in this study, and it is capable of conveying the notion of a significant, effectual, relationship between an agent and an associated disorder or disease in the host."
Professor Idle said that the Committee were defining their terms.
[5.731]Counsel next went to chapter 4, "Summaries and conclusions", under the heading "Associations and causality" on pp.30-31. The Committee stated:
"The array of information from the prospective and retrospective studies of smokers and non-smokers clearly establishes an association between cigarette smoking and substantially higher death rates."
Professor Idle agreed with this. The Committee went on:
"In this inquiry the epidemiologic method was used extensively in the assessment of causal factors in the relationship of smoking to health among human beings upon whom direct experimentation could not be imposed. Clinical, pathological, and experimental evidence was thoroughly considered and often served to suggest an hypothesis or confirm or contradict other findings. When coupled with the other data, results from the epidemiologic studies can provide the basis upon which judgments of causality may be made.
It is recognised that no simple cause-and-effect relationship is likely to exist between a complex product like tobacco smoke and a specific disease in the variable human organism."
Professor Idle said that he agreed with this last statement. The Committee went on:
"It is also recognized that often the coexistence of several factors is required for the occurrence of a disease, and that one of the factors may play a determinant role; that is, without it, the other factors (such as genetic susceptibility) seldom lead to the occurrence of the disease."
Professor Idle said he agreed with this statement also.
[5.732]Counsel then referred to the passage headed "The effects of smoking: principal findings" and the subheading "Lung cancer" on p.31, under which it was stated:
"Cigarette smoking is causally related to lung cancer in men; the magnitude of the effect of cigarette smoking far outweighs all other factors."
The following exchange then took place:
"QSo that is the conclusion they reach. Do you see that?
AI do.
QAnd have they not gone about it in an entirely appropriate way; getting a body of eminent men, reviewing all the scientific literature up to that time and reaching a conclusion on it?
AThere are two statements which we have read in the last fifteen minutes which contradict each other. One says that epidemiology can never lead to cause, and then they go on to say that reaching a cause relied on epidemiology. That is where my problem lies. The statement above says 'In conjunction with other experimental data' or 'with other data' and that is what I agree with. So they have gone about it the right way - to answer your question - but the interpretation of their findings I cannot agree with."
[5.733]Professor Idle was asked about a passage in UKHC 2000, Vol.I, paras.49 and 50, relating to the research facility at Harrogate. Professor Idle said that he had reviewed a number of papers relating to the research carried on there, mainly skin painting studies carried out with tobacco smoke condensate. He did not know if the facilities still existed, and if it did not, why not. Counsel drew attention to a passage in para.50:
"BAT [British American Tobacco] emphasised in its analysis that the purpose of Harrogate was not to establish whether tobacco condensate could produce cancer in animal test models, a fact already 'amply reported' in the scientific literature, but to identify 'the chemical constituents of tobacco smoke primarily responsible for the mouse skin tumorigenicity and to investigate cigarette design modifications which might reduce the specific tumorigenicity'."
Professor Idle said that this was his understanding of the research which had been conducted.
[5.734]Counsel then asked Professor Idle questions about IARC 2004. Professor Idle said that he was not aware of the press release and the publication of the conclusions in 2002. He agreed that, as stated in it, a scientific working group of twenty-nine experts had concluded its evaluation of the carcinogenic risks associated with involuntary smoking, with second-hand smoke also classified as carcinogenic to humans. He did not agree with it. In the summary of data reported and evaluation, at para.5.2, reference was made to IARC 1986, in which various cancers were identified as caused by cigarette smoking. "Many more studies published since this earlier Monograph support these causal links." Professor Idle did not agree with this latter statement: many more studies had been published, but they still did not establish a causal link. He was asked about other passages relating to animal carcinogenicity data, and gene mutations and chromosomal abnormalities in humans. His position on this was that he had no basis to comment on the conclusions reached by the working group, because he had not had access to the main body of the Monograph and was not aware which papers were referred to in the summary. He said that this was particularly so in respect of the statement, under the heading "Animal carcinogenicity data":
"The most compelling evidence for a positive carcinogenic effect of tobacco smoke in animals is the reproducible increase observed in several studies in the occurrence of laryngeal carcinomas in hamsters exposed to whole tobacco smoke or to its particulate phase."
He said that without references to the studies, he had no basis to comment on this statement.
[5.735]Counsel then turned to statements made in a series of articles. In Bennett et al. 1999, the introduction started with the statement:
"Classical cancer epidemiology has successfully identified populations at high cancer risk, e.g. users of tobacco products including cigarettes, cigars, and chewing tobacco. Molecular epidemiology of human cancer risk has the challenging goal of identifying high-risk individuals within these populations."
Professor Idle agreed that the authors were stating that classical cancer epidemiology had successfully identified populations of high cancer risk. In Biroš et al. 2001a the authors stated, in the introduction:
"Cigarette smoking is the most important single factor in causing lung cancer and is directly responsible for at least 90% of newly diagnosed cases [...]."
Professor Idle agreed that these researchers accepted the association and the causal effect. In Biroš et al. 2001b the authors stated, at p.410:
"Cigarette smoking is the most important single factor in causing lung cancer. [...] From this work [their research], we can consider a certain role of the p53 codon 72 single nucleotide polymorphism in susceptibility to lung cancer."
Professor Idle agreed that they were carrying on the research which he had mentioned. Denissenko et al. 1996 stated in the abstract:
"[T]argeted adduct formation rather than a phenotypic selection appears to shape the p53 mutational spectrum in lung cancer. These results provide a direct etiological link between a defined chemical carcinogen [benzo[a]pyrene] and human cancer."
The article started:
"Lung cancer is currently the leading cause of cancer death in the United States and is also the most common type of tumor world-wide. Tobacco smoking is the single most important risk factor for lung cancer."
The study ended, at p.432:
"Our study thus provides a direct link between a defined cigarette smoke carcinogen and human cancer mutations."
Professor Idle agreed that these authors were saying that tobacco smoking was the single most important risk factor for lung cancer, so here again were people working in a related field who came to a different conclusion from his.
[5.736]Hainaut and Pfeifer 2001 stated in the abstract:
"It is unquestionable that the major cause of lung cancer is cigarette smoking. p53 mutations are common in lung cancers from smokers but less common in non-smokers."
In the introduction they stated:
"Today, lung cancer is the leading cause of cancer death in the US for both women and men. It is estimated that lung cancer kills over one million people each year worldwide. It has long been recognized that the major cause of lung cancer is cigarette smoking [...]."
Professor Idle agreed that these authors accepted that cigarette smoking was a major cause of lung cancer. Hashimoto et al. 2000 stated in the abstract that their results indicated that two major subtypes of lung adenocarcinoma existed, one probably caused by tobacco smoke, and the other possibly due to spontaneous mutations. In the main text, on p.2133, they stated:
"Lung cancer constitutes one of the leading causes of cancer death in the world, and its incidence is increasing in Japan. [...] Exogenous factors, especially tobacco smoke, are established causes of squamous cell and small cell carcinomas, but other, as yet unknown, endogenous factors may be more important for adenocarcinomas."
Professor Idle agreed that these authors accepted that tobacco smoke probably caused one of the subtypes of lung adenocarcinoma and that it had been established that tobacco smoke was a cause of squamous cell and small cell carcinomas.
[5.737]Krawczak and Cooper 1998, the latter of whom was known to Professor Idle, referred to the claim in Denissenko et al. 1996 to have provided a "direct link between a defined cigarette smoke carcinogen and human cancer mutations". They wrote:
"Whilst the causal relationship between cigarette smoking and lung cancer is beyond any reasonable doubt, we nevertheless wish to take issue with Denissenko and his colleagues over the validity of their conclusions. The fundamental requirement for an epidemiological study to be sound is that a given phenomenon (in this case the spatial coincidence of in vitro benzo[a]pyrene-induced adduct formation with in vivo single base pair substitutions in the TP53 gene) which is claimed to apply to an exposed group (i.e. smoking lung cancer patients) is shown to be absent from the non-exposed group (i.e. non-smoking lung cancer patients)."
Professor Idle agreed that these were two further researchers working in his field who accepted that the causal relationship between cigarette smoking and lung cancer had been established. Pfeifer et al. 2002 stated in the introduction:
"Cigarette smoking causes 30% of all cancer deaths in developed countries [...]. In addition to lung cancer, cigarette smoking is an important cause of [other cancers]."
Professor Idle agreed that again these researchers accepted that cigarette smoking caused lung cancer.
[5.738]Rodin and Rodin 2000 stated in the abstract that it was "an almost consensus opinion that the major carcinogenic risk of tobacco smoke is in its direct mutagenic action on DNA of cancer-related genes." Professor Idle said that this was the current paradigm. The authors stated that results of their analysis of p53 mutations compiled from the IARC p53 database and from the literature pointed to a different causative link. Professor Idle said that this was "a terribly complex paper". Various different hypotheses were being mounted. Denissenko, Pfeifer and Rodin were all based in the same department at the Beckman Research Institute in Duarte, California. This was scientific debate at its most interesting, with academics at the same department debating different hypotheses in the public domain literature, a situation that was still not resolved. In summary, the authors concluded that physiological stresses (not necessarily genotoxic) aggravated by smoking were the leading risk factor in the p53-association etiology of lung cancer. Finally, counsel referred to Toyooka et al. 2003, which started with the statement:
"Lung cancer is the leading cause of cancer deaths in the world with over one million cases diagnosed every year [...], and the vast majority of cases are smoking related."
After reading this out, counsel asked whether Professor Idle saw that, to which the witness replied that he did. In concluding that cigarette smoking had not been established as a cause of lung cancer, Professor Idle agreed that his position was that he did not know.
Re-examination of Professor Jeffrey Idle
[5.739]In re-examination, Professor Idle said that the statement in MRC 1957, that the finding of carcinogenic agents in tobacco smoke was an important step forward, in that it provided a rational basis for the hypothesis of causation, might be contrasted with the position of Wynder, who had said that the importance of laboratory work was not to prove that smoking was a cause of cancer in man. EL Wynder, President, American Health Foundation, was a member of the IARC working group which prepared IARC 1986. To the extent that this report relied on the evidence from animal skin painting, in reaching a view on causation, they were at odds with Wynder, one of their participants. The working group were using a different approach to the evaluation of carcinogenicity in humans from the approach that they used in its evaluation in animals. In humans, they relied upon the epidemiology, the results of which were said to imply causality, and on nothing else. On Wynder's approach, the demonstration of the carcinogenicity of cigarette smoke condensate on mouse skin provided no evidence for determining whether or not cigarette smoking caused lung cancer in humans. The statement that there was sufficient evidence that inhalation of tobacco smoke as well as topical application of tobacco smoke condensate caused cancer in experimental animals came from studies of the inhalation of cigarette smoke by animals, particularly hamsters, mice and rats. The statement that there was sufficient evidence that tobacco smoke was carcinogenic to humans was based on epidemiology, as were similar statements that the occurrence of malignant tumours of the respiratory tract and other malignant tumours were causally related to tobacco smoking.
[5.740]In cases where there had been a specific association between a disease and a putative causative exposure, such as mesothelioma and exposure to asbestos, and angiocarcinoma of the liver and exposure to vinyl chloride monomer, the causal relationship had been established by experimentation on laboratory animals. If there were a highly specific association, one would expect to be able to establish it in the laboratory. Epidemiology, he said, pointed to experiments that should be carried out under carefully controlled conditions in a laboratory setting and, where this had been done, the hypothesis that smoking caused lung cancer in humans had failed.
[5.741]The statement in USSG 1964 that after appraising sixteen independent studies carried on in five countries over a period of eighteen years, the group concluded that there was a causal relationship between excessive smoking of cigarettes and lung cancer, was based on epidemiological studies.
[5.742]Professor Idle was asked about the suggestion that had been made, in connection with animal inhalation studies, that animals could not be compared with humans because of their much shorter life spans. He said that he was sure that researchers were aware of this and took account of it in their study designs. As previously stated by him, Laskin and colleagues exposed rats to the irritant gas sulphur dioxide mixed with the polycyclic aromatic hydrocarbon benzo[a]pyrene and reported that some rats developed squamous cell lung tumours. This report established that the rat was a species susceptible to develop squamous cell lung carcinomas. He thought that the investigators were interested in the two substances that they were applying, per se, but it could be interpreted from their paper that this operated as a form of control. In the study carried out under contract by Microbiological Associates for the Council for Tobacco Research - USA, Inc., and reported in 1984 and 1986, 20-methylcholanthrene was administered to mice as a positive control and produced squamous cell carcinoma of the lung. This led to the conclusion that if a carcinogen, something which could truly cause lung cancers, was applied to a mouse in a life time study, then it should be possible to see squamous cell carcinoma in these animals, upon the basis of the positive control experiments.
[5.743]Under reference to the most recent papers, Professor Idle said that since 1996 a controversy had developed about the role of p53 mutations, lung cancer and smoking. Denissenko et al. 1996 proposed that the pattern of p53 mutations observed in lung cancers could be reproduced in the laboratory by the incubation of normal human bronchial epithelial cells with the metabolite of benzo[a]pyrene, BPDE. They concluded that they had now established a causal link between a carcinogen and cigarette smoke and the occurrence of lung cancer. This paper generated a significant controversy and an ongoing debate in the scientific literature, which to the best of Professor Idle's knowledge was still continuing. Krawczak and Cooper 1998 wrote that Denissenko et al. and Denissenko et al. 1997 had not only failed to demonstrate that the claimed mutagenic action of benzo[a]pyrene was confined to smokers, but their data were also insufficient in general to prove that TP53 mutations associated with lung cancer were anything other than predominantly endogenous in origin. Rodin and Rodin 2000 were on the same side of the argument as Krawczak and Cooper. They proposed that oxidative stress or some other process might cause particular mutations at certain sites in the p53 gene that were observed with Denissenko et al., and these gave the cells in which they occurred a selective advantage. Rubin wrote in 2001 that there was currently sharp disagreement about the relative roles in human pulmonary carcinogenesis of the direct induction of mutations by polycyclic aromatic hydrocarbons in tobacco smoke versus the selection of endogenous mutations. The disagreement was based upon differing interpretations of base changes in codons of the p53 gene of human lung cancers. In none of the recent papers put to him in cross-examination was any evidence offered in support of statements to the effect that the causal relationship between smoking and lung cancer had been established: the authors should be regarded as treating this as the current paradigm, in the context of which their research could be assessed.
[5.744]Finally, reference was made to the statement in IARC 2004 that urine from smokers was mutagenic. While it could not be told on what research this conclusion was based, Professor Idle had given evidence that a handful of papers had reported that smokers voided a urine that was more mutagenic in the Ames test that non-smokers' urine. This, however, was at variance with experimental observations in rats, in which exposure to injections of cigarette smoke condensate produced urine that was more mutagenic by a factor of two or three than background, but when the rats were exposed to whole cigarette smoke they did not produce an elevated incidence of mutagenic urine.
Dr Arnold Cohen
[5.745]Dr Cohen, BSc, PhD, C.Chem, FRSC, MBIRA was aged 66. He was an Associate and thereafter a Fellow of the Royal Society of Chemistry (formerly the Royal Institute of Chemistry) and a member of the British Institute of Regulatory Affairs and had been admitted to the Register of Toxicologists of the Institute of Biology/British Toxicology Society and the register of Eurotox Registered Toxicologists. He explained that the British Institute of Regulatory Affairs was set up to deal with regulatory matters relating to pharmaceutical development and EU regulatory requirements when drugs were presented to the authorities for marketing authorisations. From 1963 to 1968 he headed the Editorial Department of the British Industrial Biological Research Association and was the Assistant Editor of its two publications, one of them the first European journal on Toxicology. In 1968 he served as head of the Medical Information Department of Schering Chemicals Ltd in the United Kingdom. In 1969 he founded Toxicology Advisory Services, a consultancy of which he was, and remained, sole practitioner. It provided an independent consultancy service in toxicology to industry, research organisations, government departments and international agencies in the field of pharmaceuticals, medical devices, food chemicals, agrochemicals, cosmetics and environmental and industrial chemicals. During his career he had been actively involved in the preparation of submissions and expert reports to European Union regulatory authorities on pharmaceuticals and pesticides. He explained that when a new drug was submitted to the European Union regulatory authority three expert reports were required, one of which related to toxicology. His involvement was with the toxicology programme and required the assessment of the data. From 1991 to 2002 he was a Trustee and Director of Marie Curie Cancer Care and for much of that period was a member of its Cancer Research Committee. He also served as a Director of Phogen Ltd, a joint venture biotechnology company set up between Marie Curie Cancer Care and Cantab Pharmaceuticals plc. He was also a member of various other societies including the Royal Society of Medicine and the European Society of Regulatory Affairs. He had published about thirty research papers and reviews, had been joint editor of two books on irradiated foods and had written many unsigned articles on toxicology.
[5.746]He said that he had been asked to evaluate the carcinogenicity studies reported in the scientific literature, in order to determine whether exposure of laboratory animals to cigarette smoke by inhalation or intratracheal administration resulted in the development of squamous cell carcinoma of the lung. Only those animal studies involving inhalation or intratracheal exposure to cigarette smoke for prolonged periods, i.e. six months or more, were considered by him. The six-month threshold was chosen because tumours normally were not expected until later in life, normally a year or even longer, and many studies were of only a few weeks' duration, where acute effects would have been seen. These would be totally irrelevant for the assessment of carcinogenicity. So six months was chosen as a reasonable period of exposure, so as to eliminate many short-term studies which would not have been relevant to his assessment. He reviewed reports of fifty-seven cigarette smoke inhalation and intratracheal exposure studies conducted in the mouse, rat, hamster, guinea-pig, rabbit and dog.
[5.747]Dr Cohen said that toxicity testing in laboratory animals entailed exposure of groups of animals to the test material and study of the biological response elicited under the conditions of the experiment. Typically, high doses were used in a toxicity study in an attempt to product an adverse biological response. This applied to the whole field of toxicity testing on laboratory animals. A wide range of chemicals had been submitted to toxicity testing, including drugs, food additives, pesticides and industrial and environmental chemicals, that were subject to regulatory control in many countries. In addition, lifestyle factors such as diet, alcohol, smoking and ultraviolet radiation had been submitted to toxicity testing. So the animal inhalation experiments he was considering were not unique, they formed part of a range of lifestyle animal experiments.
[5.748]He explained that there were various matters, which he described as key considerations, that needed to be considered when a toxicity study was started. An appropriate species had to be selected; and the route of exposure, the duration of exposure and the levels of exposure were dependent on the nature of the material being tested and the reason for doing the test. Control groups were very important because findings could occur in the exposed animals that were not due to treatment but due to spontaneous effects that could be picked up in the control group. For any given animal species the strain, gender, age, genetic makeup and health condition were important factors in determining the toxicological response. The route of exposure selected in a toxicity study should be dependent upon the intended human use of the test material in question or the route of ultimate human exposure. The length of a toxicity test should reflect the likely duration of exposure in humans and could range from a single dose study to daily administration over the animals' lifespan. In order to maximise the detection of carcinogenic activity of a test material, long-term exposure was necessary in animals, e.g. eighteen to twenty-four months in mice and twenty-four to thirty months in rats.
[5.749]He was asked how, if the onset of cancer in man typically occurred after the age of 50 years, this could be modelled effectively in mice and rats. He said that essentially the relative lifespans across the species were compared. In the case of a rodent with a lifespan of two years or just over, that would be deemed to be sufficient time for a carcinogenic response to develop. In the case of the dog, exposure would need to be for periods of up to ten years, and even longer with monkeys. A tumour is an age-related phenomenon linked to the age of the particular species. So fifty to seventy years in man was equivalent to one and a half to two years in the rodent and seven to ten years in the dog. He said that it was known empirically that cancers could form within the lifespan of the species in question.
[5.750]Dr Cohen went on to say that toxicity studies should be designed so as to determine the toxic potential of a test material over a wide dose range. Thus several groups, typically three, were exposed to a low, mid and high dose of the test material, the latter being well in excess of the potential human exposure level. This increased the chance of a toxic effect occurring and enabled it to be determined at what dose the effect either could not or could be seen. This helped to determine safety levels in humans, and increased the chance of an effect being manifest in the study. Various biological markers, for example general health, body weight, survival, haematology, blood chemistry, urine analysis and pathology were determined in test groups and compared with those in appropriate control groups.
[5.751]It was essential to include at least one negative control group in a toxicity study. This was a group which should be identical to the exposed group, other than receiving the treatment that the exposed group received. This provided a background measure against which the result in the test group was compared for any given toxicological end-point. A positive control group might also be included in a toxicity study in order to demonstrate the susceptibility of the animal model to a particular effect of a known agent, thereby validating the animal model for detecting the potential of the test substance to show the same effect. For example, the group might be exposed to a known carcinogen.
[5.752]There were essentially three types of negative control group: untreated control (also known as cage or shelf control), vehicle control and sham control. In untreated control the animals were left in cages, fed in the normal way and not handled in any way relating to the exposed group. In the vehicle control group, if for example what was being tested was a topically applied drug in a vehicle, the vehicle control group was exposed to the vehicle to see whether it was having any effect. In a sham control group, in the case of inhalation studies, for example, where the animals were handled in a more rigorous and robust manner than when the material is administered in the diet, they were exposed to the same procedural arrangements except that they were not exposed to the inhaled material, but were handled in exactly the same way as the exposed group. Thus any potential effect of the stressful procedure which could contribute the effects seen in the test group would be identified.
[5.753]Dr Cohen said that cancer was synonymous with a malignant neoplasm, i.e. a tumour that grew progressively, invaded local tissues, spread to distant sites (metastasis) and eventually led to death. In contrast, benign tumours grew slowly, might stop growing or regress, did not infiltrate into local tissues and did not metastasise. Benign tumours were invariably not fatal. In an adequately conducted carcinogenicity study, a statistically-significant excess or earlier onset of a particular malignant tumour in a treated group, when compared with an appropriate control group, would identify the chemical as a carcinogen in the animal model used.
[5.754]Dr Cohen was asked to comment on a passage in IARC 1986. At p.309, under the heading "Conclusions" and the subheading "(b) Carcinogenicity in animals" the report stated:
"Cigarette smoke has been tested for carcinogenicity in experimental animals by inhalation and by topical application of condensate and in other ways. Exposure of hamsters and rats to whole smoke results in the induction of malignant respiratory-tract tumours. Cigarette smoke condensate induces skin cancers in mice and rabbits after application to the skin, and lung cancers in rats after intrapulmonary injection."
This conclusion was related to a passage of text starting at p.127 under the heading "Biological data relevant to the evaluation of carcinogenic risk to humans" and the subheadings "1. Carcinogenicity studies in animals" and "(a) Inhalation of tobacco smoke". The IARC working group considered studies on mice, rats, hamsters, rabbits and dogs. Dr Cohen said that he considered all these studies "and a lot more", including studies which had been published before the Committee carried out its work in 1985. He had looked at more than twice the number of papers discussed in IARC 1986. He made it clear that his report focused purely on the inhalation studies.
[5.755]Dr Cohen was asked to consider a series of hamster studies. In Dontenwill et al. 1973, at p.1791 the authors stated:
"The fact that epithelial proliferations called 'early invasive carcinoma' [...] did not infiltrate the cartilage may be explained by the behaviour of tumor growth and cartilage."
He said that at no place in the report did the authors describe having found carcinoma without the qualification "early invasive". In Dontenwill et al. 1977 proliferative laryngeal lesions were graded as in Dontenwill et al. 1973. Stage 6 leukoplakia, the most advanced lesion, represented "early invasive carcinoma", also described as "carcinoma in situ". (These expressions are taken from a translation of the original German). The authors did not report the existence of carcinoma without the qualification "early invasive".
[5.756]In Bernfeld et al. 1974 instances were reported of laryngeal papilloma and laryngeal "microinvasive" carcinoma in two strains of hamster. Compared with either control group, laryngeal papilloma was more prevalent in the exposed groups of both strains and the increase in laryngeal "microinvasive" carcinoma was more marked in one strain. Dr Cohen said that the data were not statistically analysed. No lung tumours were reported in the exposed group of either strain; and increased incidence of non-neoplastic histopathological lesions was seen in the lungs in the exposed group of both strains. The authors did not report having found laryngeal carcinoma unqualified by the use of the word "microinvasive". In Bernfeld et al. 1979 the reported incidences of laryngeal papillomas and carcinomas (described as early carcinoma/carcinoma in situ or invasive carcinoma without distant metastasis) were set out in a table. Increased incidences in laryngeal papillomas and carcinomas were reported in the exposed groups but differences in tumour incidence between the control and exposed groups were not analysed statistically. Tumour incidence was not increased in the lungs or significantly increased in the trachea; increases in non-neoplastic histopathological changes were reported in the lungs and trachea of exposed animals.
[5.757]Dr Cohen summarised his discussion of the four hamster inhalation studies of cigarette smoke referred to above by saying that they reported an increase in laryngeal "early invasive" or "microinvasive" carcinoma (without distant metastasis). In his view, the production of laryngeal "early invasive" or "microinvasive" carcinoma in the hamster appeared to be a species-specific phenomenon; laryngeal tumours were not seen in the various mouse or rat studies, and the only species that showed laryngeal tumours was the hamster. Bernfeld also showed that one strain of hamster was more susceptible than the other in developing laryngeal tumours.
[5.758]In his evaluation of carcinogenicity studies of inhaled or intratracheally administered cigarette smoke in laboratory animals, Dr Cohen reported:
"None of the 57 inhalation and intratracheal carcinogenicity studies in the mouse, rat, hamster, guinea-pig, rabbit or dog, as reviewed in this report, showed a statistically-significant increase in squamous cell carcinoma of the lung following exposure to cigarette smoke and indeed none of the authors of these studies reported a statistically-significant increase for this carcinoma."
[5.759]Dr Cohen then turned to rat studies. IARC 1986 stated at p.194: "In one study involving long-term exposure of rats to cigarette smoke, tumours of the respiratory tract were induced." This was a reference to Dalbey et al. 1980. In this study the authors stated that their choice of a particular strain of rat was heavily influenced by the induction of squamous carcinomas in the respiratory tract after intratracheal instillations of relatively small amounts of polycyclic hydrocarbons or after bronchial implantation of pellets containing cigarette smoke condensate. They stated at p.387:
"We observed 10 respiratory tumors in 7 smoke-exposed rats. Nasal tumors occurred as 1 early adenocarcinoma and one squamous cell carcinoma. The pulmonary tumors were 5 adenomas, 2 alveologenic carcinomas and one squamous carcinoma [...]. One alveologenic carcinoma was observed in controls. [...]
Besides the description of laryngeal neoplasms in smoke-exposed hamsters [...], the present work is the only study in which an unequivocal tumor response in the respiratory tract resulted from long-term tobacco smoke exposure. The tumors in the respiratory tracts of smoke-exposed rats consisted of 5 adenomas and 5 adenocarcinomas, alveologenic carcinomas or squamous carcinomas, as compared to one alveologenic carcinoma in the control animals."
In Table 2 the authors stated that 9% of smoke exposed rats, i.e. seven individuals out of the original group of eighty, had tumours in the respiratory tract. Dr Cohen said that he believed that the authors should not have included certain tumours in that grouping, and should have shown the benign tumours and the malignant tumours in the lung not only separately but to indicate whether the animals that showed the adenomas also had adenocarcinomas. It was not known whether the lung adenomas and lung adenocarcinomas appeared in seven, six or five animals, from the data presented in the paper. The two nasal tumours should not have been included because the practice of the National Toxicology Program (NTP) guidelines at the time recommended that nasal tumours should not be lumped together with lung tumours in tumour analysis.
[5.760]The NTP guidelines were contained in McConnell et al. 1986. At p.284 the authors stated:
"The purpose of this report is to give the rationale and criteria for combining certain neoplasms and to provide guidelines for combining neoplasms and sites."
The guidelines were based mainly on lesions occurring in the F344 inbred rat and the B6C3F1 inbred mouse, both of which were widely used in carcinogenesis studies. At p.285 the authors stated:
"Table 1 contains a list of organs and tissues where combining neoplasms is or is not appropriate to obtain a better understanding of the evidence of carcinogenicity. This list comprises those organs and tissues in which neoplasia is most often observed in F344 rats and B6C3F1 mice and may or may not be appropriate for use in other strains or species."
On p.285, Table 1 set out various organ systems and neoplasms. It stated that, in respect of the nasal cavity, squamous cell neoplasms should not be combined and that, in the case of the lung, squamous cell neoplasms and bronchioalveolar neoplasms should not be combined. Dr Cohen said that the mixing of tumours of different cell types in Dalbey et al. 1980 would have been inconsistent with these guidelines, had they been published earlier.
[5.761]In IARC 1980, which set out the basic requirements for long-term assays for carcinogenicity, it was stated at p.68, in a passage relating to the analysis and reporting of categories of tumour:
"Since it appears that cancers arise independently in various parts of the body, it has become customary to treat each potential target site (brain, kidney, bladder, etc.) as a separate experiment for evaluation."
Dalbey et al. 1980 (which was submitted for publication in 1979) did not act in conformity with this custom in not treating nasal tumours and lung tumours separately. Not only did the authors mix cell types, they also mixed sites in order to get their final total. Dr Cohen also said that IARC 1980 stated at p.69 that where judgments about the grouping of lesions for statistical analysis were difficult, it was desirable to evaluate them in both ways, divided and combined. If each was statistically significantly different from its counterpart in control animals, interpretation was easier. For example, lung adenomas and lung adenocarcinomas should be analysed separately as well as combined. Dalbey et al. 1980 did not do that even though the NTP guidelines stated that for a ten-year period before their publication their approach had been widely accepted and had undergone peer review.
[5.762]Dr Cohen also criticised Dalbey et al. 1980 for not having carried out separate analyses of the effects of treatment on each separate type of tumour, contrary to the advice given in IARC 1980 at p.321 in relation to statistical tests for carcinogenicity. They had combined the control groups in order to achieve their result. He believed that in their study the comparisons should have been with the sham control group. This was closer to the exposed groups than the untreated control group, and the survival rate in the untreated control group dropped considerably, so that there were relatively few animals available in it to develop spontaneous tumours. Therefore this group was not truly representative and was not a true comparison with the exposed group in the latter three to four months of the study.
[5.763]Asked whether if the NTP guidelines had been followed this would have made a difference to the outcome of the study of Dalbey et al., in particular the finding of statistical significance of the existence of tumours in the respiratory tract, Dr Cohen said that if the two nasal tumours and the lung squamous cell carcinoma had been removed, on the basis of the guidelines, then three of the ten tumours would have been set aside, leaving seven tumours remaining, i.e. five adenomas in the lungs and two alveologenic carcinomas in the lungs. But it was not stated whether those seven tumours appeared in seven animals, six animals or five animals: it was possible that one animal had both an adenoma and an adenocarcinoma. If there were seven tumour-bearing animals and they were compared with the combined controls, there would still be statistical significance. But if the seven animals out of eighty in the group were compared, not with the combined controls but with the sham controls, Dr Cohen did not believe that the difference would have been significant. If the advice in IARC 1980 had been followed by the authors of Dalbey et al. 1980, Dr Cohen said we would have known how many animals in the Dalbey study had lung adenomas and how many had lung adenocarcinomas, and whether there were seven, six or five tumour-bearing animals. This was crucial because without that knowledge it was difficult to assess the significant difference.
[5.764]Dr Cohen said that he would have expected the working group who prepared IARC 1986 to have in mind the advice on practices set out in IARC 1980 when they came to evaluate the animal inhalation studies. Nevertheless, and despite criticism of other studies for not following such advice, they reported on Dalbey et al. 1980 without further comment. In his view, on the evidence that was before the working group and discussed in the monograph, they were not entitled to express the conclusion that exposure of rats to whole smoke resulted in the induction of malignant respiratory tract tumours.
[5.765]Dr Cohen concluded his evidence-in-chief by stating that Wynder, either on his own or as a member of a group, had not produced lung adenocarcinomas in any laboratory animal prior to 1962.
Cross-examination of Dr Arnold Cohen
[5.766]In cross-examination Dr Cohen said that he was not a smoker. He was being paid for his work as an expert witness, at his normal rate. He did not know whether, as was now stated on cigarette packets, "Smoking kills", because he was not an expert in human epidemiology. He did not know that a very large number of doctors and scientists agreed that smoking kills. He was not aware of the statement in UKWP 1998 that 120,000 people a year in Britain died from illnesses directly related to smoking. He had not read any of the scientific papers dealing with the human epidemiology. "I am not an expert in this field."
[5.767]Mr McEachran made it clear that he was not challenging the conclusion in Dr Cohen's report which stated that in his opinion "laboratory studies using whole cigarette smoke have not produced squamous cell carcinoma of the lung in experimental animals". He went on to ask Dr Cohen about IARC 1986. Dr Cohen said that he was probably aware of it in 1986. He said that IARC were a reputable organisation and were a body that disseminated information and evaluated chemicals for carcinogenicity. Their reports were put together by in-house people at IARC and also a committee that assessed the data. He agreed that the committee was made up of "top people". He was taken through the names of the members of the committee. He recognised three of the names. One of these was Sir Richard Doll, whom he described as "a major figurehead in world science". Another was Sir Richard Peto, whom he described as "a leading figurehead in epidemiology". He was taken through the description of the Committee's working methods, with particular reference to the identification of articles for evaluation and their subsequent valuation. He agreed that this was an appropriate way to approach and prepare a monograph. He explained that it was necessary to rely on animal studies of carcinogenicity because in a long-term study humans would not deliberately be exposed to the test material. He agreed that an extensive amount of work had been put into the monograph and that the Committee had "looked at a lot of research material". The references extended to sixty pages.
[5.768]Asked about his criticisms of Dalbey et al. 1980, Dr Cohen said that if only five instead of seven animals developed tumours, that would not be statistically significant even compared with combined controls. He had consulted a statistician and five out of eighty compared with one out of ninety-three would not be statistically significant at the probability level of less than 0.05 (P<0.05). In carcinogenicity studies the importance should be on the number of animals showing the tumour, rather than the number of tumours, because some animals could have multiple tumours. This was the practice accepted by IARC.
[5.769]Mr McEachran asked Dr Cohen questions about the epidemiological studies of cancer in humans considered in IARC 1986 at pp.199 to 270. He said that he knew "how epidemiology works" in broad terms. His attention was drawn to the very large numbers of people included in these studies. Counsel invited comparison with the relatively small numbers of animals used in the laboratory studies. Dr Cohen said that in the case of an animal study which was controlled one had a much better picture of what was going on. People were "exposed to all sorts of things out there", whereas an animal study was focused on a particular agent which was appropriately controlled, so when the result was obtained, it was the direct effect of that agent. Numbers were not necessarily the key to it. He did not know that less than 1% of smokers developed lung cancer in any year. Asked whether, if that was so, replication of that effect on animals would require a large number of animals, he said that carcinogenicity studies had been carried out on all sorts of chemicals and it was a standard procedure. The dose in the animals could be increased.
[5.770]In response to questions by Mr McEachran about the treatment in IARC 1986 of the relevance of duration of regular cigarette smoking to lung cancer onset rates in humans, Dr Cohen said that this was outside his area and that it was beyond his expertise to look at a statistical model. He could not comment, because he was not an expert in the field, on a finding that lung cancer incidence increased with the duration of cigarette smoking so that it was considerably higher after forty years than after fifteen. It was put to him that laboratory animals were not tested for such long periods. He said, however, that the majority of chemicals that had been shown to develop tumours in animals had been reported to show an increased risk in humans, and he could not think of any examples where the human data were in conflict with the animal data. The number of years was not relevant, it was lifespan that determined the outcome of a carcinogenic event. So two years in a rodent was the equivalent of fifty, sixty or seventy years in a human. It was in accordance with the carcinogenicity guidelines of most countries to use animals, and all the published guidelines explained that it was the lifespan of the animal in a species that mattered in determining carcinogenic potential. He did not agree that the reason why squamous cell carcinomas had not been induced in animal inhalation studies was that the exposure, albeit for most of the lifetime of the animals, was too short. Known carcinogens could induce cancers in experimental animals in a relatively short time. In one study, squamous cell carcinomas were induced in mice in twelve months with the use of 3-methylcholanthrene, a known carcinogen, in order to demonstrate whether that particular strain was capable of developing squamous cell carcinomas within the lifespan of the animals. Other compounds had produced squamous cell carcinomas in various species. Dalbey et al. 1980 mentioned in the introduction that the F344 rat was selected because it was capable of expressing and developing squamous cell carcinoma.
[5.771]Dr Cohen was asked about statements in IARC 2004 at para.5.3:
"In four out of five studies in rats, exposure to whole smoke led to modest increases in the occurrence of malignant and/or benign lung tumours. Similarly, in four of eight studies in mice with varying susceptibility to lung tumour development, exposure to whole smoke led to a modest increase in the frequency of lung adenomas. An increased incidence of lung 'tumours' has also been reported in dogs exposed to tobacco smoke [...]."
Dr Cohen said that he could not comment on these statements because he did not know which studies were referred to in the summary in IARC 2004 (which was all that had been published by then). He said that he understood "tumours" in this context to be doubtful neoplasia, which could be either tumours or pre-neoplastic lesions.
Dr Michael Lewis
[5.772]Dr Lewis, aged 55, stated that he was born in Germany and studied biology in the USA from 1970 to 1974, gaining a Bachelor of Science degree. He then went on to study medicine in Germany and became a doctor of medicine, followed by epidemiology in the USA and Canada, gaining a diploma in epidemiology from McGill University. He gained his clinical experience in Ulm in Germany, in internal medicine, and earned a diploma in tropical medicine in Hamburg. He was Assistant Professor in the Department of Epidemiology and Biostatistics at McGill University in Montréal, Canada, from 1993 to 1996. From 1993 to 1995 he was Associate Director of the Potsdam Institute of Pharmacoepidemiology and Technology Assessment, leaving the Institute as its Scientific Director at the end of 1996. He explained that pharmacoepidemiology was a branch of epidemiology which dealt with associations between medicines and their outcomes and that technology assessment dealt with the infrastructure of health care within any given country. He was currently director of a commercial firm called EPES Epidemiology, Pharmacoepidemiology and Systems Research in Berlin, specialising in consultations and conduct of pharmacoepidemiology studies. He was adjunct Reader of Epidemiology and Biostatistics at the University of Potsdam. He explained that epidemiology dealt with populations and assessing means of designing studies and capturing populations for specific questions, whereas biostatistics dealt with the more technical issues of data analysis and analysing the proportions and the distributions one finds in the population.
[5.773]Dr Lewis had been involved in several multinational projects addressing
epidemiological and pharmacoepidemiological issues, including the WHO-MONICA project and the Transnational Study on Oral Contraceptives. He explained that the WHO-MONICA project was initiated by the World Health Organization and ran from about 1982 to about 1992 in forty countries. One component looked at cardiovascular risk factors within populations and their distribution, using a survey technique; the other looked at the annual incidence of myocardial infarction in each of these areas over time. The Transnational Study on Oral Contraceptives was a multinational study involving five centres in different countries and ran for four years to determine whether or not there was an association of venous thromboembolism with oral contraceptive use, dividing oral contraceptives into various types of components, and also myocardial infarction. He had published about 150 papers and reports in scientific journals and held the Certificate for Epidemiology of the German Epidemiological Association (DAE). He was a board member of the International Society for Pharmacoepidemiology from 1991 to 1998, and was its President from 1996 to 1997. He was on the editorial boards of the journals Pharmacoepidemiology and Drug Safety and Disease Management & Health Outcomes. From 1997 to 2002 he held a faculty appointment as Adjunct Professor at the Department of Preventive Medicine of the University of Kansas Medical Center, and became Visiting Professor at the European Institute of Health & Medical Services of the University of Surrey in 1999.
[5.774]In Article 3 of condescendence it is averred that in 1992 Mr McTear was diagnosed as suffering from inoperable lung cancer. "Said cancer was caused by his smoking." Dr Lewis was asked to report whether or not epidemiological data could
be used to draw conclusions about the cause of disease in any individual. It was his opinion that epidemiological data could not be used to draw conclusions about the cause of disease in any individual.
[5.775]Dr Lewis stated that epidemiology dealt with populations and aggregate data which combined the features of many individuals. It did not deal with the individuals themselves or their specific situations. The number of new cases of any given disease occurring within a population in a year, for example, might be one in 10,000 persons. This was called an incidence rate, which defined the risk of disease in a population. The word "risk" in this context meant a predictor of what occurred in a population in terms of any type of event. The incidence rate was the number of new events for any given period of time, usually one year, occurring within the base population, which needed to be well defined. The definition might be in terms of geographical area, age or sex, for example. The expression "incidence among exposed" related to the number of events occurring within a population having a specific attribute, for example hypertension or exposure to medication. The word "exposure" included endogenous as well as exogenous factors. The expression "incidence among unexposed" related to the number of new events occurring in a population of unexposed individuals in a year. The expression "prevalence of an exposure" was the proportion of individuals exposed to a risk factor in a defined population at a given time. These expressions were used by Dr Lewis in Table 1 in his report, entitled "Incidence and prevalence in epidemiologic studies". Table 1 was as follows:
Incidence the number or rate of new events (numerator) occurring in a defined population (denominator) in a given time (i.e. a year) | I p = | new events general population | |
Incidence among exposed the rate of new events occurring in a population of exposed individuals in a year | I e = | new events exposed population | a a + b |
Incidence among unexposed the number of new events occurring in a population of unexposed individuals in a year | I u = | new events unexposed population | c c + d |
Prevalence of an exposure The proportion of individuals exposed to a risk factor in a defined population at a given time | Pe = | exposed individuals general population | |
He said that the incidence rate was an aggregate figure from millions of different individuals and told us little about the individual risk of contracting the disease in question. For example, if the incidence rate of the disease within a population in one year was one in 10,000 persons, on average each individual's risk of contracting the disease was 0.0001. Disease occurrence might be influenced by risk factors within populations. These were factors which could be consistently observed in studies to be associated with a specific health outcome. For example, hypertension was a risk factor for heart disease. Risk factors could be either endogenous, i.e. genetic, or exogenous, i.e. related to lifestyle, working environment, etc.
[5.776]Incidences of disease, Dr Lewis continued, differed within populations depending, among other things, upon age, gender, genetics, diet and other exposures. For heart disease occurrence, one could show the incidence of disease among those who had hypertension and compare it with the incidence of those who did not. If hypothetically the incidences were 100 per 100,000 among hypertensives (the exposed) and ten per 100,000 among people with normal blood pressure (the unexposed), the risk of hypertensives to incur heart disease would be ten times higher than that of non-hypertensives. This relationship was calculated by dividing the incidence rate among exposed by the incidence rate among unexposed (i.e. (100/100,000) / (10/100,000)) to show the rate ratio (ratio of two rates), which was also known as the relative risk. Dr Lewis referred to Table 2 in his report, entitled "Relative risk and risk difference". The table was in these terms:
Relative Risk The ratio of the incidence among the exposed and the incidence among the unexposed population. Its equivalent from a case-control study is called an odds ratio (OR). If the RR=1, there is no difference in risk, if RR>1, the exposure is associated with risk, if RR<1, the exposure is associated with benefit. | RR = | I e = I u | a a + b |
| c c + d |
| Risk Difference or Excess Risk
The difference in the incidences among exposed and unexposed. | RD = | I e - I u | |
The expression "odds ratio" was used in a case-control study, "relative risk" was used in a cohort context, in which a population was followed over time until the study was stopped and then the outcomes or events within the categories of exposed and unexposed individuals were counted; a cohort study was also sometimes referred to as a prospective or longitudinal study. A case-control study was based on the notion that diseases were usually rather rare events, so it would be impracticable to follow a population large enough for a long enough time to be able to accumulate enough events to enable a judgment or calculation on the relative risk to be made. So the fallback was to do a case control study in which, for example, cases were collected from hospitals and compared with a control group that was comparable to these cases in every respect except that they did not have the disease in question. The expression "risk difference" or "excess risk" was the difference in the incidence among exposed and unexposed.
[5.777]Estimates of relative risks were usually obtained through studies in which the occurrence of disease in exposed and unexposed populations was observed (in cohort or case control studies). The individuals observed generally chose their exposure themselves. This was a consideration that epidemiologists had to bear in mind, particularly in dealing with an exogenous exposure, because the investigator did not know for what reason anyone chose to become exposed to a certain medication, or to a certain lifestyle or habit, for example. The question that arose was whether there was any attribute or difference within the exposed group that determined their inclination towards exposure as compared with the unexposed group. This might be contrasted with clinical trials, where the exposure was chosen for the individual by an investigator. In observational studies, it was uncertain that those who had selected themselves for the exposure were comparable to those who had decided not to be exposed. This had been found in studies relating to hormone replacement therapy, where different results were obtained depending on whether the women had selected their exposure themselves or it had been randomly allocated to them. Further, estimates of risk were population-based figures. The individuals within these populations might belong to different groups or risk sets. The expression "risk set" denoted a group of individuals who shared attributes or a set of attributes, which had an association with outcomes.
[5.778]Asked what risk factors were associated with lung cancer, Dr Lewis said that they were smoking, cigarette smoking, socio-economic status, alcohol intake or abuse, age, gender, occupational factors, environmental factors, previous respiratory diseases and a variety of other associations. These included a family history of lung cancer, psychological factors, urban living, living in west central Scotland and poor diet. In his view, environmental tobacco smoke was not a risk factor for lung cancer.
[5.779]Dr Lewis then went on to discuss potential errors. He said that the information derived from epidemiological studies was based on population samples and was a statistical estimate. An incidence or a relative risk was a point estimate which was usually accompanied by some measure of variability, such as a standard deviation or a confidence interval. This standard deviation or confidence interval established the degree of random error. It indicated the likelihood of having obtained an incorrect result due to chance, i.e. "the confidence we can have in our results". Random error would occur in any situation in which multiple tests were done on an individual. For example, many laboratory tests on a single individual would show slightly different values for each sample, with the average value shown as a point estimate. Similarly, random error would occur in a population, in which the values of many individuals were combined.
[5.780]Dr Lewis then went on to discuss the topic of attributable fractions, also known as attributable risk percent. He said that although observational studies could not establish cause-and-effect relationships, epidemiologists might want to draw causal inferences from statistical associations observed in studies. An underlying premise of public health epidemiology was that disease incidences could be reduced by the removal or reduction of risk factors in the population. In order to estimate the quantity of disease removed from the population by the elimination of a risk factor, the concept of attributable fractions was developed. He was referred to Table 1.2 on p.17 of RCP 2000, entitled "Estimated number and percentage of deaths attributable to smoking by cause, UK 1997". He said that the figures shown under the heading "Deaths from disease estimated to be caused by smoking as % of all deaths from disease" appeared to be an example of the use of an attributable fraction.
[5.781]Whereas the relative risk (or odds ratio) compared disease occurrence within two groups (e.g. exposed and unexposed), the attributable fraction (AF), which was mathematically derived from the relative risk, calculated the fraction of cases in the population which was attributed to the exposure. There were two types of attributable fractions, one based only on the exposed population, and the other on the general population. In the hypothetical example given above, if the incidence of heart disease among hypertensives was 100 per 100,000 and among non-hypertensives ten per 100,000, the risk difference was ninety per 100,000, which was divided by the incidence among the exposed to yield 0.9 or 90%. Reference was made to Table 4 in Dr Lewis's report, entitled "Population risk measures". The Table was as follows:
Attributable Fraction (or risk percent) among exposed The proportion of cases within the exposed group attributable to the exposure | AF (exposed) | = | I e - I u I e |
Attributable Fraction (or risk percent) in the population The proportion of cases within the population attributable to the exposure | AF (population) | = | I p - I u I p |
Attributable Fraction (or risk percent) among exposed
A restatement of the attributable fraction among exposed based on relative risk. This forms the basis of the formula used for probability of causation (PC) or assigned share (AS) calculations | AF (exposed) | = | RR - 1 RR |
This meant that 90% of the cases among the exposed were attributed to the exposure. Because attributable risk percent in the population included the whole population, of which only a fraction was exposed, the attributable risk percent of the population was lower than the attributable risk percent in the exposed population. On the hypothesis that 40% was the prevalence of hypertension in the general population, this implied that 78% of all heart disease occurring in the general population would not occur if hypertension were removed. Similar calculations for the attributable fraction of exposed could be made using relative risks (RR) or odds ratios (OR) derived from case control studies. An RR of 10 yielded the same 90% attributable fraction among the exposed as was calculated from the incidences.
[5.782]Dr Lewis continued by stating that population attributable fractions were introduced into epidemiology by Levin 1953 in reference to lung cancer risk and smoking. His estimates for the percentage of all lung cancers attributable to smoking and under the assumption that smokers, had they not become smokers, would have had the same lung cancer risk as non-smokers, covered a wide range from 56.5% to 92.5%. Because the accuracy and validity of these calculations were contingent on many factors, attributable fractions were rarely reported in the epidemiology literature. They were, however, seen in the public health literature. Referred again to RCP 2000, p.17, Dr Lewis said that it was not possible to tell whether the attributable fraction, as used in Table 1.2, was the attributable fraction among the exposed or the attributable fraction among the general population: he was unable to decide what exactly the attributable fraction characteristic here referred to.
[5.783]Dr Lewis then went on to discuss what he called "problem areas". He said that the problems associated with attributable fractions included technical, computational, statistical and interpretational issues. First, the apparent simplicity of the calculation itself obscured the complexity of the underlying human biology and study populations, which in turn were designed to reflect the condition within the real populations. The estimates used in these calculations were derived from observational studies, all of which were open to confounding, bias and variability. Confounding was an attribute or a factor within a population or a group which could be associated with both the exposure and the outcome that the study was dealing with. So, for example, age was a general confounder which one would control for in the design of the study. If one was not aware of the existence of a possible confounder one spoke of residual confounding, meaning that one postulated elements that were attributes and confounders, such as, for example, genetic predisposition and so on, which might have an influence on the study estimate and which might be removed if they were known. Bias was a different type of error, and was essentially a problem in study conduct. It was a systematic error which was either based on problems in obtaining the correct information, or on exposure, for example, or on outcome. So there were diagnostic issues and issues of questioning an individual about elements of the exposure, called information bias. And there were problems in selecting the correct study populations when exposed and unexposed populations were compared. That would be selection bias. Information bias might arise through the wording of questions or through the inability of members of the study group to remember things clearly. Over-diagnosis of a particular disease in the population could give rise to problems with diagnostic bias; so would under-diagnosis. Variability was often known as random error, meaning that, with any given population, there was a certain spread of values, which amounted to an average, and, depending on how broad that spread was, determined the variability. Similarly, the sample size determined the variability that there would be in the estimate that was finally achieved. The outcome of a study was the average of the group, but no member of the group might coincide with the average.
[5.784]Relative risk estimates from clinical trials or case control studies were difficult to extrapolate to the general population, because they dealt only with specific subsets. Attributable fractions were sensitive to the definition of exposure and to the definition and the diagnosis of the medical condition under observation. For example, Levin demonstrated how exposure definitions affected risk estimates by showing that a minor redefinition of exposure in Doll and Hill 1950, which lowered the proportion of smokers among cases from 99.7% to 98.7%, reduced the risk estimate from 13.8 to 4.0.
[5.785]In Levin 1953 at pp.536-7 there was discussion of Table 5 on p.535, entitled "Lung cancer and smoking: Indicated incidence and proportion attributable to smoking in four studies." The author wrote:
"The studies of Doll and Hill and of Wynder and Graham would indicate a much greater excess incidence [of lung cancer] among smokers as compared with non-smokers. The comparative figures in Table 5 are presented chiefly to point out the different conclusions as to relative magnitude of the possible effect of smoking which may be reached from different types of data."
Three measures of the association of smoking with lung cancer were tabulated in the last three columns of the table. The first gave the ratio of incidence among smokers compared to that in the general or total population. The second was the ratio of lung cancer incidence among smokers to that among non-smokers. The third was the indicated maximum proportion of lung cancer attributable to smoking. Dr Lewis regarded the third index as being the equivalent of attributable fraction in the population. The first line of the table took Doll and Hill's figures of 99.7% of smokers among lung cancer cases and 96% among controls. The first ratio derived from these figures was 1.04, the second was 13.8 and the third was 92.5.
[5.786]At p.536 Levin stated:
"[I]n studies of the association of some environmental factor (such as smoking) with disease, the apparent extent of the association may be greatly magnified by relatively small differences between the control and test groups, when the general prevalence of the environmental factor is high. Thus, in Table 5, if the percentage of smokers in the lung cancer group in line (1) were 98.7 instead of 99.7, the indicated figure for (r) [the second index] would be 4.0 instead of 13.8. This figure is dependent, in part, on the definition of a smoker. Thus, if persons who never smoked more than 1-4 cigarettes were excluded from the category of smokers, the figures for line (1) would be those in line (6), and (r) would be only 2.8."
The table showed that line (6) used Doll and Hill's figures, excluding those who smoked 1-4 cigarettes per day. On that basis, the percentage of cigarette smokers among lung cancer cases was 96.0 and among controls was 89.5, the first index was 1.07, the second was 2.8 and the third was 61.7.
[5.787]At pp.536-537 Levin stated of the third index:
"This index is based on the assumption that smokers, if they had not become smokers, would have had the same incidence of lung cancer as that found among non-smokers. This assumes that other etiological factors are equal in the two groups (an assumption which can be further tested)."
Dr Lewis took the expression "etiological factors" to be risk factors in some way also associated with lung cancer. He accepted that the assumption that "other etiological factors are equal in the two groups" was a valid statement, but said that the assumption was not based on fact because the author had not shown that the groups were comparable. There were a number of risk factors for lung cancer, of which smoking was only one, so that if one were to remove smoking as an exposure in the population, the other risk factors would remain. A minor redefinition of exposure also had profound effects on attributable fractions.
[5.788]Dr Lewis next referred to Hsieh and Walter 1988, in the introduction to which the authors stated:
"Relative and attributable risk are common measures of association between the risk of a health outcome and exposure to a postulated risk factor. Relative risk is defined as the ratio of the rate of the disease in persons exposed to that in persons not exposed. Attributable risk is defined as the proportion of cases associated with (or attributed to) the exposure. Relative risk measures the strength of the effect of the exposure; it does not take into account the prevalence of the exposure in the population."
Dr Lewis stated that, as in his formula and the Levin formula, the prevalence had to be fed in so as to reach a figure for attributable risk. Hsieh and Walter continued:
"Attributable risk takes into account both the strength of the effect of exposure and the prevalence of the risk factor. Its use as a measure of association is useful for priority setting and policy making in public health."
Dr Lewis commented that in the taking of public health decisions, one would be guided towards dealing with a very prevalent exposure, where there was a higher attributable fraction, rather than trying to deal with an exposure which was comparatively uncommon. Hsieh and Walter continued:
"Attributable risk is also known as the etiologic fraction, attributable fraction and attributable proportion. Since attributable risk has also been referred to as the risk difference, hereafter we adopt the term attributable fraction in this presentation."
[5.789]The second problem area discussed by Dr Lewis was confounding, bias and variability. He stated that there was a vast amount of literature on the computational issues arising from confounding, bias and variability and their effects on the estimates of attributable fractions. Attempts to deal with these issues were only moderately successful, because epidemiological data were not precise. These data were based on a small sample of the population. This small sample was then used to reflect the entire population. Although the sample was composed of individuals who could have many different traits, and although all these traits were summarised in one estimate, the sample could not reflect all the differences within the population.
[5.790]Dr Lewis referred to Greenland 1988. The author of this chapter in a book to which there were a number of contributors was from the Division of Epidemiology at UCLA School of Public Health in Los Angeles, California. At p.95 the author stated:
"In his contribution to this volume, Weed has put forth a 'Popperian' evaluation of Hill's criteria for assessing causal inference. Elsewhere, he has eloquently described and prescribed a Popperian approach for the general problem of causal inference in epidemiology. In both contributions, he criticizes the notion that either causal inference or rational decision-making should be approached with methods founded on concepts of judgment, belief, opinion or subjective probability. [...] I will here argue for the hypothesis that the conflict between Popperian and more judgment-oriented epidemiologists such as Susser arises from the failure of both sides to distinguish the needs of the branch of science called epidemiology from the needs of the branch of public health called epidemiology. I will further argue that the Popperian methods proposed thus far fail to meet all the needs of either decision-making or inference, and so as yet require epidemiologists to fall back on other methods. In other words, though Popperian methods may be necessary for good scientific or decision analysis, none of the Popperian approaches described so far constitutes a sufficient system for such analyses."
At p.96 the author stated:
"Epidemiology as a science is not inherently concerned with anyone's opinion about how things are, but only how things are. It is thus understandable that Popperian epidemiologists wish to identify as scientific only statements about nature (and then only certain types), and reject from science individual beliefs or opinions about such statements. It is equally understandable that a sound methodology for practicing the science of epidemiology will be found inadequate for practicing the public-health profession of epidemiology: public health is not a science, but a form of social activism, one whose benefits appear profound enough to society that it is institutionalized and heavily subsidized by governments."
Dr Lewis said that he recognised the dichotomy between the branch of science called epidemiology and the branch of public health called epidemiology, and agreed with the view that there was a difference between these in the decision-making process. He agreed with the sentiment that public health was not a science but a form of social activism, and with the author's view that a public health activist would be concerned with communicating his or her own opinions, evaluating the opinions of colleagues and influencing the opinions of governmental figures and the public. He recognised the process, referred to by the author, whereby public health activists, on the strength of a belief, would then wish to transmit that belief to governmental figures in order to influence governmental action.
[5.791]Dr Lewis went on to state that further, one estimate could not reflect all the differences within the sample. It was a mathematical approximation which described the relationship between a disease and a risk factor. Epidemiological studies were typically short compared to the time it took some diseases to develop, particularly cancers. It was therefore not clear whether the attributable fraction reflected an excess risk due to the exposure, or whether the exposure simply moved a condition which would occur anyway forward in time. Finally, he stated, studies were performed on different populations with different methods and did not always produce the same result. It was therefore left to the discretion of the researcher to decide which study and which estimates to use in the calculation of an attributable fraction.
[5.792]The third of Dr Lewis's problem areas was that of interpretational issues. He said that the interpretational issues relating to attributable fractions within a population were causality and disease prevention. Attributable fraction calculations also touched on issues of individual attribution. The calculation of an attributable fraction assumed a cause-and-effect relationship between a risk factor and a disease. It could not be taken from an attributable fraction that it was evidence of a cause-and-effect relationship, because that notion was already embedded in the concept of attributable fraction. Although they were called "attributable", attributable fractions were derived from statistical associations (relative risk measures), which did not establish causation.
[5.793]In this context, Dr Lewis referred to Rockhill et al. 1998. In this commentary the authors considered computational and conceptual issues relevant to population attributable fraction estimation that were infrequently discussed elsewhere, with illustrations from the breast cancer literature. At p.15 they explained that they used the term "population attributable fraction" in the sense used by Greenland and Robins, who distinguished between "excess fraction" (what epidemiologists usually estimated when they computed "population attributable risk" or "population attributable fraction") and "etiologic fraction", which was not estimable without strong biologic assumptions. Dr Lewis explained that such an assumption was that observed associations had a cause-and-effect relationship.
[5.794]At p.15 the authors stated:
"The population attributable fraction is most commonly defined as the proportional reduction in average disease risk over a specified time interval that would be achieved by eliminating the exposure(s) of interest from the population while distributions of other risk factors in the population remain unchanged. This also can be interpreted as the proportion of disease cases over a specified time that would be prevented following elimination of the exposures, assuming the exposures are causal."
At p.16 the authors stated:
"Perhaps the most important aspect of population attributable fraction estimation is correct interpretation and communication."
At p.17, in a discussion of breast cancer risk factors, the authors stated:
"The population attributable fraction does not address probability of causation for a specific case of disease, nor does its estimation enable epidemiologists to discriminate between those cases caused by, and those not caused by, the risk factors under consideration."
In their conclusion, on p.18, the authors stated:
"Many public health researchers are interested in evaluating the potential population impacts of identified risk factors. For some of these evaluations, estimation of the population attributable fraction is appropriate and valuable. The assumptions underlying valid population attributable fraction estimation include the following: a causal relationship between the risk factors and disease; the immediate attainment, among those formerly exposed, of the unexposed disease risk following elimination of the exposures; and independence of the considered risk factors from other factors that influence disease risk so that it is possible to conceive of changing the population distributions of the considered factors only. Such assumptions are often not justified. Those who present population attributable fractions have a duty to ensure that estimates are correctly computed and that their limited meaning is correctly communicated, given the interest among researchers, clinicians, and the public in quantitative figures that attempt to summarize the state of etiologic knowledge about a disease."
Dr Lewis said that he agreed with all these statements.
[5.795]He went on to add that attributable fractions attempted to predict what would happen in the population if a risk factor were removed. That is, if the attributable fraction was 90% for a given risk factor and a disease, the model presumed that the removal of that risk factor would reduce the incidence of the disease by 90%. In many instances, however, as shown by studies exploring the effects of reducing blood pressure, cholesterol and cigarette smoking, the reduction in disease had been far lower than predicted by attributable risk percent calculations. The reduction of the risk factor had in general failed to reduce disease by the predicted amount.
[5.796]Dr Lewis then turned to the topic of individual causation. If the attributable fraction addressed the attributability of disease to a risk factor on a population level, what was the relationship, if any, between the attributable fraction and the individual case? Attributable fractions did not purport to deal with the individual case. Nor could they distinguish between those cases attributed to, and those not attributed to, the risk factors under consideration (Rockhill et al. 1998). However, attributable fractions had been used to develop the concept of "probability of causation", thereby seeking to move from the population level to the individual level. Probability of causation was now generally referred to as "assigned shares". One problem with assigned shares was exposure specificity. If only a single exposure was considered, high specificity must be assumed. This meant that a direct link was implied between a risk factor or an attribute and disease occurrence. Dr Lewis said, however, that most diseases were rare both in exposed and unexposed. Lung cancer, for example, was a rare disease in non-smokers, and somewhat less rare in smokers. An association for exposure to smoking, for example, which was observed to elevate annual risk from one in 10,000 in the unexposed to ten in 10,000 in the exposed, was not highly specific.
[5.797]Under reference to a diagram, Dr Lewis explained that any population that was being researched or observed in terms of a particular exposure and a particular outcome would fall into four groups: a group that was exposed and had the outcome; a group that was exposed and did not have the outcome; a group that was unexposed and had the outcome; and a group that was unexposed and did not have the outcome. In general the last group would be quite large and the first group would be quite small because most people were healthy and disease was rare in the population. He said that it was not possible to know whether group membership proved a causal connection between outcome or lack of outcome and exposure or lack of exposure.
[5.798]Dr Lewis went on to discuss heterogeneity and group memberships. He said that populations were composed of unique individuals who differed in many aspects. The assumption for individual attributability of population rates was that the likelihood of disease (or individual susceptibility) was identical for each member of an unexposed cohort or population. This was patently never the case, because it assumed that the background hazard for disease was the same in all subjects: all individuals were assumed to have precisely the same exposures. Population estimates were based on group data, an average of many individuals, which could apply only to the group and not to any particular individual. If blood pressure was measured in many individuals, no single individual need have the group's average blood pressure. Each population estimate of this sort was a group or aggregation artefact which could contain patterns and associations that did not apply to homogeneous subgroups or to individuals.
[5.799]In populations, he said, we had a baseline rate of disease occurring for which a putative causal agent was not known, and this was often called idiopathic. The background risk posed by this undetermined causal factor could not be defined, because it was unknown. When the baseline rate was compared to the rate observed among the exposed, an excess might be detected. Epidemiologists assumed that the excess in the population was due to the exposure. If this was applied to the individual, then we were again assuming that the exposure rather than the unknown agent was the cause of disease in the exposed. In the case of an exposed individual with disease, however, it was never known whether this person belonged in the "excess" or the "baseline" group.
[5.800]By the same token, he went on to say, individuals could belong to a large number of groups. The identification of an individual by age, sex and exposure did not capture all attributes which might determine risk. People were black or white, rich or poor, employed or unemployed, had unique genetic profiles and engaged in various health and lifestyle habits. Each one of these groups constituted a different risk set and would have a different attributable fraction. Each individual, who might have different characteristics such as being white, poor and unemployed, thus belonged to multiple risk sets, and had multiple attributable fractions that might be applicable to him. Further, for any given disease, the sum of all attributable fractions for all factors would exceed 100%. An individual who ceased to belong to one risk set, by ceasing to be exposed to the relevant exposure, nonetheless might remain in other risk sets. For example, taking hypertension and high cholesterol levels, both of which were risk factors for heart disease, and assuming that the relative risk for each of them is 10 and that 40% of the population had each of these exposures, so that the attributable fraction for each would be 78%, the sum of these attributable fractions would be 156%. Dr Lewis said that thus the assigned share concept did not account for heterogeneity of exposures, heterogeneity of the groups studied in observational epidemiology, or the heterogeneity of the sampling situation within one study and of several studies; nor could it account for multiple group membership of single individuals. The concept of probability of causation or "assigned shares" ignored the existence of diversity and individual differences.
[5.801]Reference was made in this context to Rothman and Greenland 1998. At p.13 the authors stated:
"There is a tendency to think that the sum of the fractions of disease attributable to each of the causes of the disease should be 100%. For example, in their widely cited work, The Causes of Cancer, Doll and Peto (1981; Table 20) created a table giving their estimates of the fraction of all cancers caused by various agents; the total for the fractions was nearly 100%. Although they acknowledged that any case could be caused by more than one agent (which would mean that the attributable fractions would not sum to 100%), they referred to this situation as a 'difficulty' and an 'anomaly.' It is, however, neither a difficulty nor an anomaly, but simply a consequence of allowing for the fact that no event has a single agent as the cause. The fraction of disease that can be attributed to each of the causes of disease in all the causal mechanisms has no upper limit: For cancer or any disease, the upper limit of the total of the fraction of disease attributable to all the component causes of all the causal mechanisms that produce it is not 100% but infinity. Only the fraction of disease attributable to a single component cause cannot exceed 100%."
Dr Lewis said that he agreed with this passage.
[5.802]Dr Lewis was referred to Callum 1998, in the introduction to which, at p.1, it was stated:
"People who have never smoked cigarettes die from diseases that smoking can cause, and to that same extent some cigarette smokers too can die of the disease but not as a result of their smoking. The methods used to estimate the number of deaths caused by smoking are all based on a proportion of deaths caused by smoking, and cannot be traced back to individuals."
Dr Lewis said that he agreed with this statement.
[5.803]Dr Lewis went on to say that another major problem in applying epidemiological data to individuals surrounded the counterfactual condition, which was the proposition that in an alternate world, where the individual was not exposed, disease would not have occurred. This was a separate concept from that of attributable fraction. It assumed an alternate setting in which the same individual remained healthy because he or she was not exposed to the putative causal agent. This, however, could never be proved because the "alternate world" in which the individual was not exposed did not exist and could not be tested. This also entailed considerations of competing risks and of rare events, i.e. the comparison of rare events with even rarer events. The assertion that the exposure caused the disease in a specific individual implied that if there had been no exposure, the individual would not have had the disease. It was unclear, however, what the individual's "alternate world" would look like if the exposure were removed. For example, if a smoker of normal weight had not smoked in an alternate world, he might have gained weight, thereby placing himself in a different risk category. Any exposure might be linked to any number of other factors which might affect the risk category in an unpredictable fashion. The counterfactual conditional therefore implied that, if the exposure had not been present, some other element of risk would not have occurred, and asserted that the individual in question did not belong to the group of unexposed who would have incurred the disease.
[5.804]This, Dr Lewis said, posited a theory counter to fact. It also neglected the fact that, whether the individual was exposed or unexposed, the initial likelihood of developing most diseases was low (for example, the lifetime risk of developing lung cancer was approximately 1 in 100 for the unexposed (non-smokers) and 10 in 100 for the exposed (smokers)). (Lifetime risk should of course be contrasted with annual risk, and Dr Lewis said that to simplify matters he took a lifetime as being 100 years.) He said that these disease likelihoods or predictions accompanied the individual through life until the individual either got the disease or ended his life without getting the disease. If he died without getting the disease (i.e. from another cause), then his disease likelihood would be zero instead of 1 in 100 or 10 in 100. If he did get the disease, his disease likelihood would be 1, although previously it had been 1 in 100 (i.e. 0.01) or, if exposed to the risk factor, 10 in 100 (i.e. 0.1). Whether an individual was exposed or not exposed, the likelihood of disease occurring was close to zero, with the unexposed likelihood slightly closer to zero than the exposed. Dr Lewis illustrated this by reference to a diagram, to demonstrate that for the unexposed group the prior likelihood of getting the disease was always 1 in 100, and for the exposed group the likelihood was 10 in 100, both of which were proportionately far removed from the end likelihood of having the disease. He said that this likelihood turned to 1 immediately for both and unexposed once disease had occurred. It was clearly not justified to argue from the fact that disease did occur that it occurred due to the exposure without taking into account the actual likelihood of disease occurrence. In both instances, the risk of developing lung cancer was very low, and it was unlikely that disease would occur in any individual, but the likelihood was not zero. Even if the exposure was withdrawn in an alternate world, the individual still might develop the disease. Conversely, on an individual level for any case of lung cancer we could, he said, posit ninety-nine "alternate worlds" in which lung cancer would not have occurred to a person who was not exposed, and nine "alternate worlds" in which lung cancer would not have occurred to a person who was exposed. Non-exposure to a specific substance was but one of the many circumstances which could have produced a situation in which no lung cancer occurred. In short, because the initial risk of lung cancer was low in any case, the likelihood that, if circumstances had been different, lung cancer would not have occurred, was high.
[5.805]Dr Lewis's conclusions were expressed in these terms:
"Epidemiological evidence cannot be used to make statements about individual causation. Firstly, the information provided in observational epidemiology is generally such that it can neither confirm [n]or refute a causal relationship, particularly when the exposure in question is not specifically associated with a certain condition. Epidemiology produces information on associations which may be used for public health decision-making and individual guidance, but it cannot provide information on the likelihood that an exposure produced an individual's condition. Secondly, the population attributable risk is a measure for populations only and does not imply a likelihood of disease occurrence within an individual, contingent upon that individual's exposure. Thirdly, the fact that cases and non-cases can emerge both from the unexposed and the exposed groups shows that the likelihood of the individual occurrence cannot be reliably predicted from his or her exposure group membership alone. Fourthly, the group estimates obscure the underlying heterogeneity of the population, so that it is entirely possible that other group memberships besides exposure, like genetic profile, socioeconomic status, workplace, diet and other exposures make a major contribution to disease occurrence. Furthermore, the question of using epidemiological data for individual causation raises the problem of identifying a particular individual who was harmed by the exposure. Models such as the assigned share concept, derived from attributable fractions, have attempted to deal with this, but suffer from the limitations mentioned above. Additionally, the attempt to identify exposure as the sole cause of disease in an individual produces a statement counter to fact in that it implies that the individual would have remained healthy if the exposure had not occurred. This is not provable and cannot be derived from epidemiological data."
[5.806]Dr Lewis was invited to comment on a number of publications. In Robins and Greenland 1989 the authors offered a mathematical definition for the probability of causation that formalised the legal and ordinary-language meaning of the term. They showed that, under this definition, even the average probability of causation among exposed cases was not identifiable from epidemiologic data. This was because the probability of causation depended both on the unknown mechanisms by which exposure affected disease risk and competing risks, and on the unknown degree of heterogeneity in the background disease risk of the exposed population. Dr Lewis was shown passages in the text of the article in which this summary was developed, and said that he agreed with them. In particular, he agreed with a passage at pp.1134-1135 in which the authors stated that the average probability of causation among exposed individuals developing disease could not be estimated from epidemiologic data without resorting to non-identifiable biologic assumptions. Furthermore, even in the absence of competing risks, the average probability of causation among all exposed cases could not be estimated. "This is because these probabilities of causation depend on (i) the unknown mechanisms by which exposure affects disease risk and competing risks, (ii) the unknown degree of heterogeneity in the background risks of disease, and (iii) the unknown degree of dependence between risk of disease and competing risks."
[5.807]Dr Lewis was next asked to consider Colby et al. 1995. At p.93 it was stated:
"There are some variations in the histologic subtypes among smokers and non-smokers (Table 7-4), with squamous cell carcinoma and small cell carcinoma showing the highest association with smoking."
Table 7-4 was headed "Histologic subtypes of carcinomas in smokers and nonsmokers". For those with squamous cell carcinoma the table showed that out of 2926 cases of squamous cell carcinoma, 98% were smokers and 2% were nonsmokers. The table was said to have been modified from reference 9, Rohwedder and Weatherbee 1974. After considering the text of this article, Dr Lewis confirmed that it did not appear to be the correct reference. The correct reference appeared to be reference 10, Rosenow and Carr 1979.
[5.808]Table 2 at p.235 of that paper listed the prevalence of the five most common lung cancers in men and women, smokers and never-smokers, as they had presented at the Mayo Clinic, Rochester, Minnesota. Table 7-4 in Colby et al. could be seen to be a modification of this table. The table in Rosenow and Carr 1979 showed that out of a total of 992 epidermoid (i.e. squamous cell) carcinomas there were 899 in men, 892 of whom were described as smokers and seven as never-smokers, and ninety-three in women, eighty of whom were described as smokers and thirteen as never-smokers. At p.233 the authors stated:
"The Mayo Lung Project of the Mayo Foundation is conducting a controlled prospective lung cancer screening program in males 45 years and older who smoke at least 20 cigarettes per day."
Dr Lewis commented that there were two pieces of information. The first was that there was a high risk project which used only exposed males, and the second was that the Mayo Clinic also captured other lung cancer cases. It was not said how these entered into the figures in the table. No definition was given of the expressions "smoker" and "never-smoker", though by inference a smoker could be taken as someone who had ever smoked, even for a short period at some earlier time in his or her life, i.e. an "ever-smoker". If, by way of illustration, and on the assumption that there was no statistical association between smoking and lung cancer, 98% of the population from which the lung cancer patients were drawn were ever-smokers, one would expect 98% of cases of squamous cell lung cancer among ever-smokers. In Dr Lewis's view there was insufficient information about the population sampled, and the general population from which it was drawn, to enable conclusions to be drawn about the relationship found between ever-smoking and epidermoid cancer. There was no indication that the authors addressed the question of whether there was a statistical association between epidermoid cancer and any other feature to be found in the members of the group, that is to say, it did not appear that they had controlled for confounding in any way.
[5.809]Returning to the passage in Colby et al. 1995, quoted above, Dr Lewis commented that the authors did not provide a statistical test. If they intended to imply that squamous cell carcinoma of the lung was statistically associated with smoking, they would not be entitled to say so on the evidence of Rosenow and Carr 1979. It was unknown where the population discussed in that paper was sampled from. Most likely, most of the information was based on the high risk exposed group, so that there was an over-sampling of individuals with the exposure and it could not be known what a random sample of lung cancer patients would look like.
[5.810]In Van Rossum et al. 2000 the authors followed up a group of British male civil servants aged 40-69 years for twenty-five years to establish whether or not differences in their socio-economic structure had some influence on the mortality experience of this cohort. They concluded that differentials in mortality persisted at older ages for almost all causes of death. Table 1 on p.179 showed aged-adjusted mortality rates per 1000 person years (number of deaths) by employment grade and mortality rate ratios for "other" grade versus administrative. The table included figures for malignant neoplasm of the lung. Dr Lewis explained that these showed a distinct gradient in the mortality experience, from lowest mortality from neoplasm of the lung in the highest socio-economic stratum, to highest mortality of neoplasm of the lung in the lowest socio-economic stratum, the overall estimate of the influence of socio-economic status being 4.08. This, he said, indicated that there was an independent influence of socio-economic status on the mortality experience from malignant neoplasm of the lung (and also, as appeared from the table, from many other causes of mortality), independent of the factors that were adjusted for, such as smoking.
[5.811]In Hart et al. 2001, which related to a study investigating differences in lung cancer mortality risk between social classes in two study groups, one from the general population of Renfrew and Paisley in the west of Scotland and the other from workers employed in the Central Clydeside conurbation, also in the west of Scotland, the authors concluded that there was a difference in lung cancer risk between social classes, in addition to the effect of smoking. This could be explained by poor lung health, deprivation and poor socio-economic conditions throughout life. Dr Lewis said that by "difference" the authors meant a statistically significant difference, and that their conclusion was consistent with that in Van Rossum et al. 2000.
[5.812]Dr Lewis was then asked to comment on Dong and Hemminki 2001. The Swedish Family-Cancer Database, with a study population of 5,520,756 offspring and their parents from 2,112,616 nuclear families, was used to systematically estimate the effects of parental and sibling cancers on the cancer risks in the individuals born after 1934. The article started with the statement that it was well documented that there was familial aggregation of cancer at practically all sites. Dr Lewis said that, in summary, the authors found, specifically for lung cancer, and looking only at parental determinants, a risk ratio of around 5 for the association of two members of a family having lung cancer, and of 13 for the association of both a parent and a sibling having lung cancer.
[5.813]In Samet et al. 1996 the authors used data from a population-based case-control study to examine the relationship between personal and family illness history and lung cancer risk. They stated that the collection of detailed information on cigarette smoking and the use of multiple logistic regression facilitated the control of the effects of smoking when the illness variables were assessed. Dr Lewis explained that this was a statistical technique which adjusted for confounding factors determined in the study, of which smoking was one. The authors found that a history of chronic bronchitis or emphysema was associated with a doubling of lung cancer risk and that if at least one parent had lung cancer the odds radio was increased fivefold. Dr Lewis referred to figures given in Table 5 on p.467, and said that these increases in risk, as shown on the table, were statistically significant.
[5.814]In Yang et al. 1999 the authors concluded that their results suggested the presence of a high-risk gene contributing to early-onset lung cancer in a population where the probands (i.e. study subjects) were nonsmokers. Dr Lewis explained that the authors had estimated the attributable fraction due to the genetic makeup first as the attributable fraction due to an environmental exposure, and postulated that the cause of lung cancer in younger probands was "a rare autosomal co-dominant gene".
[5.815]In NCI 1978 the contributors provided estimates of the fraction of cancer in the United States related to occupational factors. At p.1 they stated that if recent evidence was considered and if the full consequences of occupational exposures in the present and recent past were taken into account, estimates of the fraction of cancer incidence in the United States attributable to occupational exposure in the present and in the foreseeable future of at least 20% appeared much more reasonable than previous, lower estimates, and might even be conservative.
[5.816]Carnow 1978 stated at p.17 that there would appear to be a general consensus that cancer, particularly lung cancer, had multifactorial aetiology which included cigarette smoking, urban air pollution and occupational exposure. Separating out these factors and assessing their quantitative impact on health was critical. The author concluded at p.20:
"I noted at the onset of this discussion that any association found in the presence of such an overwhelming factor as cigarettes must be seriously considered and explained. All of the major prospective sampling studies carried out in the United States and in other countries examined by us, in addition to the regression studies we carried out, revealed a significant relationship between urbanization and lung cancer incidence, and, where benzo[a]pyrene levels were measured, an even greater relationship to levels of benzo[a]pyrene. These relationships hold, even when one standardizes for cigarette smoking, as was done in all of these studies, suggesting that air pollution is, indeed, a significant factor in the etiology of lung cancer."
[5.817]In ACC 1981 at p.13 a table was given for age-adjusted death rates per 100,000 population for selected sites for forty-two countries, derived from statistics for the years 1976 and 1977. For lung cancer in males the rate for Scotland was 108.5, which made Scotland the highest ranking country. For Ireland the rate was 61.8 and its rank was sixteenth, and for Japan the rate was 28.3 and its rank was thirty-first. Dr Lewis added the comment that at that time Japan was known to have one of the highest smoking prevalences in the world.
[5.818]In Gillis et al. 1988a male lung cancer cases and age- and sex-matched controls were interviewed between 1976 and 1981 in a case-control study of cigarette smoking habits and lung cancer in Glasgow and the west of Scotland, "an area with the highest recorded incidence in the world". The authors said that the relative risk of lung cancer increased significantly for smokers whose consumption was below twenty cigarettes per day, but did not rise significantly in those who smoked more than twenty cigarettes per day. The male lung cancer rates during the period of the study were 158 per 100,000 in the Glasgow area and 156 per 100,000 in the Renfrew/Paisley area, about 50% greater than the whole of Scotland rate in ACC 1981. At pp.41-42 the authors stated:
"The major finding in this study is the steep increase in the relative risk of lung cancer observed in West of Scotland smokers with an average consumption of 1-14 and 15-24 cigarettes daily, compared with the small increase in relative risk in smokers with a higher average daily consumption [...]. This is at variance with the majority of the literature which describes a steady increase in relative risk above an average consumption of 20 cigarettes daily. [...]
Thus, in an area of exceptionally high lung cancer incidence, there is a lack of increase of the relative risk of lung cancer at higher levels of cigarette smoking. We have been unable to explain this observation on the basis of confounding bias or artefact.
The low level of relative risk found at all levels of cigarette consumption coupled with the small increase in relative risk observed at the highest levels of smoking represent a paradox for an area with such a very high rate of lung cancer.
The existence of a higher than average proportion of heavy smokers in the West of Scotland population would not seem therefore sufficient by itself to be responsible for the high lung cancer rate. Thus the question of additional susceptibility to lung cancer in the local population is raised."
[5.819]The authors stated that the accompanying paper, Gillis et al. 1988b, attempted to place their findings in the context of a prospective cohort study of west of Scotland men with known smoking habits followed for ten and a half years. At p.46 the authors stated that the main reason for presenting the results derived from the cohort study was to establish whether the unusual finding of a flattening in the dose-response relation of cigarette smoking and lung cancer observed at the higher levels of cigarette consumption in the case-control study in the West of Scotland could be substantiated. The availability of results from both a case-control and a cohort study conducted in the same geographical area during the same period removed many of the biases inherent in the former. The fact that both studies produced dose-response relations which flattened at the higher levels of cigarette consumption suggested that the observation was not an artefact. After further discussion, the authors stated, at p.47:
"It thus appears that it is not just the West of Scotland smoker who is at an increased level of risk compared with his equal smoking counterpart elsewhere but also the West of Scotland non-smoker who may also experience a higher than expected lung cancer risk.
The flattening of the dose-response relation seen in the case-control study has not been explained by any of the smoking characteristics examined. The fact that both the size and shape of the relation can be reproduced in the cohort study leads us to believe that this is a genuine representation of the smoking and lung cancer relation in the West of Scotland.
What this might mean in terms of the aetiology of lung cancer in the West of Scotland is not known. [...]"
Dr Lewis commented that a study such as this demonstrated the need to bear in mind that geographical location might affect results, as might also membership of a risk set by reference to occupation, such as previous military service or membership of the medical profession.
[5.820]Kissen 1963b reported on a study on male lung cancer patients and non-cancer patients in three hospital chest units. The location of these units was not specified, but since the author was a research associate in psychosomatic medicine at the Southern General Hospital, Glasgow, it might be taken that they were in the west of Scotland. The author found that among the lung cancer patients as opposed to the non-cancer controls there was a lower incidence of certain childhood behaviour disorders and a high rate of concealment, or bottling up, of emotional difficulties. He stated that these findings appeared to be independent of cigarette smoking status, and of tumour histology; nor was there any apparent relationship with lack of aggression or lack of sociability. In other words, he stated, the findings supported the hypothesis that lung cancer patients had a poor outlet for emotional discharge and that they tended to conceal or bottle up their emotional difficulties. The significance of childhood behaviour disorders was that they represented early outlets for emotional discharge. In other words, the statement that lung cancer patients, in contrast to non-cancer patients, had poor capacity for emotional discharge, was supported by clinical observation in the first instance, and two subsequent independent objective measures.
[5.821]Dr Lewis said that Eysenck 1965 showed that there was an association between personality and lung cancer. At p.105 the author stated that his general conclusion from studies of personality, social behaviour and body build was that cigarette smokers on the whole tended to show extraverted behaviour patterns and that this relationship was a quantitative one, i.e. the greater the number of cigarettes smoked the greater the degree of extraversion of the smokers concerned. Dr Lewis said that Eysenck was the most prominent, and perhaps the first, person working in his field to suggest a relationship between personality and lung cancer and that in common with Kissen he found that persons with lung cancer differed in personality type from controls.
[5.822]Dr Lewis said that Horne and Picard 1979 explored the psychosocial situation of individuals who had not yet had any diagnosis of cancer, looking at stability functions, such as childhood stability, job stability and marriage stability, and composed from these a scale which was then set out as a predictor of the underlying condition. The authors stated in their conclusion at p.512:
"Smoking is well established as a risk factor for both coronary heart disease and lung cancer. In this study, psychosocial factors were one to two times as important as smoking history in predicting diagnoses of cancer.
Thus, the present data suggest that just as there are psychological risk factors for coronary heart disease [...], there may well be psychosocial risk factors for lung cancer that could be utilized in programs to prevent or detect the illness."
Dr Lewis explained that this meant that psychosocial factors were a stronger predictor of lung cancer than was smoking history in the study group.
[5.823]Knekt et al. 1996 reported on a prospective study of the association between depressiveness and subsequent incidence of lung cancer. The study population were included in the nationally representative Mini-Finland Health Survey. The authors reported that after a fourteen year observation period the relative risk of lung cancer between depressive persons and individuals with a normal depressiveness score was 3.32. Dr Lewis said that the confidence intervals showed that this was a statistically significant result and that this was an adjusted risk estimate which was not influenced by potential confounding factors such as age, education, geographic area and smoking.
[5.824]Alavanja et al. 1992 reported that pre-existing respiratory disease among lifetime non-smokers and previous cigarette smoking among former smokers who had stopped for at least fifteen years were significantly linked to lung cancer in a population-based case-control study of non-smoking women. Asthma, emphysema, pneumonia and tuberculosis appeared meaningfully related to lung cancer. Overall, a history of non-malignant respiratory disease might explain the cause of nearly 16% of the incident cases of lung cancer among non-smokers. Dr Lewis said that it was possible from these results to postulate that a history of non-malignant respiratory disease might explain the cause of some percentage of the incident cases of lung cancer among smokers also.
[5.825]Bandera et al. 2001 reviewed the epidemiological evidence for association of alcohol and lung cancer. The authors stated:
"The studies reviewed here provide some indication that alcohol and particularly beer intake may increase lung cancer risk after controlling for cigarette smoking. Although the evidence is not conclusive, it warrants additional consideration of alcohol as a risk factor in lung cancer etiology, independent of cigarette smoking."
The authors also commented that diet was an important factor to consider when evaluating the relationship between alcohol and lung cancer, because consumption of alcoholic beverages might displace other elements of the diet, particularly for heavy drinkers, and the effects of ethanol (i.e. alcohol) on appetite, digestion and absorption of nutrients were well documented. Diets high in fat and low in fruit consumption had been observed among heavy alcohol drinkers and beer drinkers. Also, smokers tended to consume more high-fat foods and less fruit and vegetables. Dr Lewis said that he accepted the authors' view that the current epidemiological evidence was suggestive of an increased lung cancer risk associated with drinking alcohol, although it remained to be established whether this was a group phenomenon or whether the link between alcohol and lung cancer was direct.
[5.826]Pollack et al. 1984 was a prospective cohort study of the relation between alcohol consumption and the subsequent occurrence of the five most frequent cancers in Japanese men in Hawaii. The analysis, which was adjusted for the effects of age and cigarette smoking, revealed inter alia a significant positive relation between alcohol consumption and lung cancer incidences, accounted for primarily by an increased risk among subjects who consumed larger amounts of wine or whiskey. The authors reported that among the subjects who drank more than forty ounces of alcohol per month, a larger proportion were current cigarette smokers, but even after adjustment for this factor, the apparent relation between alcohol consumption and lung cancer incidence remained significant. In addition, even when several categories for the number of cigarettes smoked were used as co-variates, the relation still held.
[5.827]In Darby et al. 2001 the authors (one of whom was Sir Richard Doll) examined the relationship between diet and lung cancer in a case-control study of cases of lung cancer and population controls in south-west England in which subjects were interviewed personally about their smoking habits and their consumption of foods and supplements rich in retinol or carotene. The authors reported at p.734:
"In our study, even after adjusting for smoking, for social class, and for all the other dietary factors simultaneously, we still observed statistically significant and apparently independent associations of lung cancer risk with pre-formed retinol (increase in risk with increased intake), and with fish liver oil, vitamin pills, carrots, and tomato sauce (decreases in risk with increase in intake). These specific associations have all been observed in at least some previous studies."
At p.735 they concluded that there was at least one as yet unidentified factor that was causally related to lung cancer risk and of considerable importance in terms of attributable risk, and that any such factor, or factors, were probably dietary, although not necessarily so.
[5.828]Finally, Herman and Rao 1971 investigated differences in lung cancer diagnosis among the Jews and non-Jews of Pittsburgh, Pennsylvania in the period 1953 to 1967. Dr Lewis said that they found that there were differences by religion in that there appeared to be a lower lung cancer risk among Jewish people. He said that this exemplified ethnic differences.
Cross-examination of Dr Michael Lewis
[5.829]In cross-examination, Dr Lewis said that he had been approached as an epidemiologist by lawyers acting for ITL. He had given a presentation to members of ITL in about 2001, and had provided a formal paper. He had come from Germany to give evidence. He did not know why no British epidemiologist was giving evidence. Asked whether there was "any truth in the story that the tobacco industry could not find a British epidemiologist to come and give evidence", he said he did not know. He accepted that it was generally agreed among doctors and scientists in the United Kingdom that tobacco smoking might cause lung cancer and that the evidence for this came almost entirely from epidemiological studies. He agreed that smoking consistently showed a strong association with lung cancer. On the other hand, Dong and Hemminki 2001 showed that family clustering had similarly strong associations.
[5.830]Asked about the statement by Bandera et al. 2001 that "cigarette smoking is undoubtedly the most important risk factor for lung cancer", he said that if this meant that it was the one with the strongest association found, then he agreed. Asked about the association between alcohol consumption and lung cancer, he agreed that there were studies that showed that there was no association. This was in part because it was difficult to understand, as there might be a group phenomenon of individuals who combined the two factors of smoking and alcohol consumption. Asked about various risk factors, such as diet, geographical location and socio-economic class, he said that where two or more risk factors were found together, they might or might not have some kind of combined effect. Groups with two or more risk factors might be sharing confounding associations. "We can simply observe that there are groups in the population that are at increased risk of lung cancer and that these groups combine certain factors which are themselves independently associated. But this does not allow us any statement concerning the mechanics of this." The observed association between lung cancer, smoking and exposure to asbestos could be regarded as showing a statistical synergism.
[5.831]Dr Lewis said that his evidence about the reduction of the risk factor, for example cigarette smoking, was not related to the fact that it took years for the death rates among ex-smokers to reduce to the same level as those of non-smokers. He was asked to comment on this passage in RCP 1971, p.54, para.4.11:
"Those who give up smoking cigarettes are much less likely to get cancer of the lung than those who continue; the excess risk decreases rapidly after stopping. In British doctors [...] who had stopped smoking the risk fell within five years to about one half of that of continuing smokers and after fifteen years was only three times the very small risk of non-smokers (Figure 4.3)."
He was also shown this figure, the caption to which contained the statement:
"Continuing smokers have a greatly increased risk of lung cancer but this risk is halved in those who had stopped between one and five years, and in those who had stopped fifteen years is down to about twice that of non-smokers."
He said that he accepted what was shown there, in the context that this constituted results from an observational study, as distinct from what he had said about the prediction that removal of exposure resulted in a reduction in risk. He was not suggesting that if a person stopped smoking, the risk would disappear. This was an observational approach contingent on the population under investigation and, within the context of this population, there could be seen to be a decline in risk associated with those who did not continue to smoke rather than those who did. This did not allow a distinction to be made between the characteristics of smokers and non-smokers. That was why, when looking at the attributable risk calculations, what was being dealt with was a prediction which needed to be examined by experiment. The studies he referred to in that regard took an experimental approach: certain groups were randomised to exposure and non-exposure, and therefore differences in the observational groups were equalised. This allowed the observers to focus on attributes and exposures such as blood pressure, cholesterol and cigarette smoking, but in these studies the kind of risk reduction that had been shown in the observational studies had not been shown. A statement that 90% of lung cancer cases were caused by smoking assumed causation, this was the assumption that underlay the attributable fraction calculation, which again was unproven until put to the test, and in his opinion it had not been.
[5.832]Dr Lewis said he was aware of Doll et al. 1994. Counsel asked him in the first place about the abstract. This indicated that the subjects were 34,439 British male doctors who replied to a postal questionnaire in 1951, of whom 10,000 had died during the first twenty years and another 10,000 had died during the second twenty years. Of the results, the abstract stated:
"Excess mortality associated with smoking was about twice as extreme during the second half of the study as it had been during the first half. The death rate ratios during 1971 - 91 (comparing continuing cigarette smokers with life-long non-smokers) were approximately threefold at ages 45 - 64 and twofold at ages 65 - 84. The excess mortality was chiefly from diseases that can be caused by smoking. [...]"
The conclusion, also in the abstract, was:
"Results from the first 20 years of this study, and of other studies at that time, substantially underestimated the hazards of long term use of tobacco. It now seems that about half of all regular cigarette smokers will eventually be killed by their habit."
Asked whether he accepted the results put forward by the authors, Dr Lewis said he accepted that they showed an increase of the association in the second half of the study. He did not understand the reason for that. He did not see any basis that he could reconstruct for the statement that half of all regular cigarette smokers would eventually be killed by their habit. He did not agree that the results from the first twenty years substantially underestimated the hazards of long term use of tobacco. He agreed that this particular study showed a dose relationship between the number of cigarettes smoked per day and the likelihood of developing lung cancer, and also a relationship between the length of time someone smoked and the likelihood of developing lung cancer.
[5.833]Table III in Doll et al. 1994, on p.903, was said to show the rates for seventeen types of cancer. The authors stated:
"Three types (cancers of the upper respiratory sites, lung, and oesophagus) were particularly closely related [to smoking], with the mortality in heavy cigarette smokers at least 15 times that in non-smokers [...]."
Dr Lewis commented that the table showed an analysis that he was not familiar with. They were performing a standardised test for trend which did not allow him to establish whether or not it was indeed fifteen times. In other words, they were running the test across all categories of smoking and establishing a standardised test for trend, and this was a rather unusual form of analysis. It did not give a risk ratio, which meant that he could not reconstruct from the table whether the figure of 15 was correct.
[5.834]At p.906 the authors stated, under the heading "Actuarial survival by smoking habit":
"As the observations have been made over such a long time, it has been possible to follow many men into their 10th - and a few even into their 11th - decade of life. It has, therefore, been possible to calculate "actuarial" survival curves for different categories of smoker not only throughout middle age but also into old age, with results that are reasonably reliable up to at least 85 years of age. The results from 35 years of age are shown for non-smokers and continuing cigarette smokers in figure 1, and for non-smokers and continuing light, moderate, and heavy cigarette smokers in figure 2. The most notable differences are in the proportions who die between 35 and 69 years of age, which vary from 20% in non-smokers to 41% in cigarette smokers as a whole and to 50% in those who smoke 25 or more cigarettes a day."
Dr Lewis said that he had seen the figures (i.e. graphs) and in all honesty it had always been difficult for him to understand this paper, simply because he did not see the numbers behind it. He saw the figures, he did not know what the numbers were behind them and he did not see a table that gave him the numbers, stratified for example for age groups in the way that was laid out in the figures. He could see that the trend described by the authors was there, but he was unable to know where the figures were actually coming from in terms of the real data. He had read the article many times, but it simply did not supply him with the numbers that he required in order to actually reconstruct the figures. Counsel asked whether the authors were putting forward false numbers. Dr Lewis said that was not what he was saying; he simply did not see the numbers, as would be the norm for a paper such as this, to inform the scientific reader of the numbers that were in each of these strata. They had gone straight to informing him of the fact that this was what the results were. It was traditional for scientific papers to provide the numbers so that one could satisfy oneself that the results were indeed correct.
[5.835]Dr Lewis was asked about a passage on p.908, under the heading "Discussion: causation, confounding, and chance". The authors wrote:
"In general, the results in this study for specific causes of death accord with those in many other studies. Reinforced by other evidence, they helped lead more than 30 years ago to the conclusion that the associations observed between smoking habit and mortality are chiefly causal in character (see also the more recent reviews by the US Surgeon General and the International Agency for Research on Cancer.) In most of the causal associations, smoking seems to act synergistically with other aetiological agents such as consumption of alcohol; various aspects of diet; level of blood pressure, blood lipids, or other cardiovascular risk factors; or exposure to asbestos, radon, or possibly some infective factors."
Dr Lewis said of the words "smoking seems to act synergistically with other aetiological agents" that the authors were drawing conclusions from an observational study in which they observed populations in which they noted, on the basis of other studies, that there was some statistical synergism of other shared attributes which influenced the association with lung cancer. He said that going from a population study to this statement was going beyond the evidence.
[5.836] The authors concluded the paragraph: "The quantitative effect of smoking will, therefore, vary with variation in the prevalence of these other agents." Dr Lewis commented that other factors could affect the association. The authors continued:
"In some instances smoking and other aetiological agents may also may be confounded, as with the consumption of alcohol, various aspects of personality, and perhaps some aspects of diet. Indeed, for a few causes of death the confounding between smoking and other factors may account for virtually all the observed association with smoking, in which case none of the excess mortality from those causes should be attributed to the habit. The only plausible examples of important associations that might be due to this, however, are those that involve cirrhosis, suicide, and other traumatic causes, for which the associations with smoking may be secondary to associations with alcohol and personality."
Asked whether he agreed with this paragraph, Dr Lewis said that it seemed speculative; it was part of the discussion, but he did not see where it was determined from the authors' data. The expression "plausible examples" appeared to him to be a part of what was going through the authors' minds, but not something which was actually obtained from the studies they had conducted.
[5.837]Later on the same page, the authors wrote:
"The attribution of some of the excess mortality in cigarette smokers to confounding does not, however, necessarily mean that the overall effect of smoking on all cause mortality is less than that observed, as the factors with which tobacco is confounded may also have other effects which tend to reduce mortality."
Dr Lewis said that he agreed with this observation inasmuch as, if it was reduced to population terms again, then indeed it might be so, that there were confounders that could act either way for that association.
[5.838] The authors continued:
"This is probably the case with alcohol, the consumption of which (at least in moderation) is associated with a reduced risk of ischaemic heart disease. If, as now seems likely, the consumption of a few units of alcohol a day can reduce the age specific mortality from ischaemic heart disease, then the confounding of cigarette consumption with the consumption of alcohol would mean that the total effect of cigarette smoking on ischaemic heart disease mortality is slightly more than that hitherto reported."
Dr Lewis said that they were positing this as an example, but it again implied that an association with one thing offset an association with another. This was a discussive aspect of the paper which had not been shown in any study that he knew of. It had not been confirmed one way or the other that low-level alcohol consumption in a smoking population resulted in an amelioration of overall mortality from myocardial infarction associated with cigarette smoking. He agreed with the statement at p.909 that two massive cohort studies carried out by the American Cancer Society, one in the 1960s and one in the 1980s, showed a similar increase over time in the excess mortality in cigarette smokers.
[5.839]Dr Lewis was next asked to consider passages in Callum 1998 at pp.37-38. The author stated that large social class differentials in cigarette smoking were described earlier in the paper, and that social class differentials in smoking "imply social class differentials in the percentage of deaths caused by smoking." She went on:
"Social class gradients in mortality are a well-documented and long-standing feature of UK mortality, the differential widening during the 1970s and 1980s."
Dr Lewis said that he accepted this statement, and the figures adduced in support of it.
[5.840] The author continued:
"Ideally deaths due to smoking would be estimated separately by social class and then amalgamated to provide a figure unaffected by social class differentials in mortality independent of smoking. Comprehensive, consistent and reliable data for such an exercise are unfortunately not available."
Dr Lewis said he thought that this was correct.
[5.841] The author then went on to say that the data that were available permitted a limited but illustrative exercise to be undertaken. Percentages and numbers of deaths attributable to smoking by social class for each disease and for men and women were estimated. The total obtained by adding separate social class estimates was then compared with the estimate for all classes combined. In the case of lung cancer a second estimate by social class was produced. This was said to subsume different mortality risks of smoking for each social class, with United States relative risks by educational level (derived from a study known as CPS II) acting as a crude proxy for social class. The author stated, at p.38:
"In conclusion, the figures provide no evidence of significant bias in the UK estimate of deaths caused by smoking associated by social class differentials in cigarette smoking and mortality. If anything they suggest that the estimate derived for all classes combined slightly understates deaths from smoking."
Dr Lewis said that he did not accept that this was demonstrated by the figures. He felt that it was rather a contorted exercise, inasmuch as the author used data from CPS II and transposed them to the United Kingdom. It was known from studies carried out in the United Kingdom that all showed an independent association of mortality with social class. So he could not confirm the author's conclusions, which were based on so many assumptions surrounding the attributable fractions, that data from CPS II apply to the United Kingdom, and so forth. He did not see the evidentiary aspect for the statement that the figures provided no evidence of significant bias arising from social class differentials. Studies in the United Kingdom did indeed show that social class was a risk factor. This study took estimates from the studies that showed that and proposed that certain fractions of mortality were attributable to social class. This introduced a different aspect: it went from the study estimate to the notion that, if social class differences were removed, this would be the result. The Whitehall Study (discussed in Van Rossum et al. 2000) was very well able to distinguish populations in different social classes, but he did not think that it was possible, on a population basis, to make such a distinction in the approach adopted by Callum.
[5.842]Dr Lewis said that he was aware in a general way of statistics given in MacAskill et al. 2002 that there was a marked social class gradient in Scotland, there being higher concentrations for smokers in more disadvantaged social groups. He was asked about the statistics used in Dong and Hemminki 2001, Knekt et al. 1996, Carnow 1978, Kissen 1963b and Gillis et al. 1988b; he explained how it could be seen from the statistics provided in these papers how the authors reached their conclusions. Counsel asked him whether the statistics were based on a small number of cases of lung cancer in each instance, and whether it was not very safe to rely on such small numbers for epidemiological studies. Dr Lewis said that in any group lung cancer was a rare disease, which is why estimates were used, and designated as such; the larger the numbers, the more stable the estimates.
[5.843]Dr Lewis agreed that a strong association had been shown between cigarette smoking and lung cancer, but he disagreed that the conclusion could be drawn from this that it was highly probable that smoking caused lung cancer in any individual. This was because it was necessary to look at all the other attributes and features which might also contribute or be associated with the emergence of that type of carcinoma. These could not be ruled out. The condition was one that in any event had low incidence, so there was a low likelihood of its occurring under any condition. It would not be scientific, where a disease occurred in association with more than one attribute, to conclude that it was causally connected with one of those attributes, even where the association with it was stronger.
Re-examination of Dr Michael Lewis
[5.844]In re-examination Dr Lewis said that he was aware that Professor MacRae, a biostatistician with a great deal of epidemiological experience who worked at the University of Surrey, had been giving advice in this case, but died during 2002. Dr Lewis had become involved thereafter in active preparations for giving evidence himself.
[5.845]He was asked about RCP 1971, p.55, Figure 4.3. He explained that in the observational context, reflected in this figure, the groups of individuals had self-selected themselves for the exposure by deciding to become smokers and had deselected themselves from the exposure over time. There were a core group of individuals who decided to continue to smoke. So all this was a selection phenomenon, occurring in this observational study, which did not allow it to be distinguished whether the effect being seen was a group phenomenon based on the type of individual that made a decision, or whether it actually was an exposure phenomenon. In the case of an interventional-type study or quasi-experimental study, the exposure was randomly allocated and the groups selected for "special intervention" and "usual care" were followed over time. Because this was done in a randomised way, it was possible to establish whether or not an effect could be seen based on the reduction of the exposure, independent from the characteristics of the individuals. MRFIT was a large study in the United States, with a sample of about 300,000 men. From these a group of high risk individuals were taken and were evenly distributed in "intervention" and "usual care" groups, of 12,000 each. Over a period of about twenty or thirty years multiple risk intervention was carried out by singling one randomly allocated group out for special intervention, focusing on reduction of cardiovascular risk factors, including smoking, and then looking to see whether at the end there was any reduction in overall mortality and specific mortality, such as cardiovascular mortality, but also lung cancer mortality. They found no difference in the lung cancer mortality, nor in overall mortality, when they compared the "special intervention" and the "usual care" groups, despite a good success in reducing all risk factor levels, including the smoking prevalence in the intervention group. This raised questions about the causal connection between the exposure and the disease outcome. It showed at least that the attributable fraction calculation was not valid because, under a quasi-experimental setting, no effect was seen of reducing the exposure in a randomly allocated group.
[5.846]Finally, Dr Lewis said that he was aware that there were studies that indicated that squamous cell lung cancer was found in never-smokers as well as in smokers: the table in Rosenow and Carr 1979, even though it was not accurate in terms of the population distribution, showed never-smokers with squamous cell carcinoma.
Professor Charles Platz
[5.847]Professor Charles Platz, aged 66, was a retired surgical pathologist. After completing his education, which included the degree of MD from the University of Chicago and postgraduate posts held there, he held a series of academic appointments. Between 1967 and 1975 he held successively the posts of Instructor, Assistant Professor and Associate Professor in Pathology at the University of Chicago. From 1975 to 2000 he held posts as Associate Professor and thereafter Professor of Pathology at the University of Iowa College of Medicine, before becoming Professor Emeritus in Pathology there in 2000. Alongside his academic appointments, from 1970 to 1975 he was Associate Director in Surgical Pathology at the University of Chicago. From 1975 to 1976 he was Director in Surgical Pathology at University of Iowa Hospitals and Clinics. From 1977 to 1995 he was Consultant in Pathology at the Veterans Administration Hospital, Iowa City, and from 1980 to 1992 Consultant in Pathology at the Veterans Administration Hospital in Des Moines, both Iowa. From 1982 to 1987 he was Director and from 1987 to 1994 Co-Director in Surgical Pathology at University of Iowa Hospitals and Clinics. From April 2002 he had been Consultant in the Iowa State Cancer Registry at the University of Iowa. He had also recently held some locum tenens appointments.
[5.848]His CV included a list of the conference presentations he had made, many of them on various aspects of human pathology, and a list of numerous publications of which he was author or co-author, many or most of them relating to aspects of various types of cancer. His area of research interest was the pathology of neoplastic diseases. He explained that these included benign and malignant cellular proliferations, the latter otherwise designated as cancer. Some of his research had involved work relating to lung cancer. It was a regular feature of his clinical practice over the years to examine lung tissue for the purposes of considering the diagnosis of lung cancer. He had given a number of invited lectures, relating to a variety of cancers.
[5.849]Professor Platz explained that University of Iowa Hospitals and Clinics was a large tertiary care centre. It was originally set up to care for indigent patients, but they were no longer as large a part of the patient care as used to be the case. The institution had become a fairly widely known research and treatment institution throughout the Mid-West. About half the patients were funded by insurance. Some of them were funded by Medicare, a state programme in the United States. A small percentage paid their own way. Veterans Administration (VA) hospitals were set up to care for veterans of the armed services, originally veterans of the First World War and thereafter the Second World War. To qualify for treatment, patients required to have served a specified amount of time in the armed forces. For a time all veterans were given free medical care, but thereafter limits had been introduced on the disorders or diseases which would be cared for by VA hospitals. There were also income restrictions on patients, so that the majority of the VA administration hospital patients were low-income to indigent.
[5.850]Professor Platz was asked about Randall et al. 1987. The authors of a previous study had concluded that there were virtually no meaningful differences in the use of health services between veterans and nonveterans, which suggested that healthcare planning within the VA might proceed similarly to healthcare planning for the civilian population. At p.1099 Randall et al. stated:
"Our own analyses of 1979 NHIS [National Health Interview Survey] data for male veterans suggest that VA health planning should proceed along significantly different lines than community health planning. In particular, although veterans and nonveterans may show no meaningful differences in the aggregate in the use of health services, male veterans who choose to use the VA system differ markedly in demographic, economic and health characteristics from male veterans who choose to use community health care facilities. These results indicate that VA healthcare planning must account for the distinct differences between its user population and the veteran population in general."
[5.851] After discussing the data, the authors turned to the results presented in Table 2. They said at p.1102 that these suggested that the VA patient had lower education attainment than his counterpart who used community hospitals, had less annual income than his community counterpart, was more likely to be retired because of health reasons than his community counterpart, was more likely to be out of the labour force, was more likely to live alone, was more likely to be unable to perform his usual activity because of limitations as a result of chronic conditions and was more likely to rate his health status as poor than his counterpart who used community hospitals. They went on to say:
"The above results show that the veteran who receives care in VA hospitals is quite different from his counterpart who seeks care in community facilities. The observed differences in education, annual income, labor force participation, and family structure suggest that the veteran who seeks care from the VA may have very different health care needs than the veteran who seeks care from the community. The results concerning limitations on activity and overall health status tend to confirm these other suggestive findings. [...]
The health problems of the poor and disadvantaged tend to be more numerous and more complex than those of the middle and upper income groups. Poor nutrition, inferior housing, inadequate sanitation, and the physical and psychological stresses of unemployment and deprivation all interact to intensify the health problems of the poor. The poor and less educated have higher death rates than others. For people between 45 and 64 years of age, the prevalence of chronic conditions such as arthritis, diabetes, hearing and visual impairments, heart conditions, and hypertension remains two to three times higher for those with low incomes than for others. [...]
The finding that veterans and nonveterans use hospital services at similar rates [...] does not justify the conclusion that VA and community health planning can proceed along similar lines. Instead, VA planning needs to recognise that VA facilities do not treat a representative sample of all veterans, but rather treat a unique subset of veterans that have different demographic, economic and health characteristics than veterans who seek care from the community."
Professor Platz said that the findings of Randall et al. 1987 were consistent with his own experience. He added that nutritional status was of relevance for the maintenance of the bronchial epithelium because vitamin A was involved in its repair and a deficiency in that vitamin could have implications for its maintenance.
[5.852]During the course of his evidence Professor Platz was asked to examine a biopsy slide which had been prepared from tissue taken from Mr McTear by means of the bronchoscope during the course of the procedure carried out on 10 June 1992. He used a microscope with a video attachment which enabled the slide to be seen on screens in court. He was able to indicate features of the sample as he gave his evidence. He explained that in examining such a slide he was looking for a disruption in the organisation of the normal bronchial epithelium by neoplastic epithelial cells. He described how part of the sample showed normal organisation of basal and columnar cells, with cilia on the surface, and part showed clusters of carcinoma cells. The other features which he looked for were mitotic figures, which were cells in the process of division. He indicated one such figure. He said that what he looked for in squamous carcinoma were structures called intercellular bridges and a process of maturation called keratinisation. The intercellular bridges were difficult to find, and because of this and the absence of keratinisation the squamous cell carcinoma should be described as poorly differentiated. Squamous metaplasias in the bronchus sometimes had keratin and sometimes they did not. Squamous metaplasia was a very common finding as a response to any kind of noxious stimulus or inflammation, it accompanied infections and was also part of a repair process after injury.
[5.853]Having considered and rejected the diagnosis of adenocarcinoma, Professor Platz expressed the opinion that the slide showed a sample of squamous cell bronchocarcinoma. He said that such a condition did not differ histologically as between smokers and non-smokers, as between drinkers and non-drinkers, as between persons suffering from anxiety, stress or depression and those with a different sort of personality, and those with a family history of cancer and those without. It was not possible to tell from the slide (and the other slides, which he had also examined before giving evidence) what caused Mr McTear's disease.
[5.854]Professor Platz was asked to comment on Auerbach et al. 1957 and Auerbach et al. 1961. He said that Dr Auerbach was a pathologist in the VA system and spent most of his time at the Veterans Administration Hospital in East Orange, New Jersey. He also become Professor of Pathology at New York Medical College, while remaining Consultant in Pathology at Veterans Administration Hospital. The 1957 paper reported on slides prepared from the tracheobronchial trees of 117 patients who had died and been autopsied at the Veterans Administration Hospital, East Orange, New Jersey. The material was studied only after smoking histories of the patients had been obtained. All patients dying of lung cancer were included. Those dying of other causes were included only if an adequate smoking history could be obtained. In the 1961 paper the authors stated at p.253:
"In 1957 two of us [...], with several collaborators, presented a report of progress on a study of the relative frequency of carcinoma in situ, squamous metaplasia, stratification and basal-cell hyperplasia in the lungs of nonsmokers and light and heavy smokers of cigarettes. The study was carried out on the lungs of 117 male patients dying with and without lung cancer by means of step sections of the entire tracheobronchial tree, totaling 208 sections per case. [...] All the changes mentioned above were found to be more frequent in the lungs of cigarette smokers than in those of nonsmokers, but the results of greatest interest concerned carcinoma in situ. [...]
These figures seemed to show a very definite linkage between cigarette smoking and carcinoma in situ. But they were challenged because it was claimed that we were including cases of squamous metaplasia in the category of carcinoma in situ and that our results should be re-examined on that basis. We became convinced that there was some justification for this criticism. We discovered that in the interpretation of sections of bronchial epithelium from several children our tabulations had included large recordings of carcinoma in situ. On careful re-examination it was found that the lesions observed in these cases were very different from the carcinomas in situ found in the bronchial epithelium of men who died of lung cancer. It seemed important, therefore, to restudy the whole question."
Professor Platz explained that "carcinoma in situ" referred to a change that occurs in the epithelium, out of which it was thought that invasive carcinoma would ultimately develop. Carcinoma in situ was not invading and therefore not yet capable of metastasis. The expression "carcinoma in situ" in the paper was applied to all bronchial epithelial lesions composed entirely of atypical cells and lacking cilia. The authors said that they did not mean to imply that, given sufficient time, all such lesions would inevitably become invasive.
[5.855]At p.254 of the 1961 paper the authors stated:
"Ever since 1954 the tracheobronchial tree has been dissected out of the lungs of every person examined at autopsy at the Veterans Hospital, East Orange, New Jersey. More recently, a similar arrangement was made with 11 other hospitals, most of which are in upstate New York. All this material is imbedded in paraffin and is available for study."
Altogether 402 white males, including the 117 subjects in the 1957 paper, were included in the 1961 study.
[5.856]Professor Platz commented that nothing was said about the eleven other hospitals referred to in the paper, so it was not possible to tell how many subjects, in addition to the 117 in the progress report, came from VA hospitals. It was not apparent when the arrangement with the eleven other hospitals first came into effect. The authors did not analyse whether or not the incidence of changes in the lungs differed as between patients at the VA hospital in East Orange and those at other hospitals. In very general terms the patients at a VA hospital were a selected population. It was not known in the case of such patients whether there had been exposure to toxic gas, for example, as part of their service commitment. The morphological responses might be related to irritants of more than one sort. Moreover, the VA hospital population had some features associated with low socio-economic status and with possibly inadequate nutrition, which might play a role in the disease processes of the patients, as many of them were likely to have pulmonary problems of one sort or another in the form of infection. Soldiers who served in the trenches in the First World War might have been exposed to poison gas. While the authors had addressed the relative frequency of various changes in the lungs of nonsmokers and light and heavy smokers of cigarettes, they had not addressed whether or not the incidence of lesions varied with nutritional status, socio-economic status, a family history of lung cancer or a propensity to anxiety, stress or depression. So far as Professor Platz was aware no study had been carried out along these lines addressing these questions. Nor had a study been carried out addressing whether or not the incidence of such lesions varied with the consumption of alcohol. He understood that there was an association between heavy drinking and malnutrition.
[5.857]At p.267 the authors stated:
"In this study, we found hyperplasia, destruction of cilia (or destruction of ciliated cells) and the occurrence of atypical cells all to increase greatly with the amount of cigarette smoking. We cannot escape the conclusion that a direct causal relation exists between the degree of exposure to cigarette smoke and the frequency and degree of these changes in bronchial epithelium. [...]
In our opinion the histologic evidence from this study greatly strengthens the already overwhelming body of epidemiologic evidence that cigarette smoking is a major factor in the causation of bronchogenic carcinoma."
Professor Platz said that he was unable to agree with this conclusion because the other possible factors involved in causing the changes observed in the study had not been evaluated. The authors looked at one factor and not at any others. They looked at a factor that would support the statistical evidence, referred to by them as epidemiologic evidence, and while that might be the case, Professor Platz said that he certainly did not know that it was.
[5.858]On the question how an autopsy came to be performed in any particular case, Professor Platz said that in his own experience an autopsy was carried out either with permission of the family, or if there was a potential legal issue, or if the body was unclaimed. This latter factor might select the autopsy population towards indigent individuals living in chronic care facilities.
Cross-examination of Professor Charles Platz
[5.859]In cross-examination Professor Platz says that he did not know that cigarette smoking could cause lung cancer. He was aware that in the United Kingdom the great majority of scientists and doctors and in the United States every cigarette company and the United States Government agreed that cigarette smoking could cause lung cancer. He said he was not convinced. Asked whether that put him "out on a limb", he said that it left him in the minority.
[5.860]He was then taken through Auerbach et al. 1961 in more detail than had been put to him in the course of his evidence in chief. Since, however, he did not in any way disagree with the factual findings of the authors, I do not find it necessary to repeat all of this detail here. It is sufficient to quote from pp.266-7:
"The three principal types of epithelial changes recorded were as follows: increase in number of cell rows; loss of cilia; and presence of atypical cells. [...] Taken singly, each of the three variables increased rapidly with the amount of cigarette smoking. This was true both of the number of sections showing a particular change and of the degree of the change. The proportion of sections with these changes was of the same order of magnitude or somewhat greater in men who died of lung cancer than in heavy smokers who died of other diseases.
In sections for nonsmokers such lesions as were found more often than not showed only one of the three types of change (that is, 3 or more rows of cells but cilia present and no atypical cells, cilia absent but no increase in thickness and no atypical cells, a few atypical cells but cilia present and less than 3 cell rows). Among nonsmokers there were no lesions composed entirely of atypical cells with cilia absent, extremely few lesions with cilia absent and some atypical cells and few lesions with 3 or more cell rows with some atypical cells and cilia present.
In sections from men who smoked 2 packages or more of cigarettes a day and in sections from men who died of lung cancer atypical cells were found in every lesion with 3 or more cell rows and in every lesion with cilia absent. Among these subjects, atypical cells were almost always present, even in areas with neither hyperplasia nor loss of cilia. Both in lesions with cilia present and in lesions with cilia absent the average proportion of atypical cells increased somewhat with the increasing number of cell rows.
The most striking lesions (aside from invasive carcinoma) were those composed entirely of atypical cells with cilia absent. The great majority of these were 5 or more cell rows in average depth. In other words, they exhibited all three types of change (that is, increase in number of cell rows, loss of cilia and the maximum proportion of atypical cells). None were found among men who never smoked regularly, and very few were found among light smokers, but such lesions were found in 4.3 per cent of sections from men who smoked 1 to 2 packages a day, 11.4 per cent of sections from those who smoked 2 or more packages a day and 15.0 per cent of sections from those who died of lung cancer."
Professor Platz, as I have said, did not take issue with these findings.
[5.861]He also agreed with this passage at p.267:
"It is known that cigarette smoke contains irritants, toxic substances and agents that are carcinogenic to the skin of laboratory animals. The application of irritants to epithelial tissue usually produces hyperplasia; toxic substances can destroy cells, and carcinogenic agents produce atypical changes in cells."
On the basis of the study Professor Platz was of the view that a strong association was established between the degree of exposure to cigarette smoke and the frequency and degree of the changes found in bronchial epithelium. He said that it was a question of judgment whether this constituted a causal relationship. He was not aware of any study of the other risk factors for lung cancer which showed the same graded changes to the bronchial epithelium.
PART VI: CIGARETTE SMOKING, LUNG CANCER AND ADDICTION
Causation and the law
[6.1]Before I discuss the conclusions to be drawn from the foregoing expert evidence, I propose at this stage to discuss counsel's submissions about the concept of causation. This is relevant to three averments for the pursuer: (1) that cigarette smoking can cause lung cancer; (2) that Mr McTear's lung cancer was caused by his smoking; and (3) that his lung cancer was caused by the fault and negligence of ITL. Adopting Mr Jones's terminology, I refer to these as general causation, individual causation and fault causation respectively. The burden of proving each of these is on the pursuer. The standard of proof is the balance of probabilities, not the higher standard that would be required for acceptance by scientists as proof (see for example Dingley v The Chief Constable, Strathclyde Police 2000 S.C. (H.L.) 77 per Lord Hope of Craighead at pp.89H to 90E). The following cases were referred to by counsel.
Authorities
[6.2](1)In Wardlaw v Bonnington Castings Ltd 1956 S.C. (H.L.) 26 a workman claimed damages from his employers on the ground that he had contracted pneumoconiosis through their negligence and breach of statutory duty. His duties as a steel dresser required him to work with his face in close proximity to a pneumatic hammer whose impact on the castings released particles of dangerous silica dust. Other appliances, although fitted with dust extraction plant, also caused a certain amount of the dangerous dust to permeate the air of the dressing shop. The workman averred that the employers had been negligent in failing to provide him with a respirator, and he further averred that they had been negligent and in breach of their statutory duty in regard to the maintenance of the dust extraction plant and the ventilation of the dressing shop. The workman ultimately admitted that the employers had not been negligent in failing to provide him with a respirator, and the employers ultimately admitted that they had been in breach of regulation 1 of the Grinding of Metals (Miscellaneous Industries) Regulations 1925, in relation to maintenance of some of the dust extraction plant; so that the question for decision came to be whether this breach had been a contributory cause of the pneumoconiosis.
[6.3]The House of Lords held inter alia that where there was a proved breach of a safety regulation and an injury which could be the result of that breach, the onus of proof did not, in the absence of express statutory provision, shift to an employer to prove that the injury was not caused by the breach; that in the present case there was no onus on the employers to show that their breach of statutory duty had not caused the workman's disease, but that the onus was on the workman to show affirmatively, by the ordinary standard of proof in civil actions, that on a balance of probabilities the breach of statutory duty had caused or materially contributed to his injury; and that the workman had discharged this onus and consequently the employers were liable in damages. At pp.32-33 Lord Reid said that the position could be shortly stated in this way:
"It may be that, of the noxious dust in the general atmosphere of the shop, more came from the pneumatic hammers than from the swing grinders, but I think it is sufficiently proved that the dust from the grinders made a substantial contribution. [...] It is therefore probable that much the greater proportion of the noxious dust which he inhaled over the whole period came from the hammers. But on the other hand some certainly came from the swing grinders, and I cannot avoid the conclusion that the proportion which came from the swing grinders was not negligible. [...] In my opinion, it is proved not only that the swing grinders may well have contributed but that they did in fact contribute a quota of silica dust which was not negligible to the pursuer's lungs and therefore did help to produce the disease. That is sufficient to establish liability against the appellants [...]."
[6.4] (2)In McGhee v National Coal Board 1973 S.C. (H.L.) 37 a labourer whose normal work was in pipe kilns at a brickworks was sent to work temporarily in brick kilns there. Working conditions were hotter and dustier in the brick kilns than in the pipe kilns. After he experienced irritation of the skin he was diagnosed as suffering from dermatitis. He sued his employers for damages on the ground, inter alia, that they were at fault in not providing adequate washing facilities to enable their employees to remove dust from their bodies after work. After a proof before answer the Lord Ordinary held that his employers were at fault in this respect. According to medical evidence the use of a shower bath immediately after work would have materially reduced the risk of the contraction of dermatitis. The Lord Ordinary, whose interlocutor was affirmed by the First Division, held that the pursuer had failed to establish a causal connection between his injury and the defenders' breach of duty towards him. The House of Lords held, reversing the judgment of the First Division, that as the defenders' fault had materially increased the risk of the pursuer's contraction of the industrial disease they were liable in damages to him.
[6.5]At pp.53-54 Lord Reid said:
"It has always been the law that a pursuer succeeds if he can shew that fault of the defender caused or materially contributed to his injury. There may have been two separate causes but it is enough if one of the causes arose from fault of the defender. The pursuer does not have to prove that this cause would of itself have been enough to cause him injury. That is well illustrated by the decision of this House in Wardlaw v Bonnington Castings. [...] In the present case the evidence does not shew - perhaps no one knows - just how dermatitis of this type begins."
[6.6]Lord Reid referred to the evidence about the ways in which dermatitis of this type might begin, one of which was that an accumulation of minor abrasions of the horny layer of the skin was a necessary precondition for the onset of the disease. He said that he was inclined to think that the evidence pointed to this view. But in a field where so little appeared to be known with certainty he could not say that it was proved. If it were, then the case would be indistinguishable from Wardlaw's case. He said that he could not accept the distinction drawn by the Lord Ordinary between materially increasing the risk that the disease would occur and making a material contribution to its occurrence. He concluded:
"There may be some logical ground for such a distinction where our knowledge of all the material factors is complete. But it has often been said that the legal concept of causation is not based on logic or philosophy. It is based on the practical way in which the ordinary man's mind works in the every-day affairs of life. From a broad and practical viewpoint I can see no substantial difference between saying that what the defender did materially increased the risk of injury to the pursuer and saying that what the defender did made a material contribution to his injury."
[6.7] (3)In Hotson v East Berkshire Area Health Authority [1987] A.C. 750 the plaintiff, then aged 13, fell some twelve feet while climbing a tree and sustained an acute traumatic fracture of the left femoral epiphysis. He was taken to hospital, but his injury was not correctly diagnosed or treated for five days. In the event, he suffered avascular necrosis of the epiphysis, involving disability of the hip joint with the virtual certainty that osteoarthritis would later develop. He brought an action for damages against, inter alios, the defendant health authority, who admitted negligence in failing to diagnose and treat his injury promptly. Simon Brown J found that even if the health authority had diagnosed the injury correctly and treated the plaintiff promptly there had been a high probability, which he assessed as a 75 per cent risk, that avascular necrosis would still have developed. He held that the plaintiff was entitled to damages for the loss of the 25 per cent chance that he would have made a nearly full recovery and awarded him £11,500. The Court of Appeal dismissed an appeal by the health authority.
[6.8]On a further appeal to the House of Lords, it was held, allowing the appeal, that it had been for the plaintiff to establish on a balance of probabilities that the delay in treatment had at least materially contributed to the development of the avascular necrosis and for the judge to resolve on a balance of probabilities the conflict of medical evidence as to what had caused the avascular necrosis; that the judge's findings of fact were unmistakably to the effect that on a balance of probabilities the plaintiff's fall had left insufficient blood vessels intact to keep the epiphysis alive, which amounted to a finding of fact that the fall had been the sole cause of the avascular necrosis; and that, accordingly, the plaintiff had failed on the issue of causation and no question of quantification had arisen.
[6.9] (4)In Wilsher v Essex Area Health Authority [1988] A.C. 1074 the plaintiff was born prematurely and was placed in a special care baby unit at a hospital managed by the defendants. If he was to survive, he needed extra oxygen and to ensure that the correct amount was administered it was necessary to insert a catheter into an umbilical artery so that his arterial blood oxygen levels would be accurately read on an electronic monitor. A junior doctor mistakenly inserted the catheter into the umbilical vein with the result that the monitor would give a lower reading. Neither he nor the senior registrar appreciated that the X-rays taken showed the catheter in the vein but both realised that there was something wrong with the readings on the monitor. The senior registrar inserted another catheter but into the same vein and other means of monitoring the arterial blood oxygen were also adopted. The following day the second catheter was replaced by one in the artery. Thereafter the monitoring of the arterial blood oxygen levels continued and at times during the following weeks there were periods when the levels were considered too high. The plaintiff developed retrolental fibroplasia, a condition of the eyes, which resulted in blindness. The plaintiff claimed damages from the defendant health authority for the negligent medical treatment he had received in their special care baby unit. The judge held that the defendants were liable since they had failed to prove that the plaintiff's condition had not been caused by the negligence of their employees. The Court of Appeal, by a majority, dismissed the defendants' appeal.
[6.10]On a further appeal to the House of Lords, it was held, allowing the appeal, that the onus of proving causation rested on the plaintiff; that where a number of different factors, including the administration of excess oxygen, could have caused retrolental fibroplasia, its occurrence following the defendants' failure to take a necessary precaution to prevent excess oxygen causing the condition provided no evidence and raised no presumption that it was excess oxygen rather than one of the other factors which caused or contributed to the plaintiff's condition, and that, since there was conflicting expert evidence as to whether excess oxygen in the first two days of life caused or materially contributed to the plaintiff's condition, a question on which the judge had failed to make relevant findings of fact and which could not be resolved by an examination of the evidence of transcript, the issue of causation must be retried before a different judge.
[6.11] (5)In Fairchild v Glenhaven Funeral Services Ltd [2003] 1 A.C. 32 employees had developed mesothelioma caused by exposure at work to asbestos dust. All the employees had been exposed to asbestos dust during periods of employment with more than one employer. In the Court of Appeal it was common ground that the mechanism initiating the genetic process which culminated in mesothelioma was unknown, that the trigger might equally probably be a single, a few or many asbestos fibres, that once caused the condition was not aggravated by further exposure but that the greater the quantity of fibres inhaled the greater the risk of developing the disease. The Court of Appeal concluded that, since mesothelioma was an indivisible disease triggered on a single unidentifiable occasion by one or more fibres, it could not be proved on a balance of probabilities, where a claimant had been exposed to asbestos fibres by several potential tortfeasors, which period of exposure had caused the disease. The court accordingly held that the claimant in each case had failed to establish causation against any of the defendants.
[6.12]The House of Lords allowed the claimants' appeals, holding that, where an employee had been exposed by different defendants, during different periods of employment, to inhalation of asbestos dust in breach of each defendant's duty to protect him from the risk of contracting mesothelioma and where that risk had eventuated but, in current medical knowledge, the onset of the disease could not be attributed to any particular or cumulative wrongful exposure, a modified approach to proof of causation was justified; that in such a case proof that each defendant's wrongdoing had materially increased the risk of contracting the disease was sufficient to satisfy the causal requirements for his liability; and that, accordingly, applying that approach and in the circumstances of each case, the claimant could prove, on a balance of probabilities, the necessary causal connection to establish the defendants' liability.
[6.13]Lord Bingham of Cornhill said at p.40:
"2 The essential question underlying the appeals may be accurately expressed in this way. If (1) C was employed at different times and for differing periods by both A and B, and (2) A and B were both subject to a duty to take reasonable care or to take all practicable measures to prevent C inhaling asbestos dust because of the known risk that asbestos dust (if inhaled) might cause a mesothelioma, and (3) both A and B were in breach of their duty in relation to C during the periods of C's employment by each of them with the result that during both periods C inhaled excessive quantities of asbestos dust, and (4) C is found to be suffering from a mesothelioma, and (5) any cause of C's mesothelioma other than the inhalation of asbestos dust at work can be effectively discounted, but (6) C cannot (because of the current limits of human science) prove, on the balance of probabilities, that his mesothelioma was the result of his inhaling asbestos dust during his employment by A or during his employment by B or during his employment by A and B taken together, is C entitled to recover damages against either A or B or against both A and B? [...] The crucial issue on appeal is whether, in the special circumstances of such a case, principle, authority or policy requires or justifies a modified approach to proof of causation."
[6.14]Lord Bingham said at pp.43 to 44, under the heading "Principle":
"8 In a personal injury action based on negligence or breach of statutory duty the claimant seeks to establish a breach by the defendant of a duty owed to the claimant, which has caused him damage. For the purposes of analysis, and for the purpose of pleading, proving and resolving the claim, lawyers find it convenient to break the claim into its constituent elements: the duty, the breach, the damage and the causal connection between the breach and the damage. In the generality of personal injury actions, it is of course true that the claimant is required to discharge the burden of showing that the breach of which he complains caused the damage for which he claims and to do so by showing that but for the breach he would not have suffered the damage.
9 The issue in these appeals does not concern the general validity and applicability of that requirement, which is not in question, but is whether in special circumstances such as those in these cases there should be any variation or relaxation of it. [...]"
[6.15]At p.56 Lord Bingham said:
"22 In Wilsher v Essex Area Health Authority a problem of causation arose in a different context. A prematurely-born baby was the subject of certain medical procedures, in the course of which a breach of duty occurred. The baby suffered the condition (abbreviated as RLF) of a kind which that breach of duty could have caused, and the breach of duty increased the risk of his suffering it. But there were a number of other factors which might have caused the injury. In the Court of Appeal [1987] Q.B. 730,771-772 Mustill L.J. concluded a detailed review of McGhee by making this statement of principle:
'If it is an established fact that conduct of a particular kind creates a risk that injury will be caused to another or increases an existing risk that injury will ensue; and if the two parties stand in such a relationship that the one party owes a duty not to conduct himself in that way; and if the first party does conduct himself in that way; and if the other party does suffer injury of the kind to which the risk related; then the first party is taken to have caused the injury by his breach of duty, even though the existence and extent of the contribution made by the breach cannot be ascertained.'
Omitted from this statement is any reference to condition (5) in the composite question formulated in paragraph 2 at the outset of this opinion. It was on this omission that Sir Nicolas Browne-Wilkinson V-C founded his dissenting opinion, at p.779:
'To apply the principle in McGhee v National Coal Board [1973] 1 W.L.R. 1 to the present case would constitute an extension of that principle. In the McGhee case there was no doubt that the pursuer's dermatitis was physically caused by brick dust: the only question was whether the continued presence of such brick dust on the pursuer's skin after the time when he should have been provided with a shower caused or materially contributed to the dermatitis which he contracted. There was only one possible agent which could have caused the dermatitis, viz, brick dust, and there was no doubt that the dermatitis from which he suffered was caused by that brick dust. In the present case the question is different. There are a number of different agents which could have caused the RLF. Excess oxygen was one of them. The defendants failed to take reasonable precautions to prevent one of the possible causative agents (e.g. excess oxygen) from causing RLF. But no one can tell in this case whether excess oxygen did or did not cause or contribute to the RLF suffered by the plaintiff. The plaintiff's RLF may have been caused by some completely different agent or agents, e.g. hypercarbia, intravent[r]icular haemorrhage, apnoea or patent ductus arteriosus. In addition to oxygen, each of those conditions has been implicated as a possible cause of RLF. This baby suffered from each of those conditions at various times in the first two months of his life. There is no satisfactory evidence that excess oxygen is more likely than any of those other four candidates to have caused RLF in this baby. To my mind, the occurrence of RLF following a failure to take a necessary proportion to prevent excess oxygen causing RLF provides no evidence and raises no presumption that it was excess oxygen rather than one or more of the four other possible agents which caused or contributed to RLF in this case. The position, to my mind, is wholly different from that in the McGhee case [1973] 1 W.L.R. 1, where there was only one candidate (brick dust) which could have caused the dermatitis, and the failure to take a precaution against brick dust causing dermatitis was followed by dermatitis caused by brick dust. In such a case, I can see the common sense, if not the logic, of holding that, in the absence of any other evidence, the failure to take the precaution caused or contributed to the dermatitis. To the extent that certain members of the House of Lords decided the question on inferences from evidence or presumptions, I do not consider that the present case falls within their reasoning. A failure to take preventative measures against one out of five possible causes is no evidence as to which of those five caused the injury.'
On the defendants' appeal to the House, this passage in the Vice-Chancellor's judgment was expressly approved by Lord Bridge of Harwich, who gave the only opinion, with which Lord Fraser of Tullybelton, Lord Lowry, Lord Griffiths and Lord Ackner concurred, and the appeal was allowed: [1988] A.C. 1074, 1090-1092. It is plain, in my respectful opinion, that the House was right to allow the defendants' appeal in Wilsher, for the reasons which the Vice-Chancellor had given and which the House approved. It is one thing to treat an increase of risk as equivalent to the making of a material contribution where a single noxious agent is involved, but quite another where any one of a number of noxious agents may equally probably have caused the damage. The decision of the Court of Appeal did indeed involve an extension of the McGhee principle [...]."
[6.16]Lord Nicholls of Birkenhead said, at pp.69-70:
"37 In the normal way, in order to recover damages for negligence, a plaintiff must prove that but for the defendant's wrongful conduct he would not have sustained the harm or loss in question. He must establish at least this degree of causal connection between his damage and the defendant's conduct before the defendant will be held responsible for the damage.
38 Exceptionally this is not so. In some circumstances a lesser degree of causal connection may suffice. This sometimes occurs where the damage flowed from one or other of two alternative causes. Take the well known example where two hunters, acting independently of each other, fire their guns carelessly in a wood, and a pellet from one of the guns injures an innocent passer-by. No one knows, and the plaintiff is unable to prove, from which gun the pellet came. Should the law of negligence leave the plaintiff remediless, and allow both hunters to go away scot-free, even though one of them must have fired the injurious pellet?
39 Not surprisingly, the courts have declined to reach such an unjust decision: see Summers v Tice (1948) 199 P 2d 1, a decision of the Supreme Court of California, and Cook v Lewis [1951] S.C.R. 830, a decision of the Supreme Court of Canada. As between the plaintiff and the two hunters, the evidential difficulty arising from the impossibility of identifying the gun which fired the crucial pellet should redound upon the negligent hunters, not the blameless plaintiff. The unattractive consequence, that one of the hunters will be held liable for an injury he did not in fact inflict, is outweighed by the even less attractive alternative, that the innocent plaintiff should receive no recompense even though one of the negligent hunters injured him. It is this balance ("... outweighed by...") which justifies a relaxation in the standard of causation required. Insistence on the normal standard of causation would work an injustice. Hunting in a careless manner and thereby creating a risk of injury to others, followed by injury to another person, is regarded by the law as sufficient causal connection in the circumstances to found responsibility.
40 This balancing exercise involves a value judgment. This is not at variance with basic principles in this area of the law. The extent to which the law requires a defendant to assume responsibility for loss following upon his wrongful conduct always involves a value judgment. The law habitually limits the extent of the damage for which a defendant is held responsible, even when the damage passes the threshold "but for" test. The converse is also true. On occasions the threshold "but for" test of causal connection may be over-exclusionary. Where justice so requires, the threshold itself may be lowered. In this way the scope of a defendant's liability may be extended. The circumstances where this is appropriate will be exceptional, because of the adverse consequences which the lowering of the threshold will have for a defendant. He will be held responsible for a loss the plaintiff might have suffered even if the defendant had not been involved at all. To impose liability on a defendant in such circumstances normally runs counter to ordinary perceptions of responsibility. Normally this is unacceptable. But there are circumstances, of which the two hunters' case is an example, where this unattractiveness is outweighed by leaving the plaintiff without a remedy.
[...]
43 I need hardly add that considerable restraint is called for in any relaxation of the threshold "but for" test of causal connection. The principle applied on these appeals is emphatically not intended to lead to such a relaxation whenever a plaintiff has difficulty, perhaps understandable difficulty, in discharging the burden of proof resting on him. Unless closely confined in its application this principle could become a source of injustice to defendants. There must be good reason for departing from the normal threshold "but for" test. The reason must be sufficiently weighty to justify depriving the defendant of the protection this test normally and rightly affords him, and it must be plain and obvious that this is so. Policy questions will loom large when a court has to decide whether the difficulties of proof confronting the plaintiff justify taking this exceptional course. It is impossible to be more specific."
[6.17]At p.77, paragraph 70, Lord Hoffmann said that Wilsher was correctly decided, but the grounds upon which McGhee was distinguished in that case were unsatisfactory. He went on:
"71 An alternative ground of distinction is to be found in a passage in the dissenting judgment of Sir Nicolas Browne-Wilkinson V-C in the Court of Appeal, which was approved by the House. He said that the difference was that in McGhee's case the agent of injury was the same -- brick dust -- and the only question was whether it happened before or after it should have been washed off. In Wilsher, the fibroplasia could have been caused by a number of different agencies.
72 That distinction would leave the present case on the right side of the line because the agent of injury was the same -- asbestos dust. But I do not think it is a principled distinction. What if Mr Matthews [one of the claimants] had been exposed to two different agents -- asbestos dust and some other dust -- both of which created a material risk of the same cancer and it was equally impossible to say which had caused the fatal cell mutation? I cannot see why this should make a difference."
[6.18]Lord Hutton said, at p.95:
"118 In my respectful opinion in Wilsher the House was right to hold that the majority of the Court of Appeal should not have extended the McGhee principle to apply where there were five possible candidates which could have caused the plaintiff's blindness. I consider that, as Sir Nicolas Browne-Wilkinson V-C observed [1987] Q.B. 730, 780E-F, the justification for holding a defendant liable is that the defendant created a risk and that the injury suffered by the plaintiff fell squarely within that risk. Subject to this observation on the decision in Wilsher, I wish to confine my opinion to the circumstances of these cases. It may be necessary in the future to consider whether the McGhee principle should be applied to other cases, but such decisions will have to be taken when such cases arise."
[6.19]At p.110 Lord Rodger of Earlsferry had this to say about Wilsher:
"149 Adopting the reasoning of the Vice-Chancellor, the House reversed the decision of the Court of Appeal -- and rightly so. Mustill L.J.'s extension of the approach in McGhee to a situation where there were all kinds of other possible causes of the plaintiff's condition, resulted in obvious injustice to the defendants. In particular, there was nothing to show that the risk which the defendants' staff had created -- that the plaintiff would develop retrolental fibroplasia because of an unduly high level of oxygen -- had eventuated. That being so, there was no proper place for applying the principle in McGhee. As the Vice-Chancellor decisively observed, a failure to take preventive measures against one of five possible causes was no evidence as to which of those five had caused the injury. The reasoning of the Vice-Chancellor, which the House adopted, provided a sound and satisfactory basis for distinguishing McGhee and for allowing the appeal. The year before indeed, the House had distinguished McGhee on the basis that a pursuer had not proved that the junior house officer's mistake had materially increased the risk of the particular kind of neurological damage suffered by his son: Kay's Tutor v Ayrshire and Arran Health Board 1987 S.C. (H.L.) 145."
[6.20]At p.118, in paragraph 169, Lord Rodger said:
"It is indeed plain that, as Lord Nicholls of Birkenhead has observed, considerable restraint is called for in using the principle [in McGhee]. Identifying, at an abstract level, the defining characteristics of the cases where it is, none the less, proper to apply the principle is far from easy. The common law naturally and traditionally shies away from such generalisations especially in a developing area of the law. But, having regard to the cases cited by counsel and also, in particular, to the cases and textbooks on the German law referred to in van Gerven, Tort Law, pp.444-447 and pp.459-461, I would tentatively suggest that certain conditions are necessary, but may not always be sufficient, for applying the principle. All the criteria are satisfied in the present cases."
[6.21]In paragraph 170 Lord Rodger set out these conditions, one of which was expressed in these terms:
"Fourthly, the claimant must prove that his injury was caused by the eventuation of the kind of risk created by the defendant's wrongdoing. In McGhee, for example, the risk created by the defenders' failure was that the pursuer would develop dermatitis due to brick dust on his skin and he proved that he had developed dermatitis due to brick dust on his skin. By contrast, the principle does not apply where the claimant has merely proved that his injury could have been caused by a number of different events, only one of which is the eventuation of the risk created by the defendant's wrongful act or omission. Wilsher is an example."
Submissions for Mrs McTear
[6.22]Mr McEachran submitted that it was not necessary for the pursuer to demonstrate that a particular packet of cigarettes gave rise to Mr McTear's lung cancer. It was enough for her to establish that the smoking of John Player cigarettes played a material part in the smoking which caused his death. Lung cancer did not appear to be like asbestos where one fibre could cause mesothelioma. "It appears that the longer you smoke, and the more you smoke, the more likely you are to contract lung cancer." Reference was made to passages in the evidence of Professor Friend and in IARC 1986, RCP 2000 and IARC 2004. This was the basis on which he presented his case, so he was arguing for a cumulative effect. Perhaps it was the constant invasion of tobacco smoke which caused the problem. But counsel accepted that the exact physical route for lung cancer was not yet known. He also had to deal, he said, with the fact that there had been some tobacco smoke from another source, that was the hand-rolled cigarettes ("roll-ups") which Mr McTear smoked for some time. The fact that some of the tobacco smoke was from another source did not affect liability, though it might have had something to do with the causation of his lung cancer. While the material part of the smoking "was with the defenders", because the pursuer was not able to say exactly how the cancer was started, the problem was not exactly the same as in Fairchild but was similar.
[6.23]Counsel went on to say that before Fairchild had been decided, he probably would have relied on Wardlaw as establishing that all he needed to prove was a material contribution. He said that Fairchild was a very elaborate case, and to some extent the situation in the present case was the same as in Fairchild, in that the mechanism initiating the genetic process was not known but it appeared that the more the smoking, the greater the risk. He particularly relied on the opinions of Lord Bingham and Lord Rodger. Had it not been for Fairchild, he would have relied on Wardlaw to say that, in this case, the smoking over twenty-five years or more of ITL's products could be said to have materially contributed to his lung cancer. He agreed that he did not have the problem which arose in Fairchild, which was that it was not possible to say whether it was an accumulation of fibres or one individual fibre which had triggered off the mesothelioma. Ultimately he agreed that Fairchild perhaps did not add anything to Wardlaw for present purposes. Insofar as smoking raised the problem of lack of medical science to demonstrate exactly how lung cancer was caused, the principles which Lord Rodger set out would apply in this case. But Wardlaw was sufficient for counsel on the facts of this case. He invited me to look at the matter globally and to hold that the smoking of ITL's products had materially increased the risk of Mr McTear's developing lung cancer.
Submissions for ITL
[6.24]Mr Jones submitted that the most relevant authority was Wilsher, approved and reinforced by Fairchild. The question, in counsel's submission, came to be: if it was held that smoking could cause lung cancer, did it cause Mr McTear's lung cancer? Or, as it was put in Fairchild, could it be held that but for his smoking Mr McTear would not have developed lung cancer? On the evidence individuals who did not smoke could contract lung cancer and therefore in the abstract there must be a cause or causes of it other than smoking. It was for the pursuer to satisfy me that of any of the possible causes there might be, the most probable cause was his cigarette smoking, so that if he had not smoked he probably would not have contracted lung cancer. The causes might be exogenous or endogenous. The difficulty did not arise from the evidence in this case of the kind that was addressed in either McGhee or in Fairchild, where medical science simply could not answer basic questions that required to be answered in order to meet legal tests. The result was that the legal test was adjusted to take account of the realities of medical science. The "but for" test expounded by Lord Bingham was only to be departed from in appropriate and well-defined instances, of which this was not one. The present case did not fall outside the type of case to which the normal "but for" test was applicable. Insofar as it might in any sense be a special case, it fell within the reasoning of Wilsher.
Discussion
[6.25]In the first place, I am satisfied from the authorities that, in order to establish that exposure to a substance can cause, or has caused, a condition in an individual or group of individuals, it must be shown on the evidence that, on the balance of probabilities, the condition would not have occurred but for the exposure. This applies to both exposure on a single occasion and, as contended for here, cumulative exposure. There is no suggestion to the contrary in any of the authorities, including Fairchild, in which the "but for" proposition was reaffirmed. In Wardlaw the pursuer would not have contracted pneumoconiosis but for exposure to silica dust: the problem was that some of the dust was "innocent" and some was "guilty", so it had to be decided whether the contribution made by the "guilty" dust was sufficient to establish liability against his employer. In McGhee the pursuer would not have contracted dermatitis but for exposure to dust and ashes in the brick kiln: the problem was whether the fact that the absence of washing facilities materially increased the risk of his contracting dermatitis was sufficient to establish liability against his employers (who were not liable for the initial exposure to dust and ashes). In Fairchild, the plaintiffs would not have contracted mesothelioma but for exposure to asbestos: the problem was whether, since this could have been on a single occasion, liability could nevertheless be established against each of the employers, even though it could not be said in which of the employments the exposure which caused the mesothelioma occurred. This was how Sir Nicholas Browne-Wilkinson V-C approached the question of causation in Wilsher, in the passage in his dissenting opinion which was approved in Fairchild: and Wilsher established that the burden was on the plaintiff in that case to establish which of several possible causes had probably caused the condition in question, in the sense that but for this cause the condition would probably not have occurred.
[6.26]While I shall discuss the evidence about causation later, I do not have the impression that any of the expert witnesses used the expression "cause" in a different sense from that discussed above as its legal sense. Sir Richard Doll, for example, in Doll 1997 at p.25 (see para.[5.205]) said that in epidemiology cigarette smoking was an important cause of lung cancer, as few people would have developed the disease if they had not smoked. This appears to me to be "but for" causation (to the standard of proof beyond reasonable doubt which scientists aim to achieve). It remains for consideration, however, whether, if epidemiologists hold it to be proved that an exposure causes a condition in a population, as an important but not a necessary or a sufficient cause, that can also be said to apply to an individual member of that population.
[6.27]The legal authorities to which reference was made have been concerned with the devising of a coherent set of rules, not about causation of a condition by exposure to a substance, but about fault causation. Where all the exposure is attributable to the negligence of a single employer it can readily be said that the fault has caused the consequent condition. Problems have arisen, however, where, for example, the employer has been negligent in respect of only part of an exposure, all of which has been in that employer's employment; or has materially increased the risk of contracting the condition caused by an exposure for which in itself the employer is not liable; or in exceptional circumstances, such as those in Fairchild, where on one view of the scientific evidence only one employer, or some employers, out of several, has or have been negligent in respect of the exposure which has caused the condition, and it cannot be said which of them it was. The problem considered in Fairchild does not arise from the evidence relied on in support of the cumulative process contended for by Mr McEachran; and I am not sure why that case was referred to at such length, except as the last word on "but for" causation. Mr McEachran eventually settled on Wardlaw as the authority most in point. I agree with this, if a reference to Wilsher is added. Wardlaw comes into play because, if Mr McTear's lung cancer was probably caused by his cigarette smoking, on some kind of cumulative basis, some of the exposure may have occurred at a time when ITL could be said to have been at fault and some at a time when they could not. In any event, for some period at least, there was also exposure to the smoke from at least one other manufacturer's tobacco. That is to say, in a question with ITL, some of the exposure may have been "guilty" and some "innocent". Wardlaw and McGhee established that in that event it is enough if the "guilty" exposure for which ITL could be said to be at fault made a material contribution to the contracting of Mr McTear's lung cancer; though the burden of proving this much still rests on the pursuer.
[6.28]I would add here, for subsequent discussion, that the law recognises that the application of statistical probability to individual causation may be fallacious. In the course of his opinion in Hotson v East Berkshire Area Health Authority, Lord Mackay of Clashfern discussed Herskovits v Group Health Cooperative of Puget Sound (1983) 664 P.2d 474, a decision of the Supreme Court of Washington en banc. At p.789 Lord Mackay referred to the dissenting judgment of Brachtenbach J. In Lord Mackay's summary:
"He warned against the danger of using statistics as a basis on which to prove proximate cause and indicated that it was necessary at the minimum to produce evidence connecting the statistics to the facts of the case. He gave an interesting illustration of a town in which there were only two cab companies, one with three blue cabs and the other with one yellow cab. If a person was knocked down by a cab whose colour had not been observed it would be wrong to suggest that there was a 75% chance that the victim was run down by a blue cab and that accordingly it was more probable than not that the cab that ran him down was blue and therefore that the company running the blue cabs would be responsible for negligence in the running down. He pointed out that before any inference that it was a blue cab would be appropriate further facts would be required as, for example, that a blue cab had been seen in the immediate vicinity at the time of the accident or that a blue cab had been found with a large dent in the very part of the cab which had struck the victim."
[6.29]The conclusions I draw from these authorities, as applied to the evidence in the present case, are as follows:
(1)On the matter of general causation, the burden is on the pursuer to satisfy me, on the balance of probabilities, that as a matter of fact cigarette smoking can cause lung cancer, in the sense that both in the general population and in any individual case it can be said that but for the smoking of cigarettes, lung cancer would probably not have been contracted.
(2)If so, on the matter of individual causation, the burden is also on the pursuer to satisfy me, on the balance of probabilities, that but for Mr McTear's having smoked cigarettes he would probably not have contracted lung cancer.
(3)If so, on the matter of fault causation, the burden is on the pursuer to satisfy me, on the balance of probabilities, that negligence on the part of ITL, in one or other or both of the respects averred in the pursuer's pleadings, caused or materially contributed to Mr McTear's lung cancer either by making at least a material contribution to the exposure which caused his lung cancer or by materially increasing the risk of his contracting lung cancer.
General causation and individual causation
Submissions for Mrs McTear
[6.30]Mr McEachran asked me to find it proved (1) that cigarette smoking could cause lung cancer and (2) that Mr McTear's lung cancer was caused by cigarette smoking. The United States Government, the United Kingdom Government and the World Health Organization had all accepted for many years that cigarette smoking could cause lung cancer. All the American tobacco companies accepted this, as did all the tobacco companies in the United Kingdom except for ITL. Sir Richard Doll had given evidence that it was almost universally accepted by doctors and scientists by 1957. It was taught in medical schools that cigarette smoking could cause lung cancer, and evidence about this had been given by Dr McCarroll, Dr Kerr and Sir Richard Doll. Professor Idle agreed that it was to be found in general textbooks of medicine that cigarette smoking could cause lung cancer. The public health figures were not challenged by ITL. These included the figure of 89% of lung cancer deaths being attributable to smoking, quoted in Callum 1998, RCP 2000 and UKHC 2000. Mr Davis had given evidence that smokers were far more likely to develop serious diseases like lung cancer than non-smokers. This was tantamount to admitting causation. Mr McEachran also relied on the evidence of Professor Friend and the conclusions of IARC and "the other multi-doctor studies": MRC 1957, RCP 1962, USSG 1964, RCP 1971, USSG 1971, RCP 1977, IARC 1986, USSG 1988, RCP 2000 and IARC 2004. So there was very strong evidence to support the proposition that cigarette smoking could cause lung cancer.
[6.31]Dr McCarroll said that the teaching at medical school was that the main cause of lung cancer was smoking. It was her considered view that Mr McTear died from lung cancer that was a result of cigarette smoking. She had other patients who were heavy smokers and they had tried to give up. Lots of them had tried to give up, and most of them found it very difficult. Her view was that the reason was the addictive nature of the substance. She was aware of general messages about health and in particular that nine out of ten lung cancer deaths among men were caused by smoking. She agreed with the comment in the UKWP 1998 that tobacco was a uniquely dangerous product and if introduced today would not stand the remotest chance of being made legal. In cross-examination she was taken through Mr McTear's medical notes and was asked whether she had made a detailed study of epidemiology literature and carcinogenisis as it related to smoking and lung cancer and agreed that she had not. Counsel said that this was all very interesting, but if the teaching in medical school was that smoking caused lung cancer and that teaching was accepted in this case, then she was quite entitled to make a diagnosis. The court was quite entitled to accept that, supported as it was by Professor Friend and Dr Kerr.
[6.32]Professor Friend was a distinguished clinician from Aberdeen. He gave his evidence with integrity and obvious expertise in his field. He has recently been a Clinical Professor in Medicine and Therapeutics at Aberdeen. He had been Chairman of the Government Scientific Committee on Tobacco and Health since 2000. He had been a respiratory consultant for thirty years and had seen many people with lung cancer, perhaps 3,000 over his career. Professor Friend's evidence was that, since there was a dose-response relationship between cigarette smoking and lung cancer, someone like Mr McTear, who was a heavy smoker, was at very high risk of developing lung cancer. In RCP 2000 it was stated that 89% of lung cancer patients were smokers and in Callum 1998 it was 90%.
[6.33]Professor Friend had been President of the British Thoracic Society and met some 500 to 600 physicians. He had never met a respiratory physician who did not believe that smoking caused lung cancer. Professor Friend referred to IARC 1986. This was a 400 page document which reviewed articles which took sixty pages to list. Members of the working group were of very high reputation, the Chairman was Sir Richard Doll and they were from all over the world. It took a long time for lung cancer to develop, perhaps more than thirty years. According to IARC 1986 tobacco smoke contained more than 3,800 constituents. Counsel submitted that the conclusions and evaluations in the IARC monograph were never challenged during the rest of the evidence led on both sides. The experts for ITL hardly mentioned it. According to it, the proportion of lung cancer attributable to smoking was of the order of 90%: this was also mentioned in IARC 2004, not yet available in full form.
[6.34]When asked about the statement by ITL that cigarette smoking had not been scientifically established as a cause of lung cancer, Professor Friend said that he believed that the epidemiological evidence was very strong and that it had been established beyond reasonable doubt. It was true to say that we did not know the precise mechanisms by which smoking caused lung cancer, but that did not mean that the effect did not occur. We might not know the exact chemical or biological process by which it happened, but he had no doubt that smoking caused lung cancer. This was the view reached in the various reports already referred to. Professor Friend said he believed that if a substantial number of eminent authorities came to a certain conclusion, that was bound to outweigh one's understanding of what a small number of individuals might contest in opposition to that view. Counsel submitted that this was an entirely appropriate position for an expert to take. Professor Friend said that it was highly probable that Mr McTear's lung cancer was caused by smoking.
[6.35]Counsel said that cross-examination of Professor Friend mainly consisted of putting a number of articles to him demonstrating that there were eminent scientists who did not agree with the thesis of the Medical Research Council, the Royal College of Physicians, the United States Surgeon General, and Fisher, Eysenck and Burch were among the names mentioned, but counsel suggested "this line was really exploded when Sir Richard Doll told the court that the great majority of scientists accepted in 1957 that smoking was a cause of lung cancer". In re-examination of Professor Friend it became clear that the witnesses who had given evidence to the United States Congress hearings in the 1970s and 1980s were a group of doctors from the Tobacco Research Council, which was the industry body in the United States, and they were just putting forward the tobacco industry point of view that the causal connection between cigarette smoking and lung cancer had not been established. Professor Friend said that he had never in his professional career been made aware of any strong genetic component to lung cancer development. No other risk factors had been put in detail to Professor Friend in the course of his cross-examination. He had experience of 3,000 patients. This was the basic material, people who had lung cancer. He had to see what their particular history told him.
[6.36]Of the reasons given by Professor Friend for stating that cigarette smoking caused lung cancer, Mr McEachran founded on his evidence that the risk of lung cancer diminished steadily when people had discontinued smoking. He said that once people had stopped smoking for around fifteen years, their risk of developing lung cancer approximated to that of life-long non-smokers. He said that he found this a particularly persuasive outcome. Mr McEachran also founded on Professor Friend's evidence that the incidence of lung cancer had developed in different countries at different times and in a relationship which followed quite closely the smoking habits of those countries, which seemed to him to make it much more likely that it was an environmental cause such as smoking rather than any genetic change which had led to the increase. In addition, in the United Kingdom, where the prevalence of smoking had diminished and there was a reduction in the number of men developing lung cancer, he could not see how this could happen on a purely genetic basis.
[6.37]Mr McEachran described Sir Richard Doll as a world class epidemiologist who remained the careful scientist whilst giving evidence. He relied on Sir Richard's evidence on the following matters. IARC 1986 was produced by a working group which he had chaired. The group was made up of numerous distinguished doctors and scientists, most of whom he knew, who were leaders in their fields. They concluded that smoking caused lung cancer in humans. There had never been any challenge to their evaluations and findings. The historical review in Sir Richard's Green College Lecture, Doll 1997, showed how it came to be realised that smoking caused lung cancer. The conclusion that it did was accepted by the Medical Research Council in 1957. The scientific community accepted the conclusions by the late 1950s. By 1957 the great majority of scientists and doctors accepted that smoking could cause lung cancer. This was the unchallenged evidence of Sir Richard Doll. He said that it was generally accepted in the scientific community in the 1950s that cigarette smoking was a cause of cancer. MRC 1957 effectively settled the issue as far as England was concerned. It was not until the mid 1970s, according to Sir Richard, that the media became convinced about the dangers of cigarette smoking. This change in the attitude of the media led to a much sharper reaction by the public. This related also to the start of warnings on cigarette packets in 1971. Those who expressed contrary views were a minority of scientists, who were just eccentric or wrong.
[6.38]In response to a criticism to be advanced for ITL, that Sir Richard's evidence amounted to no more than saying that the public health reports he looked at said what they said, Mr McEachran said that Sir Richard was not qualified in the disciplines from which the IARC working groups were drawn and was not open to cross-examination therefore on much of the material which formed the conclusions of these groups. In response to the criticism that no data had been presented in support of Sir Richard's view that epidemiology had established that smoking could cause lung cancer, Mr McEachran submitted that I was entitled to form a judgment on that in particular because the "multi-doctor studies" all reached that conclusion, having reviewed the evidence on which it was based. He submitted that the evidence was there. For example, he said of IARC 1986:
"It is 600 pages-worth. If they want to challenge it, they have to go into every page and see if it is wrong. But this is a report by some twenty-seven doctors from all around the world reaching this conclusion. It is extremely powerful evidence for what they conclude and their evaluation."
[6.39]Mr McEachran submitted that Dr Kerr came across as a man of outstanding competence and sharp intellectual ability. He relied on his evidence for the statements that in 98% of cases of squamous cell carcinomas the patients were smokers, it was most unusual to see a squamous cell carcinoma of the lung in a non-smoker, and the pre-invasive squamous dysplasia, the precursor lesion of invasive squamous cell carcinoma, was also frequently found in the bronchi of smokers and much less so in non-smokers. Mr McEachran submitted that Auerbach et al. 1961 was a careful and detailed study of epithelial changes in smokers and non-smokers. This supported the conclusion that there was a very strong association between dysplasia and smoking. This was followed up in Auerbach et al. 1975. Dr Kerr also referred to moderate squamous dysplasia in the biopsy taken from Mr McTear. This was frequently found in the bronchi of smokers and much less so in non-smokers, and Auerbach's research bore this out.
[6.40]Even looking at the evidence of witnesses called for ITL, who were all unbelievers, it was accepted that there was a strong association. The public health figures, which ITL did not challenge, said that 90% of male smokers who died of lung cancer died because of their smoking and heavy smokers were twenty to forty times more likely to contract lung cancer. Also unchallenged, counsel submitted, was that the risk of lung cancer was dependent on duration of smoking and was proportional to the number of cigarettes smoked. Evidence was given about this by Professor Friend, under reference to the passage from IARC 1986, p.312, quoted at para.[5.51], and the passage from USSG 1964, p.196, quoted at para.[5.96]. These, counsel submitted, were large multi-doctor survey documents making this point. In populations with a long duration and heavy intensity of cigarette usage, the proportion of lung cancer attributable to smoking was of the order of 90%. Counsel referred to IARC 1985 p.306, IARC 2004 p.10 and RCP 2000 Table 1.2. These figures, he submitted, were not challenged by ITL. For heavy smokers (those who smoked more than twenty cigarettes per day, according to Professor Friend) the risk of contracting lung cancer was twenty to forty times that for non-smokers. This appeared from Doll 1974 in which it was stated that in the survey of British doctors the mortality from lung cancer was forty times greater in those who smoked thirty-five or more cigarettes a day than in those who had never smoked at all. For a smoker who stopped smoking, it took ten to fifteen years to revert to the same risk level as a non-smoker: RCP 1962, para.28 and Figure 10. The same point was made in RCP 1971, para.4.11 and Figure 4.3. Professor Friend gave evidence that it was about fifteen years before the risk levels evened out.
[6.41]In answer to questions by me, Mr McEachran submitted that considerable weight should be placed on the fact that a proposition had come to be generally accepted. If the United Kingdom and United States Governments and the World Health Organization accepted that smoking caused lung cancer then that should carry great weight. It was extremely relevant that ITL said that they did not know whether cigarette smoking could cause lung cancer. IARC had looked at all the original research and had gone through it in detail and had concluded that cigarette smoking caused lung cancer. It was extremely powerful evidence if a group of scientists had examined the research and had reached a conclusion about it. It would be extremely difficult for a court to be taken through every formula and every graph by scientists in order to explain how they reached a conclusion. It would be much more important for scientists to be able to say what their peers thought. If a group of them looked specifically at the point and concluded, as in this case, that cigarette smoking caused lung cancer, that was the most powerful evidence that could be got to support the conclusion.
[6.42]Sir Richard Doll gave evidence that there were some people who did not accept his conclusions, but the majority did. He was not challenged in his evidence that the great majority of scientists and doctors accepted that cigarette smoking could cause lung cancer, and this fact was also accepted by ITL's experts. All that had to be demonstrated was that on the balance of probabilities cigarette smoking caused lung cancer, and those representing Mrs McTear had gone way beyond that. "The evidence is really overwhelming." It was standard teaching in medical schools that cigarette smoking caused lung cancer. An unsubstantiated theory would not be taught in medical schools. Dr McCarroll, Dr Kerr and Professor Friend had all given evidence that it was standard teaching, and again this was very powerful evidence about something that had been accepted.
[6.43]On the question of reliance on the published reports, Mr McEachran submitted that in a situation where research had come up with a thesis or a theory or a conclusion and bodies of doctors and scientists were set up to consider whether the research conclusions were valid, the results of checks and investigations carried out by these multi-doctor bodies were very powerful evidence that the initial conclusion of the researchers was valid. Professor Friend said that he was not a toxicologist nor an epidemiologist, he was a clinician who obtained information about the causes of disease from his reading elsewhere. He said that a practising physician's duty was to distil what was available from the readily accessible medical literature and to follow his practice accordingly. He had been happy to rely on reports produced by learned people for whom he had a high regard. Under reference to IARC 1986, Professor Friend said that the views expressed in it had been widely accepted by all the medical profession worldwide with only a tiny number of exceptions. He was well entitled to rely on IARC 1986. The fact that he was not an epidemiologist did not mean that he was not entitled to look at scientific papers by learned gentlemen whose views he respected. Counsel submitted that Main v McAndrew Wormald Ltd (discussed at paras.[5.12] to [5.16]) was authority for the view that Professor Friend could rely on epidemiological literature in support of his views as a physician. He was entitled to look at epidemiological evidence and to refer to such things as an IARC report to support his opinion, as a clinician who worked in the area, that smoking caused lung cancer.
[6.44]In considering whether Professor Friend was entitled to say that and rely on IARC 1986, one had to look at the background to this case. ITL did not say that cigarette smoking was not a major cause of lung cancer. They just said that it was not known. One of the original researchers was Sir Richard Doll. In Doll 1997 he went through the history of his research, the conclusion of the research and dealt with the responses by various scientists and doctors. He was not challenged on the conclusion which he reached. So, counsel said,
"We put before this court one of the scientists, an extremely eminent scientist, who had done the work and if there was to be any challenge of this, there he was in the witness box for the defenders to challenge, but their only challenge was: well, not everyone agreed with you."
Sir Richard said that he stood by everything he had said in the lecture and by the results of articles he had written relating to lung cancer and its association with smoking. Sir Richard was taken in some detail through Doll 1997 and this was not challenged in evidence.
[6.45]Counsel accepted that the main evidence for the causal link between smoking and lung cancer was epidemiological. He accepted that the biological and chemical pathways for the development of lung cancer were not yet fully understood and known, and that it was not possible by looking through a microscope at a squamous cell carcinoma to tell that that particular cancer was caused by smoking. Secondly, counsel submitted, it was proved that cigarette smoking probably caused Mr McTear's lung cancer. Mr McEachran relied on the opinion of Dr McCarroll, the opinion of Professor Friend and the evidence of Dr Kerr. Dr McCarroll, his GP, said that all the teaching she received over the years led her to believe that this was a direct result of his smoking. Her general view was that smoking did cause lung cancer and she said that it was likely that Mr McTear died from lung cancer that was as a result of cigarette smoking. Professor Friend reviewed Mr McTear's medical records and commented on his treatment. He was in no doubt that he developed primary bronchial carcinoma in 1992. A moderate squamous dysplasia was found at biopsy. From his own experience squamous dysplasia was a change found in heavy smokers and pathologists recognised it as often being a prelude to malignant change. He was quite entitled to refer to what pathologists found when they did biopsies. In his report he concluded by saying that Mr McTear developed squamous cell carcinoma of the lung in 1992 after smoking heavily for twenty-eight years and the strong probability was that this disease was caused by smoking cigarettes. In evidence he said that you could never with total accuracy define a cause in a given individual, but you could state a probability of causation. It certainly seemed likely that the probable cause here was that Mr McTear's lung cancer was caused by his heavy cigarette smoking, but that was not necessarily the only cause, and it was conceivable that some other cause might have been present in his case. So he was putting it as "highly probable".
[6.46]It was not suggested to Professor Friend specifically in relation to Mr McTear that any particular risk factor was present in this case and was the cause of his lung cancer as opposed to smoking. There was no evidence of that. If the case was that it was something to do with Mr McTear's diet, for example, then that should have been explored with Professor Friend. There had to be some averment and some evidence from the defenders, specifically relating to Mr McTear, saying that other risk factors were present in his case. There was nothing in the pleadings about them, there was nothing in the defenders' expert reports about them, they had just been brought out in the course of evidence and were not put to Professor Friend.
[6.47]Dr Kerr indicated that the type of lung cancer which Mr McTear had, i.e. squamous cell carcinoma, was very commonly found in smokers, and the figure was 98%; and that some of the pre-cancerous stages found on biopsy were also indicative that smoking caused the disease. Dr Kerr had given evidence that it was his own experience that squamous cell carcinoma was particularly associated with smokers and that the diagnosis of squamous cell carcinoma in non-smokers was exceptional. He also said that some of the non-smokers who contracted it could have done so through the inhalation of tobacco smoke in the home or at work, i.e. through "passive" smoking.
[6.48]Mr McEachran submitted that there was no direct contrary medical evidence led on behalf of ITL to refute the evidence for Mrs McTear. There was no medical evidence which said that Mr McTear died of some other cause or that cigarette smoking did not play a material part in his lung cancer. At best ITL could suggest there was evidence that there could be other factors involved in his death. A number of risk factors were mentioned in the pleadings and in the evidence in a general way, but no specific evidence was taken from any of ITL's experts which related the possible risk factors to Mr McTear's case. So there was no evidence which directly contradicted that of Dr McCarroll, Professor Friend and Dr Kerr. Accordingly the court should accept their evidence. Presumably ITL did not get their witnesses to go more closely into the various risk factors mentioned because they were liable to get the retort given by Professor Friend that by far the most significant risk factor was his smoking. Counsel referred to USSG 1964 conclusion 1: "Cigarette smoking is causally related to lung cancer in men. The magnitude of the effect of cigarette smoking far outweighs all other factors." It was probable that Mr McTear was one of the 90%, and because he was such a heavy smoker it was more than probable. Accordingly it was established that smoking caused his lung cancer.
[6.49]Mr McEachran submitted that none of the expert witnesses called for ITL was of particular distinction and none was a world expert in his subject, as Sir Richard Doll was. It was not clear why ITL had to go to Berlin, Prague and Iowa for witnesses. He suggested that they could not find suitable scientists and doctors in the United Kingdom to give the evidence they required. Perhaps they needed witnesses who did not accept the majority view that smoking could cause lung cancer, in other words who supported ITL's position on this. He suggested that I should regard with some scepticism evidence coming from a scientist from a minority group like that. None of the witnesses called for ITL said that smoking did not cause lung cancer. It was noticeable that Dr Lewis did not speak to his second report. Their position seemed to be that they did not accept that it had been proved.
[6.50]Out of the six experts, only three made reference to Mr McTear. These were Professor Gray, Professor Platz and Professor Idle. None of the six experts said that there was any cause of Mr McTear's lung cancer other than smoking. They seemed to have given evidence for three possible reasons. First, to back up ITL's "We do not know" position by showing that the biological and carcinogenic pathways had not been found and the way in which lung cancer was caused was not yet fully understood. The short answer to this was that Sir Richard Doll's evidence that smoking could cause lung cancer was not challenged, and was backed up by numerous multi-doctor studies. Secondly, to back up the position that it was not possible to demonstrate in the individual case that cigarette smoking caused Mr McTear's lung cancer, when the microscope did not tell you and there were other alleged risk factors. The answer to this was that no other cause had been suggested. Neither Dr McCarroll nor Professor Friend was cross-examined to the effect that their evidence and diagnoses were inaccurate. It was just said that they were not entitled to make a diagnosis because they were not epidemiologists. No consultant or respiratory surgeon who had practical and hands-on experience of lung cancer patients gave evidence on behalf of ITL that smoking was not a material cause of Mr McTear's lung cancer. Even ITL's witnesses accepted that cigarette smoking was the strongest risk factor for lung cancer and had the strongest associations.
[6.51]A third possible reason for their evidence was to suggest that there were a number of other risk factors associated with lung cancer. ITL's position in their written pleadings was that they could not say whether any other risk factor played a role in Mr McTear's case. Dr Cohen had gone through a number of articles where it was suggested that there were risk factors for various conditions. He did so outwith the scope of his report. He did not attempt to put any figures on any of these to say how strong was the risk and he did not attempt to relate any of them to Mr McTear. There was nothing in the evidence to demonstrate that he had a poor diet. Counsel referred to evidence given by Mr McTear on commission, when his diet was discussed in cross-examination. He submitted that there was nothing there which could suggest that there was anything wrong with his diet. At the end of the day, the evidence of Dr Cohen was left hanging in the air. No witness had come forward saying that in the case of Mr McTear a particular risk factor was very strongly present and therefore on the balance of probabilities smoking was not a material cause of his death. The court would not be entitled to hold that any of the risk factors referred to in the pleadings applied in the case of Mr McTear, because it was not pled in relation to him that any of them was a factor which applied and had some relationship with his lung cancer. There was no evidence put before the court in relation to Mr McTear's case in respect of these factors and none of them was put to Professor Friend as an alternative. So these were red herrings.
[6.52]Mr McEachran said that Professor Idle was a witness who had had tobacco funding for research. His report concentrated on the biological and carcinogenesis studies which had so far failed to show how lung cancer developed. Researchers had failed to produce squamous cell carcinoma in laboratory animals exposed to cigarette smoke. No constituent or group of constituents as they existed in cigarette smoke had been shown to be a cause of lung cancer. These conclusions were not disputed by Mrs McTear. In concluding, however, that it could not be determined whether or not smoking caused Mr McTear's lung cancer, he was approaching the matter as a chemist and a biologist, and on that basis his position was understandable. There was, however, other evidence which demonstrated that this had been established and was in line with the majority view in science and medical profession. His position was that if it was not established scientifically, he was not prepared to accept that smoking was a cause of lung cancer. This evidence should be rejected in favour of that of Sir Richard Doll and the general view in science and the medical profession that by 1957 the great majority of scientists accepted the causal link.
[6.53]Professor Idle was paid over £100,000 for his work and his evidence. One really had to wonder why it was necessary for ITL to go out of the United Kingdom and to central Europe to get a witness on this matter. Large fees like this encouraged a witness to maintain ITL's position in this case. There was a danger that such a payment would induce bias. The court should be very careful with people whose research had been funded by the tobacco industry and who had been paid large fees, it put into question their independence. So far as Professor Idle was concerned, his research had been funded by the tobacco industry and he had been paid a very substantial sum, so his evidence should be looked at critically. Counsel was, however, unable to point to any part of Professor Idle's report or of his evidence which displayed bias induced by the fact that he had been paid a fee.
[6.54]Mr McEachran made the point that Dr James did not mention Mr McTear in his report or in his evidence, so it was not exactly clear what the relevance of his evidence was. He was contacted by a New York firm of lawyers and he was another man who did not accept that smoking could cause lung cancer. Sir Richard Doll and the multi-doctor reports all accepted that the early figures for the number of lung cancer cases might be soft, but they all concluded that there had been a real increase in lung cancer mortality. Dr James agreed that he was in a minority. He accepted that the figures from 1950 onwards were likely to be reasonably accurate. The reason he stopped at the year 1950 was because that was when the cohort studies started, and obviously the figures would be more accurate thereafter, because particular people were being studied. The figures from the reports were not challenged by ITL and they suggested that the Royal College of Physicians and the United States Surgeon General were correct to proceed on the basis that there were real increases in cancer from the early part of the twentieth century.
[6.55]Mr McEachran said that Dr Lewis had expressed the opinion that epidemiological data could not be used to draw conclusions about the cause of disease in any individual. Another report by him had been lodged, in which he gave the opinion that epidemiological data did not answer the question of whether or not smoking caused lung cancer. This report was not however used in his evidence and perhaps it was obvious why, because it was so out of line with the huge majority of scientific evidence as spoken to by Sir Richard Doll. (Since this report was not referred to in evidence, and is thus not before me for consideration, I can pay no attention either to what it is said to contain or draw any conclusion as to why no reference was made to it.) Mr McEachran's response to Dr Lewis's evidence was that the argument put forward for Mrs McTear was a two-stage one. The first was that smoking caused lung cancer. That had been demonstrated and accepted in the medical and scientific community. Secondly, if that proposition was accepted, then the medical profession were entitled to proceed on it, and the individual clinicians who treated people like Mr McTear were entitled to make diagnoses based on it. Dr McCarroll, who treated Mr McTear, and Professor Friend, who looked at all the medical background evidence, were entitled to make a diagnosis in the particular case. This could be related to Dr Kerr's evidence that there was a 98% association between smoking and squamous cell carcinoma.
[6.56]Mr McEachran said that Dr Cohen was another witness who did not know whether smoking killed. He concluded that laboratory studies using whole cigarette smoke had not produced squamous cell carcinoma of the lung in experimental animals. This was not disputed, but one wondered where this evidence took the defenders when Mr Davis accepted that there was no such thing as a safe cigarette and that smokers were far more likely to develop serious diseases like lung cancer than non-smokers.
Submissions for ITL
[6.57]Mr Jones said that when he had looked at the whole evidence he would ask me to make no finding on the question whether smoking could cause lung cancer, on the basis that I had not seen sufficient, appropriate, reliable evidence to allow me to justify my making this finding. Ultimately, the pursuer had failed to prove that smoking caused Mr McTear's lung cancer.
[6.58]Mr Jones submitted that the evidence led on behalf of ITL came from well-qualified, respectable, independent scientists who had carried out appropriate research into the issue to which each testified. Mr McEachran had made no substantive attack on their evidence; he seemed to rely only on the proposition that, because they had accepted instructions from ITL and some of them, to a limited extent, had been funded in their research by the tobacco industry, they were not to be relied on. Mr Jones invited me to simply reject that proposition. On a consideration of the whole evidence the attack on the defence experts as a body was unfounded.
[6.59]Mr Jones submitted that it was of no significance that Dr James had been approached by a New York firm of lawyers. He was perfectly candid in explaining the process which led to the submission of his report in this case, including the letter to the BMJ (James et al. 1992) and his discussions with ITL's lawyers on causation. He was a forensic pathologist with considerable experience in the United Kingdom, and was a reliable and credible expert witness who had studied the literature and applied his experience and expertise in answering the questions put to him. Mr McEachran had criticised him because he did not accept that smoking could cause lung cancer. He explained, however, that for him to say that smoking caused lung cancer, it would have to be either necessary or sufficient, and it was neither. He did not use the word "cause" in the same way as it was used in the health warning he was shown. It was never explored with him whether he agreed that smoking could cause lung cancer: the question was whether he accepted that smoking did cause lung cancer. He did not agree with the suggestion that the reason why he was asked to carry out research into the period up to 1950 was that because in 1951 the cohort studies had started. He did not agree that the figures would be more accurate after 1950: he said that the figures in the RCP reports were flawed and, after a point, there was a tendency to over-diagnose lung cancer.
[6.60]Mr Jones submitted that on the face of it Professor Idle was an eminent scientist with an impressive CV. It was not suggested by Mr McEachran that he was other than an eminent scientist with an impressive CV who was well qualified to give the evidence that he gave. He was the only witness who had set out to look at all of the literature relevant to the issue of smoking and lung cancer, and indeed smoking and cancer, covering the whole of the twentieth century and into the twenty-first. He did, as experts required to do, mention in his reports all of the material on both sides of the debate, and there was no suggestion that he had failed to do that. It was quite inappropriate to criticise him, as Mr McEachran had done, as one of the people "whose research is being funded by the tobacco industry, who had been paid large fees". The only evidence that he had received funding at the University of Trondheim, where he held his present post, was that he received a small bridging grant in 1995. Mr Jones submitted that this was no proper basis for not accepting Professor Idle's evidence. The starting point was to look to the evidence and to see whether, on the face of it, it was in any sense lacking. Simply to point to fees received for an amount of work that had never been established in the evidence, but which involved looking at many articles and was conducted over a period of years, was not a proper basis for calling into question the independence of the witness, nor was his being paid a bridging grant to help him move and to start up research in a new place. No other reason had been advanced for calling into question Professor Idle's good faith and his independence, and what had been said did not constitute a proper basis on which to criticise him as a witness.
[6.61]Mr Jones said that Professor Platz was the pathologist who had in his earlier career critically reviewed the work of Auerbach in the United States, and he was also an American doctor who had worked in the VA hospitals. His expertise was unique and relevant to the case: a pathologist from the United Kingdom would have been unlikely to have these key areas of expertise. He was not finally asked to come to give evidence until shortly before he did so, and this was because Dr Kerr had referred to and relied on Auerbach and said in the course of his evidence that the catchment of VA hospitals was the general population, and Professor Platz was particularly well qualified to counter this. To describe Auerbach's study as careful was to ignore the clear evidence of flaws in the methodology which were presented in the examination-in-chief of Professor Platz and the cross-examination of Dr Kerr.
[6.62]Mr Jones submitted that Dr McCarroll was the only witness, apart from Professor Friend, who expressed a view on the cause of Mr McTear's lung cancer. She gave evidence that smoking did cause lung cancer and it was likely that Mr McTear died from lung cancer that was as a result of cigarette smoking. Counsel submitted, without intending it as a criticism of Dr McCarroll, that as a general practitioner her views on these matters were of no assistance to the court. A judgment on the general question whether smoking could cause lung cancer required consideration of the whole relevant evidence, including the epidemiological, biological, pharmacological, toxicological and genetic evidence, among other fields. Dr McCarroll professed no qualifications or experience in any of these. She had not carried out any examination of the basis for her belief that smoking could cause lung cancer. She had not studied any of the scientific literature relating to the issue, and indeed she had not heard of Doll or Peto. No doubt she genuinely held her views, and this was what she had been taught, but this did not assist my task in providing a basis for determining that question in this litigation.
[6.63]Mr Jones submitted that Professor Friend in particular, among other instances, had been used as a conduit to introduce material from disciplines that were clearly beyond his range of expertise and experience. On many occasions Professor Friend said that he should not be asked the question because he did not know the answer. There was therefore material which could not have any evidential value simply because it was being drawn out through the medium of the witness. The purpose of the evidence was to give the court an understanding which could be tested in cross-examination. It was of no assistance to the court if the witness declined to be cross-examined on a passage which he had read out from a publication. Moreover there was no evidential value in passages from a published work which had not been adopted by a suitably qualified expert as being evidence going towards an issue in the case. In the present case, the court was really taken on no journey through an understanding of the underlying science on a number of important issues and was simply given ready-made conclusions. The passages from the public health reports that were read out could not be given the status of primary evidence and had no evidential value except to the extent that they were adopted by a witness qualified to do so.
[6.64]The evidence disclosed that Professor Friend was an anti-smoking activist. This coloured his views and the evidence which he gave to the court. He made no apology for his financial contribution to and connections with ASH. He was committed to the cause of ASH and the cause of smoking prevention. He expressed the view that less reliance should be placed on research funded by the tobacco industry. He stood by statements by him in Thorax in favour of an advertising ban, and that the real enemies were not smokers themselves, but the tobacco industry. He did not meet the criteria that would qualify him as an independent expert witness on which the court could rely to give a balanced view on the issues in this case. Rather, he was giving evidence to further a public health cause. He saw it as his function to be an advocate in this case. When it was suggested to him that his report should have been supported by written reference to the primary literature, he said that he realised that this "would have made a stronger argument". When Professor Friend doubted the statement by the Prime Minister in 1964 that there was no excuse for anyone not to be aware that smoking could cause lung cancer, this was an example of a witness who was arguing a position, rather than acting independently and objectively. Professor Friend's statement that Enstrom and Kabat 2003 could not be relied upon because it was funded by the tobacco industry displayed a prejudice and a lack of objectivity. In the course of cross-examination about this study Professor Friend was unable, or unwilling, to give a straightforward answer about the meaning of "statistically significant". He did not put himself in a position by reference to his qualifications and experience to be able to assist the court on the use that was to be made of any epidemiological evidence. He had never heard of Wynder until his involvement in this case. Very often his reply to a question was that he could not help because he was not an epidemiologist.
[6.65]In his report, in expressing an opinion on the cause of Mr McTear's lung cancer, Professor Friend had advanced a number of propositions. Before examining each of these propositions, Mr Jones made two general submissions. First, no data were produced in support of these assertions. For example, when Professor Friend advanced the proposition that there was a dose-response relationship between an individual's cigarette consumption and the risk of developing lung cancer, he just said that this was the position. I was not taken to any material which I could scrutinize, in which the reasons for the conclusions were given and where the necessary criteria were laid out for judgment. This was an example of my function being usurped and of a witness failing to do what expert witnesses were required by the court to do. The assertions were ready-made conclusions, in the language of Wilkinson The Scottish Law of Evidence (see para.[5.8]). Neither in his report nor in his evidence did Professor Friend furnish the court with necessary scientific criteria for testing the accuracy of his conclusions so as to enable the court to form its own independent judgment by the application of these criteria to the facts proved in evidence (Davie v Magistrates of Edinburgh, referred to at paras.[5.5] to [5.6]). Secondly, in a number of instances, Professor Friend relied not on his own professional knowledge or experience but on what he had gleaned from those in other disciplines and from a general knowledge of what was written in the public health reports (two of which, RCP 1962 and USSG 1964, he had not read).
[6.66]The first of these assertions was the presence of squamous dysplasia found by Dr Kerr to be present in Mr McTear's biopsy sample, which Professor Friend described as a pre-malignant change often found in heavy smokers who went on to develop cancer. He acknowledged that he had learnt about this from pathologists and disclaimed any expertise in this respect, saying that a pathologist would need to be asked questions about it. In any event, such a proposition would require to be supported by evidence about studies showing what was found in heavy smokers who went on to develop cancer; these were the data that one would be looking for. Accordingly, no reliance could be placed on this item of Professor Friend's testimony. It was an assertion that could not be tested. It could only be tested by reference to an area of expertise which Professor Friend had expressly disclaimed for himself. When the point was eventually taken up with Dr Kerr, the source of the observation was to be found in part in the Auerbach material, and Mr Jones said that he could not get anywhere of course with Professor Friend on that.
[6.67]Professor Friend's next proposition was that the histological type of cancer diagnosed, of squamous cell type, was of the type where the association with smoking was particularly strong, as it was in so-called small cell carcinoma. He said that the diagnosis of squamous cell lung cancer in non-smokers was exceptional. In his evidence he said that this reflected his experience as a consultant in Aberdeen for over thirty years; in the majority of cases of lung cancer in smokers the patient had either squamous cell or small cell carcinoma, and he added that the diagnosis of squamous cell lung cancer in non-smokers was unusual, though not unknown. Counsel submitted that this evidence provided no assistance in the determination of the question whether or not Mr McTear's lung cancer was caused by his smoking. The statistical evidence, spoken to by Dr Lewis, was that the lifetime risk of developing lung cancer was approximately 1:100 for non-smokers and 10:100 for smokers. The diagnosis of lung cancer in non-smokers on these statistics was therefore unusual and the diagnosis in smokers less unusual, but we learnt nothing from this about what might have caused cancer in an individual smoker or in an individual non-smoker.
[6.68]Professor Friend's next proposition was that it could be argued that some of these unusual patients might have contracted the disease through the inhalation of tobacco smoke in the home or at work, despite not being active smokers. In his examination-in-chief the only evidence offered by him to vouch that proposition was that "a number of authorities and committees believe that is the case". In cross-examination it transpired that he knew of, but had not disclosed, the existence of Enstrom and Kabat 2003, even though he had only dipped into it. The authors of this paper concluded that the results did not support a causal relation between environmental tobacco smoke and tobacco-related mortality, although they did not rule out a small effect. But taking all of that together, no weight should be given to Professor Friend's view on the determination of the question whether Mr McTear's lung cancer was caused by his smoking. This was just a gratuitous remark which had no relevance to the question to be decided, but it was there because it was consonant with Professor Friend's general approach, which was that smoking was bad and we should be rid of it. The proposition was tendentious because it did not properly reflect the state of the debate, so far as one had been allowed an insight.
[6.69]Professor Friend's next point was that tobacco smoke contained known carcinogens. In his examination-in-chief he offered no data in support of this view. In cross-examination he said that he was aware of a number of products which included nitrosamines, benzo[a]pyrene, polonium and others, but he said that he was not a chemist when he was asked to look at a number of papers relevant to this observation. He said he was not a toxicologist, he was not an epidemiologist, he was a clinician who obtained information about the cause of disease from his reading elsewhere. When he was asked whether he had any reason to doubt the proposition that in a complex mixture, such as tobacco smoke, even if carcinogens were present, they might act in a way which was active or in a way which was inhibitory, he said that it was quite outwith his area of expert knowledge. The statement that tobacco smoke contained known carcinogens was information derived from reports he had read. Counsel submitted that in determining the issues in this case I should accord no weight to this assertion.
[6.70]Professor Friend's next proposition was that the prevalence of lung cancer was closely related to the level of consumption and epidemiological data provided clear links between historical smoking levels in different countries and lung cancer incidence. Mr Jones submitted that this assertion was both beyond Professor Friend's expertise and in any event it was unsupported by the data in this case. Professor Friend had repeatedly disclaimed qualifications as an epidemiologist, and said that he had not had an in-depth reading of the literature in the way a professional epidemiologist would have had. Part of the function of a witness of opinion was to have his evidence tested by cross-examination, and with Professor Friend it was not possible to do this because he could not give answers to counsel's questions that would test the various propositions that he had put forward. Accordingly, it could not be determined whether these conclusions were soundly based or not. He was unable to answer questions about the concept of attributable fraction, which was ultimately the keystone of his thinking in expressing the view that it was probable that Mr McTear's lung cancer was caused by smoking. When counsel had been at pains to see whether Professor Friend appreciated that this concept was such that a death could be attributed to two causes, he said that he was being taken beyond his level of expertise and would prefer that this question be asked of one of the other expert witnesses, in particular Sir Richard Doll. Professor Friend said that the foregoing proposition was based on the many reports which had already been presented in his earlier evidence. But he had looked at the summaries only in RCP 1962 and USSG 1964, and he said he was happy to rely on intelligent and sensible appraisal of these large reports. He could not say that he had read the underlying material which had been presented to the Royal College of Physicians.
[6.71]Professor Friend said that a practising physician's duty was to distil what was available from the readily accessible medical literature and to follow his practice accordingly. He had been happy to rely on reports produced by learned people for whom he had a high regard. Counsel observed that this was perfectly appropriate for a practising physician, and indeed what might be expected of him. But it became different when he came into the witness box to give evidence as an expert witness. It was no longer appropriate that he should rely just on his general knowledge of the world around him when it came to helping the court to determine issues which were disputed in the context of the litigation.
[6.72]It was useful to distinguish between the role of the practising physician and the role of the expert witness. Mr McEachran had advanced the proposition that it was quite acceptable for somebody like Dr McCarroll or Professor Friend to express these views because they diagnosed people. But the endeavour of the treating physician was to determine what was wrong with the individual. In this case what was wrong with Mr McTear was that he had squamous cell carcinoma of the lung. It was no necessary part of that diagnosis to attribute it to a cause. When it came to a dispute in litigation the causation of a disease was a different matter from what was involved in the diagnosis of the disease by a clinician in everyday practice. For all these reasons, counsel submitted that I should not rely on this passage in Professor Friend's report in considering whether or not smoking caused Mr McTear's lung cancer.
[6.73]Professor Friend's next proposition was that there was a dose-response relationship between an individual's cigarette consumption and risk of developing lung cancer. Gender differences in lung cancer risk could also be largely explicable on the basis of smoking habits. In examination-in-chief he said that the literature demonstrated a clear relationship between the number of cigarettes smoked per day and the likelihood of developing lung cancer. He said that this was demonstrated very clearly in the British Doctors Study, reported by Doll and Hill. No evidence was however given by him or by any other witness about this study, so it was not part of the evidence in this case. Once again, this evidence from Professor Friend was no more than his ipse dixit. The court had no criteria by which to form its own judgment on the question why an individual's consumption of tobacco put him at a greater risk of developing lung cancer than that of a non-smoker or someone who smoked fewer cigarettes.
[6.74]Further, the evidence before the court demonstrated that the British Doctors Study was not relevant to the determination of the question whether Mr McTear's lung cancer was caused by his smoking. Apart from the evidence of Dr Lewis, no evidence was given by any witness who was qualified to give it about the appropriateness of using population studies to determine the question whether in any given individual a particular exposure might have caused a particular disease. Sir Richard Doll was not asked about individual causation, but it was known that his views were that one could not determine causation in an individual by reference to population studies.
[6.75]The only evidence before the court that smoking caused Mr McTear's lung cancer came from Professor Friend and from Dr McCarroll. This was therefore the foundation point: one could not draw on the epidemiological material in the way that was attempted in this case, or indeed at all, to determine individual causation. But even if one could, the Doll and Hill study did not assist. Dr Lewis had given evidence which included a discussion of the west of Scotland study. This did not support the proposition that there was a dose-response relationship between an individual's cigarette consumption and a risk of developing cancer. To draw a conclusion, as Professor Friend did, from the British Doctors Study, in the face of known data to a different effect, invalidated the conclusion that he drew from it; and in any event no evidence was given about this study so I was not given an understanding of what was the reasoning which led to its conclusions, and therefore no material on which to form a view about whether the conclusions said to be drawn from it by Professor Friend were acceptable or not. In any event, Professor Friend was driven to accept that population studies did not tell us anything about an individual who was a member of that population. He agreed that an individual might smoke twenty cigarettes a day and be diagnosed with lung cancer after twenty years, whilst another individual might smoke fifty a day and never develop lung cancer. Accordingly, even if it was true that a dose-response relationship had been found in some population studies, one could not extrapolate from this to the individual.
[6.76]Professor Friend's next proposition was that in heavy smokers who ceased to smoke, the risk of subsequent development of lung cancer steadily diminished, so that within fifteen years of ceasing smoking the risks of developing lung cancer were little more than in the life-long non-smoking population. Mr Jones said in relation to this that Professor Friend did not purport to rely on his own knowledge or experience in practice for this assertion; it simply amounted to an epidemiological pronouncement outside the range of his expertise, and the court was shown no data in support of it.
[6.77]Professor Friend then said that not all smokers would develop lung cancer. It had been estimated that about 16% of smokers who continued to smoke would develop lung cancer before they reached the age of 75 years. Again, this was an estimate. It was not stated whose estimate it was, when it was made, or where it was made. The court was not told about the data on which it purported to be based, or the methodology applied. Again it was just an assertion, unsupported, from a witness who was not qualified to make a pronouncement.
[6.78]Professor Friend's next proposition was that although cigarette smoking was not the only risk for lung cancer, the proportion of lung cancer mortality attributable to smoking was estimated in RCP 2000 to be 89% in males in the United Kingdom. Counsel had four points to make about this assertion.
[6.79](1) Professor Friend did not know how the estimate that he relied on was calculated. This was a fundamental barrier to accepting this as reliable evidence, going to the causation of Mr McTear's lung cancer. If he did not know how the estimate was calculated, then there was no material from him before the court that would allow the court to consider the calculation, what one drew from it, whether it was reliable and so on.
[6.80](2) Professor Friend saw the attributable fraction of 89% for lung cancer as outweighing the other risk factors. His thinking seemed to be that although there might be a number of other risk factors, if the proportion of lung cancer mortality attributable to smoking was 89%, then that must outweigh all of the others. But as could be seen from the cross-examination of Professor Friend and from the evidence of Dr Lewis, this was a complete misunderstanding and misuse of the attributable fraction. Dr Lewis gave evidence that the attributable fraction was not a "proportion", as Professor Friend had called it, of anything, and that attributable fractions could and did total more than 100%. In considering attributable fraction two things were important: relative risk and prevalence. Dr Lewis had given evidence about these.
[6.81](3) The 89% figure came from Callum, who made the point that attributable fraction could not be read back to an individual.
[6.82](4) Professor Friend was correct to say that there were other risk factors for lung cancer, apart from cigarette smoking. Apart, however, from diet and family history of lung cancer, which he dismissed in his report and in his evidence, he singularly failed to list those of relevance to Mr McTear's case. In fact, neither Professor Friend nor any other witness called by the pursuer testified to having considered known risk factors for lung cancer by reference to Mr McTear's medical, social and family history, other than his smoking. Consequently, these other risk factors were not excluded as possible causes of his condition. In particular, Professor Friend omitted to take into account Mr McTear's family history. His mother and two paternal half siblings had lung cancer. His half brother Robert McTear died of carcinoma of the bronchus on 1 November 1978 and his half sister Jeanie McTear or Cushnaghan died on 3 January 1996 of bronchopneumonia, metastatic carcinoma and carcinoma of the lung. Mr McTear told Dr Kirsty Muirhead that his half brother had cancer. He told her that his mother died of lung cancer. Mrs McTear gave evidence that his mother had had lung cancer. Mr McTear was his mother's only son and registered her death. She died on 24 August 1963 of medastinal tumour, which according to Dr Kerr was consistent with bronchial carcinoma. The evidence was that family history was a risk factor in his case. Secondly, Professor Friend did not take into account Mr McTear's alcohol abuse. There was a statistically significant association between consumption of alcohol and lung cancer. Thirdly, there was Mr McTear's nutritional status. The evidence was that individuals who abused alcohol often suffered from a vitamin deficiency. Mrs McTear accepted that Mr McTear was undernourished, and he was so described by the Renfrew Council on Alcohol. He was given a vitamin supplement by Dr McCarroll when she treated him for his alcohol abuse. Dr Kerr explained the significance of vitamin A for the maintenance of the bronchial epithelium. Poor diet was statistically associated with lung cancer. Professor Friend also failed to take into account the relevant environmental factors. Mr McTear lived in west central Scotland and membership of that population was associated with an increased risk of developing lung cancer, independently of smoking. He was of low socio-economic status, which was associated with lung cancer independently of smoking. Professor Friend did not take into account Mr McTear's history of viral respiratory infections, particularly influenza, a history which Dr McCarroll described as unusual. One theory of carcinogenesis was that it might be caused by a virus. Professor Friend did not take into account or have any regard to Mr McTear's history of depression and anxiety. Such a history was associated with the development of lung cancer. One theory of carcinogenesis was that a depressed immune system linked to psychological factors might have a role. Professor Friend was asked in cross-examination about these risk factors. In some instances he was aware of them, in others he was not. He was not familiar with the literature. In his examination-in-chief he had said that if certain people had a genetic predisposition to developing lung cancer, they would have to start smoking before that greater risk increased, but he departed from this in cross-examination and said that he found the whole issue confusing to discuss. This condemned him, counsel submitted, as a witness on whose opinion on these matters ought not to be relied on.
[6.83]In addition to not having read RCP 1962 or USSG 1964, Professor Friend had not read USSG 1988. He said earlier in his evidence that he had read the expert reports produced on behalf of ITL, including Professor Idle's report, but it transpired in cross-examination that he had not read it. He was also unable to provide references for any of the data on which he relied in his own report, and he had forgotten the results of his own studies on smoking cessation, which came to the opposite conclusion from the proposition that the heavier the smoking, the more difficult it was for the smoker to stop smoking.
[6.84]Mr Jones submitted that, on this review of Professor Friend's evidence, he failed to meet any of the criteria set out in the authorities as being required of a witness to opinion before he or she could properly be regarded as qualified to speak on the relevant subject. He also failed to meet the test of a witness whose evidence could safely be relied on by the court. In particular, he did not supply the court with the technical or scientific knowledge necessary to enable it to understand and appreciate the relevant scientific issues in the case. He did not have an extensive and accurate state of knowledge and experience of any of the subjects involved in determining whether or not smoking could cause lung cancer, or indeed whether smoking caused Mr McTear's lung cancer. He spoke with no authority and with no experience or qualifications in the relevant disciplines. He did not furnish the court with the necessary scientific criteria for testing the accuracy of his conclusions so as to enable the court to form its own independent judgment by the application of these criteria to any facts proved in evidence. He could not be regarded as giving an objective and unbiased opinion. He was giving evidence on matters well outside his expertise and he assumed the role of an advocate. He was unable to state the facts and assumptions upon which his opinion was based and he omitted to consider material facts which could detract from his concluded opinion. Only when pressed in cross-examination did he make it clear when a particular question or issue fell outside his expertise, and of course at that point any attempt to scrutinise his evidence by cross-examination had to be abandoned. He had carried out no research on the issues in this case, did not comply with the duty to consider material which might be available in the relevant field, and did not comply with the duty not to draw conclusions based only on his own experience.
[6.85]The most flagrant example of this was in relation to familial susceptibility, where he did commit himself to a written view when he had plainly not informed himself about the relevant literature. None of the passages read out to Professor Friend in his examination-in-chief fell within his personal experience in the relevant specialist fields. In support of the foregoing observations, counsel referred to the authorities discussed above at paras.[5.2] to [5.17]. In these circumstances, counsel submitted, no reliance should be placed on the evidence of Professor Friend in determining the question either whether smoking could cause lung cancer or whether Mr McTear's lung cancer was caused by smoking.
[6.86]Mr Jones submitted that it was plain that Sir Richard Doll came to court committed to the belief that smoking could cause lung cancer and other diseases. He was neither asked, nor did he express any view, about what might have caused Mr McTear's lung cancer. He was clearly at pains to persuade the court to accept his view on general causation. He certainly had, on any view, an impressive CV, but in a sense this almost counted against him, because his career had clearly been built from the foundation of the work that he did with Hill in the early 1950s and thereafter, and one might have been forgiven for getting the impression that part of his purpose was the defence of the work that he had done over the years. This was seen most clearly in his dismissal of those who over the years had not even gone so far as to suggest that he was wrong, but had simply suggested that caution should be exercised before the scientific community finally came to the view that the statistical association was causal. Even that prompted him to dismiss whoever put up such an idea as being an eccentric, corrupt, or other descriptions.
[6.87]The pursuer sought to rely on Sir Richard's evidence for the contents, first, of the Green College Lecture, Doll 1997. The difficulty with this approach was that the lecture was essentially a memoir, a reminiscence of how it all happened. It did not purport to be a scientific document. If, during the course of reading through it, Sir Richard had been taken to the primary material of the British Doctors Study and the original Doll and Hill work, then there might have been a foundation for the court to accept the opinions expressed in the lecture. Without that, Sir Richard was in very much the same position as that of Professor Friend: he gave the court an ipse dixit, no doubt from high authority; but he had not done and was not invited to do what an expert witness had to do, which was to inform, to instruct, to process data and to give reasons for conclusions reached.
[6.88]For example, although mention was made of Doll and Hill 1950, no reference was made to the text of this article, in which the authors concluded that cigarette smoking was a factor, and an important factor, in the production of carcinoma of the lung. No evidence was given about the detailed consideration of the possibility of confounding, of the consistency of the findings in different studies, what biological relationships with amount and duration of smoking were considered, what was the size of the estimated relative risk and what was the relationship of time and place and for each sex. The court was given no insight into the material that led the researchers to their conclusion. Therefore it could not test the conclusion by anything that had been put before it in this litigation. For the purpose of exercising a judgment as to whether or not an association could be regarded as establishing a causal link, the starting point was to show what were the data on which the judgment was based. With those data, the witness would be able to demonstrate the process of reasoning that had led him to that conclusion, and the court would therefore be in a position to judge the soundness of the conclusion. Counsel referred to Dingley v The Chief Constable, Strathclyde Police (see para.[5.11]). What was missing from Sir Richard's evidence was the reasoning to support his conclusion.
[6.89]While the fact that Sir Richard's views had come to be generally accepted by a majority of those working in the field might have some weight, nevertheless, without knowing on what the views were based and why they came to be generally accepted, it was not possible to say whether or not they were right, despite the very great eminence of Sir Richard. As counsel explained, when I came to determine the question whether smoking could cause lung cancer on the evidence in this case, I would no doubt feel obliged to give reasons. It would not be sufficient reason for me to say that I found that smoking could cause lung cancer because that was the consensus view of the medical fraternity. This was particularly so where, on the part of some people, there was an acceptance that a statistical association was causal simply because it was a statistical association. For many doctors this was probably good enough as a working hypothesis: if there was a statistical association which was regarded as strong, then a doctor might well feel able to recommend to a patient that he should stop smoking, for example, and would no doubt tell the patient that smoking could cause disease. This did not take me anywhere, counsel submitted, when I had to address that question as an issue in this litigation. In other words, I did not know on what basis this consensus had been reached.
[6.90]Professor Friend accepted that there was a difference between the science of epidemiology and epidemiology as an instrument of public health. He readily accepted that if a body such as the Royal College of Physicians found a statistical association and took the view that the exposure was not of great social benefit, they would feel it their responsibility to declare that the association was causal because that would lead to an acceptable public health outcome. The evidence was that Charles Fletcher had set out to write RCP 1962 in order to persuade Members of Parliament to do something about cigarette smoking. But the report did not state by what standard of proof the Royal College of Physicians reached the conclusion that the association that had been found was causal; it was not known what was regarded as sufficient for them to declare causation and Professor Friend said that something less than the balance of probabilities could well do if it was in the interests of public health. It was for the court to decide if the public health communities' reasons were sound and should be followed, but if it was not given those reasons then there was nothing on which to found an opinion. Scientific truth was not determined by a majority vote, and issues in a litigation were not settled by reference to the number of witnesses on each side. It was not enough to point to a consensus and say that the pursuer won on the numbers. This gave no basis upon which to come to a reasoned judgment on the issue to be determined.
[6.91]It was correct to say that Sir Richard was not challenged on the conclusions he reached. There was no basis for a challenge. The evidence which led Sir Richard to his conclusions was to be found in his epidemiological studies, but none of these was before the court in evidence. There had been no evidence of the reasoning process which, as Lord Prosser said in Dingley, was the critical aspect of the evidence of an opinion witness. The pursuer relied wholly on Sir Richard's ipse dixit. At least, the data contained in Sir Richard's papers should have been open to scrutiny, and thereafter the statistical techniques which were applied to the data and the manner in which a judgment was exercised. This was on the principle that the court required to be instructed in the specialist facts of the case, the criteria for reaching conclusions and the material upon which these conclusions were reached. It would not have been an impossible task. Sir Richard could at least have been taken to those papers to which reference was made. He could have instructed me how to do epidemiology at least sufficiently to understand the reasoning which led to the conclusion. Ultimately it was for me to form the judgment, on the basis of sufficient instruction. It was not a criticism of any of the witnesses to say that this was simply lacking as a result of the approach which had been adopted in this case.
[6.92]Mr McEachran had advanced the proposition that it was enough to see what was in the public health reports and that many doctors shared the view that the association was causal. This was not the correct approach to take in the determination of issues such as the present. It amounted to a submission that the function of the court should be usurped by a majority of clinicians. If all the court had was the oracular pronouncement of a witness, no matter how eminent, then all that the court could do was give its own oracular pronouncement as an echo of what the witness had said. As the Lord President said in Davie v Magistrates of Edinburgh, that will not do.
[6.93]In addition, Sir Richard said that when he reached conclusions about causation, he took into account all of the evidence, just as the court did. This of course would include the biological evidence, the laboratory evidence and all the other factors that would feed into the ultimate conclusion. An epidemiologist, had he been going through the raw data and giving reasons for his conclusion, would no doubt have discussed what the other evidence was and how it played into the ultimate conclusion. But none of that was before the court in this case.
[6.94]It was because of the need to consider all the relevant surrounding facts and circumstances that it was appropriate to examine Sir Richard's dismissal of anybody who sounded a word of caution as worthy of no note. The opinions he expressed were forthright and definite. He was committed to his own view as early as 1949. This was on the basis of the one retrospective epidemiological study on hospital patients that he was conducting with Hill, and also on his own conviction that some of the apparent increase in lung cancer incidence was real. There was no evidence that when he formed these views he had considered that the statistical association between cigarette smoking and lung cancer might be accounted for by some confounding element. It was clear that he did not consider the constitutional hypothesis, even as a possibility to be excluded. It was plain also that nothing anyone had ever said had caused him to doubt his conviction that the statistical association between smoking and lung cancer was causal. He was scathing about those who sounded a note of caution about accepting causation as proved on the statistical evidence alone and without testing competing hypotheses. Their views were dismissed as eccentric, bizarre, nonsense or dishonest. In cross-examination he was asked about Fisher, Berkson, Seltzer, Yerushalmy, Eysenck, Burch, Oldham, Stern, Gwynne Jones, Feinstein, Passey, Little, Tokuhata, Hueper and Rosenblatt. Counsel reviewed Sir Richard's cross-examination about the views expressed by each of these individuals. He submitted that no proper reasons were given by Sir Richard for rejecting the views of any of them.
[6.95]Counsel accordingly invited me not to accept Sir Richard's evidence that the question whether the statistical association between smoking and lung cancer was causal was effectively settled by 1957. There were eminent scientists who could be seen to be expressing a note of caution, not only in the 1950s, but well into the 1960s and indeed into the 1970s. Secondly, he invited me not to hold that it was established in this case that smoking could cause lung cancer on the basis of Sir Richard's evidence. Sir Richard could not be regarded as giving an objective and unbiased opinion. He assumed the role of an advocate. He argued for what he believed as opposed to assisting the court to an understanding of the issues. He did not state the facts and assumptions upon which his opinion was based. He was not prepared to consider material facts which could detract from his concluded opinion. He did not supply the court with the technical or scientific knowledge necessary to enable it to understand and appreciate the relevant epidemiological and other scientific issues. He did not furnish me with the necessary scientific criteria for testing the accuracy of his conclusions, so as to enable me to form my own independent judgment by the application of these criteria to the facts proved in evidence. The reasoning behind his conclusions was not before the court. In the absence of any supporting primary material, his views amounted to a bare ipse dixit or a bare oracular pronouncement which could not be tested or independently appraised. On the evidence presented, therefore, I was unable to form my own judgment on these conclusions enunciated by Sir Richard. Again, counsel referred to the tests laid down in the authorities discussed above. It was not in itself a reason for rejecting an expert witness's evidence because he or she was known to have certain views on the subject in question, so long as they were able to justify those views in the witness box and be prepared to give rational grounds for rejecting any different views, or any material which might tend to contradict their own views. But Sir Richard simply dismissed alternative possibilities out of hand.
[6.96]Sir Richard had also been invited to look at IARC 1986 and IARC 2004. This amounted to no more than evidence that these documents said what they said. Although Sir Richard was Chairman of the working group which was responsible for IARC 1986, he was not asked to look at or explain the epidemiological or other scientific data that were relied on in support of its conclusions, and therefore these data too were not before the court. Further, Sir Richard was not qualified in toxicology, chemistry, biology, oncology, radiobiology or cytogenics, which were the disciplines from which the working group responsible for IARC 1986 were drawn, and presumably from which the working group responsible for IARC 2004 were also drawn. He was not open to cross-examination and did not explain to the court much of the material that informed the conclusions of these groups.
[6.97]Mr Jones said that Dr Kerr was relied on by Mr McEachran, but he was not asked questions directly about causation, although he did give some evidence which Mr McEachran prayed in aid. Dr Kerr was an experienced pathologist with a special interest in lung cancer. He thought that there was a strong association between smoking and lung cancer and there were things in tobacco smoke which caused lung cancer. In cross-examination it became apparent that his understanding about the latter point was based on a very general understanding that there were a whole variety of different chemical agents within tobacco smoke, some of which were recognised in test situations using either laboratory animals or human tissue cells in culture, where those chemicals were recognised as carcinogens because they could be shown experimentally to induce tumours in laboratory animals, and also to induce changes in animal cells, in tissue culture for example; changes which were recognised as being associated with the development of the malignant process. He did not know the literature on the animal studies well enough to comment on whether it had been possible to induce squamous cell bronchogenic carcinoma in animals by inhalation of tobacco smoke, nor was he familiar with the details of the experiments using human tissue culture. His evidence did not go beyond saying he believed that studies had been done, but he did not know the details.
[6.98]In addition to a clinical diagnosis, Dr Kerr's report addressed the relationship between squamous cell lung cancer and smoking in two ways. He stated that 98% of squamous cell lung cancers were found in smokers and, under reference to Auerbach, that squamous dysplasia was frequently found in the bronchi of smokers and much less so in non-smokers. Mr Jones submitted that insofar as he was speaking on matters going beyond clinical diagnosis and his own direct experience, Dr Kerr's evidence should be treated with caution. The reasons for this were as follows. Firstly, in his report he relied on Nasiell et al. 1987 in support of the proposition that the pre-invasive squamous dysplasia, the precursor lesion of invasive squamous cell carcinoma, was also frequently found in the bronchi of smokers and much less so in non-smokers. In examination-in-chief he particularly pointed to the data in Table 8.1 on p.217 of the paper. The table contained the statement that 23% of non-smokers with chronic inflammatory lung diseases displayed atypical metaplasia. He said that this required, however, to be read subject to the qualification that the table related to cytological changes. Counsel submitted that if the table required to be looked at with that qualification in mind for the figure of 23%, it had also to be looked at with that qualification in mind for the information on which Dr Kerr relied.
[6.99]Secondly, Dr Kerr relied on Colby et al. 1995 for the proposition that 98% of squamous cell lung cancers were found in smokers. It became apparent in cross-examination that he had not gone further than the statement in the textbook. He did not appreciate even that the data had been mis-referenced, as explained by Dr Lewis. It was also apparent from his cross-examination that it was impossible to tell whether or not the data upon which the figure was based had any statistical significance, again as explained by Dr Lewis. Dr Kerr claimed that the information in Table 2 was that squamous carcinoma in the lung was much more likely to be found in someone who had been a smoker rather than in someone who had been a non-smoker. On his interpretation, the rates of smoking in the general population had nothing to do with the paper, they were quite irrelevant to the interpretation of the data. Counsel submitted that this undermined his credit, because he misunderstood the requirements of epidemiology if one was looking for a statistical association.
[6.100]This was a matter of logic, in any event, but there was evidence from Dr Lewis about it. Dr Lewis gave reasons for expressing the view that there was insufficient information about the population sampled, and the general population from which it was drawn, to enable conclusions to be drawn about the relationship found between ever-smoking and epidermoid cancer. Counsel agreed that the way of putting his point was that without information about the study group that would enable a view to be taken as to whether or not it could be regarded as representative of the general population, it could not be determined whether or not a valid extrapolation could be made of figures relating to the study group to the general population. One would have to know what the prevalence of the exposure was in the general population in order to see whether there was either a match or a mismatch. Dr Kerr's evidence on this matter called into question his understanding and therefore his use of the epidemiological data.
[6.101]Dr Kerr also relied on Auerbach et al. 1975. But it was apparent that he had given no consideration to the question whether the population studied by the authors was representative of the general population. He was under the misapprehension that Veterans Administration Hospitals treated the general population, whereas Dr Platz's evidence, based on personal knowledge, was that these hospitals in fact treated a very specific sub-group, even of the United States veterans. Dr Platz also explained that the population had multiple health problems, in particular poor nutrition, and there was evidence from Dr Platz and Dr Kerr that this was a potential relevance to the maintenance of the bronchial epithelium.
[6.102]Mr McEachran, in relying on these papers, had submitted that the studies were "rigorously controlled". Mr Jones submitted that it was clear from Dr Lewis's evidence, about Colby et al. 1995 in particular, that they had not controlled for confounding. In re-examination of Dr Kerr on Colby et al. 1995, Mr McEachran asked Dr Kerr to compare the 98% figure in that paper with the 30% of the United Kingdom population who were current smokers. He could not say what further percentage of the population had previously smoked but had given up. Contrary to what Mr McEachran submitted, that this was a mismatch, it was like comparing apples and oranges. The figure of 30% was for current smokers in the United Kingdom, whereas the figure of 98% was of Americans presenting over an unknown period up to 1979.
[6.103]In Rosenow and Carr 1979 the diagnoses were based on sputum cytology alone. Dr Kerr gave evidence that the importance of cytological atypical cells could be difficult to determine, and indeed he said in effect that one could not draw useful conclusions about the incidence of dysplasia from Nasiell et al. 1987, upon which he founded in his report, because it was based on cytology. There was more information to be gained from a biopsy specimen. When tumours were typed on the basis of small biopsies, there was some scope for inaccuracy. In any event, without confirmation of the tumour classification on removal of the tumour, there was scope for inaccuracy. This was sufficient for him to write that it was of concern that, if 85% to 90% of patients had a diagnosis made on pre-operative specimens alone, with the likelihood of some degree of inaccuracy in tumour classification from such specimens, then epidemiological studies might be based on flawed data. Epidemiological data would be more useful if based upon more robust histological diagnosis. Further, the typing used by Rosenow and Carr was based on the 1967 World Health Organization classification. Dr Kerr gave evidence that sometimes under this classification; where histological typing was difficult, some pathologists opted for squamous cell carcinoma simply on the basis that it was the most likely one to occur. In other words, where typing was difficult, as on Dr Kerr's evidence it might well be, and where the diagnosis was based on cytology alone, there was a bias towards reporting squamous cell carcinoma.
[6.104]Dr Kerr agreed that in Auerbach et al. 1975 the study comprised 662 autopsies of men, of whom six were non-smokers. In counsel's submission, since 99% of the population studied were smokers, one could not take anything as being significant from the fact that 100% of the squamous cell carcinomas were found in smokers. This again was to do with populations. The authors of the paper did not claim that what they found was statistically significant. If the purpose of referring to Auerbach et al. 1975 was to support the figure of 98% in Colby et al. 1995, then it did not give support. Dr Kerr had also agreed that Auerbach and Garfinkel 1991 provided figures that were "in the same ball park" as the 98% in Colby et al. 1995. But in this study, which reported on 505 cases of lung carcinoma, the number of patients who had never smoked being ten, this meant that the never-smokers were 2% and the smokers were 98% of the total, but without knowing about the prevalence of smoking, one could not draw any conclusions about the significance of the figures that were brought out.
[6.105]Dr Kerr also drew on his own experience, saying that it was most unusual to see a squamous cell carcinoma of the lung in a non-smoker. But it emerged in his evidence that he would not consistently be given smoking histories of patients. He said that he would be more likely to be given a smoking history where the patient was a non-smoker. Since therefore he received samples without a smoking history, it was plain, counsel submitted, that any estimate by him of the proportion of smokers to non-smokers would be unreliable. In any event, what the evidence established was that lung cancer was a rare disease in non-smokers and a little less uncommon in smokers. This was simply a statement of the statistical association. Therefore, a pathologist would see fewer squamous cell lung cancers in non-smokers than in smokers. Accordingly Dr Kerr's experience did not advance the issue of causation.
[6.106]Finally, there was no finding that any particular proportion of squamous cell carcinomas could properly be made on the basis of Dr Kerr's evidence or on the basis of the other material before the court. Professor Platz gave evidence about Auerbach 1961. He did not take issue with the reported findings and acknowledged that they showed a strong association between the degree of exposure and the frequency and degree of changes in the bronchial epithelium. But he did take issue with the conclusion that the findings supported the judgment that a direct causal relationship existed between smoking and these changes. Dr Kerr himself accepted that all that Auerbach could show was an association. Auerbach also found a variety of changes in the lungs of non-smokers. He said that it was possible to find dysplasia in the lungs of non-smokers. So, inasmuch as there was a statistical association between smoking and lung cancer, if squamous dysplasia was a step on the way to lung cancer, then it would be expected that there would be a statistical association between squamous dysplasia and lung cancer. But this still went nowhere to resolving the question whether the relationship was one of cause and effect.
[6.107]Moreover, Auerbach's study population consisted of people who had died and had come to autopsy in United States Veterans Administration Hospitals and people who had died and come to autopsy in other hospitals. The relative proportion of these two groups was not reported. The evidence was that patients of Veterans Hospitals had had different characteristics from the general community, as described by Professor Platz. His evidence was that, to the extent to which the study population was made up of this group, the findings could not be generalised to the population at large. Apart from the fact that this was a selected sub-group, there was no evidence about their service experience which might be relevant. For example, there was the possibility of exposure to gas. Auerbach did not report on whether or not there were differences between this group of patients and the group of patients from general hospitals. This, in counsel's submission, was on the face of it a potential confounding factor. Finally, no equivalent study had been carried out to investigate whether or not there was a similar association of changes in the lung with other potential risk factors.
[6.108]Mr Jones said that Dr Lewis had prepared reports both on general causation and on individual causation and on individual causation, but he was asked questions only on the latter. Professor Lelorier, an abstract of whose evidence on epidemiology and in particular on general causation had been lodged as a production, was not called as a witness. It might have been thought that the reason for this was that an attack was going to be mounted on the sufficiency of the epidemiological evidence relied on by the pursuer. Counsel said that he was not in a position to invite me to make a positive finding on ITL's averment that the cause or causes of lung cancer had not been established. This was because a judgment on that question required to be formed on the basis of all the relevant evidence, and this was not before me.
[6.109]Since, however, it had been said that the defence was disingenuous, Mr Jones invited me to consider whether this was well-founded on the material that I had seen. Such an assertion could only be made on the basis of the evidence which had been led in this court. On the matter of specific causation, not only was this a defence put forward in good faith, it was a defence which had been made out. Counsel said that this was on the basis of his analysis of the evidence of Professor Friend, Dr McCarroll and Dr Kerr, and on the evidence of Dr Lewis. The case advanced on behalf of the pursuer on individual causation had to deal with the application of the attributable fraction. Counsel reminded me of the evidence of Dr Lewis, which demonstrated that Professor Friend was wrong to speak of "proportions" of attributable fractions.
[6.110]Mr Jones pointed out that many passages in the multi-disciplinary reports that were referred to were put to witnesses by Mr McEachran and they were simply asked to notice that these were what the authors of the reports said. So in many instances there was not even an attempt to have the witnesses adopt what was being said. Yet Mr McEachran sought to rely on those passages in his submissions. In addition, there were passages about which not a word was said during the course of evidence, but upon which Mr McEachran now sought to rely. As a simple matter of admissibility, this approach was misconceived. There were many reasons, but they were all to deal with the same considerations which arose from the authorities bearing upon the adoption of reports by expert witnesses. Such passages had not been tested in evidence, and accordingly it could not be told what reasoning might have lain behind them. So the question was, what evidential value did these passages from the multi-disciplinary reports have when they were not competently adopted by a suitably qualified witness.
[6.111]Counsel submitted that when an expert witness gave evidence, the court was interested to know: (1) the qualifications and experience of the witness; (2) information that the witness had been given about the case; (3) the investigations, if any, that the witness had carried out and the results of these investigations; (4) the assumptions that the witness might have made and the reasons for these assumptions, in order to see whether they were soundly based; (5) the methodology that the witness had applied in reaching his or her opinion; and (6) the reasons for the witness's conclusions. The witness's evidence on all of these matters must be open to being tested, not only by the cross-examiner but also by the court. It necessarily followed that the evidence on all of these matters must be understood by the court. This was because the court was: (1) interested to have the technical or scientific knowledge necessary to enable it to understand and appreciate the relevant scientific issues in the case; (2) interested to have the necessary scientific criteria for testing the accuracy of a witness's conclusions so as to enable the court to form its own independent judgment by the application of these criteria to the facts proved in evidence; (3) interested to have the relevant supporting primary material so that it could be independently appraised by the court; (4) interested to determine whether the evidence was presented as an objective and unbiased opinion and was not an exercise in advocacy; and (5) interested in being satisfied that the witness considered all material facts which could detract from the opinions expressed. None of these desiderata were met when passages from reports were simply read out or, not even having been read out during the evidence, were relied on during submissions.
[6.112]Mr Jones said that there were a number of observations that fell to be made about the reports relied upon by Mr McEachran. Most reliance had been placed on IARC 1986. Mr Jones invited me to note that it was actually written in 1985, so it was now some nineteen years since it was written. Since then, as the evidence of the expert witnesses for ITL demonstrated, science had progressed. Theories had come and gone, new studies had been done, new facts had been discovered and therefore IARC 1986 could not provide a comprehensive and up to date figure. No evidence had been led about how the authors of these reports approached the question of standard of proof, or even whether they approached it at all. One would need to know what was the purpose in the minds of the authors of these reports and what they considered as sufficient to express a definite conclusion on any matter.
[6.113]In a litigation, if a number of possibilities were given as causes of an injury or a condition, the court would expect the pursuer to establish that the cause contended for was the most likely one. Very often this was done by excluding other possible causes or leading evidence to satisfy the court that the other possibilities were less likely. It was not known whether that sort of exercise was undertaken by the authors of the multi-disciplinary public health reports and, if so to what extent and by what criteria the authors might pronounce themselves satisfied. The authorities established that an expert witness was expected to disclose any assumptions which underlay his report, if he had prepared one, or his evidence and his conclusions given in evidence. Again, it was important for the court to be able to assess whether these assumptions were well-founded and well reasoned, and for the court to form its own view.
[6.114]Examples of this could be found in the passage in MRC 1957 discussed in the evidence of Dr James. In this, it was a basic assumption that there had been a very great increase in the death rate from lung cancer. This led the authors of the report to their conclusions. The court would only be able to adopt these conclusions by accepting the basic assumption underlying them, which was that the increase in incidence was real rather than artifactual. The problem was that this was an article of faith. Even without contrary evidence, there was no basis on which the validity of the assumption could be tested. There were no underlying data to determine whether the assumption was well made, and no reasoning to determine whether the conclusion that the rise in incidence was real was soundly based. This was a fundamental problem which arose from the invitation by Mr McEachran to accept the conclusions of these reports.
[6.115]While MRC 1957 only extended to two pages, Mr McEachran had seen some weight in the fact that the reports he was relying on ran to hundreds of pages and had cited hundreds of underlying texts. In Mr Jones's submission this diminished any value they might have, because the court had not seen these pages or texts and accordingly did not know on what data the conclusions were based and whether the reasons for coming to them were sound. For the reasons given by Lord Prosser in Dingley v The Chief Constable, Strathclyde Police (see para.[5.11], it was all very well to say that the authors of these reports were eminent and drawn from a number of different countries, but it was still necessary to look behind that to see whether there was sufficient reason to rely on their conclusions.
[6.116]Another point was that a public health body, interested in avoiding risks, might very well quite legitimately ignore possibilities, when there was no evidence for them, but this was not the same approach as it was appropriate for a court to adopt, as was decided in Wilsher v Essex Area Health Authority. This could be seen in the passage in RCP 1962 discussed by Dr James, in which the possibility raised by some pathologists, that lung cancer used to be more common than mortality figures suggested, was rejected. As it was expressed in this report, such an approach might be quite justifiable as a public health advocacy tool, but it was not an accurate presentation of the material. What was entirely missing from the report was discussion and reasoning of the kind seen in the evidence of Dr James. Again, the court was being invited to take all of this as the ipse dixit of the Royal College of Physicians, with no opportunity to evaluate the material.
[6.117]Because the court had not seen the texts of reports running to some hundreds of pages, it could not be known on what assumptions they were based. In USSG 1964, for example, the committee proceeded on an acceptance that there had been a continuing rise in lung cancer as part of a trend that began before 1940. Similar assumptions would be found in other reports. Because the texts had not been explored even to the extent necessary to know what assumptions had been made, this was another reason to decline to accept their conclusions as effectively replacing my own views on the matter, when I had not been given the material to reach these views. As Lord Prosser said, litigants were entitled to a judicial pronouncement, not to an oracular pronouncement of some eminent body. This could have been done. The starting point might have been to ask Sir Richard Doll questions about epidemiology. It might or might not have been necessary to supplement his evidence with material from other disciplines but without even his evidence, reliance could not be placed on the conclusions about epidemiology which were given in the reports.
[6.118]Counsel turned to the question of what constituted a public health report. Professor Idle described IARC 1986 as a public health report destined for member Governments of the United Nations. Professor Friend described the origins of RCP 1962, under reference to Fletcher 1992. Professor Gray described reports such as those of the Royal College of Physicians and the United States Surgeon General as being part of a strategy aimed at changing people's behaviour, a mixture of propaganda and the scientific evidence upon it which it was based, but with the interpretations and the language used to describe those data biased towards the interests of the message that was being conveyed. Counsel did not suggest that there was anything untoward with this, but it had consequences for the way in which such reports were written and it might have consequences for the way that conclusions were drawn. Counsel agreed that this raised the question whether a report written for such a purpose could properly be regarded as forming part of the corpus of scientific literature to which an expert witness should have regard. Such a report was not equivalent to a scientific study or a scientific paper, but was written for a different purpose. As Professor Gray explained, the data that carried most weight were those in the primary experimental or empirical reports, the archival data. By contrast, the reports that Mr McEachran relied on were properly characterised as public health reports, and indeed at one point he appeared to accept that that was what they were.
[6.119]Dr Lewis gave evidence about the difference between the science of epidemiology and the public health profession of epidemiology. He recognised the process by which public health activists, on the strength of a belief, wished to transmit it to governmental figures in order to influence governmental action. Professor Friend gave evidence that media advocacy was the strategic use of mass media for advancing a social or public policy initiative. Although this expression was of relatively recent origin, it was understood and applied when the early public health reports were published, as could be seen from Fletcher 1992. Professor Friend accepted that one of the purposes of RCP 2000 was to persuade the Government to control tobacco. It was not surprising, counsel submitted, and not in any sense dishonourable, that the authors of this report set out to present conclusions in a way that would influence the Government and change behaviour. It was Professor Friend's belief that in general the purpose of the reports published by the Royal College of Physicians was to bring about change and apply pressure; but further, he agreed that if a body such as the Royal College of Physicians had good evidence of a strong statistical association between an exposure and a disease, he would expect it to incline towards warning the public to avoid the exposure. He was asked about passages in Gori 1989, and there was nothing in this article with which he disagreed. It was consistent with what he said was the purpose of epidemiology as a public health discipline.
[6.120]Accordingly it should be borne in mind that ultimately the purpose of such reports was to persuade, and so they were not documents like scientific papers that a court could rely on as expressing reasoned scientific conclusions. They could not be relied on as determining issues in the way that the court would determine them, and therefore they could not be relied on to assist in the determination of these issues, given that they were the only material. Even within communities particularly interested in the subject, the danger existed of confusion between "association" and "cause". Gori was saying the same thing, that there might be an acceptance that where an association was found, this should be taken as being the same as cause. This was also consistent with Professor Friend's view that where an association was found between an exposure and a disease outcome, it might be legitimate for the public health community to declare that the association was causal, if this would bring about what was regarded as a public health benefit. For all these reasons, these public health reports were not to be relied on for the purposes to which Mr McEachran would have them put.
[6.121]In summary, given the purpose of public health reports and the public health community's approach to how they should be drafted, the standard of proof applied to determine the issues addressed in a public health report could not be taken to be equivalent to or higher than that applicable to the determination of the issues in a litigation. Moreover, the views or conclusions of a committee proved no primary fact other than that the committee had reached those particular views or conclusions. So they were of no evidential value except to the extent that they had been adopted by a witness, qualified in the relevant field, who furnished the court with the necessary scientific criteria for testing their accuracy, so as to enable the court to form its own independent judgment by the application of these criteria to the facts proved in evidence.
[6.122]Counsel then turned to address Mr McEachran's submission that the "multi-doctor studies" from MRC 1957 to IARC 2004 all concluded that cigarette smoking could cause lung cancer. IARC 2004 had of course only been published in summary form in 2002. None of these reports was a study in the scientific sense, but was a review carried out by groups of members drawn from a variety of disciplines. The authors of the reports stated that the results of animal skin-painting experiments supported the proposition that the statistical association between cigarette smoking and lung cancer was causal. But Sir Richard Doll and Professor Friend said that the results of these experiments were of no value in determining whether smoking could cause lung cancer. Having regard to Professor Idle's evidence in particular, this was the correct view: skin-painting experiments were of no value in determining whether smoking could cause lung cancer. So the view which was expressed in the public health reports that the statistical association between cigarette smoking and lung cancer was causal was undermined. Considered as part of an exercise in evaluating the evidence, when this piece of evidence was taken out as being of no value, then in counsel's submission the conclusion ought properly to be regarded as undermined. In his submission, the evidence demonstrated that the public health reports could not be relied on, either as accurately recording the studies that were reviewed, or as expressing conclusions soundly based in the science.
[6.123]Perhaps one of the most representative criticisms of the public health reports was put to Professor Friend, and he was not able to refute it. This was the view expressed in Sommers 1976 that USSG 1964 dealt with the difficulty of assigning causality, but the summary and conclusions brushed these aside and assigned a causality not demonstrably evident in the text. Another example of the unreliability of public health reports to recall the studies accurately or to express conclusions soundly was found in IARC 1986. The report founded on the results of animal inhalation studies and was shown in evidence to have mis-stated the results of Dalbey et al. 1980, the study on which it relied for its conclusion that chronic exposure of rats to whole cigarette smoke resulted in the induction of malignant respiratory tract tumours, but which was shown to have adopted flawed methodology. More broadly, as Dr Cohen stated, and was not disputed, none of the fifty-seven inhalation and intratracheal carcinogenicity studies in the mouse, rat, hamster, guinea pig, rabbit or dog, as reviewed in his report, showed a statistically significant increase in squamous cell carcinoma of the lung following exposure to cigarette smoke and, indeed, none of the authors of these studies reported a statistically significant increase for this carcinoma. He also concluded that laboratory studies using whole cigarette smoke had not produced squamous cell carcinoma of the lung in experimental animals.
[6.124]Although Sir Richard Doll was the chairman of the IARC working group, he was not asked to look at or explain the epidemiological or other scientific data that were relied on in support of the conclusions of IARC 1986, so these data were not before the court. Another criticism of a public health report was the use of "really flawed" statistics in RCP 1971, as explained by Dr James. For the reasons given by him, no useful comparison could be made between the figures given in Table II in RCP 1962 and Figure 4.1 in RCP 1971.
[6.125]While Mr Jones made references to other criticisms of the public health reports, these were the main ones and I regard them as sufficient foundation for his submission. His main submission was that the passages in the public health reports relied on by the pursuer were the bare ipsi dixerunt of their authors. The court had been given only ready-made conclusions without the data on which the authors proceeded. The court had not been furnished with the necessary scientific criteria for testing the accuracy of these conclusions. None of the conclusions of the reports could be tested by cross-examination. The standard of proof, if any applied, was not enunciated. Underlying assumptions might or might not have been stated, but were not proved in this court, and in a number of demonstrated instances methodology relied on in reports, which were in turn relied on by the authors, had been shown to be flawed. In other respects the reports had been shown to have reached the conclusions which were not justified by the evidence which it had been possible to look at.
[6.126]In his submission that there was general acceptance of the proposition that smoking could cause lung cancer, Mr McEachran had placed a great deal of emphasis on the number of pages to which a report ran, or to the number of pages of references, or to the number of articles referenced. His submission was that I should be impressed by these features. Mr Jones submitted that this might be seen to count against Mr McEachran's use of these documents. If he produced a 600-page report and cherry-picked half a dozen pages to put before the court, containing passages which were useful to his case, the difficulty was that the court did not see the remaining pages and did not know what other features were being brought to bear. As a result, there was material that I did not have and could not properly use in order to assess the validity of conclusions which were finally reached and on which Mr McEachran relied. Scientific truth was not determined by majority vote and scientific debate was not decided by the number of words used in arguing a position. A court of law was not entitled to determine issues between the parties that came before it on the basis of what most people believed, or even what everybody believed, but on the material that was presented. Counsel agreed that the point could be put in this way, that one should be that much more cautious of accepting a consensus view for the very reason that that was what it was and was therefore not perhaps being examined critically at the time it was held. Once the proposition became embedded into the culture, then there was no fresh mind brought to bear upon it and it was just accepted. The fact that it was accepted told us nothing about its truth. Reference was again made to what Lord Prosser said in Dingley v The Chief Constable, Strathclyde Police, quoted at para.[5.5].
[6.127]Of course, as counsel reminded me, his position was that on the evidence, amongst serious scientists for many years and indeed up to the present day, those who had considered the evidence and had applied their minds to the issues were still engaged in a debate about the cause of causes of cancer, including lung cancer, and doubts continued to be expressed about the causal connection between cigarette smoking and lung cancer. Professor Friend said that he thought that serious scientists had always challenged the causal hypothesis as the explanation for the association between cigarette smoking and lung cancer. It was also instructive to look at what Frenk and Dar 2000, in the passage discussed in Professor Gray's evidence, had to say about the effect of consensus within the scientific community.
[6.128]Mr Jones reminded me of the passage from USSG 1964, referred to in the evidence of Professor Idle:
"Statistical methods cannot establish proof of a causal relationship in an association. The causal significance of an association is a matter of judgment which goes beyond any statement of statistical probability."
One of the problems was that when one was looking at a statistical association, the effect of confounding had to be considered. Counsel referred to the passage in Berkson 1959 discussed by Professor Idle at para.[5.487]. It was not a ground of criticism of Professor Idle that he said that, even if there was such an association between A and B that B always followed A, he would still look for laboratory evidence: on the contrary, this was the correct view. For example, if an association was discovered between drinking milk and tuberculosis, such that everybody who drank milk contracted tuberculosis and no one who did not drink milk contracted tuberculosis, on the statistics alone one might conclude that it was drinking milk that caused tuberculosis, and the public health response might be to ban milk consumption. Of course, it was not the milk that caused tuberculosis, and laboratory experimentation could be carried out to discover the nature of the relationship that the statistics had revealed. This was consistent with the approach of Hill 1966, also referred to by Professor Idle. Professor Gray, Professor Idle and Dr Lewis all emphasised the importance of considering and, where possible, eliminating potential confounding factors by the scientific method.
[6.129]Illustrations of the problem of confounding in various contexts, and of the difficulties that confounding presented in understanding the association between smoking and lung cancer, appeared in the evidence. For example, in Pollack et al. 1984, in considering the association between lung cancer and alcohol consumption, adjustment was made for the potential confounding factors of age and smoking, and in Knekt et al. 1996, in considering the association between lung cancer and depressed mood, adjustment was made for potential confounding factors of age, education, geographic area, smoking, alcohol consumption and various other potential factors. In working on the association between lung cancer and family history of lung cancer, adjustment was made for the confounding effects of age, sex, cigarette smoking and occupational and industrial exposure: Ooi et al. 1986.
[6.130]Dr Lewis gave evidence that in order to control for a particular confounder, the potential confounder must have been identified and the study designed in order to control for it. Professor Gray gave evidence about Kendler et al. 1993, in which a control method was used in examining the association between smoking and depression. Dr Lewis gave evidence that, even if lung cancer only occurred in smokers, this would still leave open the question whether smoking caused lung cancer, lung cancer caused smoking or both had some common third cause. The conclusion of Kendler et al. 1993 was that the relationship between ever-smoking and major depression was not causal but was mediated largely or entirely through genetic factors which influenced the liability to both ever-smoking and major depression. Psychological factors had been implicated in carcinogenesis and had been linked with lung cancer in the context of various theories about which Professor Idle gave evidence.
[6.131]Professor Gray gave evidence that the fact that a change was observed after a drug was discontinued did not justify the inference that the change was caused by discontinuing the drug. He went on to explain that, for example, symptoms reported by smokers after stopping smoking did not, with the exception of increased appetite and decreased heart rate, appeared to be specific symptoms attributable to the absence of nicotine, but were similar to symptoms reported by people who gave up cherished habits of many kinds, including habits which did not depend on any substance at all.
[6.132]Dr James's evidence demonstrated that the link often made between the apparent increase in the incidence of lung cancer and the increased incidence of smoking in the first half of the twentieth century was confounded by a number of other factors, including improved methods of diagnosis, the changing age profile of the population, decreased incidence of other diseases such as tuberculosis, increasing awareness of lung cancer and changes in the profile of patients admitted as in-patients to hospital. He discussed Bandera et al. 2001, a report on the link between alcohol consumption and lung cancer, in which there was discussion of the need to consider the role of diet. He also discussed Darby et al. 2001, which postulated that the associations, both positive and negative, found between lung cancer and various dietary factors were to be explained by reference to a confounder. Finally, the difficulties presented by the association between smoking and drinking, diet, and socio-economic class were discussed by Professor Lewis in cross-examination.
[6.133]From the 1950s eminent scientists, notably Sir Ronald Fisher, cautioned that the association between smoking and lung cancer might not be causal but might reflect some third confounding factor, probably genetic or constitutional in nature. Scientific work had been carried out since the 1950s which provided support for this approach. At a general level, Professor Gray gave evidence to the effect that smokers and non-smokers differed from one another genetically and in personality. Smokers tended to have different personality characteristics from non-smokers, and these had a genetic basis. Professor Gray's evidence, which was consistent with the work of Warburton, was that there was a considerable interaction between the individual's personality and environmental factors, including social factors. Moreover, individuals with particular personality traits might be likely to find that smoking was helpful to them: for example someone who was inclined to anxiety and depression might find that smoking was helpful in ameliorating these conditions, while someone inclined to be aggressive might find smoking useful because it could calm him down. Recent work had shown that genetic factors influenced smoking behaviour. Professor Gray explained that genetic inheritance accounted for about half the variance of taking up smoking and about 70% of the variance of continuing to smoke. He referred to recent literature which supported the existence of a link between genetics and smoking behaviour: Kendler et al. 1993 and True et al. 1997. The latter paper reported on results which, when taken with results from other studies, were regarded as being consistent with the conclusion of an important genetic contribution to the risk of becoming a long-term smoker in men.
[6.134]There was evidence from Professor Idle and Dr Lewis that particular aspects of an individual's personality and emotional make-up might be linked to cancer development. Dr Lewis referred to Horne and Picard 1979, and evidence was given about epidemiological studies that a family history of lung cancer was a risk factor for lung cancer.
[6.135]Sir Ronald Fisher's point could be illustrated by reference to the facts of the present case, about which Professor Gray gave evidence: Mr McTear was a man who exhibited personality traits which tended to be characteristic of smokers and which would have given him reasons for smoking. He was a man with a marked family history of lung cancer. Aspects of his lifestyle illustrated further the problem of confounding. He had a stressful lifestyle, with features which were linked to lung cancer by Kissen. He suffered from influenza and other viral infections of the respiratory tract throughout his life; such infections could impair the immune system and immunosuppression had been linked to lung cancer. Previous respiratory diseases were a risk factor for lung cancer. He abused alcohol, and alcohol consumption was a risk factor for lung cancer. Evidence about these matters was given by Professor Gray, Professor Idle and Dr Lewis. There was also the question of the importance of vitamin A for maintenance of the bronchial epithelium and the link between vitamin A deficiency and carcinogenesis, and Dr Lewis had given evidence about those of low socio-economic status living in an urban area of west Scotland being at an increased risk of lung cancer.
[6.136]It had been said in opposition to Fisher's thesis that it might be difficult to envisage how genetic factors could account for the apparent increased incidence in lung cancer over time. But the evidence before the court was that it was not possible to tell whether or not the apparent increase in incidence was real and, if it was real, to what extent it was so. So, as Dr James had explained, we were left with an unknown. Similarly, it was impossible to tell on the evidence whether or not the statistical association between smoking and lung cancer was accounted for by the constitutional hypothesis or, if that hypothesis did not account for the whole association, to what extent the association was accounted for by constitutional factors.
[6.137]Given all of this, and given that cancer was a biological, not a statistical problem, Professor Idle was well qualified to express a view on whether smoking had been established as a cause of lung cancer. He noted repeatedly the limited understanding that science had of the mechanisms of cancer and the causation of the disease. He described the various theories of cancer causation and noted how theories that were once considered highly credible had been discarded at times, then revived. He described the inability of laboratory experiments to produce lung cancer in animals exposed to cigarette smoke, and the similar failure, despite long-standing efforts, to identify what ingredient or ingredients in cigarette smoke might be responsible for the development of lung cancer. He described the need for an understanding of the basic biology of cancer and the limitations of our understanding of this. Various theories of cancer development had been advanced over the years. Some, like that of viral causation, had been put forward, then seemingly rejected, then once again considered plausible. Others, such as cancer as a protein-based disease, or the role of ciliastasis, had fallen by the wayside. Others again, such as the theory that cancer involved changes in DNA, remained current today.
[6.138]In the course of his evidence Professor Idle considered the two-stage theory which had been broadly accepted by the end of 1964; but now this theory was not accepted and instead it was thought that there was a multi-stage process. He referred to the possibility that viruses might induce cancer, and work on viruses as cancer-causing agents was very much alive and continuing. Professor Idle discussed the competition between opposing theories favoured by the McArdle laboratory and the Chester Beatty Institute relating to protein and DNA. He said that there could be no consensus where these two institutes had not reached a common view. Having examined these and other theories he gave evidence that, to date, no theory explained or could explain the origins and development of cancer.
[6.139]Both Professor Idle and Dr Cohen gave evidence that laboratory studies had not produced lung cancer in animals exposed to cigarette smoke. What was interesting, counsel submitted, was not just that squamous cell carcinoma had not been induced in the lungs of laboratory animals, but that great care had been taken to create experiments which would produce positive results. For example, researchers satisfied themselves that cigarette smoke reached the lung in the mouse model. Professor Idle looked at the question of complex mixtures, and whether any ingredient had been identified as a cause of lung cancer, and concluded that it had not. He finally concluded that, in his judgment, cigarette smoking had not been established as a cause of human lung cancer and indeed the cause of cancer was unknown. Dr Cohen gave evidence that the majority of chemicals that had been shown to develop tumours in animals had been reported to show an increased risk in humans, and he could think of no examples where the human data were in conflict with the animal data. This rather underlined an expectation that when animal experiments were being carried out, they might produce a result to confirm that cigarette smoking could cause lung cancer. Dr Cohen gave evidence that studies had been carried out on animals in whom it had been demonstrated that cancer could be induced within their lifespan. Professor Platz gave evidence that it was not possible to distinguish between a smoker and a non-smoker, or indeed an individual with any other exposure that might be associated with lung cancer, on examination of pathological material.
[6.140]Finally, Dr Lewis gave evidence about the relationship that might be expected between the incidence of lung cancer and a decrease in the prevalence of smoking. In the MRFIT (see para.[5.845]) no difference had been found in lung cancer mortality, or in overall mortality, when a comparison was made between the "special intervention" and the "usual care" groups. At least, he said, this showed that the attributable fraction calculation was not valid. Counsel explained that this point was not developed because he was not presenting an epidemiological case and this arose from cross-examination. But he described this as "completing the circle". First, there was evidence doubting whether the apparent rise in the incidence of lung cancer in the first half of the twentieth century was in fact real; then there were questions about the components of the proof of a causal connection between smoking and lung cancer; there was statistical association, but then there seemed to be a view that one needed more than a statistical association; finally, this showed that there was material which pointed to the unwisdom of relying on the attributable risk fraction as the predictor of what would happen if an exposure were removed. More generally when exposure was removed, in fact diseases associated with smoking did not decline. While none of this was developed, it did bear on the question whether a proper defence had been put forward. Mr McEachran's assertion that it could not was unsustainable, when there was at least an indication of the complexity of the issues.
[6.141]Mr Jones said that, far from having lodged nothing in this case to vouch the proposition that the cause or causes of lung cancer were not known, they had lodged literally thousands of scientific papers, amongst which were some that showed the complexity of the issue. Evidence had also been given by some of the very experts who had been advising ITL over recent years on the question whether the causal connection was established. Accordingly counsel invited me to reject as unfounded the submission for the pursuer that there was no real defence on the general causation case.
[6.142]He also invited me to hold that the defence on individual causation was not made out. On the question of what might have caused Mr McTear's lung cancer, neither Professor Friend nor Dr McCarroll, who were the only witnesses who were asked for a view on the subject, gave evidence that the court could rely on for the conclusion that it did. Mr McEachran had made the point that none of the six experts said that there was any other cause of Mr McTear's lung cancer; neither Dr McCarroll nor Professor Friend was cross-examined to the effect that their evidence and diagnoses were inaccurate, it was just said that they were not entitled to make a diagnosis because they were not epidemiologists. Mr Jones made two points about this submission. First, the attribution of an individual's cancer to a putative cause was not diagnosis. Mr McTear's diagnosis was squamous cell carcinoma of the lung. Establishing the cause of this was a separate matter from the diagnosis of the disease. The published view of Doll and Peto, which Dr McCarroll accepted as correct, was that doctors could not tell in an individual what might have caused lung cancer: Peto and Doll 1992. She accepted that where a statistical association was found between smoking and a disease, there would be no way for the medical practitioner certifying deaths to know which of the incidences of these diseases to attribute to the habit. This was a view shared by Dr James, who gave evidence about James et al. 1992. This contained the statement that the difficulty lay in applying an epidemiological and statistical association to individual cases.
[6.143]Counsel submitted, further, that there was no evidence from any epidemiologist to suggest that it would be legitimate or appropriate to apply epidemiological and statistical associations to individual cases. The only person who attempted to do this was Professor Friend, who relied on attributable fraction. It was no doubt because of this difficulty that Sir Richard Doll was not invited to express any views on individual causation; his views on this were known.
[6.144]Professor Friend was in fact cross-examined at length on other possible causes. In many cases he was unable to assist, and he certainly had not applied his mind to the question of other possible causes and the need to exclude them before coming to a conclusion about smoking. Notice was given in the pleadings for ITL of studies which reported lung cancer to be statistically associated with many factors other than cigarette smoking. Some of these factors were related to Mr McTear's case. Professor Friend accepted that there were other risk factors. Given that the starting point for the pursuer's case was epidemiology, in order for her to establish to the court's satisfaction that one rather than any other exposure in Mr McTear's life caused his lung cancer, then there would have to be some attempt in the evidence to exclude the other possible causes and to explain why they should be excluded. There was no evidence on this. Having regard to the case of Wilsher, as discussed in Fairchild, this was fatal to the pursuer's case on individual causation. Some people contracted lung cancer who had never smoked, and if it could not be said one way or the other whether Mr McTear would not have contracted lung cancer but for smoking cigarettes, then the pursuer failed.
[6.145]It was misleading to submit, as Mr McEachran had done, that even ITL's witnesses accepted that cigarette smoking was the strongest risk factor for lung cancer and had the strongest associations. Only Dr Lewis was asked about the relative strength of risk factors and so on. He did not accept the use of the expression "high material risk factor" as one used by epidemiologists. He was prepared to accept that a strong association existed between cigarette smoking and lung cancer. Under reference to Dong and Hemminki 2001, he said that familial clustering had similarly strong associations. Under reference to Gillis et al. 1988a, he said that in west central Scotland the dose-response relationship between smoking and lung cancer peaked at about twenty cigarettes per day. The authors found that in an area of exceptionally high lung cancer incidence, there was a lack of increase of the relative risk of lung cancer at higher levels of cigarette smoking, and they were unable to explain this on the basis of confounding, bias or artefact. The low level of relative risk found at all levels of cigarette consumption coupled with the small increase in relative risk observed at the highest levels of smoking represented a paradox for an area with such a very high rate of lung cancer.
[6.146]Mr Jones submitted that the submission that the association between smoking and lung cancer was stronger than any other was not made out on this evidence. There was no evidence that was relevant in this case to allow strengths of association as they might apply to Mr McTear to be assessed. The court was being invited to use the epidemiological material in order to determine causation in an individual. It was clearly illegitimate to attempt to determine the cause of Mr McTear's lung cancer by having regard to relative strengths of association, because the strength of an association was determined for populations and not individuals, and because the strength of an association could vary from population to population. No witness gave evidence that smoking was the most likely cause of Mr McTear's lung cancer by reference to the strength of association in populations. So nothing could be drawn from strengths of association. Professor Friend's reliance on the attributable fraction was simply misconceived and was not a foundation, on any view, for drawing conclusions about the cause of lung cancer in any individual and in particular in Mr McTear. This evidence, the evidence from the public health reports and the evidence of the consensus view relied on by Mr McEachran took me nowhere, Mr Jones submitted, on the matter of individual causation, because they were all about disease in populations.
[6.147]Mr Jones submitted that on every issue on which the pursuer needed to succeed in order ultimately to establish liability against the defenders, she failed, and did so for want of sufficient proof. In answer to a question by me, as to what should be the outcome if the court was unable to decide one way or the other on the evidence, counsel referred to Rhesa Shipping Co S.A. v Edmunds [1985] 1 W.L.R. 948.
[6.148]In this case, the plaintiffs' motor vessel sank. The plaintiffs sought to recover, under policies of marine insurance, against underwriters, in respect of the loss of the vessel, claiming that the loss was occasioned by a peril insured against, which included "perils of the seas". The burden of proving this, on a balance of probabilities, lay on the plaintiffs. In discussing the requirements of this standard of proof, Lord Brandon of Oakbrook, in a passage at pp.955-956, referred to Sir Arthur Conan Doyle, The Sign of Four, in which Mr Sherlock Holmes is quoted as saying to his friend Dr Watson: "How often I have I said to you that, when you have eliminated the impossible, whatever remains, however improbable, must be the truth?" His Lordship went on to say:
"In my view there are three reasons why it is inappropriate to apply the dictum of Mr Sherlock Holmes, to which I have just referred, to the process of fact-finding which a judge of first instance has to perform at the conclusion of a case of the kind here concerned.
The first reason is one which I have already sought to emphasise as being of great importance, namely, that the judge is not bound always to make a finding one way or the other with regard to the facts averred by the parties. He has open to him the third alternative of saying that the party on whom the burden of proof lies in relation to any averment made by him has failed to discharge that burden. No judge likes to decide cases on burden of proof if he can legitimately avoid having to do so. There are cases, however, in which, owing to the unsatisfactory state of the evidence or otherwise, deciding on the burden of proof is the only just course for him to take.
The second reason is that the dictum can only apply when all relevant facts are known, so that all possible explanations, except a single extremely improbable one, can properly be eliminated. [...]
The third reason is that the legal concept of proof of a case on a balance of probabilities must be applied with common sense. It requires a judge of first instance, before he finds that a particular event occurred, to be satisfied on the evidence that it is more likely to have occurred than not. If such a judge concludes, on a whole series of cogent grounds, that the occurrence of an event is extremely improbable, a finding by him that it is nevertheless more likely to have occurred than not, does not accord with common sense. This is especially so when it is open to the judge to say simply that the evidence leaves him in doubt whether the event occurred or not, and that the party on whom the burden of proving that the event occurred lies has therefore failed to discharge such burden."
Counsel submitted that, although the circumstances of that case were quite different, the approach was applicable in any case where the question was whether or not the pursuer had discharged the burden of proof on a series of issues that would lead ultimately to a determination of liability.
Discussion: (1) General Causation
[6.149]I propose to say at this point only a brief word about the expert witnesses. The demeanour of only two of them requires comment. Sir Richard Doll (who, of all the expert witnesses, was the only one not to avail himself of my invitation to be seated while giving evidence), made clear by his demeanour as well as the content of his evidence with what disdain he regarded those individuals who disagreed with his conclusion that the causal connection between cigarette smoking and lung cancer was proved. Professor Hastings, who regarded himself as an advocate for greater measures of tobacco control, carried this into his courtroom manner and his tendency to argue with counsel rather than to answer questions. I am bound to say that none of Professor Friend, Sir Richard Doll and Professor Hastings seemed to me to be mindful of the need to be independent (see para.[5.18]), and each appeared to me to engage in advocacy to a greater or lesser extent. Beyond these comments, my impression of all of the expert witnesses was that they gave evidence in a manner appropriate to their professional standing and the context of the proof. I propose therefore to concentrate principally on the content of the expert evidence, to the extent necessary to explain the views set out in the paragraphs which follow.
[6.150]Mr McEachran did not seek to argue that the causal connection between cigarette smoking and lung cancer had been established by any branch of scientific inquiry other than epidemiology. He accepted that it was established on the evidence that the process by which lung cancer developed was not yet known (see para.[6.30]). He also accepted in effect, at para.[6.56], that the averment for ITL at p.16 of the Closed Record was proved, "that over several decades, an enormous research effort has been made to produce in the laboratory the kind of lung cancer reported to be statistically associated with smoking. However, researchers have been unable to produce such cancer in test animals exposed to fresh whole smoke."
[6.151]To my mind, this means that, despite counsel's criticisms of him, no issue was taken with the substance of Professor Idle's examination-in-chief from paras.[5.484] to [5.694]. In the latter paragraph he said that it was his judgment that cigarette smoking had not been established as a cause of human lung cancer. Indeed the cause of cancer was unknown. Moreover, the mechanisms by which lung cancer developed were not known. Researchers had not produced squamous cell lung carcinoma in laboratory animals by inhalation exposure to cigarette smoke. No constituent or group of constituents, as they existed in the complex mixture which was cigarette smoke, had been shown to be a cause of lung cancer in smokers. Provided that it is borne in mind that, as stated at para.[5.484], he had been asked to give an opinion based upon his own area of scientific expertise, these appear to me to be inevitable conclusions from his very impressive survey of all the relevant literature. His area of scientific expertise did not extend to epidemiology, and he was not asked to consider epidemiological studies in the course of his investigations. Epidemiology apart, no researcher would in my view have reached a conclusion different from that of Professor Idle.
[6.152]Professor Idle's research did not appear to me to have omitted reference to any publication (apart from the epidemiological literature and the reports and other publications based on it) which might have served to undermine his conclusions, nor did it appear to me that he misrepresented the substance of any publication to which he did refer. His own conclusions seem to me to have been fairly and objectively based on the literature he had considered. Whether or not they were justified depends, of course, on what a scientist with expertise in the relevant field is to be expected to take into account. What his evidence demonstrates is not simply that there is no basis in the literature relating to any branch of scientific inquiry other than epidemiology for holding that cigarette smoking can cause lung cancer, but that an enormous amount of effort, resources and ingenuity have been devoted to the pursuit of scientific inquiry on this issue, with essentially a negative result. If regard is had to his instructions to give an opinion based upon his own area of scientific expertise, Professor Idle appears to me to have been fully justified in stating that it could not be determined whether or not smoking caused Mr McTear's lung cancer.
[6.153]No issue was taken at all with the evidence-in-chief of Dr Cohen, who conducted what I regard as a convincing evaluation of the carcinogenicity studies reported in the scientific literature, in order to determine whether exposure of laboratory animals to cigarette smoke by inhalation or intratracheal administration resulted in the development of squamous cell carcinoma of the lung. As stated at para.[5.758], he reported that none of the inhalation and intratracheal carcinogenicity studies in the various animal species there referred to, and as reviewed by him, showed a statistically-significant increase in squamous cell carcinoma of the lung following exposure to cigarette smoke and indeed none of the authors of these studies reported a statistically-significant increase for this carcinoma. I was also impressed by his critique, at paras.[5.759] to [5.764], of Dalbey et al. 1980, on which IARC 1986 relied for the statement at p.194 (see paras.[5.45] and [5.759]) that, in one study involving long-term exposure of rats to cigarette smoke, tumours of the respiratory tract were induced. His view was that on the evidence that was before the working group and discussed in the monograph, they were not entitled to express this conclusion, having regard to the defective reporting of the results in Dalbey et al. 1980. As I understood it, Dr Cohen's evidence on this matter was not disputed by Mr McEachran. The consequence is that support for the statement in IARC 1986 is no longer there. Dr Cohen's evidence therefore reinforces what I take from Mr McEachran's reliance on the epidemiology alone, which is that, this apart, no scientist with appropriate expertise who studied the relevant literature would conclude that it had been established that cigarette smoking could cause lung cancer, let alone that it caused Mr McTear's lung cancer.
[6.154]The results of experiments on animals do not necessarily apply to humans, though many in the scientific community must have regarded animal experiments as being capable of yielding results of relevance to the causation of lung cancer in humans, otherwise there could have been no justification for the expenditure of so much money and effort on animal experiments. It appears to me to be well established on the evidence that for many years epidemiological studies were regarded as serving to yield hypotheses, which could then be tested by properly constructed scientific experiments. On my reading of the evidence, it was principally on this basis, to test a hypothesis, that experiments were carried out at the Harrogate Laboratories, and not because it was already accepted by the tobacco industry that the causal connection between cigarette smoking and lung cancer had been established. It was agreed on all sides that, for ethical reasons, no scientific experiment of this kind, which would have involved, as part of a randomised controlled trial, the introduction of a group of randomly selected humans to cigarette smoking, could be conducted. So the animal experiments were of particular importance. The absence of support from the results of experiments on animals is not critical, but it is significant, because proof of the causal connection between cigarette smoking and lung cancer therefore depends solely on the conclusions to be drawn from the epidemiological studies, which on one view of the scientific approach could be regarded as yielding no more than untested hypotheses. Whatever view is taken, however, the pursuer's case stands or falls on what has been proved before me about the epidemiological studies which have led to the judgment that the causal connection is proved.
[6.155]Everything then depends on the view that I take about the evidence relating to the epidemiology of cigarette smoking and lung cancer. What is clear, from the authorities discussed in paras.[5.2] to [5.17], is that I have to consider whether the evidence of any of the expert witnesses has imparted to me special knowledge of the subject-matter of epidemiology, including published material, lying within the witness's field of expertise, so as to enable me to form my own judgment about it and the conclusions to be drawn from it. This is particularly so because it was agreed by Sir Richard Doll, and (subject to what I have to say about his expertise) by Professor Friend that the determination of the question whether or not the statistical association between cigarette smoking and lung cancer was causal itself required an exercise of judgment to be formed in light of all the available, relevant evidence. There is a statement to this effect in USSG 1964, p.20, quoted at para.[5.211] and elsewhere in this Opinion. This is: "The causal significance of an association is a matter of judgment which goes beyond any statement of statistical probability." Not only did Sir Richard Doll agree with this, he said, also at para.[5.211], that a conclusion had to be formed on the evidence as a matter of judgment, as in a court of law. He said that in addition to the strength of the association all other relevant evidence had to be considered by an epidemiologist, in the same manner as a judge would do. I am satisfied that it is not open to me to form my judgment on the evidence without being taught how to do epidemiology to a sufficient extent, and without being provided with sufficient factual material, to enable me to decide whether it is proved, at least on the balance of probabilities, not only that there is an association between cigarette smoking and lung cancer, but that the proper conclusion to draw from this is that there is a causal connection between them.
[6.156]I cannot say that I have had full instruction in this, but I have picked up some snippets along the way. What is clear to me at the outset is that epidemiology is a discrete branch of scientific inquiry, or academic discipline, with its own peculiar terminology and techniques. It is no more part of medicine than it is of public health or statistics, though it draws on and contributes to all three. I have no reason to think that Sir Richard Doll, for example, who is regarded as one of the leading figures in epidemiology, would regard a consultant physician as being qualified to express views about epidemiology without proper instruction in that discipline.
[6.157]Epidemiology, as I understand it, is in itself the study of patterns of disease occurring in human populations and the factors that influence these patterns. An epidemiologist may collect primary data, by conducting a survey, or secondary data, derived from other researchers' primary data. Consideration requires to be given to bias, such as selection bias, information bias or recall bias, and to confounding, which I understand to be a variable (usually unrecognised) that influences the observed relationship between an exposure and outcome. An exposure may be either exogenous, such as exposure to asbestos at work, or endogenous, such as a genetic defect. An association may be found between an exposure and a disease which may be judged to be statistically significant, after consideration of the confidence interval. This is a range of values likely, with a specified degree of certainty, to contain the true population figure for a variable drawn from a sample study.
[6.158]If an association between an exposure and a condition is judged to be statistically significant, after taking account of the foregoing considerations, that in itself does not constitute a judgment that there is a causal connection between the exposure and the condition. The distinction between association and causation is not always recognised, and clearly gives rise to confusion in the minds of those who are insufficiently instructed in epidemiology. The finding of an association between an exposure and a condition or disease, even if judged to be statistically significant, does not of itself connote that a causal connection between the two is established. This is a matter for a further exercise of judgment, taking account of such criteria as the consistency, the strength, the specificity, the temporal relationship and the coherence of the association (see USSG 1964, p.20, referred to at para.[5.729]). This must, I think, especially be so when, in the view of Sir Richard Doll, seen in the passage in Doll 1997 quoted at para.[5.205] cigarette smoking is not a necessary cause nor a sufficient cause of lung cancer, and Dr James at para.[5.476] agreed with this.
[6.159]The concept of relative risk requires discussion. This, as I understand it, is used to compare the incidence of a disease or condition in a group with a particular exposure to those without it. It is thus related to the concept of association, and is neutral: it does not connote that a causal connection is established. The use of the word "risk" in epidemiology appears to have led to some misunderstanding on the part of those unfamiliar with the terminology of this discipline. In ordinary language, "risk" in its primary sense refers to exposure to a hazard or danger, and carries the connotation of a potential causal connection between the risk and the subsequent misfortune or loss, should that eventuate. This has, in my view, led to a serious misunderstanding on the part of Professor Friend, who seems to have regarded the relative risk derived from a comparison of the incidence of lung cancer in smokers and non-smokers, which is such as to yield a positive association between the exposure and the disease, as connoting the establishment of a causal connection between the two. This is not so, though the relative risk may be of a magnitude such that a positive association may be judged to be strong enough for a causal connection is established.
[6.160]From what I have seen of the scientific literature, it appears possible to divide it into three categories, which I shall call the primary, the secondary and the tertiary literature. The primary literature contains, in Professor Gray's useful phrase (see para.[5.41]), the "archival data". In the field of epidemiology, it would be expected no doubt to explain the study design, the measures taken to control for bias and confounding, the statistical techniques used to determine whether or not an association has been found between an exposure and a condition or disease, such as the use of a confidence interval, and the process of reasoning which leads to any conclusions about the significance of the association and any judgment which is formed about a causal connection between the exposure and the condition or disease. There is, as I understand it, an expectation of transparency in the primary literature, so that the authors' work can be subjected to the scrutiny of their peers. Indeed, in many cases a paper is subjected to peer review before being accepted for publication in a learned journal. The scope for such scrutiny is central to the scientific process, because if a conclusion is based on sound research it should be capable of subsequent replication. A good example of this process may be found in Dr Lewis's discussion of Doll et al. 1994 at paras.[5.832] to [5.838], including the statement at para.[5.834] that he found the paper difficult to understand because he did not see the numbers behind it.
[6.161]What I call the secondary literature takes the form of review articles, where data from more than one publication in the primary literature are drawn together and re-evaluated. This process may serve to produce more reliable results, as being derived from a larger dataset which is the aggregate of the data in other studies, and may also serve to demonstrate errors or anomalies in previous studies. What I call the tertiary literature is different from the secondary literature because it involves the examination of both the primary and secondary literature without performing the kind of exercise which is done in the case of a review article. From what I have seen of them, documents such as USSG 1964 and IARC 1986 fall into this category: the authors conducted no original research themselves for the purpose of compiling the reports, nor did they subject data to the kind of process that would be used in a review article. Instead they act as compendia for summaries of numerous publications (as can be seen from the extensive lists of references), and the conclusions are therefore derived from a comprehensive, though not necessarily exhaustive, examination of all the relevant literature.
[6.162]I can say with confidence that no evidence was led about the primary literature which was sufficient to impart to me special knowledge of the relevant subject-matter and to enable me to form my own judgment about it and the conclusions to be drawn from it. This could have been done: it is clear that the survey of British doctors, on which Sir Richard Doll and colleagues have worked for many years, is regarded as a classic of its kind, both because of the pioneering nature of the research, a preliminary report of which was published as Doll and Hill 1950, and because this has been followed up with subsequent papers over several decades. I could at least have been shown these papers, which I assume disclosed the data, the statistical techniques and all the other considerations which led to the authors' conclusions, so that I could see for myself whether these conclusions were soundly based. The opportunity was there, with Sir Richard Doll in the witness box, and indeed Professor Friend for one thought that evidence would be given about this survey. Warning had been given on behalf of ITL, as early as the specification of documents referred to at para.[1.24], that Sir Richard Doll's data were of potential interest to the court. But in the event no attempt was made to show me the data.
[6.163]The fact that I have not been taken to any of the primary literature about the survey of British doctors, or indeed any other epidemiological study in which the conclusion was reached that there was a causal connection between cigarette smoking and lung cancer, appears to me to constitute a fundamental defect in the presentation of the pursuer's case. As has been seen, many were persuaded about the conclusions of Doll and Hill, but others were not. Those who were must have done so because they had the opportunity of considering what had been published about the data, the statistical techniques and so on and regarded them as sufficient to justify the conclusions. Those who were not persuaded must also have had the opportunity of considering the primary literature. I cannot believe that any scientist of any standing would have reached a view, either in favour of or against Doll and Hill, on the basis of a reading of no more than their conclusions. Yet I have no basis for saying why those who were persuaded were right to be persuaded, and those who were not persuaded were wrong. A mere head count will not do.
[6.164]This is particularly so when regard is had to Sir Richard Doll's evidence about those who disagreed with him. No attempt was made by him to explain why it was that they were wrong to disagree with him. They were all, on the face of it, people of some degree of professional standing who had put up reasoned objections to his conclusions. A reasoned response would have served to show why they were wrong. Yet Sir Richard relied before me principally on ad hominem arguments of a kind which is surely unacceptable in rational academic debate. His comments about Fisher may be read at paras.[5.215] to [5.221], about Berkson at paras.[5.222] to [5.228], about Seltzer at paras.[5.244] to [5.248], about Yerushalmy at paras.[5.229] to [5.232], about Eysenck at paras.[5.233] to [5.237] and [5.254], about Burch at paras.[5.239] to [5.243] and [5.250] to [5.251], about Oldham at para.[5.253], about Stern at para.[5.255], about Gwynne Jones at para[5.256], about Feinstein at paras.[5.258] to [5.259], about Passey at paras.[5.260] to [5.261], about Little at para.[5.273], about Tokuhata at para.[5.274], about Hueper at paras.[5.277] to [5.280] and about Rosenblat at paras.[5.268] to [5.269]. I can find little in these passages beyond assertions that those who disagreed with Sir Richard were wrong, coupled from time to time with epithets which I quite frankly found it unbecoming for a man of his stature to have chosen to use. If Sir Richard succeeded in winning over any of those whom he had previously failed to persuade, it cannot have been with these words.
[6.165]Great reliance was placed on Doll 1997, and in the course of his evidence-in-chief Sir Richard was taken over much of the text of this lecture. But I am unable to regard it as anything more than a form of memoir, in terms of self-congratulation no doubt appropriate to the occasion, but unilluminating as to the reasons why Sir Richard was right and those who disagreed with him were wrong. That is to say, he did not purport to publish his research in the lecture. While it was an interesting retrospective overview of the history of the debate, and served to establish that as a matter of fact there had been general acceptance of his conclusions, it did not attempt to enter into the merits of the debate.
[6.166]Mr McEachran's main argument, as I understood it, was that the conclusion that cigarette smoking could cause lung cancer had met with general acceptance in the scientific community by the late 1950s, was accepted by the media in the 1970s, was taught at medical schools and reflected in textbooks, and could be seen stated in a series of substantial multi-disciplinary reports, which he called the "multi-doctor studies", listed at para.[6.30], to the extent that the conclusions of IARC 1986 had never been challenged. This is all very well, but I have to say that I am reminded of the Bellman in Lewis Carroll's The Hunting of the Snark, who said: "What I tell you three times is true". But however often a conclusion may be repeated, it is only as sound as the research on which it is based, and of this I have seen none. However eminent and numerous the authors of a report may be, however many articles they may have read before preparing their texts, however many pages their reports may run to, are to no avail if I am then shown no more than the conclusions reached after all this effort. It is no good to tell me that a report is 400 or 600 pages long, and indeed to ask me to weigh the report in my hand, as Mr McEachran at one time asked me to do with UKHC 2000 Vol.II, and its list of references extends to several hundred items, without letting me see any of the text on which the conclusions are based. Indeed, as Mr Jones pointed out, the very length of a report may emphasise the inappropriateness of going simply to its conclusions: the length shows how much ground there was to cover before the conclusions could be stated. The conclusions, taken on their own, are no more than oracular pronouncements.
[6.167]Although evidence was taken from Professor Friend during his examination-in-chief about the conclusions of some of these reports, it became apparent in cross-examination that he was not qualified to express any view as to whether or not these conclusions were justified. He said repeatedly that he was not an epidemiologist: see paras.[5.95], [5.116], [5.119], [5.138] and [5.147]. I cannot regard him as being of any assistance in determining the question whether the conclusion that cigarette smoking can cause lung cancer is justified on the basis of the epidemiology. Indeed, for all the reasons given by Mr Jones in his submissions at paras.[6.64] to [6.85], I am unable to accept his evidence on any other issue of importance in this case. Sir Richard Doll was the only witness led on behalf of the pursuer who was in a position to give evidence which would enable me to form my own judgment about this issue, and for all the reasons I have given I would regard this opportunity as having been missed. I had no more than his ipse dixit. And no doubt it was because of this that the decision was taken by Mr Jones not to ask Dr Lewis, when in due course he gave evidence, about the issue of general causation: there was by then no case for ITL to answer.
[6.168]Because of these defects in the pursuer's case as presented to me there is little more that I require to say about the expert evidence bearing on general causation. I should however add that I accept the evidence of Dr James, which was subjected to little challenge, that it could not be determined how much of the apparent rise in lung cancer mortality between 1900 and 1950 was real because of changes in population; in diagnosis and treatment; in medical knowledge and practice; in the role of hospitals; in the availability of medical care and in death certification and general statistical methods. This view was based on what appeared to me to be a comprehensive review of the literature and was shared by other pathologists. In consequence, doubt is cast on any epidemiological study which states that during that period there was a correlation between an increase in cigarette smoking and a subsequent increase in lung cancer mortality. I do not think it necessary to say more about this, because I was never taken to the primary research in which such a claim may have been made.
[6.169]A remaining point is that I accepted the evidence of Professor Platz about the defects in the Auerbach studies, Auerbach et al. 1957 and Auerbach et al. 1961. These may be seen to have had defects, not only for the internal reasons to which Professor Platz pointed, but also because his own knowledge of VA hospitals served to cast doubt on the reliability of Auerbach's original data. This in turn serves to undermine Dr Kerr's reliance on Auerbach et al. 1961 and subsequent studies, Auerbach et al. 1975 and Auerbach and Garfinkel 1991, which essentially repeated the findings in the 1961 paper. Accordingly his view of the significance of squamous dysplasia may be affected. But since this was not ultimately an important part of the pursuer's case I do not think it necessary to address it further. What Professor Platz's critique of Auerbach, along with Dr Cohen's of Dalbey et al. 1980, Dr Lewis's of Colby et al. 1995 and Professor Gray's of Henningfield 1984, which I mention elsewhere, is that there is good reason from these and other examples to think that the tertiary literature cannot necessarily be relied upon. If the conclusions of papers such as these in the primary literature may on critical examination be found to be unsound, then there may be more: and in that event, if the primary literature has been accepted without criticism by the authors of the tertiary literature, the latter may not be as reliable as one would expect.
[6.170]For all these reasons, and in addition for the reasons advanced in detail by Mr Jones, which I accept, in my opinion the pursuer has failed to discharge the burden of proving, in accordance with the requirements of the law of evidence relating to expert witnesses, that cigarette smoking can cause lung cancer. I am forced to say, following Lord Brandon in Rhesa Shipping Co S.A. v Edmunds, referred to at paras.[6.147] to [6.148], that the state of the evidence is such that I simply cannot decide one way or the other whether cigarette smoking can cause lung cancer. Since the burden of proving this rests on the pursuer, she has failed to discharge this burden, and accordingly this branch of her case fails.
[6.171]I conclude this passage by emphasising that I am in no way finding that cigarette smoking cannot or does not cause lung cancer: I am simply saying that, approaching the evidence with an open mind, as I am bound to do, and applying the law relating to expert evidence, I am unable to find it proved that cigarette smoking can cause lung cancer.
(2) Individual causation
[6.172]I turn now to the question of individual causation, that is to say whether it is proved on the balance of probabilities that cigarette smoking caused Mr McTear's lung cancer, in the sense that but for his smoking of cigarettes he would not have contracted it. I require to assume, for the purpose of considering this question, that, contrary to what I have held in preceding paragraphs, the evidence led before me is sufficient to establish that cigarette smoking can cause lung cancer, i.e. I have to assume that the pursuer's case on general causation succeeds. If so, this would have been because I accepted that sufficient evidence had been led about the epidemiology relating to the association between cigarette smoking and lung cancer to enable me to form my own judgment about it and to conclude that there was a causal connection between them. Nevertheless, I bear in mind that on any view of the matter only a relatively small minority of smokers contract lung cancer: see, for example, Dr Lewis's evidence at para.[5.796].
[6.173]The question then comes to be whether, if a causal connection is established between cigarette smoking and lung cancer in the general population on the basis of epidemiology, that conclusion can be applied to the question whether an individual's, and in particular Mr McTear's, smoking of cigarettes caused his lung cancer. Putting it at its simplest, as Mr McEachran sought to do, the question is whether, if in 90% of cases of lung cancer it was caused by cigarette smoking, it could be said in any individual case that it was more likely than not that his smoking of cigarettes caused his lung cancer.
[6.174]It was not suggested that it could be established by any other means in any individual case that the lung cancer was caused by cigarette smoking. Mr McEachran agreed that the presentation of lung cancer was the same whether the individual was a smoker or a non-smoker. There was no evidence that it was possible by physical examination, by biopsy, by post mortem examination or by any other medical or scientific means to establish that in an individual case of lung cancer it was caused by smoking; or, to put it another way, without the taking of a history from the patient, it was not possible to form any opinion about the cause of his lung cancer.
[6.175]As has been seen, counsel were divided on the use of the word "diagnosis". According to the Oxford English Dictionary, "diagnosis" in its medical sense means "determination of the nature of a diseased condition; identification of a disease by careful investigation of its symptoms and history; also, the opinion (formally stated) resulting from such investigation." While I can see that the taking of a history may be relevant to the diagnosis of a condition or disease in some cases, this is not such a case, in the absence of any distinguishing features between lung cancers in smokers and lung cancers in non-smokers. I do not overlook that Dr Kerr said (at para.[5.343]) that when specimens were submitted to him for examination, he might or might not be told the smoking history of the patient, and if he was given any history at all, it would more often be in the unusual situation where such a specimen was sent to him in a non-smoker, simply to highlight the fact that he was being asked whether the patient had lung cancer and he ought to know that the patient was a non-smoker. It should be noted, however, that Dr Kerr did not say that the history assisted him in the performance of his task of diagnosis; and it may be doubted, from his account, whether it assisted the physicians. In my opinion what can properly be regarded as diagnosis in the circumstances of the present case, when considering Mr McTear's lung cancer, was that he had contracted squamous cell carcinoma of the lung. That it may have been caused by his cigarette smoking was no more part of the diagnosis than a history of a skiing accident, for example, as part of the diagnosis of a fracture of a vertebra. A history of cigarette smoking in an individual may of course be added to the statistics upon which epidemiology is based, but it is not part of the diagnosis in the individual.
[6.176]The difficulty of using statistics derived from epidemiological studies in determining causation in individual cases is well-recognised. In Callum 1998, referred to at para.[5.802], it was stated:
"People who have never smoked cigarettes die from diseases that smoking can cause, and to that same extent some cigarette smokers too can die of the disease but not as a result of their smoking. The matters used to estimate the number of deaths caused by smoking are all based on a proportion of deaths caused by smoking, and cannot be traced back to individuals."
Dr Lewis said that he agreed with this statement. In Peto and Doll 1992, referred to in the evidence of Dr McCarroll at para.[5.25], the authors stated that for most deaths that were in fact due to tobacco there was no reliable way to know that those particular deaths were due to tobacco. Even though the epidemiologist might be able to say with confidence, in the example given, that about half of the deaths from myocardial infarction were due to tobacco, "there would be no way for the medical practitioners certifying those deaths to know which ones to attribute to the habit." Dr McCarroll accepted this. Dr James's view, as stated in James et al. 1992 (see para.[5.450]) was that the difficulty lay in applying an epidemiological and statistical association between smoking and several potentially fatal diseases to individual cases.
[6.177]As Sir Richard Doll stated in Doll 1997, in the passage quoted at para.[5.205], cigarette smoking is not a necessary cause nor a sufficient cause of lung cancer, but it can be an important cause (as few people would have developed the disease if they had not smoked). If that is true in a population, then all the more so is it true in an individual case. It is striking that Sir Richard Doll was not asked for his opinion whether cigarette smoking caused Mr McTear's lung cancer; I agree with Mr Jones's submission that the inference is that this was because it was impossible to tell, on the basis of epidemiology, whether or not cigarette smoking had caused any individual case of lung cancer.
[6.178]Having regard to what I have already said about Dr McCarroll, I mean no disrespect to her when I express the view that she was not qualified to conclude that Mr McTear's lung cancer was probably caused by his cigarette smoking. As I have said, I do not regard the issue of causation as being part of her diagnosis. It may serve the purposes of a general practitioner well enough, particularly when she has been taught at medical school that most cases of lung cancer are caused by cigarette smoking, to reach such a conclusion in an individual case. But she had never had occasion to examine the underlying science, with particular reference to the question whether statistical methods used in epidemiology could be applied to the issue of causation in individual cases.
[6.179]In my view, the pursuer's case on individual causation depends on the evidence of Professor Friend. As I have said, I have to assume for present purposes that it has been proved before me, on the basis of the epidemiology, that cigarette smoking can cause lung cancer. So I assume that it has been proved that 90% of cases of lung cancer are caused by cigarette smoking. If this is taken as the starting point, then Professor Friend's clinical experience does no more than bear out the statistics upon which the epidemiology is based: it does not add to the conclusion that there is a causal connection between cigarette smoking and lung cancer. The real question is whether, notwithstanding the views referred to above, Professor Friend was correct in making use of statistics to reach conclusions in individual cases.
[6.180]I find Dr Lewis's evidence entirely convincing. It is consistent with the above views and gives extensive reasons for concluding that epidemiological data cannot be used to draw conclusions about the cause of disease in any individual. This opinion was hardly subjected to cross-examination, except in a brief passage at para.[5.843], the rest of his cross-examination being taken up with epidemiological issues. In Mr McEachran's submissions no attempt was made to argue that I should not accept Dr Lewis's conclusion, still less to discredit the extensive reasons he gave for reaching it. It is accordingly sufficient in my view to state that I accept, for the reasons given by him, and under reference to the literature referred to by him, that epidemiological evidence cannot be used to make statements about individual causation. The information provided in an observational epidemiology is generally such that it can neither confirm nor refute a causal relationship, particularly when the exposure in question is not specifically associated with a certain condition (i.e., the exposure is always associated with the condition, and vice versa). Epidemiology cannot provide information on the likelihood that an exposure produced an individual's condition. The population attributable risk is a measure for populations only and does not imply a likelihood of disease occurrence within an individual, contingent upon that individual's exposure. The fact that cases and non-cases can emerge both from the unexposed and the exposed groups show that the likelihood of the individual occurrence cannot be reliably predicted from his or her exposure group membership alone. The group estimates obscure the underlying heterogeneity of the population, so that it is entirely possible that other group memberships besides exposure, like genetic profile, socio-economic status, workplace, diet and other exposures make a major contribution to disease occurrence. The question of using epidemiological data for individual causation raises the problem of identifying a particular individual who was harmed by the exposure. While models such as the assigned share concept, derived from attributable fractions, have attempted to deal with this, they suffer from the limitations mentioned by Dr Lewis. The attempt to identify exposure as the sole cause of disease in an individual produces a statement counter to fact in that it implies that the individual would have remained healthy if the exposure had not occurred. This, as Dr Lewis said, is not provable and cannot be derived from epidemiological data.
[6.181]There is ample evidence (of which it is sufficient to refer to the papers discussed by Dr Lewis at paras.[5.810] to [5.828], that there are risk factors for lung cancer other than cigarette smoking. Some of these risk factors were present in Mr McTear's case, as submitted by Mr Jones at para.[6.135]: personality traits, family history of lung cancer, stressful lifestyle, viral infections of the respiratory tract, alcohol abuse, vitamin A deficiency, low socio-economic status and residence in an urban area of west Scotland. On the evidence, a non-smoker exposed to any or all of these risk factors can develop lung cancer. Whether or not there is a causal connection between any of these risk factors and lung cancer is a matter of judgment, which I do not require to exercise for present purposes. What is significant is that in Mr McTear's case these risk factors were present and, if epidemiology can be used, as Professor Friend sought to use it, to determine whether Mr McTear's cigarette smoking caused his lung cancer, then account requires to be taken of these other risk factors. I do not agree with Mr McEachran's submission that it was for ITL to prove that Mr McTear's lung cancer was due to some cause other than cigarette smoking. The burden of proving individual causation is on the pursuer, and in assessing the evidence of Professor Friend I am entitled to have regard to the extent to which he considered and, if so, found reasons for discounting other possible causes.
[6.182]In the end, it was demonstrated all too clearly in the cross-examination of Professor Friend that he did not understand the concept of attributable fraction and how it could not be used to determine the probability of causation in an individual. This of course was because, as he himself said repeatedly, he was not an epidemiologist; and the cross-examination only served to demonstrate that he had no real understanding of the concepts and techniques used in that branch of science.
[6.183]As Mr Jones said, no witness gave evidence, apart from that already discussed, that but for Mr McTear's smoking he would not have developed lung cancer; no witness said that it was more likely than not that his lung cancer was caused by his smoking, except on the basis of Dr McCarroll's general knowledge and on the basis of Professor Friend's misapplication of attributable fraction. For the above reasons I do not regard the evidence of either of these two witnesses as constituting an acceptable basis for holding it proved that cigarette smoking did cause Mr McTear's lung cancer.
[6.184]The problem ultimately is that, as was demonstrated by the evidence, in the state of modern science there is no way of telling whether in an individual case, such as that of Mr McTear, a lung cancer was caused by cigarette smoking. Still less is there any way of telling whether a smoker who has contracted lung cancer has in fact contracted it as a result of some cause other than smoking, or would not in any event have gone on to contract lung cancer even if he had not been a smoker. This last point is necessarily so, when there are risk factors other than smoking which have been identified as being associated with lung cancer, and when on any view of the matter about 10% of cases of lung cancer are found in non-smokers. The fallacy of applying statistical probability to individual causation has already been recognised judicially, in the passage from the opinion of Lord Mackay of Clashfern in Hotson v East Berkshire Area Health Authority quoted at para.[6.28].
[6.185]In the result, I am not in a position to hold, and do not purport to hold, that Mr McTear's lung cancer was not caused by his cigarette smoking. But I am not satisfied, on the basis of the evidence led before me, that it has been proved that it probably was caused by his smoking, in the sense that it is more likely than not that but for his smoking he would not have contracted lung cancer. The pursuer fails on this branch of the case also.
Addiction
[6.186]I turn now to consider the averment for the pursuer that:
"Tobacco is addictive in the sense that once individuals such as [Mr McTear] have started smoking it is difficult for them to wean themselves off the habit. It is more addictive than cocaine." (Closed Record p.22D-E)
This is supported by a reference in the pursuer's pleadings to USSG 1988. ITL deny these averments and aver that smoking is correctly regarded as a habit and not an addiction. They go on to aver that people choose to smoke for a variety of reasons, that smokers derive benefits from smoking, that over the years many millions of smokers have stopped smoking through choice, and that while some smokers may find it difficult to stop smoking, smokers who choose to stop smoking are able to do so.
[6.187]It should be noted that there is no reference in the pursuer's pleadings to DSM-IV or ICD-10. The position of ITL, as stated in the letter by the Corporate Affairs Director of Imperial Tobacco Group plc dated 20 January 2000, was that they agreed that nicotine could be regarded as addictive by reference to DSM-IV and ICD-10 but this did not mean that smokers were unable to stop smoking if they chose to do so (see para.[2.11]). No evidence was led about the terms of ICD-10, and the terms of DSM-IV were only referred to in the evidence of Professor Friend at para.[5.167], where he agreed that the passage in the introduction relating to the use of DSM-IV in forensic settings was in general terms the correct approach to take. This passage urged the use of caution in the drawing of conclusions from the fact that an individual's presentation met the criteria for a DSM-IV diagnosis. So I am unable to give further content to the position of Imperial Tobacco Group plc before the House of Commons Health Committee, and I must consider the averments for the pursuer on their own terms.
Submissions for Mrs McTear
[6.188]Mr McEachran submitted that the averments for ITL were an example of inappropriate pleading, having regard to the position adopted before the House of Commons Health Committee, and by Mr Davis in evidence. He relied on passages in USSG 1988 and RCP 2000. The former were brought out in the evidence of Professor Friend at paras.[5.66] to [5.73] and in the evidence of Professor Gray at paras.[5.418], [5.443] to [5.444], and the latter in the evidence of Professor Friend at paras.[5.74] to [5.83] and in the evidence of Professor Gray at para.[5.394]. Reference was also made by counsel to IARC 2004, of which only the conclusions were available at the time of the proof.
[6.189]Mr McEachran submitted that the evidence showed that it was difficult for smokers to give up smoking. The evidence was that it was nicotine in the cigarette which was the drug which caused the craving. That was the conclusion of "these two large multi-doctor reports". In further discussion Mr McEachran submitted that there were two factors working together, "the positive side, to get the benefits that smoking gives, and also the withdrawal effects from the removal of the nicotine".
[6.190]Counsel relied on Professor Friend's evidence in this regard. This, he submitted, demonstrated that there were many people who found it extremely difficult to give up smoking. They were driven by two features mentioned by Professor Friend, the need to have another cigarette, and the symptoms of withdrawal. The overwhelming evidence was that it was nicotine in the tobacco which caused addiction, the difficulty of giving up. Counsel said that he was unwilling to explore the concept of addiction further than to rely on the fact that many, if not most, cigarette smokers did indeed find it very difficult to give up.
[6.191]Mr McEachran submitted that Professor Hastings, on whose evidence he also relied, came across as an articulate and able Professor of Social Marketing, who was obviously well thought of. He succeeded in getting his message across in a number of areas. Mr McEachran agreed with my impression, that Professor Hastings was rather determined to express a point of view which was not necessarily an answer to the question he was being asked. This was, he said because he had strong views on the matter. Mr McEachran relied on his evidence for the effects of advertising, which encouraged people to keep on smoking when they might otherwise have given up in response to public health campaigns and publicity in the media about the risks to health of smoking. This meant that there was a very confused picture indeed, with different people saying different things. MacAskill et al. 2002, of which Professor Hastings was one of the authors, demonstrated why it might be particularly difficult for Mr McTear, having started smoking and being a heavy smoker, to be able to give up.
[6.192]Mr McEachran submitted that Professor Gray was prepared to accept that smoking was addictive in a descriptive sense. If this meant what was averred on behalf of the pursuer, that it was difficult for people who started smoking to wean themselves off the habit, then there was no dispute. But Professor Gray denied that nicotine was the drug which caused the addiction. He was prepared to say that it would have a contributory influence. Professor Gray's evidence represented a minority view from a tobacco man. He was a psychologist and not a doctor. Some of his research had been funded by the tobacco industry. This meant that I had to look carefully at his evidence to see whether there might be a bias towards that industry. His evidence about addiction needed to be assessed against the admission of ITL to the House of Commons Health Committee, that nicotine could be regarded as addictive by reference to DSM-IV and ICD-10. He accepted that he was out on a limb compared with many distinguished scientists and doctors.
[6.193]Mr McEachran made the point that USSG 1988 was a very impressive document. Over fifty scientists were involved and it extended to 600 pages. Their conclusions were that cigarettes were addicting and nicotine was the drug in tobacco which caused addiction. So Professor Gray was going against the views of a much larger body of scientists and doctors. In any event he accepted that a smoker might find it very difficult to stop smoking, which was the pursuer's case.
Submissions for ITL
[6.194]Mr Jones submitted that it was quite inappropriate on the evidence to seek to dismiss Professor Gray's evidence, as Mr McEachran had done, by calling him a "tobacco man". He was the only witness who was qualified to give opinion evidence on the question of addiction. He was in fact a distinguished Professor of Psychology from a leading academic institution and had researched and published extensively on a range of subjects to do with the brain and its relationship to behaviour. It was not a proper ground of criticism that he was not a doctor: he did not come to give evidence as a doctor but as a research scientist. His evidence was based on a wide reading of the literature. He had plainly given detailed consideration to the issues he was asked to address. He gave good and sufficient reasons for the opinions which he expressed. He could not legitimately be criticised for having sought and received funding from the tobacco industry, in particular for work of potential therapeutic value in relation to Alzheimer's disease. This was particularly so when he did this at a time when it was not unusual to take funding from the tobacco industry, and at a time when funding from other sources was limited. In any event, while most, if not all, of his research into nicotine received some support from the tobacco industry, this formed only one part of his very extensive body of publications. It was not correct to say that he denied the nicotine effect in tobacco: in his opinion, nicotine affected cognitive function and mood, and it was because of these effects that people chose to smoke, amongst other reasons. He denied that nicotine, or indeed tobacco, in some way affected the smoker's ability to choose whether to smoke or not. It was also said of him that he was "out on a limb". There were, however, those who supported his opinion on the addiction model: Warburton 1988a and 1988b, and Frenk and Dar 2000, in a passage which was unchallenged by Professor Friend. Indeed MacAskill et al. 2002 lent support to the functional model proposed by Professor Gray. In counsel's submission, what was important was not the "head count", but the cogency of Professor Gray's reasoning for his conclusions, which was not effectively challenged either in evidence or in submission.
[6.195]Mr Jones then turned to Mr McEachran's submission that ITL's pleadings about the addiction issue were inappropriate. After discussion at the Procedure Roll on the question whether an averment for Mrs McTear that tobacco was addictive was sufficiently specific to give fair notice of the characteristics of tobacco that were relied upon, an amendment was allowed so that the pleadings were now as quoted above. Mr Jones submitted that, on a proper construction, the averments for ITL meant that it was not true of all smokers that it was difficult for them to wean themselves off the habit. Taking the denial with its qualification, he submitted, it was clear that the defenders' response to the pursuer's case on addiction was that not every smoker found it difficult to stop and that any smoker who chose to do so could stop.
[6.196]Mr Jones went on to submit that ITL's averments were proved. Mr McTear stopped smoking. Mrs McTear stopped smoking. Sir Richard Doll, having been a smoker for twenty years, stopped smoking "without difficulty". USSG 1988 at p.466 stated:
"[T]here are approximately 41 million former smokers in the United States. Approximately 90 percent of former smokers report that they quit smoking without formal treatment programs or smoking cessation devices [...]."
Professor Gray expressed the opinion that different smokers sought different outcomes from smoking, but an individual smoker was likely to smoke for different reasons at different times, and smokers continued to smoke because of the benefits they derived from it, not because they were addicted to it. Professor Gray's views found empirical support in Professor Hastings's research in socially deprived areas of Glasgow, which found that smoking met a multitude of needs in the lives of the populations studied by the researchers.
[6.197]Replying to Mr McEachran's submission that ITL had admitted to the House of Commons Health Committee that tobacco was addictive, Mr Jones reminded me that ITL were asked questions in writing, one of which was whether nicotine could be regarded as addictive by reference to DSM-IV and ICD-10. There was no reference to either of these in the pleadings, and objection was taken to references being made to them in the evidence. Although ITL agreed that nicotine could be regarded as addictive by reference to these manuals, they said that this did not mean that smokers were unable to stop smoking if they chose to do so. Because the pursuer had no pleadings about DSM-IV or ICD-10, there was very limited evidence about the significance of the characterisation of nicotine as addictive by reference to the diagnostic criteria, but Professor Friend accepted that the criteria in DSM-IV were meant to be applied in the diagnosis of an individual by those capable of exercising clinical judgment. In addition, DSM-IV stated in terms at p.xxxiii:
"[T]he fact that an individual's presentation meets the criteria for a DSM-IV diagnosis does not carry any necessary implication regarding the individual's degree of control over the behaviors that may be associated with the disorder."
Having regard to these considerations, Mr Jones invited me to reject Mr McEachran's allegations that ITL's pleadings about addiction were inappropriate.
[6.198]Mr Jones pointed out that USSG 1988 concluded that nicotine had pharmacological effects similar to drugs such as cocaine and heroin. Reference was made to Henningfield 1984 and a number of other studies using the same methodology, which it was claimed showed similar levels of reported euphoria. RCP 2000 in turn referenced USSG 1988 and Henningfield 1984 for the same purpose. The methodology used in these studies was quite comprehensively criticised by Professor Gray in his evidence, under reference to Warburton 1988a. Accordingly, the conclusions of Henningfield 1984 and other studies adopting the same methodology could not be relied on for the proposition that tobacco had pharmacological effects similar to drugs such as cocaine and heroin. So the conclusions to this effect in the public health reports could not be relied on. Another aspect of this was that Henningfield was one of the scientific editors of USSG 1988 and he was a contributor to RCP 2000. RCP 2000 was also criticised in relation to its use of statistics on quitting.
[6.199]Mr Jones submitted that the pursuer led no witness who had any expertise on the matter of addiction. Moreover, Professor Hastings was plainly committed to the cause of tobacco control, regarded himself as an advocate for greater measures of tobacco control, and was on record as saying that the tobacco industry was to lung cancer what the mosquito was to malaria. He considered that the world would be a better place if people did not smoke tobacco. He had been an active campaigner for a ban on advertising and was a member of the Advisory Council of ASH. He was almost invariably inclined to respond to questions by making comments that were argumentative rather than by giving a direct answer to the question. His career had been in social marketing, which he described as a discipline the purpose of which was to change behaviour with a view to health benefits. All of this served to explain his perspective. His interest was in factors that might influence people's smoking behaviour.
[6.200]In any event, as the evidence turned out, and having regard to Mr McEachran's submissions, it was clear that there was little, if anything, between the parties on the substance of this part of the pursuer's case. The only difference of substance in the pleadings appeared to be that, whilst the pursuer was asserting that anybody who smoked would find it difficult to wean himself or herself off the habit, it had all along been the position of ITL that, whilst some people might find it difficult, people could, if they chose, stop smoking. Ultimately, in his submission, it was ITL's position which was made out on the evidence: it was accepted that it might be difficult for some individuals to stop smoking.
[6.201]This left the pursuer's case deficient in this important respect. It was not now, nor could it be, suggested that if Mr McTear tried to stop smoking and did not stop smoking it was because he was unable to do so. The position might have been different if it were proved that his free will to exercise a decision to stop smoking had been overcome by nicotine or something else in tobacco: one then would have to look at the case in that context. But on the evidence there was nothing left other than that some people found it difficult to stop smoking. Accordingly, counsel invited me to deal with this part of the pursuer's case by finding that some smokers might find it difficult to stop smoking, but that any smoker, if he or she chose to do so, could stop smoking. He also asked me to reject the suggestion that I should make a finding that tobacco was addictive in any sense. This was because, first, there were a number of different definitions of the word "addictive". If I made a finding that some people might find it difficult to stop smoking when they were smokers, that disposed of the issue between the parties and did not introduce the difficulties and confusion that the use of the word "addictive" would introduce. Secondly, counsel asked me expressly to decline to make a finding that "tobacco is more addictive than cocaine" on the basis that no evidence had been led in support of this.
Discussion
[6.202]Although counsel claimed that the parties were not far apart on the question of addiction, the foregoing account of their submissions may make them seem to be further apart. I can say at the outset that the averment for the pursuer that tobacco is more addictive than cocaine is not proved: the pursuer led no evidence in support of this apart from the references to heroin and cocaine in the passages in USSG 1988 referred to in the evidence of Professor Friend (paras.[5.66], [5.67] and [5.72]). Professor Friend was not, however, qualified to express any view about this. As he said himself, at para.[5.72], he was not an addiction specialist and not a psychiatrist, he had only had the opportunity to read some of the literature (i.e. the reports referred to above). He nevertheless said that he believed that nicotine resulted in a very strong addiction for many people, which he clearly regarded as being "an intense physical addiction, as a result of a chemical process which had been very carefully studied". In cross-examination, at paras.[5.162] to [5.171], Professor Friend demonstrated not only a lack of familiarity with the relevant literature, but also a forgetfulness about literature in which he had participated, BTS 1990 and Lennox et al. 2001, which would support the conclusions that ability to stop smoking did not appear to be affected by daily cigarette consumption, sex, age, or heaviness of smoking, but there was a significant inverse association with a level of social deprivation. I am not therefore prepared to accept Professor Friend's evidence about addiction, primarily because this did not appear to me to lie within his field of expertise.
[6.203]By contrast, Professor Gray appeared to me to be well qualified to give evidence about addiction, and I found his evidence to be persuasive. I reject the criticism of him that he was a "tobacco man". I detected no bias in his evidence, which appeared to me to be presented with moderation, internal coherence and appropriate reference to authority. Rose et al. 2000 gave support for his view that, as far as the pleasure and satisfaction of smoking were concerned, the principal route did not involve nicotine, but lay somewhere else in the complex behaviour that was smoking a cigarette. Support for the view that smoking had an intrinsic anti-depressant action was found in Kendler et al. 1993, and there was laboratory evidence that nicotine could have the effect of reducing anxiety. Accordingly Professor Gray's overview that nicotine and smoking tobacco had a remarkably broad spectrum of activity in alleviating negative mood and emotion, including depression, irritability and anxiety was supported by the literature. This justified the functional view which he favoured.
[6.204]Professor Gray's criticisms of the "addiction" model appeared to me to have force. I was particularly impressed by the criticism of Henningfield 1984. As had been brought out in Warburton 1988a, Henningfield's histograms when re-plotted on the same scale did not provide strong support for Henningfield's conclusion. Nicotine could then be seen to be, at best, a weak euphoriant and did not act like other compounds in the maintenance of other kinds of substance self-administration. Professor Gray also considered the question of tolerance and contrasted withdrawal symptoms from quitting smoking and from quitting heroin. His discussion of these supported the view that the behavioural and psychological changes observed in quitting smokers were more reasonably interpreted as reflecting non-specific dysphoria consequent upon disruption of a habit and loss of the pleasure or other benefits the habit provided.
[6.205]I was impressed above all by Professor Gray's critique of the mechanistic view embodied in the proposition that smokers did not smoke out of choice but because they became addicted to nicotine. As he pointed out, under the normal humanist view of life people chose to do things. The mechanistic view was not supported by the data about the number of people who had given up smoking. Support for the functional view was found in Warburton 1988b. Among the functional effects of smoking, of particular relevance in Mr McTear's case were those concerned with mood control. If smoking tobacco alleviated depression, not because it had a direct antidepressant effect, but rather because, for a habitual smoker, deprivation of smoking had a depressant effect, this could explain Mr McTear's behaviour on the occasions when he temporarily gave up smoking. There was little by the way of direct challenge to this evidence in cross-examination. He said that it was not possible to say why one smoker succeeded in quitting while another did not, though the answer might lie in the smoker's individual circumstances. He agreed that it could be taken from MacAskill et al. 2002 that people in lower socio-economic groups in Scotland were more likely to smoke and less likely to give up. But, as he pointed out, this observation was consistent with the functional model.
[6.206]Professor Gray's evidence accordingly is consistent with the averment for the pursuer that once individuals such as Mr McTear have started smoking it is difficult for them to wean themselves off the habit. It provides no support for the proposition that tobacco is more addictive than cocaine, or more addictive than heroin for that matter. There is no evidence before me which provides support for the conclusion in USSG 1988 that the pharmacological and behavioural processes that determine tobacco addiction are similar to those that determine addiction to drugs such as heroin and cocaine. Indeed, insofar as this relied on Henningfield 1984, it lacked a sound scientific basis.
[6.207]What I take particularly from Professor Gray's evidence, and his preference for the functional model, is that it retains the element of choice. The ability to choose is a central feature of the individualist philosophy of the common law which I discuss in Part VII. The word "addiction" is of questionable use in describing some forms of repetitive behaviour which the individual may or may not wish to alter. In everyday parlance it has come to be applied to such behaviour as shopping, for example, and even in its more scientific use it appears to be capable of being applied to behaviour such as gambling which does not involve the ingestion of any substance (though no doubt effects on the chemistry of the brain would need to be considered). If "addiction" can be applied in such a wide sense it ceases to be useful for any occasion, such as the present, when precision of meaning is required, though it may serve a legitimate purpose in the public health context. Even in that context, the definition of "addiction" has changed over time: USSG 1964, in the passage quoted at para.[5.163], said that the tobacco habit should be characterized as an habituation rather than an addiction. I prefer to concentrate on the behaviour and thought processes that the word has been used to describe.
[6.208]The evidence of Professor Hastings appears to me to add nothing for present purposes. The fact that individuals may be exposed to advertising, and even influenced by it, does not mean that they are precluded from exercising a free choice. Advertising simply adds to the complexity of the individual's decision-making process. People are well-accustomed to weighing up mixed messages, and to making their own decisions and choices. In any event Professor Hastings himself disclaimed any such mechanistic account of the influences to which an individual such as Mr McTear might be exposed. For an individual to say that he has found difficulty in altering or giving up a habit, as Mr McTear did of his smoking, because he is "addicted", appears to me to be little more than an attempt to absolve himself of individual responsibility for his own decisions and choices. In my view a smoker such as Mr McTear makes a deliberate choice as to whether to start smoking, whether to continue smoking or to stop smoking, and indeed whether or not to smoke a cigarette on any particular occasion. The fact that smokers such as Mr McTear may find it difficult to give up does not appear to me to deprive them of the element of free will which is fundamental to the individualist philosophy of the common law.
PART VII: LIABILITY
[7.1]Although I have held that the pursuer has not discharged the burden of proving that cigarette smoking can cause lung cancer and, if so, that it caused Mr McTear's lung cancer, so that the pursuer's case on both general causation and individual causation fails, I have nevertheless to consider whether ITL should be found liable on the assumption that, contrary to what I have held, the pursuer has succeeded in both these respects. It should be borne in mind that the remainder of this Part proceeds on this hypothesis.
Negligence
Submissions for Mrs McTear
[7.2]Mr McEachran began his submissions on liability by saying that this was a defective product liability case, but the Consumer Protection Act 1987 did not apply because a special exemption was made for cigarettes at section 10(7)(f). Accordingly the matter proceeded at common law. This was as summarised in Salmond & Heuston, The Law of Torts (21st edn., 1996), p.296:
"Before 1932 it was extremely doubtful whether there was any liability on the part of a manufacturer of goods to the ultimate consumer or user with whom there was no contractual relationship, when there was no fraud, when he did not know the article to be dangerous, and when it did not belong to the category of things dangerous per se. But in that year the decision of a majority of the House of Lords in Donoghue v Stevenson, an appeal from the Court of Session, established that in such circumstances the manufacturer might owe a duty to the ultimate consumer."
[7.3]Counsel founded therefore primarily on Donoghue v Stevenson 1932 S.C. (H.L.) 31. In this case the pursuer brought an action of damages against a manufacturer of ginger beer, averring that she had been poisoned by ginger beer, which was bought from a retail dealer in an opaque sealed bottled in which it had left the manufacturer's premises, and which contained a decomposed snail. The House of Lords held, by a majority, that where the manufacturer of a product intended for human consumption sent it out in a form which showed that he meant it to reach the ultimate consumer in the form in which it left his factory, with no reasonable possibility of intermediate examination by the retailer or consumer, and with the knowledge that want of reasonable care on his part in the preparation of the product might result in injury to the consumer, the manufacturer owed a duty to the consumer to take such care, and would be liable to the consumer in damages if he or she suffered injury through the failure to take such care.
[7.4]Lord Atkin said, at p.43:
"The sole question for determination in this case is legal. Do the averments made by the pursuer in her pleadings, if true, disclose a cause of action? I need not restate the particular facts. The question is whether the manufacturer of an article of drink sold by him to a distributor, in circumstances which prevent the distributor or the ultimate purchaser or consumer from discovering by inspection any defect, is under any legal duty to the ultimate purchaser or consumer to take reasonable care that the article is free from defect likely to cause injury to health."
[7.5]At p.57, Lord Atkin said:
"If your Lordships accept the view that this pleading discloses a relevant cause of action, you will be affirming the proposition that by Scots and English law alike a manufacturer of products, which he sells in such a form as to show that he intends them to reach the ultimate consumer in the form in which they left him, with no reasonable possibility of intermediate examination, and with the knowledge that the absence of reasonable care in the preparation or putting up of the products will result in an injury to the consumer's life or property, owes a duty to the consumer to take that reasonable care."
[7.6]At pp.59-60, Lord Thankerton said:
"There can be no doubt, in my opinion, that, equally in the law of Scotland and the law of England, it lies upon the party claiming redress in such a case to show that there was some relation of duty between her and the defender which required the defender to exercise due and reasonable care for her safety. [...] The special circumstances from which the appellant claims that such a relationship of duty should be inferred may, I think, be stated thus, namely, that the respondent, in placing his manufactured article of drink upon the market, has intentionally so excluded interference with, or examination of, the article by any intermediate handler of the goods between himself and the consumer that he has, of his own accord, brought himself into direct relationship with the consumer, with the result that the consumer is entitled to rely upon the exercise of diligence by the manufacturer to secure that the article shall not be harmful to the consumer. If that contention be sound, the consumer, on her showing that the article has reached her intact, and that she has been injured by the harmful nature of the article owing to the failure of the manufacturer to take reasonable care in its preparation prior to its enclosure in the sealed vessel, will be entitled to reparation from the manufacturer.
In my opinion, the existence of a legal duty under such circumstances is in conformity with the principles of both the law of Scotland and the law of England."
[7.7]Lord Macmillan said, at p.72:
"It must always be a question of circumstances whether the carelessness amounts to negligence, and whether the injury is not too remote from the carelessness. I can readily conceive that, where a manufacturer has parted with his product and it has passed into other hands, it may well be exposed to vicissitudes which may render it defective or noxious, for which the manufacturer could not in any view be held to be to blame. It may be a good general rule to regard responsibility as ceasing when control ceases. So, also, where between the manufacturer and the user there is interposed a party who has the means and opportunity of examining the manufacturer's product before he re-issues it to the actual user. But where, as in the present case, the article of consumption is so prepared as to be intended to reach the consumer in the condition in which it leaves the manufacturer, and the manufacturer takes steps to ensure this by sealing or otherwise closing the container so that the contents cannot be tampered with, I regard his control as remaining effective until the article reaches the consumer and the container is opened by him. The intervention of any exterior agency is intended to be excluded, and was in fact in the present case excluded."
[7.8]Counsel said that he referred to Donoghue v Stevenson as establishing that in such circumstances the manufacturer might owe a duty to the ultimate consumer. He founded particularly on the speech of Lord Atkin as effectively applying the wider "neighbourhood" principle propounded in this case to manufacturers. Counsel submitted that the manufacturers' duty had been given a broad interpretation and was not limited to food and drink, but extended to any item capable of causing damage, such as an article of clothing: Grant v Australian Knitting Mills Ltd [1936] A.C. 85. The appellant in this case contracted dermatitis of an external origin as a result of wearing a woollen garment which, when purchased from the retailers, was in a defective condition owing to the presence of excess sulphites which, it was found, had been negligently left in it in the process of manufacture. The presence of the deleterious chemical in the garment was a hidden and latent defect, and could not be detected by any examination that could reasonably be made; nothing happened between the making of the garment and its being worn to change its condition; and the garment was made by the manufacturers for the purpose of being worn exactly as it was worn in fact by the appellant. It was held, applying the principle of Donoghue v Stevenson, that these facts established a duty to take care as between the manufacturers and the appellant for the breach of which the manufacturers were liable in tort. In delivering the judgment of the Privy Council, Lord Wright said at p.105:
"The principle of Donoghue's case can only be applied where the defect is hidden and unknown to the consumer, otherwise the directness of cause and effect is absent: the man who consumes or uses a thing which he knows to be noxious cannot complain in respect of whatever mischief follows, because it follows from his own conscious volition in choosing to incur the risk or certainty of mischance."
[7.9]Counsel submitted that cigarettes were themselves defective because they had elements in them which caused death. Knowledge by the manufacturer that there was a risk of serious injury to the health of the consumer was obviously vital to establish liability: there was no need to prove exactly how that risk came about. So far as lung cancer was concerned, it was enough to establish that serious scientists were raising significant concerns that tobacco smoking was liable to cause damage to health, especially lung cancer: to hold otherwise would be to put the consumer at the mercy of the "flat earther", because otherwise the manufacturer could wait until all scientists were convinced before taking action.
[7.10]Sir Richard Doll had given unchallenged evidence that by about the date of MRC 1957 at least the great majority of scientists accepted the link between tobacco smoking and lung cancer. ITL founded on evidence that some scientists did not accept the Doll thesis, but he had described them as mistaken and eccentric. Considering that no challenge had been put forward to IARC 1986 and later reports, it was clear that he was right, even though in 1964 there were a few who did not accept the hypothesis. ITL employed scientists and they were aware of the state of knowledge, both in the industry and among scientists. ITL were aware of the early reports. In addition there was the evidence about Dr Bentley's report following a meeting in 1958. So it was established that ITL were aware in the late 1950s of the risk of lung cancer. At the latest by 1957 ITL were aware that their product was liable to cause lung cancer to smokers and accordingly to cause death. It was their duty to cease manufacture, at least until they had managed to remove the carcinogen or carcinogens from the tobacco smoke that led to lung cancer. They seemed, despite this duty, to have continued with the manufacture for reasons of profit. They thus became liable to anyone like Mr McTear who suffered injury when he started smoking after that time. ITL had to take their victim, Mr McTear, as they found him. No doubt many smokers of their products were drinkers, were unemployed, were depressed, and had been convicted of drink-related offences. ITL would be aware of the level of smoking in the socio-economic class to which Mr McTear belonged.
[7.11]Counsel next referred to Wright v Dunlop Rubber Co Ltd (1972) 13 K.I.R. 255. The plaintiffs in this case commenced employment with the first defendants (Dunlops) in December 1946 and March 1947 respectively. They alleged that they had contracted cancer of the bladder as a result of being exposed, during the course of their employment, to Nonox S, a chemical containing carcinogenic substances manufactured by the second defendants, Imperial Chemical Industries Limited (ICI) and sold to the first defendants. In May 1949 Dunlops were warned that they might have a grave problem of bladder cancer. They stopped using Nonox S. In 1966 the plaintiffs were diagnosed as suffering from the disease. In actions for damages the plaintiffs alleged negligence against both defendants, and further alleged breaches of section 47 of the Factories Act 1937 against Dunlops. Both defendants denied negligence, breach of duty and causation. O'Connor J. gave judgment for the plaintiffs against both defendants. He held inter alia that ICI should have withdrawn Nonox S before the end of 1946 and that Dunlops enhanced the risk of injury to the plaintiffs by failing from 1960 onwards to advise all employees employed before 1949 to submit themselves for screening. ICI appealed as to liability.
[7.12]The Court of Appeal held, dismissing the appeal, that the manufacturer of a chemical product owed to the purchaser's employees a duty to take all reasonable steps to satisfy himself that the product was safe in the sense that there was no substantial risk of any substantial injury to health on the part of persons who were likely to use it or to be brought into contact with its use, the method of use being such as was at least reasonably to be expected as normal and proper; that ICI knew, or ought to have realised, before either of the plaintiffs entered the employment of Dunlops, that Nonox S was, or contained, a carcinogenic substance involving a real risk of causing cancer of the bladder to persons working in rubber factories in which it was used; and that, in failing to cease manufacturing and supplying Nonox S at that time, ICI were negligent. The following passages in the judgment of the court, read by Sachs L.J. and Lawton L.J., were referred to in the discussion before me.
[7.13]At p.266 the court summarised the contentions of the parties on the negligence issue as follows:
"The plaintiffs' argument, broadly stated, is that at all material times (which in the circumstances of this case means the 1940s) ICI knew: first, that the A and B amines, particularly the B amine, were dangerous carcinogens in both bulk and trace; secondly, that the free amines in Nonox S included the A and B amines; thirdly, that the free amines in Nonox S would volatilise at temperatures over 1020C; fourthly, that in Dunlops' factories Nonox S would be under heat at temperatures over this figure; fifthly, that in the course of production in those factories dust would be dispersed into the atmosphere when bags of Nonox S were emptied and when the Banbury mixers were charged with raw rubber and Nonox S; and, sixthly, that the rubber-making processes would give off a large amount of fumes. Knowing what they did, it was submitted, ICI should have appreciated the nature and extent of the risks to which they were subjecting Dunlops' workers and should have either withdrawn Nonox S or, at the very least, have given them a warning about its carcinogenic properties. Their failure to do either was alleged to be negligence.
ICI did not dispute that they had this knowledge. What has been in issue was the inferences which could, or should, have been drawn from it. Their main contention has been that at no time before 1949 did they know, or could have been reasonably expected to have known, that the free amines in Nonox S could cause bladder cancer amongst workers in Dunlops' factories."
[7.14]After considering the evidence as to ICI's knowledge, the court concluded, also at p.266, that the contemporaneous documentary evidence proved that from about 1942 onwards ICI knew that very small amounts of amine in the atmosphere, whether as dust or fumes, were a grave hazard to the health of those who came into contact with them. At p.267 the court turned to the question:
"Having this knowledge, would ICI, if they had given positive thought to the matter, have appreciated the risks to which Dunlops' workers would be exposed in handling Nonox S? If yes, what should they have done?"
After reviewing the evidence bearing on this question the court said, at p.268:
"It follows, in our judgment, that the warnings given in the medical literature in the 1920s and the 1930s should have made ICI think about risks in use; and they may probably have had this result because, as we have found, they did consider the risks to which their own workers were exposed in handling Nonox S."
[7.15]At p.271 the court reached the following conclusions on the negligence issue:
"In the judgment of this court, ICI long before 1949 were in a position to appreciate that Dunlops' workers were at risk. It is difficult to say when, on balance of probabilities, they should have appreciated this. The trial judge put the date at 1940, which is perhaps earlier than we would feel able to put it on the evidence before us. The date to which we are disposed is by the year 1943; though we cannot rule out an earlier date as a possibility. Clearly, they were in that position well before either of the plaintiffs entered their employment with Dunlops. Had they given thought to the risk to Dunlops' workers, as manifestly they should have done, some action by them was called for. The least they should have done was to have warned Dunlops of the suspicions which they had. The giving of a warning would probably have resulted in Dunlops giving up buying Nonox S: this is what happened in July 1949 as soon as ICI had told them about the risks. ICI in fact did nothing; and the two plaintiffs worked in an atmosphere contaminated with the A and B amines without any protection of any kind, with the result that they both, years later, were found to be suffering from bladder cancer.
In coming to this conclusion we have gone further than O'Connor J., who found for the plaintiffs on the basis that had ICI at any time after 1940 asked themselves whether it was safe for workmen in the rubber industry to be exposed to the B amine they would have been obliged to admit that they did not know and on that narrower ground were liable in negligence. We agree with that approach; but we have founded our conclusions on the basis that ICI actually had the relevant knowledge."
[7.16]The court then turned, at pp.271-273, to consider the relevant law, in these terms:
"What, then, are the consequences in law? The relevant principle of law by which the question whether or not ICI were in breach of a duty owed to the plaintiffs falls to be decided seems to be clear, viz., that the duty of the manufacturer to the purchaser's workmen in a case such as this is the same as the duty of a manufacturer towards his own workmen, subject only to one proviso. That proviso is that the manufacturer knows how the goods are going to be used by the purchaser. So far as the present case is concerned, the proviso creates no difficulty for the plaintiffs. While ICI did not know all the details of the processes of rubber manufacture in which Nonox S was used by Dunlops, they were not unaware of anything which was material for present purposes. There was no suggestion that Nonox S was used by Dunlops in any unexpected or unusual way, or that any of the relevant factors, such as the temperatures at which the processes were conducted, were not known or could not readily have been discovered by ICI. No problem arises in this appeal in connection with the opportunity for intermediate inspection by Dunlops. Thus, we do not have to consider the question which has sometimes arisen in the application of the Donoghue v Stevenson [...] principle. For ICI have not raised any suggestion, and in this appeal have expressly disclaimed the suggestion that, if ICI ought to have foreseen the risk to the plaintiffs arising from the use of Nonox S by Dunlops, Dunlops should also have foreseen that risk. We do not, therefore, have to consider what, if any, effect such a contention, if it were established, would have on the question of ICI's liability to the plaintiffs.
ICI, then, owed a duty to Dunlops' employees in respect of Nonox S. What was the extent of the duty? It was a duty to take all reasonable steps to satisfy themselves that Nonox S was safe: 'safe' in the sense that there was no substantial risk of any substantial injury to health on the part of persons who were likely to use it or to be brought into contact with its use, the method of the use being such as was intended or contemplated or was at least reasonably to be expected as a normal and proper use.
It is obvious that the answer to the question: 'What are reasonable steps?' must depend upon the particular facts. It is obvious, also, that the duty is not necessarily confined to the period before the product is first produced or put on the market. Thus, if, when a product is first marketed, there is no reason to suppose that it is carcinogenic, but thereafter information shows, or gives reason to suspect, that it may be carcinogenic, the manufacturer has failed in his duty if he has failed to do whatever may have been reasonable in the circumstances in keeping up to date with knowledge of such developments and acting with whatever promptness fairly reflects the nature of the information and the seriousness of the possible consequences.
If the manufacturer discovers that the product is unsafe, or has reason to believe that it may be unsafe, his duty may be to cease forthwith to manufacture or supply the product in its unsafe form. It may be that in some circumstances the duty would be fulfilled by less drastic action: by, for example, giving proper warning to persons to whom the product is supplied of the relevant facts, as known or suspected, giving rise to the actual or potential risk. Factors which would be relevant would be the gravity of the consequences if the risk should become a reality, and the gravity of the consequences which would arise from the withdrawal of the product. In the present appeal, we do not, however, have to consider that question: for it is not suggested on behalf of ICI that, if they ought to have realised the carcinogenic qualities of Nonox S before the time when the plaintiffs were exposed to it, they could, or would, have refrained from at once ceasing its manufacture and supply, as they in fact did in August 1949.
The principal issue with which we are concerned in this appeal is thus essentially simple. It can be simply stated, and, as we think, simply and shortly answered. The question is whether ICI, before the end of 1946, when the plaintiff Mr Wright was first employed by Dunlops, knew or ought to have realised that Nonox S was, or contained, a carcinogenic substance involving a real risk of causing cancer of the bladder to persons working in rubber factories in which Nonox S was used.
If the plaintiffs fail to establish that the answer to that question is 'Yes', their claim fails. If the plaintiffs succeed on that issue, then, subject to the question of causation, their claims succeeds. O'Connor J. held that the plaintiffs succeeded on that issue. We agree with him. Our own examination of the evidence has led us to the same basic findings of fact as he made; indeed, as already stated, we have made an important additional finding about knowledge. This means that negligence has been proved."
[7.17]Counsel submitted that, while the tobacco manufacturers would not have any knowledge that their product was carcinogenic until the work done by Sir Richard Doll and others, starting in 1950, there were risks of a significant number of deaths, and the only reasonable step which reasonable manufacturers would have taken in the 1950s would have been to cease manufacture until the problem had been dealt with. This submission applied to all tobacco manufacturers in the United Kingdom, who all ought reasonably to have ceased production by 1957. If the tobacco manufacturers had ceased manufacture, this would have focused everybody's minds on getting a solution to the problem. What had happened was that it had been allowed to continue and there were now more than 120,000 deaths a year from smoking, on the basis of the unchallenged public health figures. It was not relevant, in looking to see what a reasonable manufacturer would do, to consider what the Government position was as a matter of public health. The complaint was that ITL continued to manufacture, and if cigarettes had not been available in 1964 Mr McTear would not have been able to smoke them. The risks had been established by epidemiology, and were accepted by the scientific and medical community by 1957. This was an extremely dangerous product, and if it was going to kill people, then the duty was to cease production. It was not legitimate to say in response that smoking was socially acceptable and regarded as a source of pleasure, nor that it had beneficial effects primarily in the area of mental health.
[7.18]Counsel accepted that the scope of a duty of care had to be examined according to the standards at the time, and what might be reasonable for a manufacturer to do now was not necessarily the same as would have been reasonable for the manufacturer to have done fifty years before. But given that the risk was the same then as now, he submitted that the duty on the manufacturer was no different. It was not reasonable for a manufacturer who found that his product was capable of causing such serious harm to leave it to the public authorities to make it unlawful for him to sell the product or restrict its sales, and unless and until they did that to continue selling the product. Wright v Dunlop Rubber Co Ltd was an example of a case where an obligation fell on the manufacturers to take action once they discovered that a substance was carcinogenic, and the action was to withdraw it. In Thompson v Smith's Shiprepairers (North Shields) Ltd [1984] 1 Q.B. 405 it was held that the test to be applied in determining the time at which an employer's failure to provide protection constituted actionable negligence was what would have been done at any particular time by a reasonable and prudent employer who was properly but not extraordinarily solicitous for his workers' safety in the light of what he knew or ought to have known at the time. This afforded an example of the focus on the date when the defender should reasonably have foreseen a risk of injury, which in the present case was in the 1950s and in particular 1957.
Submissions for ITL
[7.19]Mr Jones started his submissions by saying that if I was with him on either general or individual causation, then it was not necessary to go further. But it was nevertheless necessary to consider all of the issues, including the legal issues, so he proceeded to address me on them. Even if I were persuaded that Mr McTear's lung cancer was caused by his smoking of ITL's cigarettes, the real issue was whether or not he suffered injury as a result of a breach of a duty of care owed to him by ITL, that is to say whether, but for the breach of a duty of care owed to him by ITL, he would not have contracted lung cancer. There was no such thing as negligence or liability in the air: Overseas Tankship (UK) Ltd v Morts Dock & Engineering Co Ltd (The Wagon Mound) [1961] A.C. 388 at p.425. Liability could not be isolated from its context. There had to be a complete picture of cause and effect before negligence or breach of duty could be discussed.
[7.20]In addressing the central issue, he invited me to consider two preliminary questions to help clarify the two key issues of fact. The first of these was the relevance of knowledge of the health risks associated with smoking; and the second was the relevant date for assessing whether or not Mr McTear suffered injury as a result of a breach of a duty of care owed to him by ITL. On the first question, if Mr McTear smoked ITL's cigarettes, knowing of the link between smoking and lung cancer that was being talked about, then he could not blame ITL if in fact he contracted lung cancer as a result of smoking in that state of knowledge. In those circumstances one could say either that ITL did not owe him any relevant duty of care, or that they were not in breach of any duty of care owed to him, or that any breach of their duty of care to him did not cause his injury, or that he was volens. In the cases these various possibilities crossed over and sometimes excluded each other, but ultimately they arrived at the same point, which was the absence of liability on the part of the defenders.
[7.21]I observed that it could not be said that ITL did not owe a duty of care to Mr McTear as they would to any ultimate consumer of their products, but what needed to be looked at was the content of the duty. Mr Jones said that this raised an interesting jurisprudential point. In the cases sometimes the result was that a defender or defendant was absolved from blame because there was no liability. This result was variously described as coming about sometimes because there was no duty of care in the circumstances; or sometimes because there was a duty of care, but there was not a breach of the particular formulation of that duty. It could be put either way. For his purposes, ultimately in this case it really did not matter, because he would be concentrating on the content of any duty of care. His hesitation in accepting my way of putting it was that we came back to the problem of there being no such thing as negligence in the air. One might say that as a matter of principle there was a duty to avoid acts and omissions which it was reasonably foreseeable would be likely to injure one's neighbour, but this only had any practical application when one came to determine whether a breach of a duty of care had caused injury. This might be a rather impractical philosophical answer, but it was a reflection of the views that were expressed in some of the cases. Ultimately it was necessary to identify just what particular duty was to be performed in any case, without looking at the broader question, because that ultimately was what the court was concerned with.
[7.22]Mr Jones submitted that there was a breach of a duty of care in Donoghue v Stevenson because there was no opportunity for intermediate inspection of the contents of an opaque sealed bottle, so that the purchaser was not aware that there was a snail in the bottle. If the purchaser bought the bottle knowing that there was a snail in it, there would be no action for breach of any duty to take care to avoid a snail getting into the bottle during manufacture. If there was an opportunity prior to consumption for becoming aware of whatever the harmful defect might be, there was no breach of duty. Counsel referred to Grant v Australian Knitting Mills Ltd, supra.
[7.23]Reference was next made to Titchener v British Railways Board 1984 S.C. (H.L.) 34. According to the report, the Occupiers' Liability (Scotland) Act 1960, section 2, provides inter alia:
"(1)The care which an occupier of premises is required, by reason of his occupation or control of the premises, to show towards a person entering thereon in respect of dangers which are due to the state of the premises or to anything done or omitted to be done on them and for which the occupier is in law responsible shall, except in so far as he is entitled to and does extend, restrict, modify or exclude by agreement his obligations towards that person, be such care as in all the circumstances of the case is reasonable to see that that person will not suffer injury or damage by reason of any such danger.
(3)Nothing in the foregoing provisions of this Act shall be held to impose on an occupier any obligation to a person entering on his premises in respect of risks which that person has willingly accepted as his; and any question whether a risk was so accepted shall be decided on the same principles as in other cases in which one person owes to another a duty to show care."
[7.24]In this case a girl aged 15 was struck by a train while crossing a railway line. She raised an action of damages against British Railways Board averring that they had failed in terms of section 2 of the 1960 Act to take reasonable care to maintain a fence made of sleepers, which separated the public street from the embankment on which the line was situated. It was established after proof that there had been gaps in the fence through which persons could easily reach the line and that the defenders had known that persons did walk across the line by that route. The pursuer admitted in evidence that she had so crossed the line on several previous occasions with her boyfriend. She had known that it was dangerous to do so and that she should have looked out for trains on the occasion of the accident, as she had done previously. The Lord Ordinary disbelieved her when she said that she would have been prevented from crossing the line by an ordinary post and wire fence. The Lord Ordinary, Lord Ross, assoilzied the defenders. In the course of his Opinion the Lord Ordinary at pp.40-41 quoted a passage from the cross-examination of the pursuer in the course of which she said:
"Well, before my accident I never ever thought that it would happen to me, that I would never get hit by a train, it was just a chance that I took."
He added the comment:
"A person who takes a chance necessarily consents to take what comes."
[7.25]The pursuer reclaimed and an Extra Division adhered to the Lord Ordinary's interlocutor. The pursuer appealed. The House of Lords held:
(1)That the duty of the occupier of premises under section 2(1) of the 1960 Act was to show such care as in all the circumstances was reasonable to see that the person entering on them would not suffer injury; in the case of the operator of a railway the existence and extent of a duty to maintain a fence beside the line depended on the circumstances, including the age and intelligence of the person entering on to the line and the nature of the locus. (2) That, in relation to the appellant, the Lord Ordinary was entitled to hold that the respondents owed no duty to her to maintain the fence in a better condition than it was on the grounds that she was aware of the danger, that on-coming trains could be seen for a quarter of a mile and that she had not averred any complaint as to the way in which the train had been operated.
(3)That the Lord Ordinary and the Extra Division were also correct in holding that even if the respondents had failed in their duty to maintain the fence the appellant had failed to prove as a matter of probability that the accident would have been prevented had the fence been maintained.
(4)That the Lord Ordinary was also correct in holding that the respondents had established a defence under section 2(3) of the 1960 Act which merely stated the principle of volenti non fit iniuria in that the appellant was well aware of and accepted the risk of crossing the line while trains were being operated properly.
[7.26]At p.52 the Lord Chancellor, Lord Hailsham of St. Marylebone, said:
"To my mind the crucial fact in this appeal was that no averment was or could have been made against the respondent Board that the train which struck the appellant was being driven otherwise than in a perfectly proper manner. If such an averment had been made and proved the respondent Board would have been liable on the lines of the well-known passage of Denning L.J.'s judgment in Slater v Clay Cross Co Ltd [1956] 2 Q.B. 264 at p.271. But, on the facts and evidence in this case, once it was accepted that there was no negligence on the part of the driver of the train, it seems to me that the pursuer's claim, which was based solely on the condition of the fence, was doomed to failure, if only because, on her own admissions, she had voluntarily accepted the risk whatever it was which she incurred by crossing the line, provided only that it was a 'risk of danger from the running of the railway in the ordinary and accustomed way'.
On this analysis of the facts it is possible to formulate the result either by saying that, at the critical moment, that is when the appellant crossed the line, the respondent Board owed no duty to the appellant, or that the duty they owed to the appellant had been discharged by the time she crossed the boundary fence, or that the accident was not caused by any breach of duty on the part of the respondent Board, or alternatively that, having assumed the risk involved, the respondent Board was covered by the doctrine volenti non fit iniuria."
[7.27]At pp.54-55 Lord Fraser of Tullybelton said:
"The duty under section 2(1) was considered by your Lordships' house in McGlone v British Railways Board 1966 S.C. (H.L.) 1 where Lord Guest said at p.15 'The duty is not to ensure the entrant's safety but only to show reasonable care. What is reasonable care must depend "on all circumstances of the case"'. One of the circumstances is the age and intelligence of the entrant. That appears from the provision in section 2(1) that the duty is to show 'such care as in all the circumstances of the case is reasonable to see that that person will not suffer injury' (emphasis added). The question in each case relates to the particular person who has entered upon the premises. The submission of counsel for the respondents was that they did more than enough to discharge their obligations to this appellant because the fences along the north and south sides of the line, notwithstanding that they had gaps, gave her warning that if she went on she would be entering upon railway premises. She was well aware, as she admitted, of the danger of walking across or along the line, and she said that when doing so she normally kept a lookout for trains. By giving her that warning, the respondents were, said Mr Morison [senior counsel for the respondents], doing more than they were obliged to do, because this appellant already knew that the railway was there, and therefore needed no warning. Counsel accepted that the logical conclusion of this argument was that, as the appellant had no need of a warning, the respondents could have left their premises near the bridge completely unfenced without being in breach of any duty towards her. A fortiori they had no duty to do more than they did.
The Lord Ordinary accepted that argument, and in the Division Lord Hunter agreed, although only with some hesitation.
I must emphasise that the question in this appeal is not whether the respondents, and other operators of railways if any there be, have as a general rule a duty to the public to maintain fences beside their lines in good condition or at all. The existence and extent of a duty to fence will depend on the circumstances of the case including the age and intelligence of the particular person entering upon the premises; the duty will tend to be higher in a question with a very young or a very old person than in the question with a normally active and intelligent adult or adolescent. The nature of the locus and the obviousness or otherwise of the railway may also be relevant. In the circumstances of this case, and in a question with this appellant, I have reached the opinion that the Lord Ordinary was well entitled to hold, as he did, that the respondents owed no duty to her to do more than they in fact did to maintain the fence along the line. I reached that view primarily because the appellant admitted that she was fully aware that the line existed, that there was danger in walking across it or along it, that she ought to have kept a lookout for trains, and that she had done so when crossing the line on previous occasions."
[7.28]Lord Fraser went on to consider additional features of the case which he regarded as important. He then said, also at p.55:
"There was therefore no special danger peculiar to the locus of the accident, and no criticism was made by the appellant of the way in which the particular train was being operated. [...] Taking all these circumstances together I consider that the respondents did not owe the appellant a duty to maintain the fence in better condition that it was. If it were necessary to do so I would hold that they owed her no duty to provide any fence at all."
[7.29]At pp.55-57 Lord Fraser went on to consider additional grounds on which the Lord Ordinary and the Division had based their decisions. First, he held that the Lord Ordinary had correctly decided that, even if the respondents were at fault in failing to maintain the fence and to repair the gaps in it, the appellant had failed to prove, as a matter of probability, that if the respondents had performed their duty in those respects, the accident would have been prevented. He then said:
"Secondly, the Lord Ordinary held that the respondents had established a defence under section 2(3) of the 1960 Act by proving that the appellant had willingly accepted the risks of walking across the line. As Lord Reid said in McGlone, supra, subsection (3) merely puts in words the principle volenti non fit iniuria. That principle is perhaps less often relied upon in industrial accident cases at the present time than formerly, but so far as cases under the 1960 Act are concerned, the principle is expressly stated in section 2(3) and there is no room for an argument that it is out of date or discredited. If the Lord Ordinary was entitled to sustain this defence, the result would be that, whether the respondents would otherwise have been in breach of their duty to the appellant or not, the appellant had exempted them from any obligation towards her. [....] On this matter I am of opinion, in agreement with Lord Hunter, that the Lord Ordinary was well-founded in sustaining this defence. The reasons for doing so are in the main the same as the reasons for holding that the respondents were not in breach of their duty. The appellant admitted that she was fully aware that this was a line along which trains ran, and that it would be dangerous to cross the line because of the presence of trains. She said in cross-examination 'it was just a chance I took', and the Lord Ordinary evidently accepted that she understood what she was saying. She was in a different position from the boy in McGlone, supra, who did not have a proper appreciation of the danger from live wires - see Lord Reid at p.13 and Lord Pearce at p.18. As I said already the appellant did not suggest that the train which injured her had been operated in an improper or unusual way. The importance of that is that the chance which she took was no doubt limited to the danger from a train operated properly, in the 'ordinary and accustomed way' - see Slater v Clay Cross Co Ltd [1956] 2 Q.B. 264, per Denning L.J. at p.271. Had there been evidence to show that the train which injured the appellant was driven negligently, like the train in Slater's case, the risk which materialised would not have been within the risks that the appellant had accepted. But there is nothing of that kind here. In my opinion therefore the defence under section 2(3) is established."
[7.30]Counsel submitted that the duty of a manufacturer of goods was to show such care as in all the circumstances was reasonable, so there was no distinction to be made between that duty and the duty of an occupier of premises. The pursuer in Titchener voluntarily accepted the risk, whatever it was, which she incurred by crossing the line. In a case involving a manufacturer and consumer, the duty was not to ensure the consumer's safety, but it was only to show reasonable care, and that depended on all the circumstances of the case. Likewise, the occupier of premises had no duty to ensure the safety of a person coming on to land and effectively, once that person knew of the existence of danger, there was no duty on the part of the occupier to do more. Mr McEachran had submitted in effect that warnings might not have been heeded by Mr McTear, so that it was the duty of ITL to erect an "impenetrable barrier" by ceasing production. This was analogous to what was being argued for the pursuer in Titchener. But the duty was to exercise reasonable care, having in mind the reasonable person as the person to whom that duty was owed, an adult who on an objective view would act reasonably in all the circumstances. So, even although in Titchener an impenetrable barrier might have had the effect of keeping her off the railway, there was no duty to erect one when her knowledge was that she was "taking a chance" by going onto the line.
[7.31]It was important, counsel submitted, to consider the factual basis upon which all of the judges in the House of Lords held either that there was no breach of duty, or that the maxim volenti non fit iniuria applied, because the pursuer had taken a chance. This was consistent with the policy of the law, that once an individual was aware that there was a risk in what they were doing, then the consequences of the risk fell on him, because he could choose whether or not to take the risk. The cases on volenti non fit iniuria, where the acceptance was of a future risk, where there had not yet been negligence, such as driving carelessly, could be contrasted with the type of circumstance found in Titchener, where the alleged fault had already taken place, in that case the state of the fence. These circumstances were important in determining as a matter of fact whether the pursuer had accepted a risk, waived a claim and so on. It was sometimes very difficult to get to volenti non fit iniuria, because by the time one was looking at that one had already decided that there was no breach of a duty of care. Counsel submitted that Titchener afforded an insight into the general policy of the common law, which was founded on the notion of individual freedom, and the notion that the individual took responsibility for his own actions. The common law recognised that individuals were entitled to do things which involved risk to their health or well-being, but if they did so they must accept responsibility for the consequences of their actions.
[7.32]These principles could be seen in action in Tomlinson v Congleton Borough Council [2004] 1 A.C. 46. In a country park owned and occupied by the first defendant and managed by the second defendant (Cheshire County Council) was a lake that had formed in a disused quarry. It was meant to attract many visitors in hot weather. Swimming in the lake was prohibited, and the defendants displayed prominent notices reading "Dangerous Water: No Swimming" and employed rangers with the duty of giving oral warnings against swimming and handing out safety leaflets. The first defendant, aware that the notices were frequently ignored and had little effect in preventing visitors to the park from entering the water and that several accidents had resulted from swimming in the lake, intended planting vegetation around the shore to prevent people from going into the water but had not yet done so because of a shortage of financial resources. On a hot day the plaintiff, aged 18, went into the lake and from a standing position in shallow water dived and struck his head on the sandy bottom, breaking his neck. He claimed damages against the defendants, alleging that the accident had been caused by their breach of the duty of care that they had owed to him as a trespasser under section 1 of the Occupiers' Liability Act 1984. The judge, on a preliminary issue as to liability, found that there had been nothing about the lake that made it any more dangerous than any other ordinary stretch of open water and that the danger and risk of injury from diving in it where it was shallow had been obvious. He dismissed the plaintiff's claim. The Court of Appeal by a majority allowed an appeal by the plaintiff.
[7.33]On appeal by the defendants, the House of Lords held, allowing the appeal, that (Lord Hutton dubitante) any risk of the plaintiff suffering injury had arisen not from any danger due to the state of the defendants' premises or to things done or omitted to be done on them within section 1(1)(a) of the 1984 Act but from the plaintiff's own misjudgment in attempting to dive in too shallow water; that that had not been a risk giving rise to any duty on the defendants; and that, in any event, it had not been a risk in respect of which the defendants might reasonably have been expected to afford the plaintiff some protection under section 1(1)(c).
[7.34]At pp.81-86 Lord Hoffmann said:
"32 That leaves paragraph (c) [of section 1(3) of the Occupiers' Liability Act 1984]. Was the risk one against which the council might reasonably be expected to offer the plaintiff some protection? The judge found that 'the danger and risk of injury from diving in the lake where it was shallow were obvious'. In such a case the judge held, both as a matter of common sense and following consistent authority (Staples v West Dorset District Council (1995) 93 L.G.R. 536, Ratcliff v McConnell [1999] 1 W.L.R. 670 and Darby v National Trust [2001] P.I.Q.R. P372), that there was no duty to warn against the danger. A warning would not tell a swimmer anything he did not already know. Nor was it necessary to do anything else. 'I do not think,' said the judge, 'that the defendants' legal duty to the plaintiff in the circumstances required them to take the extreme measures which were completed after the accident.' Even if Mr Tomlinson had been owed a duty under the 1957 Act as a lawful visitor, the council would not have been obliged to do more than they did."
[7.35]After summarising the opinions delivered in the Court of Appeal, Lord Hoffmann went on:
"34 My Lords, the majority of the Court of Appeal appear to have proceeded on the basis that if there was a foreseeable risk of serious injury, the council was under a duty to do what was necessary to prevent it. But this in my opinion is an over-simplification. Even in the case of the duty owed to a lawful visitor under section 2(2) of the 1957 Act and even if the risk had been attributable to the state of the premises rather than the acts of Mr Tomlinson, the question of what amounts to 'such care as in all the circumstances of the case is reasonable' depends upon assessing, as in the case of common law negligence, not only the likelihood that someone may be injured and the seriousness of the injury which may occur, but also the social value of the activity which gives rise to the risk and to the cost of preventative measures. These factors have to be balanced against each other.
35 For example, in Overseas Tankship (UK) Ltd v Miller Steamship Co Pty (The Wagon Mound (No.2)) [1967] 1 A.C. 617, there was no social value or cost saving in the defendant's activity. Lord Reid said, at p.643:
'In the present case there was no justification whatever for discharging the oil into Sydney Harbour. Not only was it an offence to do so, but it involved considerable loss financially. If the ship's engineer had thought about the matter, there could have been no question of balancing the advantages and disadvantages. From every point of view it was both his duty and his interest to stop the discharge immediately.'
36 So the defendants were held liable for damage which was only a very remote possibility. Similarly in Jolley v Sutton London Borough Council [2000] 1 W.L.R. 1082 there was no social value or cost saving to the Council in creating a risk by leaving a derelict boat lying about. It was something which they ought to have removed whether it created a risk of injury or not. So they were held liable for an injury which, though foreseeable, was not particularly likely. On the other hand, in The Wagon Mound (No.2) [1967] 1 A.C. 617 Lord Reid, at p.642, drew a contrast with Bolton v Stone [1951] A.C. 850 in which the House of Lords held that it was not negligent for a cricket club to do nothing about the risk of someone being injured by a cricket ball hit out of the ground. The difference was that the cricket club were carrying on a lawful and socially useful activity and would have had to stop playing cricket at that ground.
37 This is the kind of balance which has to be struck even in a situation in which it is clearly fair, just and reasonable that there should in principle be a duty of care or in which Parliament, as in the 1957 Act, has decreed that there should be. And it may lead to the conclusion that even though injury is foreseeable, as it was in Bolton v Stone, it is still in all the circumstances reasonable to do nothing about it."
[7.36]After contrasting the 1957 and 1984 Acts, Lord Hoffmann turned to the balance under the 1957 Act. He said, at para.39, "I accept that we are concerned with the steps, if any, which should have been taken to prevent any kind of water accident." He also said that "there is obviously some degree of risk in swimming and diving, as there is in climbing, cycling, fell-walking and many other such activities." He decided that the financial cost of taking preventative measures was not a significant item in the balancing exercise. Then at para.41 he said:
"There are two other related considerations which are far more important. The first is the social value of the activities which would have to be prohibited in order to reduce or eliminate the risk from swimming. And the second is the question of whether the council should be entitled to allow people of full capacity to decide for themselves whether to take the risk."
[7.37]After discussing the social value of the activities, Lord Hoffmann, under the heading "Free will" said:
"44 The second consideration, namely the question of whether people should accept responsibility for the risks they choose to run, is the point made by Lord Phillips of Worth Matravers M.R. in Donoghue v Folkestone Properties Ltd [2003] Q.B. 1008, 1024, para.53 and which I said was central to this appeal. Mr Tomlinson was freely and voluntarily undertaking an activity which inherently involved some risk. By contrast, Miss Bessie Stone (Bolton v Stone [1951] A.C. 850), to whom the House of Lords held that no duty was owed, was innocently standing on the pavement outside her garden gate at 10 Beckenham Road, Cheetham when she was struck by a ball hit for six out of the Cheetham Cricket Club ground. She was certainly not engaging in any activity which involved an inherent risk of such injury. So compared with Bolton v Stone, this is an a fortiori case.
45 I think it will be extremely rare for an occupier of land to be under a duty to prevent people from taking risks which are inherent in the activities they freely choose to undertake upon the land. If people want to climb mountains, go hang-gliding or swim or dive in ponds or lakes, that is their affair. Of course the landowner may for his own reasons wish to prohibit such activities. He may [...] think that they are a danger or inconvenience to himself or others. Or he may take a paternalist view and prefer people not to undertake risky activities on his land. He is entitled to impose such conditions, as the Council did by prohibiting swimming. But the law does not require him to do so.
46 My Lords, as will be clear from what I have just said, I think that there is an important question of freedom at stake. It is unjust that the harmless recreation of responsible parents and children with buckets and spades on the beaches should be prohibited in order to comply with what is thought to be a legal duty to safeguard irresponsible visitors against dangers which are perfectly obvious. The fact that such people take no notice of warnings cannot create a duty to take other steps to protect them. I find it difficult to express with appropriate moderation my disagreement with the proposition of Sedley L.J. [2003] 2 W.L.R. 1120, 1135, para.45, that it is 'only where the risk is so obvious that the occupier can safely assume that nobody will take it that there will be no liability'. A duty to protect against obvious risks or self-inflicted harm exists only in cases in which there is no genuine and informed choice, as in the case of employees, or some lack of capacity, such as the inability of children to recognise danger (Herrington v British Railways Board [1972] A.C. 877) or the despair of prisoners which may lead them to inflict injury on themselves: Reeves v Comr of Police of the Metropolis [2000] 1 A.C. 360.
47 It is of course understandable that organisations like the Royal Society for the Prevention of Accidents should favour policies which require people to be prevented from taking risks. Their function is to prevent accidents and that is one way of doing so. But they do not have to consider the cost, not only in money but also in deprivation of liberty, which such restrictions entail. The courts will naturally respect the technical expertise of such organisations in drawing attention to what can be done to prevent accidents. But the balance between risk on the one hand and individual autonomy on the other is not a matter of expert opinion. It is a judgment which the courts must make and which in England reflects the individualist values of the common law."
[7.38]At paras.48 and 49 Lord Hoffmann referred to defensive measures taken by the council officers to prevent the council from being held liable to pay compensation. He said that "local authorities and other occupiers of land are ordinarily under no duty to incur such social and financial costs to protect a minority (or even a majority) against obvious dangers". In any event there was little evidence that defensive measures had had much effect on diving injuries. He then concluded by saying:
"50 My Lords, for these reasons I consider that even if swimming had not been prohibited, and the council had owed a duty under section 2(2) of the 1957 Act, that duty would not have required them to take any steps to prevent Mr Tomlinson from diving or warning him against dangers which were perfectly obvious. If that is the case, then plainly there can have been no duty under the 1984 Act. The risk was not one against which he was entitled under section 1(3)(c) to protection. [....]"
[7.39]Lord Hutton, at pp.88-91, said:
"57 I thought for a time that [the reasoning of Ward L.J. in the Court of Appeal] was persuasive, but I have concluded that it should not be accepted because I consider that it is contrary to a principle stated in the older authorities which is still good law. In Stevenson v Glasgow Corporation 1908 S.C. 1034, 1039 Lord McLaren stated:
'in a town, as well as in the country, there are physical features which may be productive of injury to careless persons or to young children against which it is impossible to guard by protective measures. The situation of a town on the banks of a river is a familiar feature; and whether the stream be sluggish like the Clyde at Glasgow, or swift and variable like the Ness at Inverness, or the Tay at Perth, there is always danger to the individual who may be so unfortunate as to fall into the stream. But in none of these places has it been found necessary to fence the river to prevent children or careless persons from falling into the water. Now, as the common law is just the formal statement of the results and conclusions of the common sense of mankind, I come without difficulty to the conclusion that precautions which have been rejected by common sense as unnecessary and inconvenient are not required by the law.'
58 In Glasgow Corporation v Taylor [1922] 1 A.C. 44, 61 Lord Shaw of Dunfermline stated:
'Grounds thrown open by a municipality to the public may contain objects of natural beauty, say precipitous cliffs or the banks of streams, the dangers of the resort to which are plain.'
Lord Shaw then cited with approval the words of Lord McLaren in Stevenson v Glasgow Corporation 1908 S.C. 1034, 1038 that 'in a town, as well as in the country, there are physical features which may be productive of injury to careless persons or to young children against which it is impossible to guard by protective measures'. I think that when Lord McLaren referred to physical features against which 'it is impossible to guard by protective measures' he was not referring to protective measures which it is physically impossible to put in place; rather he had in mind measures which the common sense of mankind indicates as being unnecessary to take. This statement echoed the observation of the Lord President, Lord Dunedin, in Hastie v Edinburgh Magistrates 1907 S.C. 1102, 1106 that there are certain risks against which the law, in accordance with the dictates of common sense, does not give protection - such risks are 'just one of the results of the world as we find it'.
59 Stevenson v Glasgow Corporation and Hastie v Edinburgh Magistrates (which were not concerned with trespassers) were decided almost a century ago and the judgments are couched in old-fashioned language, but I consider that they express a principle which is still valid today, namely, that it is contrary to common sense, and therefore not sound law, to expect an occupier to provide protection against an obvious danger on his land arising from a natural feature such as a lake or a cliff and to impose a duty on him to do so. In my opinion this principle, although not always explicitly stated, underlies the cases relied on by the appellants where it has been held that the occupier is not liable where a person has injured himself or drowned in an inland lake or pool or in the sea or on some natural feature."
[7.40]After referring to other cases in which the judgment of Lord Shaw in Glasgow Corporation v Taylor had, expressly or implicitly, been applied, Lord Hutton concluded by saying:
"65 Therefore I consider that the risk of the plaintiff striking his head on the bottom of the lake was not one against which the defendants might reasonably have been expected to offer him some protection, and accordingly they are not liable to him because they owed him no duty. I would add that there might be exceptional cases where the principles stated in Stevenson v Glasgow Corporation 1908 S.C. 1034 and Glasgow Corporation v Taylor [1922] 1 A.C. 44 should not apply and where a claimant might be able to establish that the risk arising from some natural feature on the land was such that the occupier might reasonably be expected to offer him some protection against it, for example where there was a very narrow and slippery path with a camber beside the edge of a cliff from which a number of persons had fallen. But the present is not such a case [...]."
[7.41]In the course of his opinion Lord Hobhouse of Woodborough said, at p.94:
"74 Returning to the facts of this case, what more was it reasonable to expect of the defendants beyond putting up the notices and issuing warnings and prohibitions? It will not have escaped your Lordships that the putting up of the notices prohibiting swimming is the peg which the claimant uses to acquire the status of trespasser and the benefit of the suggested more favourable duty of care under the 1984 Act. But this is a case where, as held by the judge, all the relevant characteristics of this mere were already obvious to the claimant. In these circumstances, no purpose was in fact served by the warning. It told the claimant nothing he did already know [...]. There was no danger; any danger did not arise from the state of the premises; any risk of striking the bottom from diving in such shallow water was obvious; the claimant did not need to be warned against running that risk; it was not reasonable to expect the occupier to offer the claimant (or any other trespasser) any protection against that obvious risk."
[7.42]At pp.96-97, in para.81, Lord Hobhouse said:
"[I]t is not, and never should be, the policy of the law to require the protection of the foolhardy or reckless few to deprive, or interfere with, the enjoyment by the remainder of society of the liberties and amenities to which they are rightly entitled. Does the law require that all trees be cut down because some youths may climb them and fall? Does the law require the coastline and other beauty spots to be lined with warning notices? Does the law require that attractive waterside picnic spots be destroyed because of a few foolhardy individuals who choose to ignore warning notices and indulge in activities dangerous only to themselves? The answer to all these questions is, of course, no. But this is the road down which your Lordships, like other courts before, have been invited to travel and which the councils in the present case found so inviting. In truth, the arguments for the claimant have involved an attack upon the liberties of the citizen which should not be countenanced. They attack the liberty of the individual to engage in dangerous, but otherwise harmless, pastimes at his own risk and the liberty of citizens as a whole fully to enjoy the variety and quality of the landscape of this country. The pursuit of an unrestrained culture of blame and compensation has many evil consequences and one is certainly the interference with the liberty of the citizen."
[7.43]Counsel submitted that when it came to the alleged duty to cease manufacture, the court had to look at all the facts and circumstances of the case and determine what was reasonable in that context. The principle that the individual should be free to choose risks, and if he did so that he must take the responsibility if harm resulted, applied even where the risk was one of death. The balance between risk on the one hand and individual autonomy on the other was recognised by the courts in Scotland, like those in England, and reflected the individualist values of the common law here. The principles of the English common law of tort and the Scottish common law of delict were likely to be the same, as for example in the field of employment law. Tomlinson was an example of a case where there was not even a duty to warn against risks which were obvious. An individual's responsibility required that it was for the individual, when he made his choices, to satisfy himself whether or not there was a risk, and if so what it was, and then to decide whether he was going to run it.
[7.44]Reference was next made to Reeves v Commissioner of Police of the Metropolis [2000] 1 A.C. 360. The deceased in this case was held in a police cell in the custody of the defendant's officers, who had been alerted to the risk that he might commit suicide, although a doctor who examined him soon after his arrival at the police station stated that he showed no evidence of any psychiatric disorder or clinical depression. Taking advantage of the officers' inadvertence in leaving the flap of the cell door open, the deceased tied his shirt through the spy-hole on the outside of the door and hanged himself. In an action for negligence begun by the plaintiff as administratrix of his estate, the defendant raised the defences of, inter alia, novus actus interveniens and contributory negligence under the Law Reform (Contributory Negligence) Act 1945. The judge found that the defendant's officers were in breach of a duty of care to take reasonable steps to prevent the deceased's suicide but held that since he was of sound mind his deliberate act entitled the defendant to rely on the suicide as a novus actus interveniens, and accordingly dismissed the action. On the issue of contributory negligence the judge assessed the deceased's responsibility at 100%. The Court of Appeal, by a majority, allowed the plaintiff's appeal on the grounds that the duty of care to the deceased existed irrespective of his state of mind, that his suicide, being the very act against which the defendant had been required to guard, did not constitute a novus actus interveniens, and that in all the circumstances it was inappropriate to reduce the award of damages to reflect the deceased's responsibility for his loss.
[7.45]On the defendant's appeal, a majority of the House of Lords held that a deliberate and informed act intended to exploit a situation created by a defendant did not negative causation where the defendant was in breach of a specific duty imposed by law to guard against that very act; that those entrusted with the custody of prisoners had a duty to take reasonable care for their safety while in custody whether they were of sound or unsound mind; and that, accordingly, since the defendant was admittedly in breach of duty, the deceased's act in taking his own life did not entitle the defendant to rely on the defences of novus actus interveniens or volenti non fit iniuria. The House, however, held, in allowing the appeal, that "fault" within the meaning of section 4 of the Act of 1945 could include intentional acts as well as negligence; that the deceased had responsibility for his own life and since his intentional act while he was of sound mind was a substantial cause of his death, the defence of contributory negligence succeeded; and that, having regard to all the circumstances, responsibility for the suicide should be apportioned equally between the deceased and the defendant and the damages reduced accordingly.
[7.46]At pp.367 to 368 Lord Hoffmann said:
"The commissioner appeals to your Lordships' House. Mr Pannick argued two points on his behalf. The first was the question of causation: was the breach of duty by the police a cause of Mr Lynch's death? The way he put the answer was to say that the deliberate act of suicide, while of sound mind, was a novus actus interveniens which negatived the [causal] connection between the breach of duty and the death. He said at first that he was going to argue the application of the maxim volenti non fit iniuria as a separate point. But when it came down to it, he accepted that if the breach of duty was a cause of the death, he could not succeed on volenti non fit iniuria. I think that is right. In the present case, volenti non fit iniuria can only mean that Mr Lynch voluntarily caused his own death to the exclusion of any [causal] effect on the part of what was done by the police. So I think it all comes to the same thing: was the breach of duty by the police a cause of the death? [...]
On the first question, Mr Pannick relied upon the general principles stated in Hart and Honoré, Causation and the Law, 2nd ed. (1985), p.136:
'the free, deliberate and informed act or omission of a human being, intended to exploit the situation created by a defendant, negatives [causal] connection.'
However, as Hart and Honoré also point out, at pp.194-204, there is an exception to this undoubted rule in the case in which the law imposes a duty to guard against loss caused by the free, deliberate and informed act of a human being. It would make nonsense of the existence of such a duty if the law were to hold that the occurrence of the very act which ought to have been prevented negatived causal connection between the breach of duty and the loss. This principle has been recently considered by your Lordships' House in Environment Agency (formerly National Rivers Authority) v Empress Car Co (Abertillery) Ltd [1998] 2 W.L.R. 350. In that case, examples are given of cases in which liability has been imposed for causing events which were the immediate consequence of the deliberate acts of third parties but which the defendant had a duty to prevent or take reasonable care to prevent.
Mr Pannick accepted this principle when the deliberate act was that of a third party, but he said that it was different when it was the act of the plaintiff himself. Deliberately inflicting damage on oneself had to be an act which negatived causal connection with anything which had gone before.
This argument is based upon the sound intuition that there is a difference between protecting people against harm caused to them by third parties and protecting them against harm which they inflict upon themselves. It reflects the individualist philosophy of the common law. People of full age and sound understanding must look after themselves and take responsibility for their actions. This philosophy expresses itself in the fact that duties to safeguard from harm deliberately caused by others are unusual and a duty to protect a person of full understanding from causing harm to himself is very rare indeed. But, once it is admitted that this is the rare case in which such a duty is owed, it seems to me self-contradictory to say that the breach could not have been a cause of the harm because the victim caused it to himself."
At the top of p.369 Lord Hoffmann added:
"The duty, as I have said, is a very unusual one, arising from the complete control which the police or prison authorities have over the prisoner, combined with the special danger of people in prison taking their own lives."
[7.47]Lord Hope of Craighead said, at pp.379-380:
"It is unusual for a person to be under a duty to take reasonable care to prevent another person doing something to his loss, injury or damage deliberately. On the whole people are entitled to act as they please, even if this will inevitably lead to their own death or injury. As a general rule the common law duty of care is directed towards the prevention of accidents or of injury caused by negligence. The person to whom the duty is owed is, of course, under a corresponding duty to take reasonable care for his own safety. If he is in breach of that duty, his damages may be reduced on the ground of his contributory negligence. But if he injures himself by intentionally doing deliberately the very thing which the defendant is under a duty to prevent him doing negligently, he may find that he is unable to recover any damages. He may be found to have assumed the risk of injury, on the principle of volenti non fit iniuria. Or it may be held that the chain of causation was broken by his deliberate act, in which case his claim will be defeated on the principle of novus actus interveniens. Or it may simply be that his loss, injury and damage will be held to have been caused wholly by his own fault with the result that there will be no room even for a reduced award on the ground of contributory negligence."
[7.48]Counsel said that he referred to this case because of the emphasis on the individualist philosophy of the common law and the principle that people of full age and sound understanding must look after themselves and take responsibility for their actions. In a case such as that of Reeves, the duty arose because of the special relationship which existed and was a reflection of the nature of that special relationship. The relationship between a manufacturer and a consumer did not fall into this type of special category.
[7.49]Counsel submitted that this was consistent with Scottish authority. In Law Hospital NHS Trust v Lord Advocate 1996 S.C. 301 a patient suffered from irreversible damage to the cerebral cortex and fell into a persistent vegetative state in 1992. Permanently insensate, the patient remained alive only because feeding and hydration were provided to her artificially and because of the nursing care she received in a hospital. Medical experts opined that her case was useless and that there were no useful avenues of treatment to explore. The patient was unable to consent to treatment ceasing and her family agreed with the experts that the treatment should stop. The hospital raised an action, concluding for declarator that the proposed course of terminating nutrition and hydration and all other life sustaining treatment to the patient would not be unlawful. In the course of his opinion the Lord President, Lord Hope, said at p.306:
"It may be helpful if I were to describe at the outset what I consider to be the function of the Court in a case of this kind. It belongs to a group of cases which have been recurring with increasing frequency in recent years where the courts are being asked to give their authority to actions to be taken by medical practitioners which raise acute questions of moral or ethical principle. Medical science has now advanced to such a degree that many techniques are now possible which only a generation ago would have been unthinkable. The ability to prolong life by artificial means has reached such a stage that it is possible to nourish the body and preserve it from disease so that life in the clinical sense may be continued indefinitely. Invasive techniques such as those of sterilisation are also possible without the slightest risk of any other physical injury than that which is to be inflicted deliberately. Where the patient is of full age and capable of understanding and consenting to the procedures which on medical advice are for his or her benefit, or decides to refuse medical treatment, the right of self determination provides the solution to all problems, at least so far as the court is concerned. It is not in doubt that a medical practitioner who acts or omits to act with the consent of his patient requires no sanction or other authority from the court. The patient's consent renders lawful that which would otherwise be unlawful. It is not for the court to substitute its own views as to what may or may not be in the patient's best interests for the decision of the patient, if of full age and capacity."
Counsel submitted that this was an example of the court's recognition of the fundamental right of self determination. This was consistent with the "individualist philosophy" of the law described by Lord Hoffman.
[7.50]Against this background, counsel submitted, in the present case it was critical for the pursuer to establish, first, that Mr McTear was not aware of the health risks associated with smoking when he started smoking and, secondly, that by the time he became aware of these risks something irrevocable had happened. This was that there must have been some change which had occurred within him that was eventually going to lead to a diagnosis of lung cancer: this was to be regarded as the moment when he suffered damage. Counsel referred to this as the time when he contracted lung cancer, although it might have been, so far as the evidence disclosed, at any time, long or short, before he was actually diagnosed as having lung cancer. Without establishing these two things, the pursuer's case inevitably failed, because she failed to establish that there was any breach of duty on the part of ITL which caused Mr McTear's lung cancer.
[7.51]This brought counsel on to a preliminary question, which was to do with establishing the relevant date for assessing whether or not Mr McTear suffered injury as a result of breach of duty on the part of ITL. Mr McEachran had submitted that the date of breach should be 1957, but Mr Jones submitted that this was just wrong. It was wrong to consider the question of duty in the abstract. The correct question was whether or not Mr McTear suffered injury as a result of any breach by the defenders of a duty of care owed to him and then, if so, to consider when he suffered injury. That then was the moment of the breach.
[7.52]Counsel referred to Hamilton v Fife Health Board 1993 S.C. 369 in support of this submission. A child was born in 1976 and died three days later in consequence of injuries sustained by it while in utero which were allegedly caused by negligent acts on the part of the doctors attending the child's mother. The parents of the child brought an action against the health board seeking damages for loss of the child's society. The defenders argued that the action was irrelevant as the child had not been a person for the purposes of the 1976 Act at the time when the injuries were sustained. The Lord Ordinary held that personal injuries could only be sustained by a person and that the child had not been a person at the relevant time. The pursuers reclaimed.
[7.53]It was held by the First Division, reversing the judgment of the Lord Ordinary, that the case depended on the construction to be placed upon section 1(1) of the Damages (Scotland) Act 1976, that there could be no liability until both damnum and iniuria concurred, but once the child was born and became a person the necessary concurrence was established and the child acquired the right to sue the person whose breach of duty resulted in its loss; and it followed that the defenders were liable to pay damages to the pursuers in accordance with section 1(1) of the 1976 Act. Lord McCluskey said at p.382:
"As the act or omission must be one giving rise to liability to pay damages, there can be no liability until both damnum and iniuria concur. There can be no liability to pay damages until there is a person in respect of whose loss the claim to damages arises."
Lord Caplan said, at p.388:
"However the duty is not breached nor does a right of action arise at the point when the careless act is committed (assuming there were such an act). The duty which rests on a person charged with taking care is not the academic responsibility of not being negligent but rather the duty not to cause harm by negligence. The delict is only committed when the initial negligent act actually causes harm. That is to say the concurrence of iniuria and damnum is required. Thus as Lord Reid said in Watson v Fram Reinforced Concrete Co (Scotland) Ltd 1960 S.C. 92 at p.109:
'The ground of any action based on negligence is a concurrence of duty and damage and I cannot see how there can be that concurrence unless the duty still exists and is breached when the damage occurs.'
As Phillips J. puts it in de Martell v Merton & Sutton Health Authority [1993] Q.B. 204 at p.218:
'The duty in the law of negligence is not a duty to exercise reasonable care to avoid risk of causing injury. It is the duty not to cause injury by want of reasonable care.'"
[7.54]Counsel also referred to Watson v Fram Reinforced Concrete Co (Scotland) Ltd 1960 S.C. (H.L.) 92. In this case a workman, who had been injured through the breaking of a defective part in the machine with which he was working, brought an action of damages against his employers, and later convened as second defenders the manufacturers of the machine, who had supplied it to his employers, on averments to the effect that the accident had been caused by the fault of the manufacturers in that they failed to supply his employers with a machine which was safe for use by their servants. The machine had been supplied on 7 July 1955 and the accident had happened on 9 August 1956, but the manufacturers were not convened in the action until 25 March 1959. The House of Lords held that the three-year limitation period provided by section 6(1)(a) of the Law Reform (Limitation of Actions &c.) Act 1954 ran from the date when the workman suffered the injury and that, accordingly, the action against the manufacturers was not time-barred.
[7.55]Lord Reid said, at pp.109-110:
"It appears to me that default in the sense of breach of duty must persist after the act or neglect until the damage is suffered. The ground of any action based on negligence is the concurrence of breach of duty and damage, and I cannot see how there can be that concurrence unless the duty still exists and is breached when the damage occurs. Suppose that the damage occurred a year or two years after the manufacture and sale of the article: then undoubtedly the injured person can sue. But how could he sue if the manufacturer could say that his default had ceased a year before the injured person ever came near the dangerous article? Whatever be the true view with regard to the act or neglect, I think that the appellant is entitled to say that the respondents' 'default giving rise to the action' existed at the time when he suffered his injuries."
[7.56]Lord Keith of Avonholm, at pp.112-113, said:
"Now this is a Donoghue v Stevenson type of case, and such a case undoubtedly introduces specialities into the law of negligence. But, on any view, I see difficulty in saying that there was negligence at the date of supply. At that date on the pursuer's pleadings there was no reason why the manufacturers should have known of the dangerous state of the strut. It can hardly be expected that they had a legal duty to take it to pieces and inspect it before sending it out. Undoubtedly there was an act of carelessness on the part of some workman when the pin was welded to the strut and the manufacturers would be vicariously responsible for that carelessness. But can it be said that at either date there was an act of negligence in the legal sense? The manufacturers owed a duty to anyone who should handle the machine to take reasonable steps to see that it was safe. They owed a duty not to injure, but until someone was injured there was no breach of duty. Only then could it be said that an act of negligence had been committed. That, I think, necessarily follows from the judgment of this House in Donoghue v Stevenson."
Then, after analysing the decisions in Heaven v Pender (1883) 11 Q.B.D. 503, Donoghue v Stevenson and Grant v Australian Knitting Mills Ltd, Lord Keith said, at p.113:
"Applying the ratio of these decisions there was, in my opinion, no act, neglect or default within the meaning of the statute affecting the pursuer until he was injured. A fortiori there was no act, neglect or default giving rise to his action before that date. It was then for the first time that there arose a breach of duty which made its impact on the pursuer. Time, in my opinion, commenced to run against the pursuer under the statute from that date."
[7.57]Lord Denning, at pp.115-116, under reference to Donoghue v Stevenson, said:
"I think the true principle is contained simply in this: 'You must not injure your neighbour by your fault.' It is the doing of damage to him which, in my opinion, is the breach of duty giving rise to the action. It is no doubt correct to say, as Lord MacMillan did say (at p.71), that the manufacturer 'is under a duty to take care in the manufacture of these articles.' That is a duty which he owes to all those who may have occasion to use the article: and it is a duty which is broken at the time when he is negligent in making the article. But it is not a breach of duty to any particular individual. And it is not that breach of duty which gives rise to the action. There is another duty also to be considered: and that is the duty which Lord Atkin put in this wise (at p.44): 'You must not injure your neighbour': which I would expand so as to say that there is a duty on every man not to injure his neighbour by his want of reasonable care. This is a duty which he owes, not to the world at large, but to his neighbour. It is broken only when his neighbour is injured and not before. Then, and then only, is there a breach of duty giving rise to an action."
[7.58]Mr Jones said that the intriguing question which arose in this case was that Mr McTear might or might not have started smoking in 1964. If he did, then that clearly was the earliest date on which he could have suffered injury as a result of any breach of duty on the part of ITL. At some time, which in counsel's submission was when he started smoking, but even if it was not, he became aware of the health risks said to be associated with smoking. At that moment there was no breach of duty on the part of ITL, even assuming that there had earlier been some breach because of a failure to warn. This was because the authorities showed that once he knew of the risks then there was no need to warn him. In counsel's submission, it would have to be found that Mr McTear contracted lung cancer before the moment when any putative breach on the part of ITL came to an end, because unless there was that concurrence of damnum and iniuria, there was no liability on their part.
[7.59]This of course proceeded on the assumption, contrary to counsel's primary submissions on the facts, that it was held that smoking could cause lung cancer and caused Mr McTear's lung cancer. In that event, I would be relying on the epidemiology, and the evidence was that after about fifteen years' cessation, the risk returned to normal. So I could not find that by the time that the breach of duty ceased, Mr McTear had inhaled enough cigarette smoke to constitute a material contribution to a subsequent development of lung cancer, unless the "guilty exposure" occurred within about fifteen years before Mr McTear was diagnosed as having contracted lung cancer. Even assuming that Mr McEachran was correct in his submission that Mr McTear became aware of the risks to health associated with smoking in 1971 by reason of the Government health warnings appearing on cigarette packets, and attempted to stop smoking then, any contribution made by the hypothetical negligence of ITL would have ceased to have effect between 1981 and 1986. Mr McTear was diagnosed as suffering from lung cancer in 1992, and there was reason to suppose that he might have had diagnosable lung cancer in 1991. If he had stopped smoking at any time up to 1975, on that evidence the risk would have returned to normal.
[7.60]Counsel's main submission, however, was that it could not be determined on the evidence when there was a concurrence of iniuria and damnum. Without such evidence, there could be no liability. There was no evidence that when Mr McTear consumed his first cigarette or packet of cigarettes, or had smoked for the first month after he began, that made any material contribution to his subsequent lung cancer. Without such evidence, it was not possible to determine when he contracted lung cancer in the sense counsel had advanced. It could not be determined that he contracted lung cancer at any time before he became aware of the health risks said to be associated with smoking, and it could not therefore be decided that his lung cancer was attributable to any breach of duty on the part of ITL, because the date of the concurrence of alleged breach and injury could not be determined.
[7.61]Mr Jones accepted that, if I were to hold that Mr McTear was unaware of the risks to health associated with smoking until some time after he started smoking, and that from the outset a material contribution was being made to the lung cancer he eventually contracted, then he would be in more difficulty. But, he submitted, there was no evidence to that effect. Indeed the evidence was to the opposite effect, that the risk returned to normal after about fifteen years. On any view, Mr McTear was aware of the risk long before 1975, so there was no breach of duty after that date and therefore there could not have been a concurrence of injury and breach of duty when he first contracted his lung cancer. On this basis, there came a time when there was no continuing breach of duty on ITL and from that moment on Mr McTear took the risk of injury. The causal connection between the breach and the lung cancer was, in these circumstances, broken.
[7.62]The test, counsel submitted, was whether, but for Mr McTear's smoking up until the moment he became aware of the risks to health, he would not have contracted lung cancer. The idea of individual responsibility carried with it the freedom to choose among various options. The law proceeded on the basis that the consumer to whom a manufacturer might have to have regard was a reasonable man, because that was the only way in which the law could sensibly operate. Such a man would do what was reasonable in the circumstances. The moment that Mr McTear contracted his lung cancer was the moment at which it fell to be determined whether there existed any duty owed by ITL to Mr McTear, and if so what was its nature. It was essential for the pursuer to prove, not only that Mr McTear was unaware of the health risks associated with smoking when he started, but also that prior to the date when he became aware of the health risks he had already contracted lung cancer or a material contribution had already been made to his contracting lung cancer. Mr McTear's continuing smoking once he was aware of the health risks was entirely his responsibility. ITL could have no liability to Mr McTear from the moment that he became aware of the health risks associated with smoking unless in some sense the damage was already done. It could not be said that they were at fault thereafter unless it was established that, when Mr McTear started smoking, the nature of cigarettes was such that he would not be able to stop, ITL knew this, Mr McTear did not and therefore they were in breach of a duty to warn him of it.
[7.63]None of that was made out in the present case. There was no evidence that ITL had any reason to believe that anybody who started smoking might be unable to stop. On the evidence, some people might find it difficult to stop, but there was no evidence that Mr McTear did not know that when he started smoking. Without that foundation, any case based on inability to stop smoking simply failed. On the evidence, the pursuer's case was perilled on showing that Mr McTear was damaged by the time he first became aware of the health risks said to be associated with smoking. The very earliest date for that would be 1964, and there was nothing on the evidence that would allow the court to hold that to be proved.
[7.64]Counsel then turned to look at the content of any duty of care. It followed from the individualist philosophy that the common law did not in general impose a duty on manufacturers not to produce or sell goods, the use or consumption of which involved risks to health. The legislature might intervene to regulate or even prohibit the manufacture and sale of particular commodities, but that did not trench upon the individualist assumptions of the common law. The policy of the common law in the context of product liability was not that all risk should be eliminated but, consistently with the underlying principle of individual autonomy, that consumers should not be exposed to dangers of which they could not reasonably be expected to be aware. In Donoghue v Stevenson the manufacturer was in breach of duty, not simply because there was a snail in the ginger beer bottle, but because the bottle was opaque and the dangerous snail was unlikely to be discovered by any intermediate inspection before the consumer poured the ginger beer into her glass. If the risks associated with the use of the product were patent, it was up to the consumer to decide whether or not he or she wished to use or consume the product.
[7.65]Counsel referred to the speeches of Lord Atkin, Lord Thankerton and Lord MacMillan in Donoghue v Stevenson, quoted at paras.[7.4] to [7.7]. Counsel submitted, on the basis of these passages, that the absence of any reasonable opportunity for inspection or intermediate examination was an essential feature of the type of liability identified in that case. If the policy of the law were to eliminate risk to the consumer, the possibility or the opportunity for intermediate inspection would be an irrelevant consideration in determining the existence and scope of a duty of care owed by the manufacturer to the consumer, because the opportunity for inspection could not be said necessarily to eliminate the risk. Because the consumer should be free to choose whether or not to run risks, then the opportunity for intermediate inspection became relevant. Until the decision in Donoghue v Stevenson in the Court of Session, the only line of authority which permitted recovery where a consumer was injured by a product was where it was established that the product was dangerous in itself. Donoghue v Stevenson introduced for the first time the possibility of recovery where injury was caused by a defective product. The decision assimilated this area of the law, so that liability for defective products and liability for dangerous products moved forward together, according to the same principles; and the duty then of the manufacturer was to take such care as was reasonable in the whole circumstances. This could be seen from the speech of Lord Atkin in particular.
[7.66]The scope of the principle in Donoghue v Stevenson was stated by Lord Wright in Grant v Australian Knitting Mills Ltd and by Lord Keith of Kinkel in Murphy v Brentwood District Council [1991] 1 A.C. 398. In the latter case the House of Lords held inter alia that, while the principle in Donoghue v Stevenson applied to impose a duty on the builder of a house to take reasonable care to avoid injury or damage, through defects in its construction, to the persons or property of those whom he ought to have in contemplation as likely to suffer such injury or damage, that principle as stated extended only to latent defects.
[7.67]Lord Keith of Kinkel said at p.464:
"[A]n essential feature of the species of liability in negligence established by Donoghue v Stevenson was that the carelessly manufactured product should be intended to reach the injured consumer in the same state as that in which it was put up with no reasonable prospect of intermediate examination: see per Lord Atkin, at p.599; also Grant v Australian Knitting Mills Ltd [1936] A.C. 85, 103-105, per Lord Wright. It is the latency of the defect which constitutes the mischief. There may be room for disputation as to whether the likelihood of intermediate examination and consequent actual discovery of the defect has the effect of negativing a duty of care or of breaking the chain of causation [...]. But there can be no doubt that, whatever the rationale, a person who is injured through consuming or using a product of the defective nature of which he is well aware has no remedy against the manufacturer."
[7.68]Lord Jauncey of Tullichettle said, at p.492:
"In the 40 years after Donoghue v Stevenson it was accepted that the principles enunciated by Lord Atkin were limited to cases where there was physical damage to person or to property other than the property which gave rise to the damage and where there was no reasonable opportunity of discovering the defect which ultimately caused the damage: Grant v Australian Knitting Mills Ltd [1936] A.C. 85, Farr v Butters Brothers & Co [1932] 2 K.B. 606."
At pp.494-5 Lord Jauncey said that two matters emerged clearly from Lord Atkin's speech in Donoghue v Stevenson, one of which was "that the duty only extended to articles which were likely to be used before a reasonable opportunity of inspection had occurred."
[7.69]Counsel then turned to consider the duties of a manufacturer who produced a product, the use or consumption of which involved inherent risks. He submitted that such a manufacturer had a duty to act reasonably in all the circumstances. Reference was made first to Holmes v Ashford [1950] 2 All.E.R. 76. In this case a hairdresser treated the plaintiff's hair with a dye, and as a result the plaintiff contracted dermatitis. The dye had been delivered to the hairdresser in labelled bottles together with a small brochure of instructions. Both the labels and the brochure contained a warning that the dye might be dangerous to certain skins, and a recommendation that a test should be made before it was used. The hairdresser had read the labels and the brochure and was aware of the danger, but he made no test and did not warn the plaintiff. The plaintiff claimed damages against the hairdresser and the manufacturers, and was awarded judgment against both. On appeal by the manufacturers, the Court of Appeal held that a manufacturer who put a dangerous article on the market must take reasonable steps to prevent any person coming into contact with it from being injured, but it was not necessary in every case that precautions should be taken to ensure that the ultimate recipient of the article was warned of the danger; in the present case the manufacturers had given the hairdresser a warning which was sufficient to intimate to him the potential danger of the dye, and it was not necessary that they should have warned the plaintiff; and, therefore, they had discharged the duty which was on them.
[7.70]Tucker L.J. said, at p.77:
"A number of authorities have been cited to us by counsel for the plaintiff in support of the proposition that a manufacturer who puts a dangerous article on the market must take reasonable precautions to ensure that the ultimate recipient is warned of the danger. I think that that is not the correct way of stating the proposition. Every person who puts on the market a dangerous article (and the learned judge has found this to be a dangerous article) must take reasonable steps in all the circumstances. This is not an article the nature of which can be ascertained by intermediate examination, and, therefore, it is an article which requires some warning. The question in this case is: Was the warning attached to this bottle a sufficient and adequate warning to be given in cases where the material is supplied to hairdressers for use on their customers? We must presume that the material is supplied to reasonable people, and the first defendant has said that he read the warning, appreciated what it meant, and ignored it. I find it, therefore, impossible to hold that the warning which was, in fact, given in the present case was insufficient."
[7.71]Counsel submitted that this case yielded the proposition that the manufacturer must take such steps as were reasonable in all the circumstances, and the presumption that the product was supplied to reasonable people. If people did not act responsibly, then that was their choice and they must take the consequences. As a general proposition, where it could reasonably be presumed that the consumer knew or ought to know of a risk inherent in using a product, there was no duty on the manufacturer either to warn or to withdraw the product. Provided that the ordinary consumer was in a position to make an informed choice, the law left him to make that choice: he was free to consume or not to consume the product in question.
[7.72]Counsel contrasted the position of the ordinary consumer with that of an employee. He submitted that Wright v Dunlop Rubber Co Ltd did not yield the general proposition that if a manufacturer learned that his product was associated with the risk of contracting fatal diseases and death, he had a duty to withdraw the product from the market until he had eliminated the risk. The statement that the duty of the manufacturer to the purchaser's workmen in a case such as Wright was the same as the duty of a manufacturer towards his own workmen, subject to the proviso that the manufacturer knew how the goods were going to be used by the purchaser, put Wright into the category of cases where there was a relationship between the alleged wrongdoer and the claimant such as to affect the content of the duty of care and consequently the exercise of the duty of care. As in Tomlinson, the relationship was in a special category, because the employee was not free to choose whether or not to use the substance, and in any event had no knowledge of its nature. An employee did not have freedom to exercise choice. He had to do the work that his employer instructed him to do. As it was put in Tomlinson, where there was a relationship of a particular nature which brought particular duties, there might be a duty to protect the other person even against obvious risks or self-inflicted harm.
[7.73]Wright v Dunlop Rubber Co Ltd was considered by the Supreme Court of Victoria in Thompson v Johnson and Johnson Pty Ltd [1991] 2 V.R. 449. The plaintiff sued the defendants, who were manufacturers and distributors of a particular brand of tampon manufactured in New Zealand, and purchased by the plaintiff in November or December 1980 in Australia and used by her soon after, alleging negligence resulting in personal injuries to her in the form of toxic shock syndrome. In dismissing the plaintiff's appeal against the decision of Vincent J., the Appeal Division of the Supreme Court of Victoria held: (1) The duty of care in such a case as the present could not be categorised as being merely a duty to warn or alternatively to withdraw a product from the market. The duty was a duty to take reasonable care to avoid injury or harm being suffered by those using the product as intended. In each case it would be necessary for the tribunal of fact to determine whether in all the circumstances those marketing the goods failed to take reasonable care and whether that failure was a cause of the injury suffered by the user. (2) After a reported case of toxic shock syndrome in New Zealand in October 1980, the first defendant's position in Australia was still not to be equated with that of the manufacturer of the equivalent tampon in the United States. (3) The recommendation of the National Health and Medical Research Council (NHMRC) whether or not to give a warning was a relevant fact to be taken into account when determining whether reasonable care had been exercised. (4) It had not been established that within the relevant period of time the defendants were in breach of their duty of care by failing to give warning on or in packets of their tampons or by paid advertisement through the means of the print and electronic media. (5) Having regard to all relevant matters including the evidence of reluctance on the part of the Health Department in New Zealand to forward a draft letter prepared on behalf of the American manufacturer to medical practitioners in New Zealand, but rather a preference for handling such communications itself, the trial judge was in error in concluding that the defendants were in breach of their duty of care by failing to write to all Australian medical practitioners before the plaintiff's illness advising them of the risk of a relationship of toxic shock syndrome to the use of the tampons.
[7.74]At p.488 the Appeal Division considered a submission on behalf of the appellant that the trial judge should have found, and erred in not finding, that in the circumstances of the case the respondents were not in breach of any relevant duty of care owed by them to the appellant. The court said:
"The threshold question in considering the matter is to determine the scope of the duty of care owed by the respondents as distributors and manufacturers of Carefree Super tampons used by the appellant being one of the class of persons who could be reasonably foreseen to be purchasers and users of that product.
That a duty of care was owed by the respondents to the appellant was not disputed by the respondents. The tampons used by the appellant and manufactured by the second respondent and distributed by it to the first respondent and by it in turn to the public for purchase by that section of them using the same was of a nature, kind and composition as designed and intended. It was not part of the appellant's case that it suffered from any defect of fault brought about in its preparation or distribution as to give rise to consideration of that type of duty of care as was considered, for example, in Donoghue v Stevenson [1932] A.C. 562 and Grant v Australian Knitting Mills Ltd [1936] A.C. 85.
However, where the manufacturer and/or distributor of the product ought reasonably to have foreseen that there was a risk of injury, which was not far-fetched, in the sense referred to by Lord Reid in The Wagon Mound (No.2) [1967] A.C. 617 at pp.643-4 and by Mason J., as he then was, in Wyong Shire Council v Shirt (1980) 146 C.L.R. 40, at pp.46-7, there exists a relationship between the respondents and the appellant as a member of the class of persons likely to purchase and use the products so manufactured and distributed which gave rise to a duty of care by the respondents to the appellant.
The question is, 'what is the scope of that duty of care?' Is it to take reasonable care to avoid injury to the appellant from her use or continued use of the product? If such is the duty then in determining whether the respondents were in breach of their duty it is necessary to evaluate the magnitude of that risk and all other relevant circumstances and matters in order to determine whether the respondents' response to the risk was reasonable or whether it was such as to constitute a breach of the duty owed: see Wyong Shire Council v Shirt, at p.47. If, however, as was contended for on behalf of the appellant the scope of the duty was to warn the appellant as being a member of the class of persons to whom the duty was owed, of the risk involved in using or continuing to use Carefree Super tampons then, putting aside any question of causation in the event of a breach of their duty, the appellant would be entitled to succeed."
[7.75]The court then went on to consider a number of previous decisions, including Wright v Dunlop Rubber Co Ltd before continuing, at pp.490-492:
"It is a question of fact in each case whether the duty owed has been breached. It is not a question of law. The manufacturer and retailer must act reasonably in placing its product on the market. The almost infinite variety of circumstances forbid any categorical exegesis of the manner of performance of the relevant duty of reasonable care.
Accordingly the duty of care cannot be categorised in the circumstances of such a case as this as being merely a duty to warn or alternatively to withdraw the product from the market. The duty is a duty to take reasonable care in the Donoghue v Stevenson sense to avoid injury or harm being suffered by those using the product as intended. In some circumstances a discharge of such duty of care might require and demand that the product be withdrawn from the market so as to prevent it being used. In other circumstances in order to discharge the duty it might be necessary to give adequate warning as to the risks involved in its use. It does not follow that the failure to warn with respect to those risks will necessarily constitute a breach of duty. In each case it will be necessary for the tribunal of fact to determine whether in all the circumstances those marketing the goods failed to take reasonable care and whether that failure was a cause of the injury suffered by the user.
It follows that the fact that no warning was given in all the circumstances of this case must be examined in the light of the duty of the manufacturer and distributor to take reasonable care. In Wyong Shire Council v Shirt, at pp.47-8, Mason J. said:
'In deciding whether there has been a breach of the duty of care the tribunal of fact must first ask itself whether a reasonable man in the defendant's position would have foreseen that his conduct involved a risk of injury to the plaintiff or to a class of persons including the plaintiff. If the answer be in the affirmative, it is then for the tribunal of fact to determine what a reasonable man would do by way of response to the risk. The perception of the reasonable man's response calls for a consideration of the magnitude of the risk and the degree of probability of its occurrence, along with the expense, difficulty and inconvenience of taking alleviating action and any other conflicting responsibilities which the defendant may have. It is only when these matters are balanced out that the tribunal of fact can confidently assert what is the standard of response to be ascribed to the reasonable man placed in the defendant's position.
The considerations to which I have referred indicate that a risk of injury which is remote in the sense that it is extremely unlikely to occur may nevertheless constitute a foreseeable risk. A risk which is not far-fetched or fanciful is real and therefore foreseeable. But, as we have seen, the existence of a foreseeable risk of injury does not of itself dispose of the question of breach of duty. The magnitude of the risk and its degree of probability remain to be considered with other relevant factors.'
In his judgment the learned trial judge said, [1991] 2 V.R. 449, at p.468:
'Lying at the heart of this matter, however, is the necessity to ensure, as far as possible, that consumers are not unnecessarily or, through no fault of their own, unknowingly exposed to the risk of injury or other adverse consequences being suffered by reason of their use of products available to them in the marketplace.'
Again he said, at p.469:
'As a general proposition it appears to me to be obvious that where possible consequences of the contraction of a condition include death, even though the risk of any contraction may be very small, a potential purchaser is, at least, entitled to know of the existence of that risk and to be able to choose whether or not it will be accepted.'
If by those expressions his Honour meant that a manufacturer and/or distributor of goods to which such a risk as last referred to is attached and which risk would not ordinarily be apparent [...] has a duty or an obligation in order to satisfy that entitlement to warn of such risk as distinct from a duty to take reasonable care, we would disagree. If such was the case it would promote the duty to take reasonable care to an absolute duty to warn of such risk. The consequences of risk, which possibly may result in death, does not of itself give rise to a duty or obligation to warn of the risk. However, it would be a very material consideration to be regarded along with other material considerations when assessing whether the duty to take reasonable care in all the circumstances had been fulfilled."
[7.76]The court then went on to consider what they regarded as material considerations. Among these was the position of the NHMRC, of which the court said, at p.494:
"Whether or not the NHMRC recommended that a warning be given was not determinative of the question of reasonable care, for to accept that proposition would permit the respondents to abrogate the duty of reasonable care owed by them. It is not the response of such a body which determines whether a person in the position of the respondents is or is not negligent. That is for the courts to decide. However, it is a relevant fact to be taken into account when determining whether reasonable care has been exercised."
[7.77]The Appeal Division concluded this passage of their opinion, also at p.494, in these terms:
"The evidence was that in October and November 1980 there was much publicity about the matter of toxic shock syndrome. The fact was that the appellant was a reader of newspapers and regarded herself as having a fair general knowledge through the media but nevertheless she was unaware of toxic shock. These facts were relevant to the question whether a reasonable response by the respondents to the knowledge of the risk concerned called for the placing of advertisements in newspapers and/or advertising by means of the electronic media and whether a failure to do so constituted negligence.
Having regard to all these matters we have concluded that it was not established on the evidence that within the time frame in the circumstances of this case the respondents were in breach of the duty of care owed by them to the class of persons of whom the appellant was a member, by failure to give warning on or in packets of Carefree Super tampons or by paid advertisements [through] the means of the print and electronic media of the risk of the use of such tampons being associated with the onset of toxic shock syndrome."
The Appeal Division also decided that the trial judge was in error in concluding that the respondents who were the manufacturers and distributors of the product were in breach of the duty owed by them by failing to write to all medical practitioners in Australia before the plaintiff's illness advising them of the risk of the relationship of the onset of toxic shock syndrome to the use of tampons by menstruating women.
[7.78]Counsel submitted that this case demonstrated that a duty to warn was imposed where a danger was unknown; but it was a duty simply to warn adequately and not to insure against it. This duty might arise if the manufacturer knew or ought to know something which the consumer did not know and could not reasonably be expected to know, but if the existence of a risk was common knowledge as a result of information which was in the public domain, then the manufacturer might not be under any duty even to give a warning. In all cases it was for the consumer to make an informed choice. The authorities established that a manufacturer of consumer goods produced to meet a demand would not normally be acting unreasonably in continuing to produce and sell them, even if they involved risk, unless the risk was hidden from the public. It was enough to give a warning of risks to health. There was a duty on the manufacturer to warn, in the sense of giving information; the consumer should be made aware of any risk inherent in the use of the product so that he could exercise the choice whether to use the product or not. There was no authority for the proposition that the manufacturer had any duty to do more than inform, and in particular to persuade or shock or cajole. On the evidence in the present case, insofar as ITL were under a duty to give warnings of risks to health, they fulfilled this duty from 1971 onwards when Government health warnings first appeared on cigarette packets. These were not only sufficient for this purpose in general, but were in fact sufficient in the case of Mr McTear, who became aware of the risks to health caused by smoking in 1971, if not before.
[7.79]Counsel submitted that Wright v Dunlop Rubber Co Ltd laid down no strict rule about cessation of manufacture, it simply reiterated that a manufacturer should do what was reasonable in the whole circumstances of the case. Counsel next referred to Graham Barclay Oysters Pty Ltd v Ryan (2002) 211 C.L.R. 540. A representative action was brought in the Federal Court of Australia on behalf of a group of consumers who had contracted the hepatitis A virus after eating oysters harvested from the waters of Wallis Lake in New South Wales. The waters had been polluted by human faecal contamination which in turn contaminated the oysters. The applicants alleged that the grower of the oysters (GBO), the distributor (GBD), the local government authority for the area in which Wallis Lake was located (the council), and the State government were liable in negligence for the harm suffered. They also claimed that GBO and GBA were liable under various provisions of the Trade Practices Act 1974 (Cth), and an individual applicant brought a personal claim against GBO under sections 74B and 74D of that Act. The representative applicants succeeded against each respondent in negligence but failed in respect of claims based on sections 52, 71, 74C and 75AD of the Trade Practices Act. The individual succeeded in his personal claim under the Act. On appeal by the State and the council to a Full Court on the issue of existence of a duty of care to consumers of the oysters and by GBO and GBD on the issue of breach of the relevant duty of care and of sections 74B and 74D of the Act, all but the council's appeals were dismissed. On further appeal to the High Court of Australia, it was held, inter alia, by a majority that neither GBO nor GBD had breached its duty of care to the consumers.
[7.80]In the course of his opinion, Gaudron J. said, at p.571, para.64, contrasting the provisions of the Trade Practices Act 1974 and the general law of negligence:
"Although different concepts inform the law of negligence, ordinarily there is a duty to warn only if there is a foreseeable risk that a person will be led to believe that something is safe when it is not."
[7.81]McHugh J. said at p.583, para.101:
"The Barclay companies accepted that they owed oyster consumers a duty of care to ensure that the oysters were safe for human consumption. The issues in relation to the Barclay companies related to the scope of the duty of care that they owed to oyster consumers and whether there was a breach of that duty."
In the course of his consideration of these issues McHugh J. said at p.585, para.106:
"The duty of care owed by a manufacturer or producer to a consumer is a duty to take reasonable care to avoid injury to the consumer [footnote reference to Donoghue v Stevenson [1932] A.C. 562 at 599, per Lord Atkin]. To formulate the duty in more specific terms invites error because it is likely to mix a question of law (whether a duty existed) with a question of fact (whether a breach occurred). If the duty is formulated in specific terms, the issue on breach is whether the duty has been performed in accordance with the terms of the duty as formulated. But, as Wyong Shire Council v Shirt [footnote reference to (1980) 146 C.L.R. 40 at 47-48, per Mason J., Stephen and Aickin J.J. agreeing] shows, the question of breach is far more complex than an affirmative or negative answer to the question whether the defendant carried out the duty as formulated. It involves evaluating and weighing a number of competing considerations."
[7.82]After discussing the competing considerations, McHugh J. concluded, at p.587, para.113:
"In my opinion, the steps that the Barclay companies took [in suspending the harvesting of oysters for a period of several days during and after the heavy rain which led to the human faecal contamination] were a reasonable response to a very low risk of viral contamination. Reasonable care did not require them to go to the expense of conducting sanitary surveys - even if they could have done so effectively - or shutting down their business indefinitely or labelling their oysters with a warning concerning the risk of viral contamination. In nearly a century, no previous outbreak had occurred. What they did was in accordance with industry practice and at the time was a reasonable response to the slight possibility that consumers would suffer harm because of viral contamination caused by the heavy rain that occurred in November 1996."
[7.83]Gummow and Hayne JJ. said at pp.611-612, para.192:
"A duty of care that is formulated retrospectively as an obligation purely to avoid the particular act or omission said to have caused loss, or to avert the particular harm that in fact eventuated, is of its nature likely to obscure the proper inquiry as to breach [footnote reference to Brodie v Singleton Shire Council (2001) 206 C.L.R. 512 at 627-628 [309]]. That inquiry involves identifying, with some precision, what a reasonable person in the position of the defendant would do by way of response to the reasonably foreseeable risk. As Isaacs A-CJ observed in 1924, '[n]o conclusion of negligence can be arrived at until, first, the mind conceives affirmatively what should have been done' [footnote reference to Metropolitan Gas Co v Melbourne Corporation (1924) 35 C.L.R. 186 at 194]. The trial judge and the majority of the Full Court in the present case failed to identify with the necessary precision, by reference to considerations of the nature of those indicated in Wyong Shire Council, the reasonable response to the risk of harm that existed. In so failing, their Honours fell into an error of law."
[7.84]After discussing various courses of action, Gummow and Hayne JJ. said at p.614, para.201:
"Therefore, in practical terms, the alternatives open to the Barclay companies were (i) to cease harvesting and selling oysters after the November 1996 rainfall event until a sanitary survey was conducted and testing revealed an acceptable risk; or (ii) to sell oysters with a warning as to their possible viral contamination; or (iii) to cease growing oysters at Wallis Lake entirely, and, perhaps, to establish operations in pristine waters elsewhere. Given the attitude of both the Council and the State, and the apparent similarity between the November 1996 rainfall and previous rainfall events, option (i) effectively would have required the cessation of harvesting for an unspecified, potentially indefinite, period following any such heavy rainfall. Option (ii) is likely to have had the same effect as ceasing to sell oysters altogether. Option (iii) was not explored in any detail during argument and would have required relocation to some unspecified waterway isolated from human beings. Each of the three courses of action would have been either entirely destructive of, or highly disruptive to, the business of the Barclay companies. Each represents alleviating action of the most difficult, expensive and inconvenient type. According to the settled principles propounded in Wyong Shire Council, such alleviating action can only be required by the law of negligence if the magnitude of the risk and the degree of probability of its occurrence are great indeed."
At p.615, para.202, Gummow and Hayne JJ. said:
"Notwithstanding the significant magnitude of the risk of harm that eventuated in this case, the degree of probability of its occurrence cannot be said to justify the difficult, expensive and inconvenient alleviating action contended for by the consumers."
[7.85]Counsel submitted that this case afforded an example of the reinforcement in another jurisdiction of the correct approach, which was that there was no absolute duty to warn or to cease manufacture. Both that case, and Wright v Dunlop Rubber Co Ltd, were entirely consistent with the general proposition that a manufacturer of a product, the consumption of which might involve risk, had a duty to act reasonably in all the circumstances, but this did not dictate any particular result. On the contrary, a manufacturer of consumer goods would normally not be acting unreasonably in continuing to produce and sell them, even if consumption of them should involve risk, unless the risk was hidden from the public.
[7.86]Counsel went on to submit that the starting point in considering whether or not there was a duty to warn was to articulate the proposition about the risks or dangers attaching to the use of a product which it would be proper to make on the basis of the current state of the science. It was only against such a background that one could assess whether or not in all the circumstances it was incumbent upon the manufacturer to issue a warning. Once the risks were properly articulated, the extent to which knowledge of them was already in the public domain was an important consideration in determining whether or not a manufacturer who had not issued a warning had fulfilled his duty to act reasonably in all the circumstances. The cases established that there was in general no duty to warn in respect of risks which were patent or which one could reasonably anticipate would be discovered by intermediate inspection. In general, a manufacturer had no duty to warn of risks of which it would be reasonable to expect an ordinary consumer to be aware.
[7.87]Counsel referred to Bogle v McDonald's Restaurants Ltd [2002] E.W.H.C. 490 (Q.B.). In a trial of generic issues arising from the pleaded cases of a group of claimants suing for personal injuries caused by the spillage of hot drinks served by the defendant (McDonald's), the generic issues included:
"(5)Whether there was a duty upon the defendant to warn its customers as to the risk of scalding from hot drinks.
(6)If there was such a duty, whether the defendant was in breach of it."
Field J. discussed these generic issues at paras.63-69 of his opinion. At para.64 he noted the contentions for the claimants that there was a duty to warn for various reasons, including:
"(5)Whilst some customers might be aware of the risk, the duty to warn arises because some may not be aware of the risk."
[7.88]At para.65 Field J. said:
"I think it a fair inference that small children very rarely buy or intentionally consume coffee and tea in McDonald's Restaurants. (It is certainly the case that in all the claims that have been brought, the hot drinks were bought by an adult.) In my opinion, McDonald's could therefore expect that the great majority of those who bought hot drinks in their restaurants would be in their teenage years or above. In my judgement, these customers could be taken to know that the coffee and tea they were buying was hot and could cause a nasty scalding injury if it spilled on someone. Most customers would not know precisely how hot the drink was, but they would know that tea and coffee is made with very hot water. Nor would most customers know just how severe the scalding injury could be, but they would know that it could be very painful and serious. They would also know that drinks occasionally get spilled in restaurants such as those run by McDonald's."
[7.89]At para.67, he said:
"Whether McDonald's were negligent in not warning their customers depends on an objective assessment of all the circumstances, including the risk of injury and the customers' appreciation of those matters that gave rise to the risk. As I have said, I am quite satisfied that those who bought coffee and tea could be taken to know that such drinks sometimes get spilled and are served at temperatures which cause serious and painful injury if they come into contact with someone's skin. I accordingly find that there was no duty on McDonald's to warn their customers about the risk posed by the temperatures at which tea and coffee were served, notwithstanding the warnings they gave to their employees and the fact that from 1995 a warning has been printed on the cups."
[7.90]Counsel submitted that in this case the court adopted the approach of what it was reasonable to do in the whole circumstances. This was consistent with the general approach in the leading authorities. Reference was next made to Hodge & Sons v Anglo-American Oil Co (1922) 12 Ll.L.R. 183. In the first action the plaintiffs who were barge repairers in London claimed damages arising out of an explosion on the Anglo-American Oil Company's oil tank barge Warwick, when she was being repaired by the plaintiffs, to whom she had been sent for that purpose by the defendants Messrs Miller & Co. As a result of the explosion several lives were lost and considerable damage done. In the second action, which was in the nature of a test action, the plaintiff, a boilermaker employed by Messrs Hodge & Sons, claimed damages for personal injuries caused by the explosion.
[7.91]In the course of his opinion Bankes L.J. said, at pp.184-185, after narrating the circumstances:
"It is in these circumstances that the question of liability arises. The Anglo-American Oil Co were, in my opinion, under a double duty, (a) the duty of using reasonable means for securing the efficient cleaning out of the tank, and (b) the duty of giving any necessary warning of the dangerous character of the tank even after a proper and sufficient cleaning. The first duty, in my opinion, extended to all those who necessarily came into contact with the tank in the course of carrying out the repairs, including therefore the plaintiff Willmott. With regard to the second duty, a warning would not, in my opinion, be required where the person who would otherwise be entitled to warning was already aware of the danger, or [...] might reasonably be assumed to be aware of it. Messrs Miller obviously required no warning; they were perfectly well aware of the danger. Messrs Hodges were in relation to the Anglo-American Oil Co in a different position to Messrs Miller: but I assume that the Anglo-American Oil Co were aware that the barge was being sent to Messrs Hodges for repair. If so, Messrs Hodges would be entitled to a warning unless they, like Messrs Miller, are to be taken to have been aware of the danger. Having regard to what must be the state of knowledge among ship and barge repairers on the Thames as to the danger of dealing with cleaned petrol tanks, I think that the Anglo-American Oil Co were entitled to assume that Messrs Hodges needed no warning as to that danger. [...]
I do not think that the present is a case in which the Anglo-American Oil Co were under any duty to Messrs Hodges' workmen to give them any individual warning. Whether a warning to an employer of the dangerous character of an article sent to him for repair is a sufficient warning to the workmen directed by the employer to carry out those repairs must be a question of fact depending upon the particular circumstances of each case. There are in this case, in my opinion, no such special circumstances as placed the Anglo-American Oil Co under any duty to give any warning to the plaintiff Willmott or to the other employees of Messrs Hodges."
[7.92]In the course of his opinion Scrutton L.J. reviewed the cases bearing on the question whether a warning ought to have been given, and at p.187 he said:
"But all the cases cited distinguish the case of a thing in its nature dangerous without warning, described by Lord Shand in Caledonian Railway Co v Mulholland [1898] A.C. 216, at p.292, citing the argument of the present Lord Dunedin, then Lord Advocate, as 'an instrument noxious or dangerous in itself which might produce an accident from the mere handling of it,' and by Lord Dunedin himself in Dominion Natural Gas Co v Collins [1900] A.C. 646:
'What that duty is will vary according to the subject-matter of the things involved. It has, however, again and again been held that in the case of articles dangerous in themselves such as loaded firearms, poisons, explosives, and other things ejusdem generis, there is a peculiar duty to take precaution imposed upon those who send forth or instal such articles when it is necessarily the case that other parties will come within their proximity.'"
[7.93]At p.188 Scrutton L.J. went on to say:
"The law, therefore, seems to be:
(1) That if the barge which has carried petrol is an article dangerous in itself, it is the duty of the owners to take proper and reasonable precautions to prevent its doing damage to people likely to come into contact with it. These precautions may be fulfilled by entrusting it to a competent person with reasonable warning of its dangerous character, if that danger is not obvious. If such precautions are not taken, the owner will be liable to third persons with whom he has no contact for damage done by the barge, which they could not have avoided with reasonable care.
(2)If the barge which has carried petrol is not dangerous in itself, but becomes dangerous because it has been insufficiently cleaned, and the owner is ignorant of the danger, the owner is not liable for damage caused by it to persons with whom he has no contract. (Earl v Lubbock [1905] 1 K.B. 253)
(3)In the case of a thing dangerous in itself, where either the danger is obvious or the owner has given proper warning to the person entrusted with it, not being his servant, the owner is not liable for negligence of such person causing injury to a third party; such negligence is nova causa interveniens."
[7.94]Counsel submitted that a distinction could be drawn between Hodge & Sons and Wright v Dunlop Rubber Co Ltd, because in Hodge & Sons the employers could be assumed to know of the danger, whereas in Wright the employers in fact did not know of the danger and could not be assumed to know of it. If the consumer had the relevant knowledge, then there might be no duty to give a warning; and Hodge & Sons demonstrated that there was a distinction between the relationship between a manufacturer of a product and the consumer, and that of an employer and an employee. Tomlinson supported the submission that it was not necessary that the claimant should know the precise nature and extent of the risk, and once he appreciated that there was some risk it fell to him to satisfy himself as to its nature and extent, and it was assumed that he would do so.
[7.95]Applying these considerations to the present case, counsel submitted, it would suffice if it could reasonably be assumed by ITL by the relevant date, that is the date when Mr McTear started smoking, whenever that was, that the ordinary consumer would be aware of a link between smoking and lung cancer, because he would then know that by smoking he was running a risk of fatal disease. By contrast with an employee, if a consumer was aware that the product which he was contemplating consuming was linked with a fatal disease, then that was sufficient to place the onus on him to decide whether or not he was prepared to "take a chance", in the expression used in Titchener, without seeking further advice or information about the precise nature and extent of the risks. If the manufacturer could reasonably take it that consumers in general were aware that the product was linked with a fatal disease, then it was sufficient for them reasonably to assume that the onus was on ultimate consumers to determine whether they were prepared to take a chance and consume the product. This was consistent with what was said in Grant v Australian Knitting Mills Ltd, and with Titchener. It was also consistent with Woods v Multi-Sport Holdings Pty Ltd (2002) 208 C.L.R. 460.
[7.96]In the latter case a player was struck in the eye by the ball when batting in a game of indoor cricket. He suffered serious injury and sued the owner/operator of the facility at which the game was played. It was not disputed that the defendant owed a duty to take reasonable steps to avoid the risk of injury to players arising from the dangers involved in playing indoor cricket. The plaintiff contended that the defendant was in breach of that duty in failing to warn him or to display signs warning of the dangers of the game, in particular of the risk of serious eye injury, and in failing to provide him with eye protection equipment. The High Court of Australia held, by a majority, that there were no grounds for rejecting the trial judge's finding (a) that the defendant's duty of care did not require it to provide the plaintiff with a helmet that would have protected him against the risk of injury to his eyes; or (b) that the risk of a player being struck was so obvious that reasonableness did not require the defendant to warn players about the specific risk of eye injury.
[7.97]It is sufficient to quote from the opinion of Gleeson C.J. In discussing the appellant's complaint of a failure to provide a sign to warn of the dangers of indoor cricket, and, in particular, the risk of serious eye injury, he referred at p.470, para.31 to the dangers of indoor cricket, and at p.471, para.32, to the expression "inherent risks" used by the trial judge to describe risks which are "by their nature obvious to persons participating in the sport", and described the risk of being hit by a cricket ball during the course of play as a risk of that kind. At para.34, Gleeson C.J. referred to the heightened risk of a particular type of eye injury because of the more malleable quality of the ball used in indoor cricket, by comparison with that used in outdoor cricket, which would allow it to impact on the eye surface rather than injure the bones around the socket. He referred to the conclusion of the trial judge that reasonableness did not require a warning, which was expressed in these terms:
"I do not consider that in these circumstances, where being hit in any part of the body including the head, is an obvious risk, that there is any duty to warn of the specific risk of serious eye injury."
[7.98]At p.472, para.39, Gleeson C.J. said:
"Because the concept of foreseeability in the law of negligence has been taken to embrace risks which are quite unlikely to occur, and to mean only that a risk is not one that is far-fetched or fanciful, many of the cases which discuss the approach to be taken by a tribunal of fact in deciding whether there has been a breach of duty of care speak in terms of balancing the magnitude of the risk with the cost of inconvenience of preventing it. But, as Mason J. pointed out in Wyong Shire Council v Shirt [footnote reference to (1980) 146 C.L.R. 40 at 47], ultimately the question of fact is what a reasonable person, in the position of the defendant, would do by way of response to the risk."
[7.99]At pp.473-474 Gleeson C.J. said:
"43As to the matter of the warning, the trial judge dealt with the appellant's case as it was put to her. The case was that there should have been a warning of the dangers associated with indoor cricket and, in particular, the danger of serious eye injury. It is useful to reflect upon what exactly might have been the content of the warning. There was no reason to limit it to the risk of head injury, much less eye injury. There was one particular respect in which the type of eye injury suffered at indoor cricket can be different from the type suffered at outdoor cricket, but there were probably also a number of respects in which the risk of back injury, or concussion from collisions, might be different from the risks associated with outdoor cricket. The risk that, in the confined space in which the game was played, any player, batsman or fielder, might receive a severe blow to any part of the head, including the eye, was, the trial judge found, obvious and well known to the appellant. It was argued that the appellant was not aware of the precise nature, and full extent, of the risk. But warnings of the kind here in question are not intended to address matters of precision. Judge French concluded that the risk of a player being struck in the face by a cricket ball was so obvious that reasonableness did not require the respondent to warn the players about it.
44Judge French, and the Full Court, were criticised in argument for their reliance on what Judge French described as the comment of Kirby J. in Romeo v Conservation Commission (N.T.) (1998) 192 C.L.R. 431 at 478 that:
'Where a risk is obvious to a person exercising reasonable care for his or her own safety, the notion that the occupier must warn the entrant about that risk is neither reasonable nor just.'
45It is right to describe that observation as a comment. It is not a proposition of law. What reasonableness requires by way of warning from an occupier to an entrant is a question of fact, not law, and depends on all the circumstances, of which the obviousness of a risk may be only one. And, as a proposition of fact, it is not of universal validity. Furthermore, the description of a risk as obvious may require closer analysis in a given case. Reasonableness would not ordinarily require the proprietor of an ice skating rink to warn adults that there is a danger of falling; but there may be some skaters to whom such a warning ought to be given. Nevertheless, as a generalisation, what Kirby J. said is, with respect, fair comment. That is how Judge French and the Full Court understood it, and they did no more than indicate that they regarded it as apposite to the present case. There is no error in that."
[7.100]By contrast, counsel referred to Bow Valley Husky (Bermuda) Ltd v Saint John Shipbuilding Ltd [1997] 3 S.C.R. 1210. In this case, Saint John Shipbuilding Limited (SJSL) constructed an oil rig for Bow Valley Husky (Bermuda) Limited (BVHB) which was to conduct drilling operations off the east coast of Canada. A heat trace system was required in order to prepare the rig for winter operations. The purpose of a heat trace system was to prevent the rig's pipes or "mud lines" from freezing. The heat trace system which was installed was supplied by Raychem Canada Limited and Raychem Corporation (Raychem). This system was chosen after consultation with Raychem representatives because it had a self-regulating heater. Raychem's heat trace system used Thermaclad wrap to keep moisture from the insulation and heat trace wire. The specification for the Raychem heat trace system required the installation of a ground fault circuit breaker system, the purpose of which was to cut off the power in the event of an electrical fault, to prevent arcing of the heat trace wire. The ground fault circuit breaker system initially installed by SJSL was unsuitable, and a functioning system was not installed on the rig until after the incident which formed the basis of the case. During the drilling of an exploratory well a fire broke out on the oil rig, causing damage to cables.
[7.101]In a subsequent litigation, the trial judge held inter alia that SJSL was liable in tort for breach of duty to warn of the inflammability of Thermaclad. He also held that the defendant Raychem was liable in tort for breach of its duty to warn. When the case reached the Supreme Court of Canada, it was held by a majority that SJSL's appeal with regard to the duty to warn should be allowed. The majority of the court held that BVHB was not entitled to claim against SJSL on the basis of the tort duty to warn, by reason of provisions of the contract between them. The majority did not however disagree with what was said by the minority of the court about the duty to warn.
[7.102]The opinion of the minority was delivered by McLachlin J., who said at pp.1229-1230:
"SJSL argues that in order for a duty to warn to arise, there must be an 'informational imbalance' between the manufacturer or supplier and the party who is owed the warning. SJSL submits that the plaintiff BVHB knew as much about the inflammability of the Thermaclad as it did.
The law may be simply stated. Manufacturers and suppliers are required to warn all those who may reasonably be affected by potentially dangerous products: Lambert v Lastoplex Chemicals Co [1972] S.C.R. 569, and Hollis v Dow Corning Corp. [1995] 4 S.C.R. 634. This duty extends even to those persons who are not party to the contract of sale: Rivtow Marine Ltd v Washington Iron Works [1974] S.C.R. 1189. The potential user must be reasonably foreseeable to the manufacturer or supplier - manufacturers and suppliers (including a builder-supplier like SJSL) do not have the duty to warn the entire world about every danger that can result from improper use of their product.
The plaintiff BVHB was clearly within the class of persons that SJSL and Raychem ought to have known might reasonably be affected by the use of Thermaclad. SJSL was in a contractual relationship with BVHB, and Raychem had directly approached BVHB's predecessor [...] to encourage the use of its products in the construction of the rig.
The defendant SJSL submits that there is an additional requirement for a duty to warn: a knowledge imbalance between the manufacturer or supplier and the consumer. It goes on to argue that since BVHB knew about the inflammability of Thermaclad no duty to warn arose. The Court of Appeal held that knowledge may be a defence, but only where the plaintiff can be viewed as accepting the risk (volenti non fit iniuria).
I agree with the Court of Appeal that knowledge that there may be a risk in some circumstances does not negate a duty to warn. Liability for failure to warn is based not merely on a knowledge imbalance. If that were so every person with knowledge would be under a duty to warn. It is based primarily on the manufacture or supply of products intended for the use of others and the reliance that consumers reasonably place on the manufacturer and supplier. Unless the consumer's knowledge negates reasonable reliance, the manufacturer or supplier remains liable. This occurs where the consumer has so much knowledge that a reasonable person would conclude that the consumer fully appreciated and willingly assumed the risk posed by use of the product, making the maxim volenti non fit iniuria applicable: Lambert, supra.
The evidence establishes that the plaintiff BVHB knew that Thermaclad would burn under some circumstances. The defendants SJSL and Raychem, however, had much more detailed knowledge of the specific inflammability characteristics of the Thermaclad. Raychem gained this knowledge through its own testing as manufacturer. SJSL gained it through its request to Raychem for information on Thermaclad's inflammability. BVHB did not have the degree of knowledge necessary to negate reliance on SJSL and Raychem. SJSL and Raychem did not demonstrate that BVHB accepted the risk of using Thermaclad. It follows that both SJSL and Raychem owed BVHB a duty to warn [...]."
[7.103]Mr Jones submitted that the approach of McLachlin J. was more restrictive than that in Murphy v Brentwood District Council and in the Australian cases. It left wholly out of account any consideration of what it was reasonable for the manufacturer to do in the whole circumstances. McLachlin J. had, he submitted, started with a consideration of the loss and asked what the manufacturer ought to have done to avoid the loss. It was in this context that she started by looking at the knowledge that was actually possessed by the claimant. He submitted that this approach was not consistent with the United Kingdom authorities, particularly Murphy v Brentwood District Council. Once it was acknowledged that, where there was an opportunity for intermediate inspection and where the approach was to consider what it was reasonable for the manufacturer to do and to assume, in the whole circumstances of the case, about the consumer of its products, then it could be seen that the approach of McLachlin J. was wholly inconsistent with that of the United Kingdom courts. It was also inconsistent with the approach in Graham Barclay Oysters Pty Ltd v Ryan, Thompson v Johnson and Johnson Pty Ltd, Woods v Multi-Sport Holdings Pty Ltd and Bogle v McDonald's Restaurants Ltd. McLachlin J. had left out of account any possibility that the plaintiff might fail because there was no duty to warn in the particular circumstances, and went straight to the question whether the consumer fully appreciated and willingly assumed the risk posed by use of the product. As could be seen in Titchener, under the approach in the United Kingdom, it was not necessary to have a full appreciation and willing assumption of the risk posed for the maxim volenti non fit iniuria to apply.
[7.104]Counsel next turned to two English cases which, he submitted, supported the proposition that a manufacturer had a duty to do what was reasonable in the whole circumstances, making reasonable assumptions about its consumers. Reference was made in the first place to London Graving Dock Co Ltd v Horton [1951] A.C. 737. In this case an experienced welder who had for a month been carrying out work on a ship as an employee of sub-contractors engaged by ship-repairers in occupation of the ship, sustained injuries, without negligence on his part, owing to the inadequacy of certain staging, constituting an unusual danger, of which he had full knowledge and which, despite complaints, the ship-repairers had not remedied. It was held by a majority in the House of Lords that, the welder being an invitee, his knowledge of the unusual risk exonerated the ship-repairers from liability for the damage sustained by him and that it was not essential to their defence to establish that he was volens in that he was not under any feeling of constraint in accepting the risk.
[7.105]At p.749 Lord Porter summarised the facts in Donoghue v Stevenson, and at p.750 he said:
"Your Lordships' House held that, assuming the facts alleged to be true, the manufacturer would have escaped if it was natural to expect that the intermediate vendor would take care to see that the contents were in order. The pursuer, however, could recover from the manufacturer because such an examination was not to be expected. The law required the latter to be careful not to run the risk of injuring a person whom he contemplates or ought to contemplate as likely to be injured by his negligence, but an examination by the retail vendor, if rightly expected, could be relied upon by the manufacturer and would have been a complete answer to the claim. Still more so would knowledge by the purchaser of the true position, whether such knowledge was actual or such as the circumstances would warrant the manufacturer to assume. The defence did not have to show that the pursuer drank the contents with a full knowledge of the risk: it would have been enough if examination and consequent knowledge was to be expected. To that extent an argument based on Donoghue v Stevenson seems less forcible than the more obvious contention founded upon the relationship of invitor and invitee. Neither ground, in my opinion, supports the conclusion that the appellants were in breach of their duty of care."
[7.106]Secondly, in Lewis v University of Bristol [1999] E.W.C.A. Civ. 1569, the plaintiff was a research assistant employed by the University of Bristol. She was an experienced molecular biologist. She was using an ultra violet transilluminator to photograph DNA gel in a laboratory when she was exposed to an excessive dose of ultra violet light and suffered serious burns to her face and neck. For some years she had used an ultra violet transilluminator known as a TL33 without mishap. Shortly before this event, and without her knowledge, this machine had been replaced by the University by a more powerful machine of similar appearance. The machine was manufactured by the third party, Ultra Violet Products Limited, who had supplied an instruction book with the machine.
[7.107]The first opinion in the Court of Appeal was delivered by Otton L.J., who accepted a submission that the TM40 was manufactured for a niche market. It was not a product created for general consumer use. It was a product created for exclusively scientific uses. After a reference to Holmes v Ashford he said:
"It is thus in my view a simple question of fact and degree in every case whether a manufacture[r] has given sufficient warning in all the circumstances when supplying a dangerous piece of equipment. [...] If the question is asked: what ought the reasonable manufacture[r] to foresee and what steps should he reasonably take?, the answer to my mind is clear. These manufacturers could reasonably foresee that the university would adequately instruct anyone who might use the machine - and in particular the research assistants - and they could not reasonably have foreseen that the university would allow the machine to put into circulation and use without adequate warning."
[7.108]The Lord Chief Justice, Lord Bingham of Cornhill, said that he agreed that the third party could not reasonably be expected to foresee the possibility that an expert professional buyer such as a scientific department of a university would make a machine such as the TM40 transilluminator available for use by its staff without, if necessary, familiarising itself with the potential hazards of such a machine and the safety precautions necessary to counter those hazards, and without taking steps to warn its staff of the dangers and to give instruction on the safe operation of the machine.
[7.109]Mr Jones submitted that this case constituted another example of the application of the proposition that the starting point was not what the plaintiff knew or did not know, but what it was reasonable, in the whole circumstances of the case, for the manufacturer to do and to assume.
[7.110]Turning to the present case, counsel submitted that the link between smoking and lung cancer was firmly in the public domain by September 1964, which was the earliest date that liability could arise. The publicity given to this link was one factor. It was also relevant that the Government had since 1956 publicly asserted that it would take steps to ensure that members of the public were informed of the link and associated risks and took active steps to inform the public. The actions of the Government were an important part of the context within which the question whether or not ITL had acted reasonably in the whole circumstances had to be assessed.
[7.111]The importance of common knowledge of the risks associated with smoking in assessing whether or not cigarette manufacturers had acted reasonably in not issuing warnings had been recognised in other jurisdictions. Reference was made to seven cases.
[7.112] (1)In Létourneau v Imperial Tobacco Ltd (1998) 162 D.L.R. (4th) 734, the plaintiff began smoking in 1964, attempted unsuccessfully to quit in 1973 and 1980, and finally quit in 1996, with the aid of nicotine patches. She brought an action against two tobacco companies for the cost of the patches. The evidence showed that in 1964, smoking was considered a habit rather than an addiction. In the Court of Quebec, Pokomandy Q.C.J. held, dismissing the action, that the tobacco companies were not obliged in 1964 to warn of the danger of addiction, nor to warn that smoking was habit-forming, since this was well-known. In any event, the plaintiff's loss was not caused by any failure to warn, since she continued to smoke with knowledge of the risks.
[7.113]In the course of his opinion (as translated in the report), the judge said, at pp.744-747:
"A manufacturer, in addition to liability for any danger or hidden defect resulting from a flawed design in goods offered for sale to the public, or the improper use of materials used in the manufacture of the said goods, or the defective assembling of the goods, also has the duty to sufficiently inform the purchaser or end user of the dangers or special nature of the goods that may render them unfit for a particular purpose.
Thus, the manufacturer which sells its goods to the general public has the duty to warn the consumer of any risks and dangers associated with its use.
The scope and content of the duty to warn varies according to circumstances, the nature of the goods and the knowledge of the purchaser. [...]
This duty to warn and provide information aims to compensate for the consumer's lack of knowledge with respect to the true nature of products, how to use them, or certain consequences arising out of use which the manufacturer is presumed to know.
The objective is to place the customer in the position of the normally prudent, knowledgeable and well-informed person. If the substance or object is universally recognised as being dangerous or the user is aware of the dangerous nature of a product or has used it for a sufficiently long period that any additional information would be superfluous, the failure to warn or inform will not be deemed a fault of the manufacturer.
In other words, manufacturers are under no obligation to warn end users of their products with respect to facts which are generally known, that is so well known in the community that they are more or less beyond dispute.
Thus, the Court will review the particular facts of each case in order to determine the scope of the manufacturer's duty to warn with respect to the product, the circumstances and the party in question."
[7.114]After reviewing the evidence relating to the state of public knowledge that smoking cigarettes constituted a health hazard, and the display of messages stating that smoking cigarettes was harmful to health, the judge said:
"The consumer, having been informed by such warnings of risk to health associated with smoking cigarettes, is under a duty to become informed and seek advice with respect to the specific and foreseeable consequences for him or her of such use. The manufacturer has the duty to inform, but not to advise."
After consideration of the petitioner's personal circumstances, the judge said, at p.746:
"As an adult, she must assume the consequences of having chosen an activity whose risks and dangers were known."
[7.115]After discussion of the petitioner's complaint that the respondents should have informed her that she risked becoming addicted to nicotine by smoking over a long period of time, the judge said, also at p.746:
"The only warning under the circumstances that could have been given is that long-term, heavy smoking could be very habit-forming and that consequently quitting smoking could prove to be difficult.
However, that was already known, not only as a result of cigarette-smoking, but also of several other pleasant activities practised intensively over a long period of time.
The manufacturer is not obliged to warn of dangers that are clearly known to all.
The argument of the petitioner to the effect that she was unaware of the consequences of the habit of smoking is not very convincing when placed within the context of the overall evidence.
In fact, any reasonable person who acts, undertakes an activity or engages in behaviour of any nature is presumed to assume the consequences of his or her choice, which implies a minimal duty to educate oneself in advance of the risks and benefits at stake.
If the petitioner did not do so and voluntarily or carelessly ignored the consequences of smoking, including the subsequent difficulty of stopping, instead considering only its present aspect, she must now assume the consequences of such a choice."
[7.116] (2)Heine v Reemtsma Cigarettenfabriken GmbH 2 O 294/02 was a decision of the Second Chamber for Civil Matters of the Arnsberg Regional Court, Germany, announced on 14 November 2003. I was informed that it was under appeal. A translation of the judgment was prepared for the present proceedings. According to the first paragraph:
"The Plaintiff claims damages and compensation for pain due to harm to his health from smoking 'Ernte 23' brand cigarettes manufactured by the Defendant. He furthermore seeks information about the addition of addiction-promoting substances and a finding with regard to consequential damages. He hereby cites the Defendant's failure to provide warnings, product manipulation and a fundamental flaw in the cigarette product."
[7.117]At pp.13-15 of the translated opinion the court held that there was no liability from the point of view of producer liability due to a fault in construction or instruction. They said:
"There is no construction fault in cigarettes. Cigarettes are not a faulty product, in spite of the health risks arising from their consumption. The dangers arising from this have indisputably been known to consumers and the Plaintiff for a long time and were consciously accepted. Everyone knows that in the long term smoking can lead to serious, potentially even fatal harm to health, that it can lead to addiction which makes it hard to stop smoking. Consumers cannot justifiably expect that cigarettes are constructed in such a way that they do not give rise to these dangers. For instance, in the jurisdiction which this chamber follows it has long been recognised that the producer does not have to avert dangers which are typically linked with the use of a product and known to the users or recognised and accepted by them [...]. The decisive aspect therefore is that smokers are responsible for their own acts. They must themselves bear the consequences of their independent behaviour and cannot pass them on to the cigarette manufacturers."
[7.118]Further down p.14, the court said:
"The Defendant has also not committed a so-called instruction fault by neglecting warnings on his products. The Plaintiff did not concretely assert that the Defendant had not met the legal duty of information and this is not evident. There are no further duties of information for the Defendant.
The manufacturer of a product must only indicate the most important features. He must not meet any special duties of information if certain product risks are generally known.
However, all risks linked with the consumption of cigarettes have been known to the consumers for a long time. This also includes the possible addictive effect of cigarette consumption. This does not concern special knowledge - such as how health is harmed by cigarette consumption. Therefore the judiciary has basically unanimously rejected a further duty of information [...]. Thus there does not have to be separate information about an allegedly addiction-increasing effect of additives. Because the effect of these substances, i.e. in lay terms that smoking is addictive - as always - is not news to the consumer."
[7.119] (3)Lund v J.L. Tiedemanns Tobaksfabrik A.S., H.R. - 2002 - 00753a, 31 October 2003, was a decision of the Supreme Court of Norway. A translation of the judgment was prepared for the present proceedings. The case concerned a request for a declaratory judgment finding that a tobacco manufacturer was liable for damages on a strict liability basis with respect to an injured party who after over 40 years of cigarette smoking developed lung cancer and died. The leading opinion was delivered by Judge Flock, with whom the other members of the Supreme Court agreed. At para.47 he said:
"The parties have in their arguments before the Supreme Court concentrated to a large degree on what knowledge of the health risks of smoking the normal consumer had during the space of time from 1950 to 1975. The appellant has acknowledged that the knowledge of both the general public as well as that of [the deceased] Robert Lund of the risks in 1975 had been brought to such a level that continued smoking after that took place at his own risk."
[7.120]The judge then went on to review the evidence, commenting, in para.49:
"The parties are in agreement that the question of the relationship between smoking and damage to health is not related to what the individual injured party - Robert Lund in our case - knew or did not know."
After referring to the publication of various reports, including one by the Norwegian General Director of Health in 1964, the judge concluded, at para.56:
"Despite the fact that extremely many cigarette smokers continued not to accept the consequences of the medical knowledge that the research had brought to light, I am of the opinion that the consumers had in any event received such information in 1964 concerning health damage that a normally intelligent person would include it in his assessment of how he wished to conduct his life. Such as I see it, there cannot be any doubt that Robert Lund's smoking after this point in time took place at his own risk."
[7.121]The judge then turned to consider the ten year period between 1954, when Robert Lund began smoking the particular brand of tobacco in question, to 1964. He said, at para.63:
"My overall impression of the material that was submitted on the situation from the first half of the 1950s up to 1964 is that medical science at that time had still not secured reliable knowledge concerning a direct causal relationship between cigarette smoking and lung cancer and other serious injuries to health."
At para.64, however, he concluded:
"During this last 10-year period prior to the final conclusions being able to be drawn, the relationship between smoking and damage to health was not unknown to the average man or woman. However due to the lack of completely clear evidence it was to a greater degree than later left to the individual as to the extent to which one wished to believe what one read and heard now and then about the harmful effects of tobacco. And then as now, it was completely up to the individual as to whether one chose to take the chance. What is crucial for me is that it also must have been generally known at the time that cigarette smoking could involve a risk of serious health damage, and that the risk of such damage in any event to some extent would increase if the consumption of cigarettes was large. Such as I view the case, no more fine-meshed of an analysis is needed on this point."
[7.122] (4)Cruz-Vargas v R.J. Reynolds Tobacco Company 348 F.3d 271 (1st Cir.2003) was a decision of the United States Court of Appeals, 1st Circuit. Relatives of a deceased smoker brought a negligence and strict liability suit against a tobacco company, alleging that it was responsible for his death. The action was brought in the United States District Court for the District of Puerto Rico. There was evidence that "the average consumer in Puerto Rico during the 1950's, during the 1960's" was aware both of health risks, such as cancer and cardiovascular disease, associated with smoking and that "smoking was or could be difficult to quit".
[7.123]In discussing the evidence regarding common knowledge, the Court of Appeals said at pp.275-276:
"[5, 6] This case calls for us to evaluate application of the common knowledge doctrine in the context of tobacco litigation. The doctrine stems from the principle that a manufacturer cannot be held liable under either strict liability or negligence for failure to warn of a danger commonly known to the public. See, e.g., Guevara v Dorsey Labs., Div. of Sandoz, Inc., 845 F 2d 364, 367 (1st Cir. 1988) ('The duty to warn in general is limited to hazards not commonly known to the relevant public'); Aponte Rivera v Sears Roebuck, 44 P.R. Offic. Trans. 7, 144 D.P.R. 830 (1998) ('[A] manufacturer need not warn of a hazard if the average consumer ordinarily has knowledge of the dangers of the product.'). [...]
[7, 8] A products liability plaintiff alleging failure to warn must prove
'(1) the manufacturer knew, or should have known of the risk inherent in the product; (2) there were no warnings or instructions, or those provided were inadequate; (3) the absence of warnings made the product inherently dangerous; (4) the absence of adequate warnings or instructions was the proximate cause of plaintiff's injury.'
Aponte Rivera, 44 P.R. Offic. Trans. at 6. Under the common knowledge doctrine, however, a defendant neither breaches a duty nor causes the product to be inherently dangerous when the allegedly omitted warning concerns a danger of which the public is well aware. [...]
The crux of appellants' entreaty on appeal is that neither the strict liability nor the negligence claim requires any affirmative showing, and thus the burden rested entirely on Reynolds. Whether or not this is a correct view of the law, after searching the record we have found no evidence which supports appellants' allegations that there was a lack of common knowledge and thus we are compelled to find that Reynolds met its burden in any event."
[7.124] (5)In Roysdon v R.J. Reynolds Tobacco Company 849 F.2d 230 (6th Cir. 1988), a smoker and his wife brought an action against a tobacco manufacturer to recover for disease allegedly caused by smoking. The United States Court of Appeals, Sixth Circuit, inter alia affirmed the dismissal by the United States District Court for the Eastern District of Tennessee of the plaintiffs' failure to warn claim. At p.236, para.10, the Court of Appeals said:
"[T]he district court took judicial notice that
'tobacco has been used for over 400 years and that its characteristics have also been fully explored. Knowledge that cigarette smoking is harmful to health is widespread and can be considered part of the common knowledge of the community.'
Roysdon, 623 F.Supp. at 1192. Remembering that this action was limited to the ten years preceding the filing of this complaint [on 5 July 1984], we think this approach was appropriate. The extensive information regarding the risks of smoking available to the public during that time precluded the existence of a jury question as to whether cigarettes are unreasonably dangerous. We find that whether there was knowledge regarding Mr Roysdon's specific medical problem is irrelevant in light of the serious nature of the other diseases known at that time to be caused by cigarette smoking."
[7.125] (6)Paugh v R.J. Reynolds Tobacco Company 834 F.Supp. 228 (N.D.Ohio 1993) was a decision of the United States District Court, N.D.Ohio, E.D. In the course of her opinion, the district judge said, at pp.230-231:
"The dangers posed by tobacco smoking have long been within the ordinary knowledge common to the community. In fact, tobacco is specifically mentioned in the Restatement (Second) of Torts as an example of a product which is not defective merely because the effects of smoking may be harmful. Rest. (2d) of Torts §402A(i)."
[7.126]After referring to various authorities, including Roysdon v R.J. Reynolds, the district judge said at p.231:
"[E]specially in light of the Sixth Circuit's holding in Roysdon, this Court finds that the better-reasoned decisions are those finding the dangers of smoking to have been common knowledge. Much as in the case of alcohol, users of tobacco products have made a consumer choice in the face of health risks that are common to ordinary knowledge. [...] That some ignore or underestimate these risks has little bearing on the extent to which knowledge of the dangers [is] salient within the community. Therefore, because the risks posed by smoking are an inherent characteristic of cigarettes, and because knowledge of these risks has been common to the community since well before 1966, Paugh's allegations are insufficient to support her claim for damages caused by a product in an 'unsafe and defective' condition [...]."
[7.127] (7)In Tompkin v American Brands 219 F.3d 566 (6th Cir. 2000). The widow of a former smoker brought a product liability suit against cigarette manufacturers. The United States District Court for the Northern District of Ohio granted summary judgment to the manufacturers. The plaintiff appealed. The United States Court of Appeals, Sixth Circuit, held inter alia that "fact questions precluded summary judgment on design defect and failure to warn claims under the Ohio Products Liability Act (OPLA)". So far as the failure to warn claim was concerned, the question for the Court of Appeals was whether there was an issue to be tried. In reaching their decision on this, the Court of Appeals required to make certain assumptions in favour of the plaintiff: as explained at p.575 they required to credit the report and deposition of Dr Whelan, relied upon by the plaintiff, as true and to read all inferences in the light most favourable to the plaintiff. OPLA expressly exempts from liability products whose dangers are regarded as "common knowledge". Specifically, a defendant is not liable for a purported design defect when "the harm for which the claimant seeks to recover compensatory damages... is recognised by the ordinary person with the ordinary knowledge common to the community."
[7.128]In the course of their opinion, at pp.572-575, the Court of Appeals said:
"[3]At the outset, we think it necessary to frame properly the issue we must decide. The pertinent issue here is not whether the public knew that smoking was hazardous to health at some undifferentiated level, but whether it knew of the specific linkages between smoking and lung cancer. Public awareness of a broad-based and ambiguous risk that smoking might be tenuously connected to lung cancer does not suggest 'common knowledge' of the known scientific fact that cigarette smoking is a strong precipitant of lung cancer. [...] It is one thing to be aware generally that a product might have an attenuated and theoretical connection with a deadly disease like lung cancer; it is another altogether to comprehend that it is the cause of an overwhelming majority of lung cancer cases [...]. The 'common knowledge' requirement is emasculated if a defendant may show merely that the public was aware that a product presented health risks at some vague, unspecified, and undifferentiated level.
Viewing the 'common knowledge' issue through the proper lenses, we conclude that a rational jury could find the absence of 'common knowledge,' between 1950 and 1965, of the nature of the link between smoking and lung cancer. While Dr Whelan concedes that an overwhelming majority of the public was aware that smoking was dangerous to health, and that opinion polls even showed an awareness of some connection between smoking and lung cancer [...], she nevertheless concluded that there was 'no reason to believe' that the public had any understanding of the nature of this connection. [...]
Surely, if the ordinary person had an understanding of the harms of cigarette smoking that was wildly disproportionate to its actual danger, one may not characterize such misunderstanding as 'common knowledge.' The requirement that the public have 'common knowledge' - as opposed to broad familiarity, or some other more generalized standard - informs that substantial incongruence between perceived and actual risk precludes a 'common knowledge' finding. [...]
In short, crediting the report and deposition of Dr Whelan as true and reading all inferences in the light most favorable to Mrs Tompkin [...] we hold that a rational factfinder could reasonably conclude that the public did not have 'common knowledge' of the strong connection between cigarette smoking and lung cancer between 1950 and 1965."
[7.129]Counsel submitted that these authorities were consonant with the United Kingdom approach, which was that, in individualist philosophy, the individual was well enough served if he was given such information as a normally intelligent person would include in his assessment of how he wished to conduct his life, thus putting him in the position of making an informed choice. Where risks were common knowledge, no liability arose from failure to give a warning. It was enough if the average consumer had sufficient knowledge to know that he took a chance. It was a question of fact whether there was publicly available information amounting to common knowledge.
[7.130]Counsel submitted that the underlying policy of the law could also be seen in Pelman v McDonald's Corporation 237 F.Supp.2d 512 (S.D.N.Y.2003). In this case, parents brought an action on behalf of their children against fast-food corporations and restaurants, alleging violations of state consumer protection laws and negligence in connection with the children's over-consumption of fast-food products. The United States District Court, S.D. New York, dismissed the action, holding inter alia that the defendants owed no duty to warn consumers of the products' well-known attributes. At p.520 District Judge Sweet set out the causes of action alleged by the plaintiffs, two of which were expressed in these terms:
"Count III sounds in negligence, alleging that McDonalds acted at least negligently in selling food products that are high in cholesterol, fat, salt and sugar when studies show that such foods cause obesity and detrimental health effects.
Count IV alleges that McDonalds failed to warn the consumers of McDonalds' products of the ingredients, quantity, qualities and levels of cholesterol, fat, salt and sugar content and other ingredients in those products, and that a diet high in fat, salt, sugar and cholesterol could lead to obesity and health problems."
[7.131]In discussing count III, at pp.532-533 the judge said:
"[14] [...] It is well-known that fast food in general, and McDonalds' products in particular, contain high levels of cholesterol, fat, salt and sugar, and that such attributes are bad for one.
[...] If a person knows or should know that eating copious orders of super- sized McDonalds' products is unhealthy and may result in weight gain (and its concomitant problems) because of the high levels of cholesterol, fat, salt and sugar, it is not the place of the law to protect them from their own excesses. Nobody is forced to eat at McDonalds. [...]
As long as a consumer exercises free choice with appropriate knowledge, liability for negligence will not attach to a manufacturer. [...] Plaintiffs have failed to allege in the Complaint that their decisions to eat at McDonalds several times a week were anything but a choice freely made and which now may not be pinned on McDonalds."
[7.132]In discussing count IV, at pp.540-541, the judge said:
"[19] [...] In Liriano v Hobart Corp., 92 N.Y.2d 232 [...] (1998), the New York Court of Appeals summarized the current State of New York law with regard to a manufacturer's liability for failure to warn in a products liability case:
'A manufacturer has a duty to warn against latent dangers resulting from foreseeable uses of its product of which it knew or should have known. A manufacturer also has a duty to warn of the danger of unintended uses of a product provided these uses are reasonably foreseeable... [A] manufacturer may be liable for failing to warn against the dangers of foreseeable misuse of the product... A manufacturer's superior position to garner information and its corresponding duty to warn is no less with respect to the ability to learn of... misuse of a product....' [...]
[21, 22] In duty to warn the cases, New York recognises two circumstances that would preclude a finding of proximate cause: (1) obviousness and (2) the knowledgeable user. [...]
[23] Pursuant to the 'open and obvious' exception, a manufacturer may not be liable for a failure to warn if the risks were sufficiently obvious to the user without a warning. [...]
[24] The open and obvious defense will not apply 'when there are aspects of the hazard which are concealed or not reasonably apparent to the user...". Liriano, 92 N.Y.2d at 241-42 [...]
[25] Because of the difficulty in administering this test, the question of whether a danger is open and obvious is usually a jury question unless only one conclusion may be drawn from the established facts. [...]
[26] As discussed above, the Complaint fails to allege that the McDonalds' products consumed by the plaintiffs were dangerous in any way other than that which was open and obvious to a reasonable consumer."
Counsel submitted that the approach in Pelman would be followed in the United Kingdom.
[7.133]So far as Mr McEachran's submission about cigarettes as being a "defective product" was concerned, Mr Jones made the point that the pursuer did not aver and had not sought to prove that the cigarettes allegedly smoked by Mr McTear were anything other than ordinary cigarettes. This case did not concern the introduction into the product of some extraneous substance as a result of a manufacturing error. It would not be in dispute that ITL did have a duty to take reasonable care to avoid contamination, on ordinary Donoghue v Stevenson principles. This was not, however, such a case: the issue was whether or not ITL had any duty in relation to risks inherent in the ordinary and intended use of the product. The appropriate analogy was with, for example, foods rich in fat, the consumption of which carried inherent health risks, as in Pelman's case.
[7.134]Mr Jones then turned to the circumstances of the present case. Counsel reiterated his submission, based on the individualistic philosophy of the common law, that in general it was for individuals to decide what goods and services they wished to purchase and consume. It was for them to decide whether or not any risk associated with the particular activity was one which they wished to take. It was not in general for the court to determine that any particular consumer product should not be available for purchase. Various factors emerged from the evidence. Cigarettes were at all relevant times widely enjoyed and socially acceptable. In the 1960s, the majority of adults in the United Kingdom smoked. USSG 1964, referred to in Professor Friend's evidence, discussed the significant beneficial effects of smoking. Professor Gray described the benefits which smokers might derive from smoking: most smokers reported that they enjoyed smoking. Mr McTear's evidence, given on commission, was that this was why he smoked. Smokers described how they smoked for one or more of a range of beneficial effects related to sensory enjoyment, mood control and increasing alertness. In MacAskill et al. 2002, of which Professor Hastings was one of the authors, it was found that smoking was, for many of the subjects of the study, their main pleasure, and met a multitude of needs in the lives of the study population.
[7.135]Counsel submitted that in order to determine whether or not in all the circumstances ITL acted unreasonably in not withdrawing their products from the market or in not issuing a warning, it was necessary in the first place to identify what the state of the science at the relevant time would justify as the appropriate understanding of any risk. In his submission the pursuer had not led any appropriate evidence upon which the court could reach a reasoned conclusion on the state of the science today, and by the same reasoning she had not led any evidence upon which the court could reach a reasoned conclusion about the state of the science as at, for example, September 1964. It was, in any event, relevant to the question of reasonableness that, even if the majority of scientists had concluded that smoking could cause lung cancer, there continued to be serious scientists who were arguing caution, at least in accepting the causal hypothesis, and some who were proposing alternative explanations.
[7.136]The attitude of the Government and the public health authorities was relevant to the issue of reasonableness in not withdrawing the product from the market and not issuing a warning. There was no suggestion from the Government that smoking should be banned or that cigarettes should be withdrawn from sale. There was no evidence that the Royal College of Physicians were recommending prohibition of the sale of cigarettes. All the recommendations in RCP 1962 were designed to lead to the consuming public being informed. The stated policy of the Government at the relevant time was to ensure that adults knew the facts about the dangers of smoking and to discourage children and young people from acquiring the habit. This could be seen from the report of the Ministry of Health for the year ended 31 December 1962, referred to in the cross-examination of Professor Hastings. By the late 1960s it had become policy to seek to discourage smoking by campaigns directed to making it appear unfashionable, but it remained Government policy, as it did today, to recognise that people had a right to choose whether or not to smoke. The views of the Government might not, counsel submitted, as a general proposition, be determinative of the question whether a manufacturer who continued to sell his product was in breach of his duty of care, but in the circumstances of this case the views of the Government were a factor of some weight. It was not in general the business of the common law to dictate what goods and services might lawfully be sold and purchased, although the legislature and, under delegated powers, the executive might regulate or even prohibit the sale and purchase of particular goods and services. The question whether the sale and purchase of particular goods and services should be prohibited raised issues of policy which were not in general for the courts to address in the context of delictual liability. By 1964 the Government was taking active steps, pursuant to its policy, to inform the public.
[7.137]A further consideration which was relevant, counsel submitted, was that ITL were, and remained, a substantial company upon which many people relied for their livelihood. Given that the Government then and now regarded smoking as a legitimate choice for individuals to make, it was not incumbent on ITL in all the circumstances unilaterally in effect to cease trading. Counsel stressed the word "unilaterally", because the evidence was that all the other cigarette manufacturers continued to trade, and this was a relevant consideration for ITL to have had in mind were there any question of ceasing manufacture. These, counsel submitted, were all relevant facts and circumstances, but of course they had to be seen in the context of public awareness at the relevant time or times. On the question of public awareness, Mr Jones invited me to find, under reference to the material set out in Part III, that the 1954 and 1956 ministerial statements, publication of MRC 1957, RCP 1962 and USSG 1964 and the ban on television advertising of cigarettes in 1965 were all significant media events widely covered in the press throughout the country, and that the coverage of smoking and health issues was not confined to these significant news stories. The media coverage effectively constituted reminders throughout the 1950s and 1960s that there were risks associated with smoking.
[7.138]The starting point was the evidence of Professor Hastings that the health evidence about tobacco was well known and publicised by the 1960s, that there was considerable publicity about the health consequences of smoking during the 1960s, and that Mr McTear must have been aware of it. This was because of the extensive media coverage at the time. Professor Hastings said that in effect any member of the public must have been aware of the publicity that was being given to the health consequences of smoking. Mrs McTear said, consistently with the evidence of Professor Hastings, that the first disease she could remember being linked with smoking was lung cancer. While Professor Hastings was quite content to recognise that people were bound to have been aware of publicity given to the health risks associated with smoking, his concern was that other messages, and in particular advertising, would influence people towards smoking. Counsel did not criticise him for having this approach, but in his submission this was quite different from the approach of the law: the law did not require that the manufacturer should set out to change people's behaviour. That was left to public health bodies and people like Professor Hastings. In addition, he had a tendency to judge comments in newspapers, and Government policy and actions in the 1950s and the 1960s, from the standpoint of his current understanding of the science and of more recent practice in the field of social marketing. But his general conclusions about the depth and breadth of the penetration of public awareness, particularly in the early 1960s, were well founded. They were amply supported by the vast quantity of media reporting of the issue of smoking and health that had been agreed by way of joint minute.
[7.139]More generally, it emerged from the evidence of Professor Hastings that the media covered events and other matters which were considered to be of interest to readers, listeners and viewers. In the 1950s and 1960s it would have been of interest to many members of the public that smoking was being linked with fatal diseases. The press took an interest in research on matters of topical interest, as could be seen by reference to the reporting of the work of Doll and Hill. The media also took an interest in the views of the medical profession on topical issues of the day. There were some reports in the 1950s on the views of the medical profession on the health risks associated with smoking. In January 1953 a television programme presented by Dr Fletcher called "The tobacco habit" described the evidence on the link between smoking and lung cancer: he was the secretary to the committee which produced RCP 1962. The programme was commented on in newspapers such as the Daily Mirror and the Sunday Pictorial.
[7.140]The ministerial statement in the House of Commons in 1954, that the statistical evidence pointed to smoking as a factor in lung cancer, made it clear that the Government was giving a warning that there was a risk of lung cancer associated with smoking cigarettes, albeit that the warning was qualified in certain respects. This statement was widely reported in newspapers targeted at all social strata. The ministerial statement in the House of Commons in 1956 was again a significant news story which was widely and prominently reported. It included a public announcement by the Government that it was going to take steps to ensure that the public were kept informed. The statement was reported in the Daily Record and the Evening Times, among other newspapers.
[7.141]The publication of MRC 1957 and the ministerial statement in the House of Commons were again widely reported in newspapers, including the Daily Record, the Evening Citizen, the Evening Times and the Paisley Daily Express. It was covered also on radio and television. The report was widely anticipated in the press throughout the United Kingdom, and following its publication was also widely reported. The reports referred to the ministerial statement that once the risks were generally known, everyone who smoked would have to be relied upon, as a responsible person, to assess them and act as he thought best.
[7.142]The publication RCP 1962 received extensive publicity. There were reports in the Daily Record, the Evening Times, the Evening Citizen and the Sunday Post, among other newspapers. Following publication of the report the Government embarked on a campaign. Publicity material was supplied by the Ministry free of charge to local authorities and to other organisations. In 1965, television fillers were being shown on ITV free of charge to the Government.
[7.143]Not only was central Government taking responsibility on itself and encouraging local authorities to do specific things, there were local initiatives. There was a vigorous campaign waged in Paisley, for example, in the first half of the 1960s. Reference was made to reports in the Paisley Daily Express and the Paisley and Renfrew Gazette. There were reports of an anti-smoking clinic being opened in Paisley in February 1965.
[7.144]There was also widespread coverage of the publication of USSG 1964. In counsel's submission the public awareness was such that at the very latest by the time of publication of this report it could be taken that the public knew about the health risks, and in particular the association between smoking and lung cancer. On 30 January 1964 the Prime Minister, Sir Alec Douglas-Home, said in the House of Commons: "I do not think there is any excuse for anyone not to know the connection between cigarette smoking and cancer." Not only could this be regarded as a responsibly expressed view, but a tobacco manufacturer such as ITL was entitled to rely on it when thinking about what reasonably to do in the light of emerging knowledge about the link between smoking and lung cancer.
[7.145]Against this background of public awareness and the other facts and circumstances counsel had referred to, he submitted that there was no duty on ITL to cease production or to put out warnings. While there were no Government health warnings on cigarette packets until 1971, it was clear that the Government and various public health bodies were putting out repeated warnings during the 1950s and into the 1960s about the link between smoking and lung cancer, and indeed the media coverage of the significant events was intended to be and was in effect a series of public health warnings. Professor Hastings had accepted that any member of the public must have been aware of the publicity that was being given to the health consequences of smoking in the 1960s.
[7.146]There was no evidence that the tobacco industry sought to contradict the public health message. Sir Richard Doll's evidence was that in the United Kingdom the tobacco industry did not seek to challenge it. Counsel invited me to sustain the objection to the line of evidence from Professor Hastings about statements from the tobacco industry. There was no notice in the pleadings of any argument that public awareness of the public health warnings was in some way affected by statements from the tobacco industry. Had it been the pursuer's intention to argue that public awareness of the public health warnings as at September 1964 had been in some way affected by industry statements, this line should have been foreshadowed in the pleadings, and notice should have been given of the industry statements to be relied upon by her in that regard. Not only were there no averments to this effect, there was no averment that Mr McTear was influenced in his decisions about smoking by any statements by the tobacco industry. He made no reference to this when he gave evidence on commission, and there was no averment that ITL were in breach of any duty by virtue of any statement made by them.
[7.147]In any event, counsel submitted, the evidence did not support the proposition that awareness of the public health warnings as at September 1964 was in any way influenced by industry statements. This could be seen by reference to the evidence of Professor Hastings, summarised above. Even in the 1950s when those in the tobacco industry were calling for caution, any member of the public who became aware of a report of such a statement would also be aware that the statement was a response to the announcement which had given rise to the report, and would accordingly have been aware of the health risks about which warning was being given, as well as the fact that these warnings were being given by the Government and public health authorities. The fact that such an individual might have been made aware of the position of the tobacco industry still left him with the relevant information to enquire further if he wished or, if not, to make a choice about future action. For the purposes of the duty of care it was sufficient that it could reasonably be assumed that the ordinary consumer would have been aware of the warnings about smoking and health being given by the Government and the public health authorities. Counsel made it clear that he was not saying that as a matter of assertion, no comment was made by the tobacco industry in 1962 or 1964; his submission was that if Mr McEachran wished to make out that the tobacco lobby group contradicted the conclusions, it was for him to bring the evidence on which he relied, and none had been brought out.
[7.148]Counsel concluded his submissions on the issue of public awareness by referring to the pleadings for ITL on this issue:
"At all material times, and in particular by 1964, the general public in the United Kingdom, including smokers and potential smokers, were well aware of the health risks associated with smoking, and in particular of the view that smoking could cause lung cancer. There was, at all material times, extensive coverage in the media in the United Kingdom of smoking and health issues. At all material times there were numerous articles on smoking and health in the print media throughout the United Kingdom."
As counsel pointed out, these averments were met by a general denial, but in the event it had proved possible to agree many thousands of newspaper articles and publications in the other media which clearly vouched them. In addition, reliance was placed on the pursuer's own expert, Professor Hastings, for the above propositions taken from his evidence about the level of public awareness in the United Kingdom at the relevant time.
[7.149]Mr Jones submitted that it was not clear what finding I was being invited to make about the nature of advertising, or about ITL's expenditure on advertising and promotion. The pleadings on advertising were limited, and there was very limited evidence before the court about the nature of cigarette advertising by ITL, or in general, at the relevant time. There was, however, evidence that in April 1962, following the publication of RCP 1962, the tobacco industry voluntarily restricted their television advertising to the period after 9pm. In June 1962 the industry agreed with the Independent Television Authority that television advertising would be governed by a code which excluded advertisements which suggested that cigarette smoking was inseparable from masculinity, that it was a desirable recreation for young people, that it was a socially acceptable habit, that it produced ecstatic pleasure or that it was enjoyed by popular heroes or heroines. It could not be taken from this that advertising previously suggested, for example, that cigarette smoking was inseparable from masculinity or recreation for young people. This would have to be demonstrated by reference to advertisements. In any event, given that I had sustained an objection, there was no live issue in the present case.
[7.150]Since, however, that Mr McTear had given evidence on this matter at commission without objection, counsel went on to submit that in addition to the restrictions on television advertising in 1962, in November 1962 the tobacco industry agreed to apply the same restrictions to other advertisements, and in June 1964 a new code for television advertising was promulgated containing further restrictions. So by the time Mr McTear started smoking in September 1964 or later it was difficult to see what there was for him to fall for.
[7.151]In response to Mr McEachran's submissions about the contrast between ITL's advertising expenditure and direct government expenditure, counsel submitted that this was not a direct comparison because the costings on the public health side did not take into account the publicity through the mass media, nor local authority expenditure. In any event ITL, like other tobacco manufacturers, operated in a competitive market, selling a lawful product which was at all relevant times widely socially acceptable. They were entitled to promote their products within the law and within any relevant advertising codes of practice and any voluntary restrictions accepted by them. Professor Hastings accepted that advertising performed the function of strengthening brand identity. Mr Davis gave evidence that ITL's advertising was aimed primarily at the smokers of other manufacturers' cigarettes, to persuade them to convert to ITL's products. Counsel submitted that the relevant question was whether or not it could reasonably be assumed at the relevant time, September 1964 or later, that the ordinary consumer was aware of the warnings which the Government and public health authorities were putting out to the public. If they were, then the fact that ITL were advertising their products was irrelevant.
[7.152]Both on the pleadings and on the evidence, the tobacco manufacturers, including ITL, were deriving their information from the same published sources as were available to the public. There was nothing to which they were privy which was not publicly available and which might therefore place them under a duty to provide information which the public did not otherwise have. ITL had no better or greater knowledge than the average consumer, and they gained it at precisely the same time as the average consumer did, and in the same way. In addition, the Government were relying on the same material at the same time. The foundation of the pursuer's case was based on the published reports, starting with MRC 1957. There was no evidence that the public would have been any better informed than they already were, by reason of the publicity given to these reports, if ITL had printed warnings on cigarette packets or in advertisements that smoking could cause fatal diseases. On the evidence, when Mr McTear started smoking in 1964 or later, ITL's products carried no hidden danger, such that they were under a duty to give warnings about it. The public awareness that smoking was linked with health risks, and in particular lung cancer, was so widespread that ITL had no duty to give warnings about it. The same level of public awareness ruled out any duty to cease manufacture.
[7.153] Turning to the issue of fault causation, Mr Jones submitted that the first question which arose from the argument for the pursuer, that Mr McTear would not have developed lung cancer but for ITL's breach of duty, was whether, if ITL had ceased manufacturing, Mr McTear would not have smoked. Mr Jones submitted that the onus was on the pursuer to establish, not only that ITL were in breach of a duty owed to Mr McTear, but that, if they had not been in breach of that duty of care, he would not have contracted lung cancer; or, to take the principal formula as that derived from Fairchild, the onus was on her to establish that, but for ITL's breach of duty, Mr McTear would not have contracted lung cancer.
[7.154]Counsel referred to McWilliams v Sir William Arrol & Co 1962 S.C. (H.L.) 70. In this case, a workman was killed when he fell a distance of seventy feet from a steel lattice tower which was in the course of erection at a shipyard. After evidence had been led, it was found proved that both his employers, who were independent contractors in charge of the operation of erecting the tower, and the occupiers of the shipyard were in breach of their respective duties to provide a safety belt. It was also found proved that, even if a safety belt had been provided, the deceased would not have worn one. In making this finding, the Lord Ordinary held that the onus was on the pursuer to prove that the deceased would have worn a safety belt had one been provided. The House of Lords held, affirming the judgment of the First Division, that the onus was on the pursuer to establish, not only the breach of duty, but also the causal connection between the breach of duty and the accident; that what the deceased would have done, if a safety belt had been provided, was a matter of inference from the appropriate facts, and that, in the present case, the inference was that he would not have worn a belt; further that there was no obligation on the employers to instruct or exhort him to wear a safety belt; and that, accordingly, liability had been established.
[7.155]It is sufficient to quote from the speech of Lord Reid who said, after referring to the evidence, at p.81: "So it seems to me to be a natural, and indeed almost inevitable, inference that he would not have worn a belt on this occasion even if it had been available." At p.83 Lord Reid said:
"It has been suggested that the decision of this House in Wardlaw v Bonnington Castings Ltd 1956 S.C. (H.L.) 26 lays down new law and increased the burden on pursuers. I do not think so. It states what has always been the law - a pursuer must prove his case. He must prove that the fault of the defender caused or contributed to the damage which he has suffered. But proof need not be by direct evidence. If general practice or a regulation requires that some safety appliance shall be provided, one would assume that it is of some use, and that a reasonable man would use it. And one would assume that the injured man was a reasonable man. So the initial onus on the pursuer to connect the failure to provide the appliance with the accident would normally be discharged merely by proving the circumstances which led to the accident, and it is only where the evidence throws doubt on either of these assumptions that any difficulty would arise. Normally, it would be left to the defender to adduce evidence, if he could, to displace these assumptions. So, in practice, it would be realistic, even if not theoretically accurate, to say that the onus is generally on the defender to show that the man would not have used the appliance, even if it had been available. But in the end, when all the evidence has been brought out, it rarely matters where the onus originally lay: the question is which way the balance of probability has come to rest."
[7.156]Counsel submitted that the pursuer's case was that if ITL had ceased to manufacture, Mr McTear would not have smoked and would not have contracted lung cancer. The difficulty in deciding this came about because of the lack of evidence. Without evidence from Mr McTear to the effect that, if ITL's cigarettes were not available on the market, he would simply never have smoked, then the case did not get off the ground. His first smoking experiences involved taking cigarettes from any source, not a specific brand. Over a period of years half of his smoking consumption was of Old Holborn hand-rolling tobacco, which rather tended to negate any suggestion that, if ITL's cigarettes had not been available, he would simply never have smoked. He had smoked before he started smoking the John Player brand of cigarettes, and he was smoking roll-ups, on any view of the evidence, right up until the time that he stopped smoking altogether. The pursuer's position, that if ITL had ceased manufacture, Mr McTear would not have contracted lung cancer as a result of their fault, was untenable. If he was going to contract lung cancer anyhow, then the fault had not caused it. For the pursuer to establish fault causation, it was necessary to prove that if the defenders had ceased manufacture Mr McTear would simply not have smoked and therefore would not have contracted lung cancer as a result of smoking, or in any event, he would not have smoked enough to cause lung cancer. It was not clear which of these was being argued for. There was no authority to vouch the proposition that one should proceed on the assumption that everybody else did everything that they should have done, so there was no foundation for assuming that all the United Kingdom tobacco manufacturers would have ceased production in 1957. What had to be done was to look at the particular breach and ask what the result would have been if it had not occurred. The difficulty was that there was no evidence about what Mr McTear would have done had ITL's products not been available. McWilliams was authority for the need to show a causal connection between the breach and the damage, and the burden of proving this was on the pursuer. The present case was a fortiori of McWilliams, because there was evidence from Mr McTear which supported the inference that he would in any event have started smoking, continued to smoke and increased the amount he smoked; and if it was smoking that caused his lung cancer, that the result would not have been any different.
[7.157]Mr Jones said that it was not clear whether a warnings case was still being advanced. Mr McEachran's submissions had appeared to suggest that if the Government health warnings which first appeared on cigarette packets in 1971 had appeared at the time when Mr McTear was starting to smoke, he would not have started to smoke. The first problem arising from this was that in order to determine whether the performance of a duty by ITL to warn would have had the result that Mr McTear would not have started smoking, and therefore whether it could be said that but for the breach he would not have contracted lung cancer, it was necessary to decide what was the state of the science. Only when that was determined could one determine what would have been the appropriate warning. The next question was, if Mr McTear had been given the warning, what would have been the result. In order to establish fault causation, it would be necessary to say that if he had seen warnings on cigarette packets he would never have started smoking. If there was a duty to put on a warning, then that must be to reflect the science at the time, and if that was done, then there would have to be evidence that the consumer, seeing such a warning, would have been deterred from starting to smoke; and there was simply no evidence to that effect.
[7.158]If the pursuer's case was that a 1971-type warning would have been sufficient to have deterred Mr McTear in 1964, it would be necessary for her to establish that when he started smoking regularly in September 1964 or thereafter, he was not in fact already aware that smoking was believed to be a cause of lung cancer; and that if he had been made so aware such a warning would have deterred him from starting to smoke. If Mr McTear had the information, as counsel submitted he did, that cigarette smoking could cause lung cancer before he starting smoking, that was enough for him to make an informed choice.
[7.159]Counsel submitted that the next question for consideration was whether it was proved that Mr McTear smoked a sufficient quantity of ITL's products to have caused or materially contributed to his lung cancer. The starting point for consideration of this question was whether Mrs McTear had proved how much of ITL's products Mr McTear consumed.
[7.160]I have already discussed counsel's submission that there was no reliable factual evidence on which I could make any finding as to: (1) the date when Mr McTear started smoking products manufactured by ITL; (2) how long he smoked ITL's products; (3) how much of ITL's products he smoked from time to time; and (4) the proportion of ITL's products he may have smoked compared with other products such as hand-rolling tobacco and cigarettes produced by other manufacturers. Counsel further submitted that there was no expert evidence that Mr McTear smoked sufficient of ITL's products over a sufficient period to have contributed to his lung cancer. There was no evidence that he smoked ITL's products during any time when he was unaware of the association between smoking and lung cancer. The only evidence about a dose-response relationship between smoking and disease was that of Professor Friend, and he accepted that this was general evidence about populations and that the dose-response relationship did not apply to individuals. He accepted that somebody could smoke fifty cigarettes a day for years and never develop lung cancer, for example. Dr Lewis also gave evidence that the generality of the dose-response relationship did not apply to the population of West Central Scotland.
[7.161]Mr Jones submitted that the question of difficulty in stopping smoking ("addiction") would only arise if it was held that smoking caused Mr McTear's lung cancer, and that ITL were in breach of a duty of care to Mr McTear when he contracted lung cancer or when he had consumed sufficient of their products to have materially contributed to his lung cancer. The pursuer's case now seemed to be that, if Mr McTear became aware that there were health risks associated with smoking before he contracted lung cancer and before he consumed a sufficient quantity of ITL's products to contribute materially to his condition, ITL were liable because Mr McTear continued to smoke until the time came when he contracted lung cancer or until smoking materially contributed to it, because he found it difficult to stop.
[7.162]It might be that this was the reason for the pursuer's argument that ITL had to take their victim as they found him as a consumer of their products. Mr Jones submitted that this was not a principle of liability: it was a doctrine applicable to questions of remoteness of damage, and it did not open the door to liability. Counsel referred to the decision of the First Division in McKillen v Barclay Curle & Co Ltd 1967 S.L.T. 41. In this case, a plumber's mate who fractured a rib when he was descending a three-step staging maintained that tuberculosis from which he was found to be suffering had been reactivated by the accident. In an action against his employers it was held that the accident was caused by their negligence, and damages, including damages in respect of his tuberculosis, were awarded. The defenders reclaimed on the measure of damages and maintained inter alia that the reactivation of the pursuer's tuberculosis was not a foreseeable consequence of the accident for which the defenders were bound to compensate him. The First Division held inter alia that the doctrine of reasonable foreseeability had no relevance to the measure of damage once liability had been established, since the party guilty of negligence must take his victim as he found him. The Lord President (Lord Clyde) said at p.42:
"In my opinion it has never been the law of Scotland that a man guilty of negligence towards another is only liable for the damage in respect of physical injuries which a reasonable man would foresee as likely to follow from it. On the contrary it has always been law of Scotland as I understand it that once a man is negligent and injures another by his negligence he is liable for all the damage to the injured man which naturally and directly arises out of the negligence. He must take his victim as he finds him, and if his victim has a weak heart and dies as a result of the injury the negligent man is liable in damages for his death, even although a normal man might only in the same circumstances have sustained a relatively trivial injury. [...] The doctrine of reasonable foreseeability with all its subtle ramifications may be applied in determining questions of liability [...]. It has no relevance once liability is established and the measure of damage is being determined."
[7.163]Counsel submitted that in any event there was no credible and reliable evidence that before 1992 Mr McTear made any serious attempt to stop smoking and found it difficult to do so. He did stop smoking when he was diagnosed as suffering from lung cancer, and there was no evidence that he found that difficult. As Professor Gray said, he stopped in 1992 because he was motivated to stop.
[7.164]Further and in any event, even if there were such evidence that Mr McTear tried to stop and found it difficult, the law, counsel submitted, did not absolve individuals of their legal responsibilities on account of a subjective belief that it was difficult to meet such responsibilities. Counsel referred to Morris v Murray [1991] 2 Q.B. 6. In this case, after drinking alcohol during the whole of the afternoon, the plaintiff and his friend decided to go on a flight in the friend's light aircraft. The plaintiff drove the car which took them to the airfield and he helped to start and refuel the aircraft, which was piloted by the friend. Shortly after take-off the aircraft crashed, killing the pilot and severely injuring the plaintiff. In an action against the pilot's personal representatives for personal injuries, the judge, in giving judgment for the plaintiff, held that the defendants had succeeded on their plea of contributory negligence but not their alternative plea of volenti non fit iniuria. On the defendants' appeal, the Court of Appeal held, allowing the appeal, that the plaintiff willingly embarked upon the flight, knowing that the pilot was so drunk as to be incapable of discharging a normal duty of care; that the danger in embarking upon the flight was both obvious and great and the plaintiff was not so drunk as to be incapable of appreciating the nature and extent of the risk involved, and, therefore, he was to be taken to have fully accepted the risk of serious injury and implicitly discharged the pilot from liability for negligence in relation to the flying of the aircraft; and that, accordingly, the maxim volenti non fit iniuria applied as a defence to the plaintiff's claim. At pp.16-17 Fox L.J. said:
"If the plaintiff had himself been sober on the afternoon of the flight it seems to me that, by agreeing to be flown by Mr Murray, he must be taken to have accepted fully the risk of serious injury. The danger was both obvious and great. [...] None of [the facts] suggests that his facilities were so muddled that he was incapable of appreciating obvious risks. [...] I think he knew what he was doing and was capable of appreciating the risks. [...] I think that in embarking upon the flight the plaintiff had implicitly waived his rights in the event of injury consequent on Mr Murray's failure to fly with reasonable care."
[7.165]Counsel referred to this passage in support of a submission that there was no evidence that when Mr McTear was aware of the risks that were being warned of, he was incapable of stopping smoking. He would have to get to that point before he could be said to have continued to smoke as a result of ITL's breach of some duty owed to him. The matter was more complicated than that, because in any event, if he became aware, as he clearly did, then at that stage any breach of a duty to warn flew off, so there was no fault causation. What the pursuer would have to do would be to say that there was a continuing breach of another kind, that he was incapable of stopping and that the breach on the part of the defenders was in not having warned him that, once he stopped smoking, he was unable to stop. This was wholly missing in the case in any event. Counsel's main submission was that "difficulty" was not a good reason in law for not performing the duties that were incumbent upon an individual. As Professor Gray said, Mr McTear could have stopped, and it was really a question of motivation: there was nothing to prevent him from stopping.
[7.166]In answer to a question by me, Mr Jones submitted that there was no distinction between the civil law and the criminal law where it came to the general proposition that individuals were responsible for their own actions. Counsel referred to Galbraith v HM Advocate (No.2) 2002 J.C. 1, in which the law of diminished responsibility was reconsidered by a court of five judges, of whom I was one. In delivering the Opinion of the Court, the Lord Justice-General (Lord Rodger of Earlsferry), said at p.17, para.44:
"It is, of course, impossible to attempt to describe the ambit of the doctrine of diminished responsibility without even attempting to describe the operation of the doctrine itself. A common theme in the cases where judges have left the issue to the jury is that they involve some abnormality of the accused's mind. While philosophers continue to debate the timeless questions - about the nature of the relationship between mind and body and about the extent to which individuals have control over their actions - our law proceeds on the basis that an adult person of sound mind has sufficient control over his acts, and over his omissions to act, as to be responsible for them in law. Criminal acts and omissions are punished accordingly."
During the discussion about this case, I observed that I could not see anything unjust in attributing the same responsibility for the purposes of the civil law as was attributed for the purposes of the criminal law. One had to assume that the individual was a reasonably well-informed and reasonably responsible member of the public. Mr Jones agreed that this would be consistent with the chapter of his submissions which related to the way in which one had to approach the question of the information that was available to the public.
Discussion: (1) Negligence
[7.167]Although it is averred on behalf of the pursuer, at p.25A-B of the Closed Record, that it was "the duty of the defenders prior to 1964 and thereafter to warn persons smoking their products, or who may be intending to start smoking their products of the facts that smoking was addictive and could cause lung cancer, such as by printing clear warnings on their cigarette packets or in advertisements that smoking could cause fatal diseases", and that it was breach of this among other duties that ultimately caused Mr McTear's lung cancer, as can be seen from the foregoing summary this did not form any significant part, if at all, of Mr McEachran's submissions on the issue of negligence.
[7.168]This appears to me to be inevitable, given the state of the evidence, which is reflected in my finding in fact at para.[4.230] that Mr McTear was aware, in common with the general public, well before 1971, and indeed by 1964, when he said he started smoking, of the publicity about the health risks associated with smoking, and in particular the risk of lung cancer. At para.[4.227] I have stated that I am not prepared to hold it proved that it was ITL's products that Mr McTear smoked at any time prior to 1971. That was of course the year in which Government health warnings first appeared on cigarette packets. I have also held it proved that tobacco is "addictive" in no more than the sense averred by the pursuer, that once individuals have started smoking it is difficult for them to wean themselves off the habit, and, at para.[4.229], that Mr McTear did not in fact become "addicted" to tobacco except in this sense. In these circumstances I do not think it necessary to discuss further the case based on an alleged failure to give warnings. I would only comment that there appears to me to be no justification for a criticism which appeared to be made of ITL, in common with other tobacco manufacturers, that the warnings they printed originated not with themselves but with the Government. I can see no force in this: the point is that the warnings were there to be read, as indeed they were by Mr McTear.
[7.169]Accordingly, I now turn to consider the averment for the pursuer on which Mr McEachran founded, also at p.25A-B of the Closed Record, that it was "the duty of the defenders to take reasonable care not to manufacture tobacco products, including John Player cigarettes for sale to members of the general population such as the deceased", and it was "their duty to take reasonable care not [to] sell such products directly or indirectly to consumers such as the deceased."
[7.170]The starting point for Mr McEachran's submissions about the applicable law was Donoghue v Stevenson, paras.[7.3] to [ 7.7]. This case established that the manufacturer of a product intended for consumption owed a duty to the ultimate consumer of the product to take reasonable care that the consumer should not suffer harm by reason of any act or omission on the part of the manufacturer which he should reasonably foresee as being liable to cause such damage. Breach of this duty is negligence, so that the manufacturer becomes liable in reparation to the consumer for any harm caused by it. This is, however, only the starting point. While the decision in Donoghue v Stevenson was of fundamental importance in establishing that a duty of care may be owed by a manufacturer to a consumer, and indeed owed in many other relationships, it did not establish the content of the duty beyond stating that it is to take reasonable care.
[7.171]What appears to me to be the more useful approach is that advanced by Mr Jones, which is to consider whether, assuming that Mr McTear suffered harm as a result of smoking ITL's products, this was caused by a failure on their part in a duty to him to exercise reasonable care. What has to be examined is the content of such duty. In relation to Mr McTear this cannot have existed earlier than 1964, which on his own account is when he started to smoke, or 1971, which is the earliest date at which I am prepared to hold that he was proved to have been smoking John Player cigarettes.
[7.172]Assuming for present purposes that cigarette smoking can cause lung cancer, and that tobacco can therefore be described as a dangerous product, I can find no support in the authorities for the proposition that as soon as they became aware of this ITL had a duty effectively to cease manufacture. They could only have had such a duty if the law held that a manufacturer must ensure the safety of the consumer. The cases do not support this approach. In Holmes v Ashford, referred to at paras.[7.69] to [7.70], the Court of Appeal went no further than to hold that every person who put on the market a dangerous article must take reasonable steps in all the circumstances.
[7.173]In Donoghue v Stevenson the circumstances were that the ginger beer, and the snail, were contained in an opaque sealed bottle, and there was no opportunity for intermediate inspection of its contents. In Grant v Australian Knitting Mills Ltd, para.[7.8] it was emphasised that Donoghue v Stevenson only applied where the defect was hidden and unknown to the consumer. Reference may also be made to Murphy v Brentwood District Council, in the passage from the speech of Lord Keith quoted at para.[7.67]. As Lord Keith said, an essential feature of the species of liability in negligence established by Donoghue v Stevenson was that it was the latency of the defect in a carelessly manufactured product which constituted the mischief: there could be no doubt that a person who was injured through consuming or using a product of the defective nature of which he was well aware had no remedy against the manufacturer.
[7.174]As Mr Jones submitted, the proposition that there is no duty to warn of risks of which the ordinary member of the relevant class of people may reasonably be assumed to be aware applies not only in the context of product liability, but also in other circumstances involving risk: see for example Hodge & Sons v Anglo-American Oil Co, quoted at paras.[7.90] to [7.93], and Tomlinson v Congleton Borough Council, quoted at paras.[7.32] to [7.42]. Wright v Dunlop Rubber Co Ltd (see paras.[7.11] to [7.16]) does not appear to me to be of any assistance to the pursuer, for two reasons: first, because ICI knew or ought to have realised that there was a real risk to employees of Dunlops, of which neither Dunlops nor their employees were aware, arising from the use of the product; and secondly because as employees the plaintiffs were obliged to use substances which Dunlops as their employers instructed them to use in the course of their employment, and this formed part of the circumstances of which ICI ought to have taken account in the exercise of reasonable care.
[7.175] The circumstances which appear to me to be relevant to the present case are as follows. Tobacco and tobacco products have at all material times lawfully been sold to adult members of the population in the United Kingdom. The manufacture and sale of tobacco products support a substantial industry. ITL are a substantial company with numerous employees and their activities no doubt make a substantial contribution to the economy. The demand for their products may be related to the evidence that smoking gives pleasure and may have social benefits. USSG 1964, pp.354-356, quoted at para.[5.163], referred to "significant beneficial effects of smoking primarily in the area of mental health". There is no suggestion in this case that cigarettes manufactured by ITL have at any time contained any substance other than what the public would normally expect as a constituent of a cigarette, so this is not a case of a latent defect of the kind that was discussed in Donoghue v Stevenson and Grant v Australian Knitting Mills Ltd: smokers of ITL's cigarettes were consuming products in a state in which ITL intended that they should reach the consumers and which the consumers themselves intended to consume in that state. There cannot thus be said to have been a "defect" in their products of which the consumers of their products were not also aware. ITL became aware in the same way as the general public did, from published reports, of the association between cigarette smoking and lung cancer from 1950 onwards. The Government have from the outset relied on the provision to the public of information and education about the risks to health, in particular lung cancer, associated with cigarette smoking. Apart from the imposition of restrictions designed to prevent the sale of cigarettes to persons other than adults and the use of fiscal measures designed, in part, to act as a deterrent to purchase, the Government have left it to individuals to decide whether or not to smoke cigarettes. It is not irrelevant that by section 10(7)(f) of the Consumer Protection Act 1987 tobacco is excluded from the expression "consumer goods" and thus from the general safety requirement under the Act.
[7.176]While it could hardly be disputed, and indeed was accepted by Professor Hastings, that the general public would be aware, because of all the publicity referred to in Part III, of the association between cigarette smoking and lung cancer, or at least of the serious risks to health attributed to smoking, I understood Mr McEachran to submit that the impact of this publicity was lessened by the continued appearance of advertisements for cigarettes and by statements made by the tobacco industry that it had not been proved that the association amounted to a causal connection between cigarette smoking and lung cancer. As has been seen, the issue was by no means as open-and-shut as Sir Richard Doll, for example, believed it to be. If Sir Ronald Fisher and other critics seriously disagreed with him, this would quite properly be taken into account by ITL, and it would be part of the normal process of press coverage that opposing views be reported. I have no reason to think that the general public in the United Kingdom were not well aware that both sides of an argument might appear in the media - indeed they might well expect this to happen - or were unable to weigh up the competing arguments and decide what to make of them. Although, at para.[5.337], Professor Hastings spoke of the difficulty of making such decisions, he also accepted that readers of newspapers might be expected to have a certain degree of sophistication. What is important is that the information about the association between cigarette smoking and lung cancer was available to the general public, and each individual could decide what to make of it and how, if at all, to act upon it. In my view, each individual at all material times was in a position to make an informed choice whether to start, to continue or to stop smoking; and Mr McTear in particular not only made such an informed choice but could be seen to have acted on it on occasions when he chose to stop smoking on various occasions from 1971 onwards and then chose to start smoking again.
[7.177]I reject the insidious suggestion which, if not expressly advanced, was at least implicit in aspects of the pursuer's case based on the evidence of Professor Hastings, to the effect that because he was in a lower socio-economic class Mr McTear was somehow to be regarded as more a victim of circumstances and as having less than full responsibility for his own choices and actions. This lay behind Mr McEachran's submission that ITL had to take their victim as they found him. No doubt, as brought out in MacAskill et al. 2002 and the evidence of Mr Davis and Professor Hastings, the prevalence of smoking is, for whatever reason, higher among members of lower socio-economic classes. But that does not, in my view, support an approach which would accord less individual responsibility to such people as Mr McTear. In Holmes v Ashford, quoted at paras.[7.69] to [7.70], it was held that a person to whom a product is supplied for consumption may be presumed to be reasonable. There is a statement to similar effect in McWilliams v Sir William Arrol & Co, referred to at paras.[7.154] to [7.156]. Likewise, a subjective view by an individual that it may be difficult for him to give up smoking does not absolve him of his responsibilities under the common law.
[7.178]The policy of the law in a society such as ours seems to me to be entirely clear. Adults of full age and not suffering from legal incapacity are equal in the eyes of the law. They have equal rights and duties, freedoms and responsibilities. Each of them is presumed to be reasonable, and to have the responsibility of making reasonable choices, not least in matters affecting his or her safety, health and welfare. This approach is fundamental to the workings of our society. It is reflected, for example, in the equality of individuals as members of the electorate, and in the approach of the criminal law, which is to treat all individuals as having full criminal responsibility in the absence of special circumstances (see Galbraith v HM Advocate (No.2), referred to at para.[7.166]). Individuals are assumed to be reasonably well informed and reasonably responsible members of society.
[7.179]At the centre of my thinking is the individualist philosophy of the common law, described by Lord Hoffmann in Tomlinson v Congleton Borough Council, in the passage quoted at para.[7.46]. As he said, people of full age and sound understanding must look after themselves and take responsibility for their actions. There is no duty to save people from themselves. If they are, or may reasonably be supposed to be, in possession of information about harm which they may suffer if they choose to follow a particular course of action, the responsibility is theirs alone. They have the right of self determination which was recognised in Law Hospital NHS Trust v Lord Advocate, quoted at para.[7.49]. If, in knowledge that they are taking a chance, as the pursuer did in Titchener v British Railways Board, they expose themselves to a risk of harm, there is no breach of any duty of care. As was said in Grant v Australian Knitting Mills Ltd (para.[7.8]), "the man who consumes or uses a thing which he knows to be noxious cannot complain in respect of whatever mischief follows, because it follows from his own conscious volition in choosing to incur the risk or certainty of mischance." In Murphy v Brentwood District Council Lord Keith, in the passage quoted at para.[6.67], said that a person who was injured through consuming or using a product of the defective nature of which he was well aware had no remedy against the manufacturer. It is not difficult to find instances today of people who, rather than blaming themselves for the consequences of their own decisions, seek to negate responsibility by claiming that a condition, such as obesity or addiction to a controlled drug, has just happened to them, independently of their own volition, or is someone else's fault, as was claimed in Pelman v McDonald's Corporation, referred to at paras.[7.130] to [7.132]. For sound reasons the law gives no countenance to such a tendency. The individualist philosophy requires that individuals must live with the legal consequences of their own informed choices.
[7.180]The approach of the common law in the United Kingdom is consistent with the approach in the Australian cases to which reference was made, Thompson v Johnson & Johnson Pty Ltd, referred to at paras.[7.73] to [7.77], Graham Barclay Oysters Pty Ltd v Ryan, referred to at paras.[7.79] to [7.84] and Woods v Multi-Sport Holdings Pty Ltd, referred to at paras.[7.96] to [7.99]. I agree with counsel's reasons for distinguishing the Canadian case of Bow Valley Husky (Bermuda) Ltd v Saint John Shipbuilding Ltd, referred to at paras.[7.100] to [7.103]. It is not without significance that the view I have formed about the effect of public awareness of the publicity about the health risks associated with smoking, particularly lung cancer, has led to similar results in actions against tobacco manufacturers in other jurisdictions, in the cases referred to at paras.[7.112] to [7.128]. As counsel put it, all of these cases support the view that the individual is well enough served if he is given such information as a normally intelligent person would include in his assessment of how he wishes to conduct his life, thus putting him in the position of making an informed choice.
[7.181]For these reasons in my opinion there was no lack of reasonable care on the part of ITL at any point at which Mr McTear consumed their products, and the pursuer's negligence case would accordingly fail.
(2) Fault causation
[7.182]Since I have held as a matter of fact that Mr McTear was aware, in common with the general public, well before 1971 of the publicity about the health risks associated with smoking, and in particular the risk of lung cancer, and since I am not prepared to hold it proved that it was ITL's products that he smoked at any time prior to 1971, so that by the time he is shown by acceptable evidence to have started smoking the John Player brand of cigarettes he was already aware of the publicity about the health risks, it does not appear to me to be necessary to consider the issue of fault causation in relation to the pursuer's warnings case. I propose therefore only to consider the issue of fault causation in relation to the averment that it was the duty of ITL to take reasonable care not to manufacture tobacco products, including John Player cigarettes, for sale to members of the general population such as Mr McTear and that it was their duty to take reasonable care not to sell such products directly or indirectly to consumers such as Mr McTear. For this purpose I require to assume, contrary to what I have held in preceding paragraphs, that ITL were negligent in this regard. I also require to assume that but for smoking cigarettes Mr McTear would not have contracted lung cancer, and that ITL's cigarettes made a material contribution to his contracting lung cancer. The latter assumption is fraught with difficulty, because even if I were to hold it established, on the basis of the epidemiology, that cigarette smoking can cause lung cancer, there is still no evidence as to the process by which smoking causes lung cancer in an individual: but I assume for present purposes that the process is cumulative. On this assumption, if an individual smokes the products of more than one manufacturer over many years, the products of any one manufacturer which he smokes for more than a negligible period and in more than a negligible quantity may be regarded as making a material contribution to his contracting lung cancer.
[7.183]But the main problem for the pursuer is that there is no basis upon which I could hold it established that, if ITL had not manufactured cigarettes at any material time, so that Mr McTear did not smoke their products and accordingly their products could not have made a material contribution to his contracting lung cancer, it would have made any difference. It could only be said that ITL's products made a material contribution if, by not smoking them, Mr McTear would have reduced his overall consumption. On the contrary, all the evidence is that Mr McTear would have started smoking when he did, and would have continued to smoke, for the same length of time and in the same quantities, as he in fact did. I cannot see that anything other than the impossibility of buying tobacco in the United Kingdom would have prevented him from doing this. It is not part of the pursuer's case on Record that the other tobacco manufacturers should or would have followed suit, though Mr McEachran advanced a somewhat improvised submission to this effect. The result was that it was not explored at all in the evidence whether such a result could have been feasible, even if desirable. And what would have prevented tobacco from being brought into the country? This would have required effective Government action. Attempts at prohibition of substances which people enjoy using and strongly desire to use are notoriously ineffective. On the evidence I am satisfied that, even if ITL were negligent in the manner alleged, this would have made no difference to Mr McTear's contracting lung cancer, and as a result he would have been in the same position as the pursuer in McWilliams v Sir William Arrol & Co.; failure to provide a safety belt is not negligence if it would not in any event have been used.
Volenti non fit iniuria
[7.184]I turn finally to consider the fourth plea-in-law for ITL which, so far as material, is in these terms:
"The deceased having willingly accepted as his own any risk to his health from smoking cigarettes, the defenders should be assoilzied."
This plea invokes the maxim volenti non fit iniuria. This maxim has featured in some of the cases and submissions discussed in the previous section, but I was also separately addressed on it by counsel, and I think it appropriate to treat it as a separate topic. Although, for convenience, Mr McEachran addressed me on it first, it was not in dispute that the burden of proving it is on the defenders.
Submissions for Mrs McTear
[7.185]Mr McEachran submitted that this expression meant that a legal wrong was not done to someone who was willing. The onus of proving that Mr McTear was volens rested on ITL. For the defence to apply, they required to show that Mr McTear, with full knowledge of the nature and extent of the risk that he ran, freely and voluntarily agreed to incur it. He must be both sciens et volens: there must be both knowledge of the risk and evidence of acceptance of the risk. ITL must be able to show that there was full appreciation of the danger of the situation. Counsel submitted that there was a long line of established authority to vouch these propositions. He referred to five cases.
[7.186] (1) In McCaig v Langan 1964 S.L.T. 121 a passenger in a motor car suffered serious injuries in an accident while the car was being driven by a friend. He brought an action of damages against the driver of the car who admitted that the accident was caused by his fault. The defender averred that when the pursuer entered the car he knew that the defender's ability to drive had been so affected by drink as to endanger his passengers' safety and he also knew that the car was so overcrowded as to render the safe steering and control of the car difficult. The defender further averred that the pursuer knew that because of both the drunkenness of the driver and the overcrowding of the car he ran a risk of grave injury by allowing himself to be driven in the said car, and by entering the car he voluntarily accepted the said risk. In these circumstances, the defender pleaded inter alia that the pursuer had voluntarily accepted the risk of sustaining such injuries as he did sustain. It was held by Lord Kilbrandon that these averments were relevant.
[7.187]At p.124 Lord Kilbrandon said:
"I now turn to the plea of volenti non fit iniuria. I will adopt, from the many explanations of that maxim, a passage from the opinion of Lord MacDermott in Kelly v Farrans Ltd [1954] N.I. 41 quoted in Charlesworth, 4th edition, section 1156:
'The question raised by a plea of volenti non fit iniuria is not whether the injured party consented to run the risk of being hurt, but whether the injured party consented to run that risk at his own expense so that he and not the party alleged to be negligent should bear the loss in the event of injury. In other words, the consent that is relevant is not consent to the risk of injury but consent to the lack of reasonable care that may produce that risk.'
Whether the inference ought to be drawn in the absence of express consent that a person must be supposed to have given the relevant consent can only be decided as a question of fact [...]. If a person steps into a car in order to be driven by a driver who is, to his knowledge, so drunk as to be unable to drive the car safely, as is averred here by the defender, it may be proper to draw the inference that that person must appreciate that the driver is incapable of exercising reasonable care, and so he consents to the lack of it. That would satisfy Lord MacDermott's test, and the plea would be established."
Lord Kilbrandon then went on to hold that it was plain from the authorities that the plea might, in suitable circumstances, be established in a case such as that before him.
[7.188] (2) In Nettleship v Weston [1971] 2 Q.B. 691 the plaintiff, an experienced driver, agreed to give a friend's wife some driving lessons in her husband's car, after satisfying himself that the car was insured against risk of injury to a passenger. During the course of one driving lesson the learner lost control of the car which collided with a lamp standard. The learner was shortly afterwards convicted of driving without due care and attention. The plaintiff, who was injured in the collision, brought an action for damages in respect of the learner's negligence. The trial judge dismissed the plaintiff's claim on the grounds inter alia that he had voluntarily assumed the risk of injury. The Court of Appeal, in allowing the appeal, held inter alia that the plaintiff, by checking on his position under the car insurance before agreeing to give the lessons, had shown expressly that he did not consent to run the risk of injury which might occur through the learner's known lack of skill, so that she could not rely on the defence of volenti non fit iniuria to bar his claim.
[7.189]At p.701 Lord Denning M.R. said:
"This brings me to the defence of volenti non fit iniuria. Does it apply to the instructor? In former times this defence was used almost as an alternative defence to contributory negligence. Either defence defeated the action. Now that contributory negligence is not a complete defence, but only a ground for reducing the damages, the defence of volenti non fit iniuria has been closely considered, and, in consequence, it has been severely limited. Knowledge of the risk of injury is not enough. Nor is a willingness to take the risk of injury. Nothing will suffice short of an agreement to waive any claim for negligence. The plaintiff must agree, expressly or impliedly, to waive any claim for any injury that may befall him due to the lack of reasonable care by the defendant: or, more accurately, due to the failure of the defendant to measure up to the standard of care that the law requires of him."
[7.190] (3)In White v Blackmore [1972] 3 All.E.R. 158 the deceased, an experienced "jalopy" racing driver, was participating in jalopy races. During one race, in which he was not participating, he stood next to the spectators' enclosure rope. The rope became entangled in the rear wheel of a car and it, and the stakes to which it was attached, were pulled out. The deceased was catapulted into the air, and subsequently died of his injuries. The trial judge held that the defendants were negligent in tying all the ropes to one stake, and were therefore in breach of the common duty of care owed by an occupier of land to visitors under section 2 of the Occupiers' Liability Act 1957. The trial judge, however, dismissed the claim on the ground that the defence of volenti non fit iniuria applied, having regard to the terms of warning notices about the dangers of motor racing which were displayed at the entrance and around the track. On appeal, the Court of Appeal held that the doctrine of volenti non fit iniuria did not apply to a case where the risk of injury arose, not from participation in the dangerous sport of motor racing, but from the organisers' failure to take reasonable precautions for the safety of visitors to the meeting. A visitor to a motor race meeting did not willingly accept the risk of injury due to the organisers' defaults in ensuring his safety; since the deceased did not have full knowledge of the risk he was running from the faulty layout of the ropes, he had not willingly accepted the risk of injury arising from the defendants' default; accordingly the doctrine did not afford a defence to the wife's claim.
[7.191]Lord Denning M.R. said at p.164:
"No doubt the visitor takes on himself the risks inherent in motor racing, but he does not take on himself the risk of injury due to the defaults of the organisers. People go to race meetings to enjoy the sport. They like to see the competitors taking risks, but they do not like to take risks on themselves. Even though it is a dangerous sport, they expect, and rightly expect, the organisers to erect proper enclosures, and to do all that is reasonable to ensure their safety. If the organisers do everything that is reasonable, they are not liable if a racing car leaps the barriers and crashes into the crowd: see Hall v Brooklands Auto-Racing Club [1933] 1 K.B. 205. But, if the organisers fail to take reasonable precautions, they cannot excuse themselves from liability by invoking the doctrine of volenti non fit iniuria; for the simple reason that the person injured or killed does not willingly accept the risks arising from their want of reasonable care: see Slater v Clay Cross Co. Ltd [1956] 2 Q.B. 264, Wooldridge v Sumner [1963] 2 Q.B. 43 at 69, Nettleship v Weston [1971] 2 Q.B. 691 at 701.
In this case Mr White was quite unaware that the organisers had been negligent. He never willingly accepted the risk of injury due to this default. They cannot rely on volenti non fit iniuria."
[7.192] (4) In Fowler v Tierney 1974 S.L.T. (Notes) 23 a young woman was injured in a collision with a motor car when she was travelling as a pillion passenger on a motor scooter. She brought an action claiming damages against the driver of the motor scooter. The defender pleaded, inter alia, volenti non fit iniuria. The Lord Ordinary, Lord Maxwell, held it proved that the defender did evince an initial reluctance to give the pursuer a lift, but he did inform her that he had only a provisional licence, either by using those actual words or words to equivalent effect, and that something was said by the defender relating to the pursuer taking a risk or to it being her fault if anything happened.
[7.193]In repelling the defender's plea of volenti non fit iniuria Lord Maxwell, at p.24, after referring to various authorities, including McCaig v Langan, said:
"In the normal volenti case there is required, I think, proof that the pursuer has knowingly submitted himself to some special or exceptional risk in such circumstances that the court can infer from the whole facts that he is consenting to run the risk of the other party's negligence at his own expense or, to put the matter in another way, that he is consenting to lack of reasonable care on the part of the other party. While not of itself sufficient to make such a case, it is, I think, an essential element of such a case that there should be knowledge of the nature and extent of the special or exceptional risk. [...] I have held that the pursuer knew that the defender was a learner-driver and, to that extent, no doubt knew that he was of limited experience. But there is no suggestion on the pleadings or in evidence that the pursuer knew, or had reason to know, that he was unable or unlikely to exercise normal standards of reasonable care [...]."
[7.194] (5) In Winnik v Dick 1984 S.L.T. 185 the respondent, a passenger in a motor car who was injured in an accident, raised an action of damages against the driver, the appellant, who had been convicted of an offence under the Road Traffic Act 1972. The men had been drinking together in public houses for most of the day and when the respondent entered the appellant's car to return home, he knew that the appellant was drunk. The appellant contended that he was not liable in damages to the respondent inter alia because the respondent had voluntarily accepted the risk of an accident.
[7.195]The Lord Justice-Clerk, Lord Wheatley, at pp.187-188, reviewed the Scottish cases, including McCaig v Langan and Fowler v Tierney, before concluding:
"From these expressions of view as to what is involved in the maxim so far as the law of Scotland is concerned, I can find no support for, but rather refutation of, the contention that its effect here is to establish that on this journey there never was any duty on the defender as the driver of the car to take reasonable care quoad the pursuer [...]. In my opinion the effect of the maxim was not to relieve the defender from any duty to take care quoad his passengers. On the contrary the maxim proceeds on the basis that there is duty to take care and not be negligent, but the successful establishment of the maxim means that the pursuer has accepted the risk of the defender's negligence in the exercise of his legal duties and has absolved the defender from the consequences arising from that negligence."
[7.196]On the basis of these authorities Mr McEachran submitted that the plea would only succeed if Mr McTear had agreed expressly or impliedly to waive any claim for any injury that might befall him. While the cases referred to related to accidents, the same considerations arose where what was alleged was continuous negligence having a cumulative effect. It was necessary to identify the risk and to see whether there was evidence that Mr McTear consented to a lack of reasonable care on the part of ITL. As was said in Letang v Ottawa Electric Railway Co [1926] A.C. 725, there had to be a finding that he freely and voluntarily, with full knowledge of the nature and extent of the risk he ran, impliedly agreed to incur it.
[7.197]In order to succeed ITL would need to show that Mr McTear, when he started smoking, knew not just that it was possibly bad for him, but that there was a real risk that he would contract lung cancer. Counsel founded on a concession by Mr Davis that Mr McTear might know about the risks associated with smoking, but not about the causation of lung cancer. There must be real difficulty in demonstrating that when Mr McTear started smoking he knew that it could cause lung cancer. Mr McTear denied that when he gave evidence on commission. This was supported by the evidence of Professor Hastings: the picture was of an evolving new line of argument, and there was a big difference between views and arguments being offered to the public and an acceptance by the manufacturers and the Government that the product could bring with it a risk. Taken at its highest, what was present here was the possibility of knowledge on the part of Mr McTear of a view that "smoking might not be good for you". The manufacturers of a product, counsel submitted, could only rely on volenti non fit iniuria when they themselves had taken steps to warn a user of the possible risk associated with the product, by putting a warning on cigarette packets such as "Smoking kills" and something to the effect that liability was excluded. It was unacceptable for ITL to have spent millions of pounds promoting a positive image of their product and encouraging smokers to continue to smoke products and then rely on the plea. The "clean hands" doctrine pointed the other way.
[7.198]On the evidence, it was not generally accepted in 1964 that there was a risk. At best the public were aware of the debate about smoking and health. The manufacturers did not accept that any risk had been proved, they did not give any warning of it and they spent huge sums on advertising and promotion. While much would come down to the view which the court took of the level of public awareness at this time, in order to allow the plea to stand it would have to be accepted, on the balance of probabilities, that when Mr McTear started smoking he knew that he was running the risk of contracting lung cancer. By the time warnings were placed on cigarette packets in 1971, Mr McTear was addicted and finding it difficult to stop. It could not be said that he had freely given consent thereafter. The plea could only succeed if it was shown that at the time of starting to smoke Mr McTear was aware of the risk and, as was established by Fowler v Tierney, that there was a lack of reasonable care by ITL. There was no basis for saying that he showed consent to such a lack of reasonable care. For the plea to succeed ITL had to show that Mr McTear took the risk of lung cancer, that he accepted that risk, and that he consented to their negligence by waiving any rights to make a claim. Warnings of the type that appeared in 1971 were not enough, because there was no reference made to lung cancer or the risk of death, such as now appeared on cigarette packets.
Submissions for ITL
[7.199]Mr Jones submitted that the issue of the volenti non fit iniuria only came into play if I were to hold that ITL had a duty to withdraw their products from the market and that if they had done so Mr McTear would not have contracted lung cancer. This was so because if the duty only was to warn, then on counsel's approach to the case (with which, as I have already stated, I agree) ITL were not in breach of their duty for reasons he had advanced. Therefore one did not reach the question of volenti non fit iniuria, one stopped at the point of there being no breach of a duty of care. Counsel said he could see that volenti non fit iniuria might be a live issue if there had been a breach of a duty to withdraw the product from the market. In that event, I should sustain the plea for ITL. The questions to be considered were, first, whether Mr McTear knew of the health risks associated with smoking; and, secondly, whether or not he accepted the risks. The knowledge in question was knowledge that Government and public health authorities were warning that smoking carried with it a risk of lung cancer.
[7.200]Counsel referred to Imperial Chemical Industries Ltd v Shatwell [1965] A.C. 656. The respondent in this case was employed as a shot firer in a quarry. There was to be a test of the electric wiring connecting explosive charges. Contrary to instructions that testing must be done from a shelter, the respondent and another shot firer carried out a test in the open and in the result they were both injured. The House of Lords held that where two fellow-servants combined to disobey an order deliberately though they knew the risk involved, volenti non fit iniuria was a complete defence if the employer was not himself at fault and was only liable vicariously for the acts of the fellow servant. At p.673, Lord Reid said:
"It was argued that in this case it has not been shown that George [Shatwell] had a full appreciation of the risk. In my view it must be held that he had. He knew that those better qualified than he was took the risk seriously. He knew that his employers had forbidden this practice and that it had then been prohibited by statutory regulation. And he knew that his employers were taking strong measures to see that the order was obeyed. If he did not choose to believe what he was told I do not think that he could for that reason say that he did not fully appreciate the risk. He knew that the risk was that a charge would explode during testing, and no shot firer could be in any doubt about the possible consequences of that."
Counsel submitted that this was authority for the proposition that it was not necessary that Mr McTear should have had any more precise knowledge of the risks involved than that the Government and public health authorities were warning that smoking carried with it a risk of lung cancer. This could be related to Titchener v British Railways Board, where it was held to be sufficient to know that one was taking a chance, without knowing of the precise chain of possible events or precise nature of the outcome.
[7.201]On the question of acceptance of risk, counsel submitted, under reference to the authorities referred to by Mr McEachran, that where the negligence which finally came about was prospective, something like a waiver of liability was necessary before it could be said that the injured person was volens. So, where a passenger got into a motor car with a driver who had been drinking, at that moment there had been no negligent driving, but it was possible to infer a waiver of liability from the whole facts and circumstances of the case. Counsel submitted, however, that this was not such a case: this was a case like that of Titchener, where the alleged negligence had already been committed, the act had been done and there was nothing more to happen by way of negligence. This was why in Titchener their Lordships were at pains to point out that there was no question of the train having been negligently driven, for example. In Grant v Australian Knitting Mills Ltd it was said that the man who consumed or used the thing which he knew to be noxious could not complain in respect of whatever mischief followed, because it followed from his own conscious volition in choosing to incur the risk or certainty of mischance. In counsel's submission, this would be the case even if the dangerous nature of the product was attributable to some negligence during manufacture. So a person who bought a bottle of ginger beer knowing that it had a snail in it could not complain, even if the snail was only in the bottle because of the negligence of the manufacturer.
[7.202]From the time that Mr McTear became aware of the health risks, no later than 1971, he continued to smoke cigarettes. His continued smoking from then on, in knowledge of the health risks, was volens. In the absence of evidence that his smoking of ITL's cigarettes during the period when he was unaware of the risk caused or materially contributed to his lung cancer, the pursuer's case failed. In Reeves v Commissioner of Police for the Metropolis the House of Lords held that a police authority could not rely on volenti non fit iniuria to resist liability for breach of a duty to take reasonable care to prevent a prisoner, while in police custody, from taking his own life deliberately, but Lord Hope said that it was unusual for a person to be under a duty to take reasonable care to prevent another person doing something to his loss, injury or damage deliberately: on the whole, people were entitled to act as they pleased, even if this would inevitably lead to their own death or injury.
[7.203]As counsel had already submitted, it was not alleged that ITL had a duty to prevent Mr McTear from smoking. He might for example have obtained tobacco products from other sources, including other manufacturers or foreign sources or even illicit sources. What was averred in the pleadings was that they had a duty to refrain from marketing their products, so to give effect to a plea of volenti non fit iniuria in this type of case would not be inconsistent with the existence of the duty.
Discussion
[7.204]The maxim volenti non fit iniuria, literally translated, means, as Mr McEachran submitted, that a legal wrong is not done to one who is willing (or, perhaps preferably, one who consents). Invocation of the maxim is predicated on the assumption that negligence has otherwise been established and that if the defender's plea fails the pursuer must succeed. It is for this reason that the burden of proving it is on the defender who invokes it.
[7.205]The authorities do not seem to me to permit an entirely confident exposition of what must be proved in order for the plea to succeed. As can be seen from the cases referred to by Mr McEachran, it may be variously stated that the pursuer has voluntarily assumed the risk of the defender's negligence; or he has consented to a lack of reasonable care on the part of the defender that may produce the risk of injury; or he has agreed, expressly or impliedly, to waive any claim for any injury that may befall him due to the lack of reasonable care by the defender; or he has willingly accepted the risks arising from the want of reasonable care on the part of the defender, in awareness of the defender's negligence; or that he is consenting to lack of reasonable care on the part of the defender and to run the risk of the defender's negligence at his own expense; or that he has accepted the risk of the defender's negligence in the exercise of his legal duties and has absolved the defender from the consequences arising from that negligence. All of these ways of giving effect to the maxim may amount to the same thing, which is consent to the lack of reasonable care on the part of the defender and acceptance of the risk of harm arising therefrom. The consent may of course be inferred from the whole circumstances. I do not take it from the authorities that the pursuer need have expressly in mind the concept of negligence on the part of the defender, but he must knowingly consent to such conduct as may objectively be held to amount to negligence.
[7.206]I can see that the maxim may readily be applied in a situation where the pursuer's consent precedes the defender's negligent conduct, as in the road traffic and similar cases referred to by Mr McEachran, and Shatwell's case referred to by Mr Jones. There is, however, much greater difficulty where the conduct has taken place already before the pursuer becomes aware of it. I recognise that in Titchener's case, for example, Lord Hailsham in particular was willing to consider that the maxim applied where the pursuer was aware of the circumstances giving rise to the risk and decided to take a chance in going onto the railway. But it appears to me to be a more correct analysis that where conduct on the part of the defender has given rise to a risk which the pursuer then decides knowingly to accept as his own and to take a chance on it, there is no negligence on the part of the defender. This is what was meant in Grant v Australian Knitting Mills Ltd by saying that a man who had consumed or used the thing which he knew to be noxious could not complain in respect of whatever mischief followed. So if in Donoghue v Stevenson the pursuer knew, because the bottle was transparent or for some other reason, that there was a snail in the ginger beer, any harm that ensued would be attributable, not to the negligence of the defender, but to her own conscious volition in choosing to incur the risk or certainty of mischance. This is, in essence, the approach which has found favour with me on the main issue of liability: there is no liability in negligence for the supply of a potentially harmful product if the consumer, in knowledge of its potential for harm, nevertheless chooses to consume it.
[7.207]It is very hard to see in what circumstances it would be open to me to hold that ITL had been negligent, but that the plea of volenti non fit iniuria should nevertheless succeed. Most obviously, consideration of the plea would arise on the basis that, notwithstanding the printing of warnings on cigarette packets and awareness on the part of the general public of the risks to health associated with smoking, ITL were negligent in not ceasing to manufacture cigarettes and to supply them for sale to the public. (This is of course contrary to what I have already held.) But in that event the very circumstances relied on in support of the plea of volenti non fit iniuria would already have been discounted in deciding that there was negligence. On this necessary hypothesis, I do not see how the plea could effectively be engaged, separately from consideration of the question whether ITL were negligent, let alone succeed. It is this paradox which is central to the difficulty I perceive.
[7.208]For these reasons I prefer to take the view that, as can be seen from my summary of counsel's submissions, the issues I have been asked to consider under this heading are the same as those which arise and of which I have already taken account in the context of the question whether ITL were negligent; and if I had found that they were, I would not have been disposed to sustain the defenders' fourth plea-in-law.
PART VIII: DAMAGES
[8.1]Regardless of the outcome of this action, I must assess the damages which it would have been appropriate to award to Mrs McTear in the event of success. As I have said, this action was originally raised by Mr McTear, and after his death Mrs McTear was sisted in his room and place. Since then she has been the pursuer in this action as an individual and as executrix of Mr McTear. She claims damages under three heads.
[8.2]The relevant statutory provisions are contained in the Damages (Scotland) Act 1976 (as amended) and the Administration of Justice Act 1982. Section 1 of the 1976 Act (as amended by section 1 of the Damages (Scotland) Act 1993) provides inter alia:
"(1)Where a person dies in consequence of personal injuries sustained by him as a result of an act or omission of another person, being an act or omission giving rise to liability to pay damages to the injured person or his executor, then, subject to the following provisions of this Act, the person liable to pay those damages (in this section referred to as 'the responsible person') shall also be liable to pay damages in accordance with this section to any relative of the deceased, being a relative within the meaning of schedule 1 to this Act.[...]
(4)If the relative is a member of the deceased's immediate family (within the meaning of section 10(2) of this Act) there shall be awarded [...], such sum of damages, if any, as the court thinks just by way of compensation for all or any of the following -
(a)distress and anxiety endured by the relative in contemplation of the suffering of the deceased before his death;
(b)grief and sorrow of the relative caused by the deceased's death;
(c)the loss of such non-patrimonial benefit as the relative might have been expected to derive from the deceased's society and guidance if the deceased had not died,
and the court in making an award under this subsection shall not be required to ascribe specifically any part of the award to any of paragraphs (a), (b) and (c) above."
In terms of section 10(2) and schedule 1 Mrs McTear, who immediately before his death was Mr McTear's wife, is a member of his immediate family.
[8.3]Had Mr McTear survived and pursued the action to a successful conclusion, he would have been entitled inter alia to an award of solatium at common law, i.e. compensation for pain and suffering and loss of the amenities of life. Section 2 of the 1976 Act (as substituted by section 3 of the 1993 Act) provides inter alia:
"(1)Subject to the following provisions of this section, there shall be transmitted to the executor of a deceased person the like rights to damages in respect of personal injuries (including a right to damages by way of solatium) sustained by the deceased as were vested in him immediately before his death. [...]
(3)In determining the amount of damages by way of solatium payable to an executor by virtue of this section, the court shall have regard only to the period ending immediately before the deceased's death."
Section 2A of the 1976 Act (as inserted by section 4 of the 1993 Act) makes provision inter alia for the executor (or in this case executrix) of a deceased person to be sisted as pursuer in an action brought by the deceased before his death. It may be noted that while the provisions of the 1993 Act referred to above came into force on 18 April 1993, i.e. after the date of Mr McTear's death on 23 March 1993, section 6(6) of the 1993 Act gave these provisions retrospective effect to July 1992, so that instead of being extinguished by his death Mr McTear's claim for solatium transmitted to Mrs McTear as his executrix.
[8.4]Finally, section 8 of the 1982 Act provides inter alia:
"(1)Where necessary services have been rendered to the injured person [defined by section 7 as including a person who has died in consequence of personal injuries sustained] by a relative in consequence of the injuries in question, then, [...] the responsible person shall be liable to pay to the injured person by way of damages such sum as represents reasonable remuneration for those services and repayment of reasonable expenses incurred in connection therewith."
[8.5]Mr McEachran invited me to make awards under three heads, which I shall refer to respectively as "the section 1(4) claim", "the section 2(1) claim" and "the section 8(1) claim". It may be noted that while on Record there is a claim for expense incurred in connection with Mr McTear's funeral, which would have fallen within the provisions of section 1(3) of the 1976 Act, this was not pursued before me and I was not invited to make any award under this head. I should perhaps also note that in his submissions Mr McEachran, in addressing me on the section 2(1) claim, erroneously referred to section 1A of the 1976 Act (as inserted by section 2 of the 1993 Act), which is not concerned with the transmission to an executor of a deceased person's right to damages by way of solatium. At one point in his submissions Mr McEachran sought to rely on section 9A of the 1976 Act (as inserted by section 5 of the 1993 Act), but in subsequent discussion he accepted that it was not open for him to do so and he departed from this part of his submissions.
Submissions for Mrs McTear
[8.6]In addressing me on the section 1(4) claim Mr McEachran took as his starting point the decision of the Extra Division, delivered by Lord Marnoch, in Shaher v British Aerospace Flying College Ltd 2003 S.C. 540. The pursuers in that action made section 1(4) claims for the death of their son, a trainee pilot aged 19, in a flying accident. The defenders reclaimed against the Lord Ordinary's awards of £35,000 to each parent. In the course of the reclaiming motion the pursuers invited the Extra Division to take account of recent jury awards in deciding whether the Lord Ordinary's awards should stand. In the course of their opinion, at pp.542-543, para.[6], the court said:
"As it seems to us, there is clearly a huge gulf not only between the level of judicial awards and the level of two recent jury awards in respect of the loss of an adult child but between the level of judicial awards and the level of recent jury awards so far as bereavement generally is concerned. This, in turn, is reflected by a similar gulf as between the submissions advanced on behalf of the defenders and appellants, on the one hand, and, on the other hand, those advanced on behalf of the pursuers and respondents. We would be less than frank if we did not immediately concede very real difficulty in finding a way to bridge that gulf. In attempting to do so, however, we remind ourselves at the outset that, since the decision of the House of Lords in Girvan v Inverness Farmers' Dairy 1998 S.C. (H.L.) 1, there can be no doubt whatever that the court is encouraged to look for guidance to jury as well as to judicial awards of damages. I refer, in particular, to what is said by Lord Clyde at p.25:
'In a system in which damages may be assessed in different cases either by a jury or by a judge it is essential, not only for the profession, but also for the court both in the making of awards and in the consideration of awards which have been made, for there to be available a convenient record of awards by juries as well as by judges.'
Indeed, as Lord Hope of Craighead makes clear at p.7 of the Report, the 'overall philosophy' of Scottish practice is that the assessment of damages is first and foremost a matter for a jury. We, ourselves, might go further and suggest that it is this very philosophy which gives to awards of damages in this area their essential legitimacy. These awards, as it seems to us, should in the end reflect the expectation of the society which the legal profession serves and represents, rather than be simply an invention of that profession. On the other hand, we see immediately the force of Lord Kingarth's observations [in McManus's Executrix v Babcock Energy Limited 1999 S.C. 569] anent the danger of relying on only one jury award and the desirability of finding some consistent pattern as between a number of such awards. In this connection, a wide disparity between jury and judicial awards was not, it seems, foreseen by the House of Lords in Girvan and, indeed, the assumption made by Lord Hope of Craighead at p.17 of the Report is that jury and judicial awards would fall within the same 'relatively narrow range of figures'."
[8.7]The Extra Division decided that recent jury awards for bereavement demonstrated that judges had become "out of touch with awards made by juries in the exercise of their proper function", but they did not go so far as to establish that awards to parents of adult children under section 1(4) should be taken to lie between £30,000 and £35,000 for each parent, which was the basis upon which the Lord Ordinary had proceeded; that there was the possibility that other jury awards in this area might disclose a broader and different pattern which could prove more reliable and the sums awarded should not be regarded as representing any sort of tariff; and that a fair and proper award to each parent was £20,000. Mr McEachran invited me to take account of the cases referred to in Shaher in which jury awards were made.
[8.8]Reference was next made to the decision of Mr J Gordon Reid, Q.C., sitting as a temporary judge of this Court, in Murray's Executrix v Greenock Dockyard Co Ltd 2004 S.L.T. 346. The deceased in that case died as a result of mesothelioma caused by exposure to asbestos. The deceased and the pursuer married in 1959 when they were both 21, having met when they were about 17. When he died, they had been married over 41 years, and had one child. The marriage had its ups and downs, and for a time during the 1980s was difficult. The deceased was drinking heavily and the pursuer had left the matrimonial home with their daughter to give him a "wee fright", but returned after two weeks. He undertook to cut back on his drinking and normal married life was resumed. The temporary judge was satisfied that the marriage was generally happy and that there was a close loving relationship between them. Over the last ten years before his death she looked after the deceased and was devoted to him and in his last year organised her day so that she could be with him. The deceased was a heavy smoker and had a breathless turn in 1999. During the course of subsequent investigation the mesothelioma was diagnosed. He underwent radiotherapy (three fractions). His GP subsequently recorded that pain did not seem to be a problem. The temporary judge took the view that in the last year of his life the deceased was less unfortunate than some mesothelioma sufferers. He did not suffer quite as much pain and discomfort as some did. The temporary judge awarded £20,000 to the pursuer in respect of her section 1(4) claim, and £47,500 to her as executrix in respect of her section 2(1) claim for solatium.
[8.9]In McManus's Executrix v Babcock Energy Ltd 1999 S.C. 569 the deceased died of mesothelioma caused by exposure to asbestos. He was aged 55 when he died, and prior to the onset of any symptoms he had a close family relationship with his wife and two sons. About nine months before his death he developed shortness of breath which caused him to go to his general practitioner. Shortly thereafter he was told that he had mesothelioma and that he had been six and eighteen months to live. He had operative treatment in May 1996 to try and reduce the size of the tumour. He underwent chemotherapy between June and September 1996, with unpleasant side effects, and when it ended he suffered considerable pain. Lord Kingarth inter alia awarded his widow £20,000 in respect of her section 1(4) claim, and £50,000 in respect of her claim as the deceased's executrix for solatium under section 2(1).
[8.10]Finally, Mr McEachran referred to the decision of Lord Cameron of Lochbroom in McLean v William Denny & Bros Limited 2004 S.L.T. 422. In that case the deceased died at the age of 75 from mesothelioma. He developed symptoms of breathlessness, coughing and tiredness before the mesothelioma was diagnosed a few months before his death. The Lord Ordinary was satisfied that there was substantial distress and anxiety endured by his widow in contemplation of the deceased's suffering before his death, and that this included an appreciable period of time prior to the actual intimation of a confirmed diagnosis. He was also satisfied that the nature of the death itself and the loss of her husband did cause and continue to cause her very substantial grief and sorrow. Finally, he took into account that the deceased appeared to be a fit and reasonably healthy man prior to the obvious symptoms of mesothelioma, and that his widow and he enjoyed a very close and happy relationship which would have continued in the normal course for a reasonable length of time but for his death. He decided that an appropriate award of damages in respect of the section 1(4) claim was £28,000.
[8.11]In respect of the section 2(1) claim, Mr McEachran referred to evidence from Mr McTear that Mrs McTear forced him to go the doctor when he first started to feel the effects of the lung cancer in about April 1992. He was sent to Crosshouse Hospital where a bronchoscopy was carried out. This and other tests led to the diagnosis of cancer in May 1992. He received one course of chemotherapy, but no radiotherapy. He also said that he was put on painkillers, but was not initially suffering from pain, the pain just gradually came with the months. By the time he was giving evidence he was taking morphine and steroids. By that time also he was wearing a pulser to help alleviate the pain. His sleep was disturbed. He went to Bristol and to Edinburgh Royal Infirmary in search of treatment. It was at Edinburgh that the radiotherapy was carried out in November 1992. It helped his breathing.
[8.12]Mrs McTear's evidence was that she caused her husband to go to the GP because he was not eating regularly, he was losing weight and was off-colour. When his cancer was diagnosed her husband was unhappy. He underwent courses of chemotherapy and radiotherapy. Thereafter there was shortness of breath and pain, for which he required morphine. The pain appeared gradually months after the diagnosis, maybe about September 1992, and from then onwards he required morphine. He required nursing attendance in the later stages. By the end he needed help and was brought his food and medication. He was mostly bed-ridden. I was also reminded of the evidence of Dr McCarroll, who said that in the months leading up to his death Mr McTear experienced an unusual amount of pain, which was difficult to control. She confirmed that Mrs McTear provided services to her husband, particularly in the last months of his life. Reliance was also placed on Professor Friend's report, referred to at paras.[4.85] to [4.94].
[8.13]Having regard to the authorities and jury awards referred to above, and to this evidence, Mr McEachran invited me to award £35,000 in respect of the section 1(4) claim and £47,500 in respect of the section 2(1) claim for solatium. He also invited me to award £8,000 in respect of the section 8(1) claim.
Submissions for ITL
[8.14]Mr Jones addressed me first on the section 1(4) claim. On behalf of ITL he acknowledged that Mrs McTear was fond of Mr McTear and loyal to his memory. He invited me, however, to take into account a number of features of her life with him. First, throughout their marriage, Mr McTear drank to excess. Only in the 1990s, and indeed the late 1990s, and at the insistence of Mrs McTear, did he take positive steps to bring his drinking under control. Secondly, he regularly assaulted her and their children, and did damage to property at the family home. In addition to incidents which led to his being convicted for criminal offences, there were occasions when the police had to be called to deal with domestic incidents involving Mr McTear. Thirdly, he was in prison at least during the periods from 6 August 1984 to 5 December 1984, from 18 September 1986 to 14 October 1986, from 10 November 1986 to 26 November 1986, from 16 March 1987 to 24 April 1987, from 30 April 1987 on a sentence of three months' imprisonment and from 24 July 1987 on a sentence of six months' imprisonment. Fourthly, there were in addition periods during the 1980s when Mr and Mrs McTear lived apart. At one point she obtained an interim interdict to exclude him from the family home. Fifthly, Mr McTear blamed Mrs McTear when he was accused of benefit fraud. He lied to her and repeatedly broke promises which he had made to her about his behaviour. Sixthly, the nature of their relationship was, he submitted, perhaps illustrated by the fact that, when Mrs McTear started work, she did not tell Mr McTear and felt it necessary to conceal from him that she was doing so. Over the years, she worked in order to support herself and her family, and also to pay for Mr McTear's drink, cigarettes and fines. He made little effort to support his family, regularly giving up employment without apparently having any new job to go to. He regularly behaved in such a manner as to lead to dismissal. Mr Jones recognised that, after Mr McTear's illness had been diagnosed, this brought him and Mrs McTear together. No doubt, in their earlier married life, she was fond of him to the extent that she stuck with him, but that had to be counterbalanced by the fact that she had him excluded from the house.
[8.15]In respect of the section 2(1) claim for solatium, Mr Jones asked me to take into account features of Mr McTear's illness which distinguished the present case from McManus's Executrix. First, he submitted, unlike the deceased Mr McManus, Mr McTear did not undergo any operation to treat his cancer. He received a single dose of mustine at the time of his diagnosis. In November 1992 he underwent a course of radiotherapy at the Western General Hospital in Edinburgh. There was no evidence that he suffered from any unpleasant side effects as a result of the radiotherapy. Secondly, from the date of his diagnosis until October 1992, his principal physical symptom was breathlessness and any pain was well controlled by drugs. In October 1992 he required to be admitted to hospital for six days for treatment of an infection. In January 1993 he was again admitted to hospital, this time for five days for treatment of a further chest infection. Thirdly, on 11 February 1993 he was pain free on the particular drug treatment then prescribed for him, and in that month he was well enough to go for a two week holiday to Malta. Following his return from holiday on 8 March 1993 he suffered a sudden collapse and dyspnoea after lifting a television set. Fourthly, he died in Ayrshire Hospital on 23 March 1993, having been admitted on the previous day after being bed-ridden from 19 March. Mr Jones did not suggest any alternative figures, and he did not direct any submission specifically to the section 8(1) claim.
[8.16]Mr McEachran invited me to assess interest at 4% per annum on 75% of the figure to be awarded in respect of the section 1(4) claim and at 8% per annum on the figures to be awarded in respect of the section 2(1) and section 8 claims, in each case from the date of Mr McTear's death to the date of decree. Mr Jones did not advance any contrary submission.
Subsequent events
[8.17]After I had made avizandum it came to my notice that the First Division had decided reclaiming motions against the section 1(4) awards in McLean v William Denny & Bros Ltd 2004 S.C. 656 and Murray's Executrix v Greenock Dockyard Co Ltd 2004 S.L.T. 1104. The former was the leading case. The First Division held, affirming Lord Cameron's judgment, that he had not erred in law and in particular was entitled to proceed on the basis that judicial awards for bereavement had been too low, and that the "base figure" in McManus's Executrix required to be considered afresh. There was no inconsistency between his findings and his decision, and no ground for interfering with his award. The award of £28,000 was accordingly upheld. The court observed, under reference to Shaher v British Aerospace Flying College Ltd that, if there were a number of jury awards which indicated a level or range of awards a jury might be expected to make, that would be important evidence for a judge making an assessment. In general, judicial awards in bereavement cases had been on the low side, including awards to widows, but because of the paucity of jury awards, no definite conclusion could be drawn from them as to the extent to which judicial awards should be increased; however, the "base figure", in the case of sudden death, that is without allowing for head (a) of section 1(4), should in the absence of special features be in the region of £25,000. In Murray's Executrix v Greenock Dockyard Co Ltd it was held that the award to the pursuer in respect of a section 1(4) claim was unreasonably low and that £28,000 would be more appropriate, it having been unnecessary to distinguish between her and the widow in McLean. There was no reclaiming motion against the award in respect of the pursuer's section 2(1) claim for solatium, which accordingly remained at £47,500.
[8.18]In view of the decisions of the First Division, I put the case out By Order for further discussion. Mr McEachran submitted that the matter had to be looked at from the point of view of the widow. All the evidence was that Mrs McTear was devoted to her husband and it was this loss on which the court had to put a figure. He submitted that, having regard to her loss of society, having to observe her husband going through all the stages of death and all the events leading up to that, I should award £28,000 under this head. Mr Jones adhered to a written supplementary submission, in which it was pointed out that the marriage in McLean was described by the court as "very happy". Likewise, apart from a difficult period in the 1980s, the marriage in Murray was also described as "generally a happy one". It was submitted that the present case exhibited "special features", such as were contemplated in McLean, which were those features to which attention had been drawn in counsel's previous submissions. These features, taken together, would justify the view that an appropriate award in the present case under section 1(4) should be materially lower than the awards in Murray and McLean.
Discussion
[8.19]In deciding what would be an appropriate award in respect of the section 1(4) claim, I recognise that it is appropriate to take account of jury awards in comparable cases. I note, however, that all the jury awards which Mr McEachran relied upon were before the Extra Division in Shaher, and for that matter before the temporary judge in Murray and the Lord Ordinary in McLean, and two of them before the Lord Ordinary in McManus's Executrix. I have already mentioned the figures which it was thought appropriate to award in each of those cases. I also bear in mind that, as was pointed out in Murray and in McLean, jury awards to a parent for the death of a child or to a child for the death of a parent are not directly relevant when considering a claim by a widow for the death of her husband. In any event, the figure of £28,000 which the First Division thought appropriate in McLean and Murray for an award to a widow under all three of heads (a), (b) and (c) of section 1(4), in the absence of special features, must now be my starting point. In the end, however, my award must be based on my assessment of the considerations which emerge from the evidence in the present case.
[8.20]In the first place, in considering the section 1(4) claim, I accept that Mrs McTear was genuinely fond of her husband, despite his serious ill-treatment of her. This is a feature of many such marriages, and since Mrs McTear's affections are a subjective matter for her, I see no need to make any further comment about it. I accept also that she experienced grief and anxiety in contemplation of Mr McTear's suffering before his death and grief and sorrow caused by his death. He was only 49 years old at the time of his death, and I have no reason to suppose that the marriage would not have persisted, no doubt with ups and downs as before, for many years. It is accordingly appropriate to recognise that Mrs McTear has lost such non-patrimonial benefit as she might have derived from Mr McTear's society and guidance if he had not died. I am not, however, able to place as much weight on this as I would have done if the marriage had been continuously happy. I believe that a jury would adopt the same approach. Overall, in my opinion, an award of £25,000 under this head would be appropriate.
[8.21]Turning now to the section 2(1) claim for solatium, I have the benefit of comparative figures derived from McManus's Executrix and from Murray's Executrix. Lung cancer is often a painful and distressing terminal illness. In Mr McTear's case, I am satisfied that he suffered from breathlessness and a progressive decline in his strength. I am also satisfied that he experienced pain, even though it may, to a significant extent, have been controlled by drugs. He also had to undergo the various treatments I have mentioned. There is some force to Mr Jones's submissions, and I accept that Mr McTear suffered to a lesser extent than did Mr McManus, on whose case Mr McEachran principally relied. Nevertheless, I think it appropriate that the pain, suffering and loss of the amenities of life experienced by Mr McTear should be reflected in a substantial award of solatium, which I would assess at £45,000.
[8.22]I am satisfied that Mrs McTear rendered services to Mr McTear during his final illness and it is appropriate that they be recognised by an award under section 8. I see no reason to differ from the figure suggested by Mr McEachran, so I assess the award under this head at £8,000. I also accept that interest should be awarded as proposed by Mr McEachran, which appears to me to be in accordance with the usual practice.
[8.23]My assessment of damages, with interest to 31 May 2005, is therefore as follows:
| Section 1(4) claim | £25,000.00 |
| Interest thereon | 9,141.78 |
| Section 2(1) claim for solatium | 45,000.00 |
| Interest thereon | 43,880.55 |
| Section 8 claim for services | 8,000.00 |
| Interest thereon | 7,800.99 _________ |
| Total damages | £138,823.32 |
PART IX: CONCLUSIONS AND RESULT
Conclusions
[9.1]I now set out my main conclusions, which should be read in conjunction with the passages of discussion to which cross-references are given.
[9.2]It is not in dispute that Mr McTear died of lung cancer (para.[1.4]). I accept that he smoked the John Player brand or brands of cigarettes manufactured by ITL for many years, as part of his consumption of cigarettes. I am not, however, prepared to hold it proved that it was ITL's products that Mr McTear smoked at any time prior to 1971. I do not accept that he smoked John Player brand cigarettes exclusively from the early 1970s onwards until the last few years of his life. I conclude that he smoked a significant quantity of roll-ups made from Old Holborn tobacco along with his smoking of John Player brand cigarettes for many years, perhaps as many as twenty years, but I am not able to decide in what proportion he divided his smoking between John Player brand cigarettes and roll-ups. They both made a material contribution to his total consumption from about 1971 onwards (para.[4.228]).
[9.3]Mr McTear started smoking no earlier than 1964. I am satisfied that advertising had nothing to do with his reasons for starting to smoke. He started smoking because it was socially acceptable and most young people started smoking as part of becoming adults (para.[4.226]). I am prepared to accept that Mr McTear found it difficult to wean himself off his habit once he had started smoking and in that sense could be described as addicted. I do not accept that he was for this reason unable to stop smoking (paras.[4.229] and [6.202] to [6.208]). The averment that tobacco is more addictive than cocaine is not proved.
[9.4]I am satisfied that at all material times, and in particular by 1964, the general public in the United Kingdom, including smokers and potential smokers, were well aware of the health risks associated with smoking, and in particular of the view that smoking could cause lung cancer (para.[3.1] and Part III generally). I am also satisfied that Mr McTear was aware, in common with the general public, well before 1971 of the publicity about the health risks associated with smoking, and in particular the risk of lung cancer. Therefore by the time he is shown by acceptable evidence to have started smoking the John Player brand of cigarettes he was already aware of the publicity about the health risks. As with many other aspects of his life, he chose to ignore it (para.[4.230]).
[9.5]The pursuer can succeed in this case only if she proves all of the following (paras.[1.5] and [6.29]):
(1)That cigarette smoking can cause lung cancer, in the sense that both in the general population and in any individual case it can be said that but for the smoking of cigarettes lung cancer would probably not have been contracted (general causation).
(2)That cigarette smoking caused Mr McTear's lung cancer, in the sense that but for his having smoked cigarettes he would probably not have contracted lung cancer (individual causation).
(3)That Mr McTear smoked cigarettes manufactured by ITL for long enough and in sufficient quantity for his smoking of their products to have caused or materially contributed to the development of his lung cancer.
(4)That Mr McTear smoked cigarettes manufactured by ITL because ITL were in breach of a duty of care owed by them to him.
(5)That such breach caused or materially contributed to Mr McTear's lung cancer either by making at least a material contribution to the exposure which caused his lung cancer or by materially increasing the risk of his contracting lung cancer (fault causation).
[9.6]There is no direct evidence that ITL, as a company, have ever accepted that there was a causal connection between smoking and disease, and the evidence before me does not satisfy me that this is the inference which should be drawn (para.[2.76]). The fact that they have never sought to challenge the public health message, that cigarette smoking does cause lung cancer, does not in my opinion constitute such an admission (para.[2.78]). Accordingly, in my opinion, ITL are entitled to put the pursuer to proof of her averment that cigarette smoking can cause lung cancer (para.[2.80]).
[9.7]I must base my decisions about questions of fact on the evidence, and that alone (para.[1.8]). It is not open to me to take account of any passage in any document, the terms of which were not agreed, and to which reference was not made in the course of the evidence of any witness (para.[1.37]). It is not within judicial knowledge that cigarette smoking can cause lung cancer: this is an issue which I am duty-bound to approach with an open mind and to decide on the basis of the evidence led before me; and the burden of proving it is on the pursuer (para.[1.12]).
[9.8]The law relating to expert witnesses is as discussed at para.[5.17]. Above all, the purpose of leading the evidence of any expert witness should have been to impart to me special knowledge of the subject-matter, including published material, lying within the witness's field of expertise, so as to enable me to form my own judgment about that subject-matter and the conclusions to be drawn from it.
[9.9]The pursuer relies on epidemiology to prove general causation. I have not been sufficiently instructed by the expert evidence relating to this discipline to be able to form my own judgment as to whether or not this averment is proved. Special knowledge of this subject-matter was not imparted to me, so as to enable me to form my own judgment about it. The pursuer has accordingly failed to prove this averment (paras.[6.149] to [6.171]).
[9.10]In any event, the pursuer has failed to prove individual causation. Epidemiology cannot be used to establish causation in any individual case, and the use of statistics applicable to the general population to determine the likelihood of causation in an individual is fallacious. Given that there are possible causes of lung cancer other than cigarette smoking, and given that lung cancer can occur in a non-smoker, it is not possible to determine in any individual case whether but for an individual's cigarette smoking he probably would not have contracted lung cancer (paras.[6.172] to [6.185]).
[9.11]In any event there was no lack of reasonable care on the part of ITL at any point at which Mr McTear consumed their products, and the pursuer's negligence case fails. There is no breach of a duty of care on the part of a manufacturer, if a consumer of the manufacturer's product is harmed by the product, but the consumer knew of the product's potential for causing harm prior to consumption of it. The individual is well enough served if he is given such information as a normally intelligent person would include in his assessment of how he wishes to conduct his life, thus putting him in the position of making an informed choice (paras.[7.167] to [7.181]).
[9.12]In any event, there is no basis upon which I could hold it established that, if ITL had not manufactured cigarettes at any material time, so that Mr McTear did not smoke their products and accordingly their products could not have made a material contribution to his contracting lung cancer, it would have made any difference. On the contrary, all the evidence is that Mr McTear would have started smoking when he did, and would have continued to smoke, for the same length of time and in the same quantities, as he in fact did. Fault causation would therefore not in any event be established (paras.[7.182] to [7.183]).
[9.13]On my interpretation of the law relating to the maxim volenti non fit iniuria, and in the circumstances of this case, I would not have been disposed to sustain the fourth plea-in-law for ITL, if the pursuer had otherwise succeeded on the foregoing issues (paras.[7.204] to [7.208]).
[9.14]The damages which I would have awarded, had the pursuer succeeded, would have been £25,000 for her claim for compensation under section 1(4) of the Damages (Scotland) Act 1976 (as amended), £45,000 for her claim under section 2(1) of the Act as Mr McTear's executrix for solatium for the pain, suffering and loss of the amenities of life experienced by him, and £8,000 for her claim under section 8(1) of the Act for services rendered by her to him during his final illness (paras.[8.20] to [8.22]). With interest to 31 May 2005 the total award of damages would have been £138,823.32 (para.[8.23]).
Result
[9.15]In my opinion therefore, for all the foregoing reasons, the pursuer's case fails on every issue on which I would have needed to find in her favour were I to hold the defenders liable to her in damages. I accordingly sustain the second and third pleas-in-law for the defenders and assoilzie them from the conclusions of the summons.