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OUTER HOUSE, COURT OF SESSION [2005] CSOH 69 |
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OPINION OF LORD NIMMO SMITH in the cause MRS MARGARET McTEAR Pursuer; against IMPERIAL TOBACCO LIMITED Defenders:
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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:
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Paragraph |
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PART I: |
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[1.2] |
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[1.5] |
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[1.11] |
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[1.13] |
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[1.30] |
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[1.31] |
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[1.32] |
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[1.33] |
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[1.35] |
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PART II |
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[2.1] |
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[2.7] |
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[2.10] |
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[2.15] |
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[2.23] |
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[2.52] |
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[2.54] |
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[2.55] |
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[2.62] |
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[2.75] |
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PART III: |
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[3.2] |
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[3.6] |
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[3.11] |
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[3.28] |
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[3.45] |
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[3.54] |
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[3.58] |
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[3.61] |
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[3.63] |
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[3.66] |
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PART IV: |
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[4.3] |
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[4.67] |
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[4.85] |
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[4.95] |
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[4.112] |
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[4.124] |
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[4.169] |
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[4.174] |
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[4.194] |
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[4.200] |
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[4.222] |
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[4.226] |
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PART V: |
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[5.2] |
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[5.12] |
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[5.15] |
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The evidence of expert witnesses: |
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[5.20] |
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[5.24] |
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[5.27] |
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[5.100] |
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[5.184] |
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[5.189] |
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[5.211] |
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[5.304] |
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[5.305] |
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[5.326] |
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[5.339] |
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[5.349] |
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[5.370] |
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[5.373] |
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[5.435] |
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[5.447] |
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[5.448] |
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[5.475] |
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[5.480] |
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[5.698] |
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[5.739] |
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[5.745] |
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[5.766] |
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[5.772] |
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[5.829] |
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[5.844] |
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[5.847] |
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[5.859] |
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PART VI: |
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[6.1] |
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[6.2] |
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[6.22] |
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[6.24] |
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[6.25] |
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[6.30] |
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[6.57] |
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[6.149] |
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[6.172] |
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[6.186] |
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[6.188] |
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[6.194] |
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[6.202] |
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PART VII: |
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[7.2] |
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[7.19] |
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[7.167] |
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[7.182] |
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[7.184] |
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[7.185] |
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[7.199] |
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[7.204] |
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PART VIII: |
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[8.6] |
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[8.14] |
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[8.17] |
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[8.19] |
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PART IX: |
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[9.1] |
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[9.15] |
PART I: PRELIMINARIES
[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.
[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.
[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
[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.
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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.
(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.
[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.
[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.
[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".
[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".
[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".
[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".
[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".
[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.
[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;"
(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.
(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
[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."
[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
[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.
[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:
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
Additional Criteria
- use despite harmful effects
- relapse following abstinence
- recurrent drug cravings
- 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:
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.
[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.
[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.
[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
[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, th