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OUTER HOUSE, COURT OF SESSION [2008] CSOH 67 |
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OPINION OF LORD CARLOWAY in the cause WILLIAM HYNES Pursuer; against SIMON LOBNITZ and OTHERS Defenders: ________________ |
Pursuer: TG Marshall, solicitor advocate
of Thompsons
Defenders: (1st and 5th
defenders):
Defenders: (2nd to 4th,
6th & 7th defenders): Summers; Biggart
Baillie LLP
1 May 2008
Background
[1] The
pursuer was born on
[2] It is admitted (no 34 of process) by each defender that, during his employment with them, the pursuer experienced exposure to asbestos sufficient to cause asbestos disease. It is admitted by the first and fifth defenders (31 and 33) that they employed the pursuer for 44 and 27 months respectively and that his exposure to asbestos was as a result of their fault. It is admitted by the second, third, fourth, sixth and seventh defenders (32) that the pursuer's exposure during their employment of him was caused by their fault. These defenders also admit the periods of exposure as 64 months with the second defenders, 4 months with the third defenders, 3 months with the fourth defenders, 13.5 months with the sixth defenders and 12.5 months with the seventh defenders. The defenders accepted that, for pragmatic reasons, a joint and several decree could be made in the circumstances of this case; without prejudice to their position in other litigations. The defenders were all agreed that the appropriate apportionment, in the event of liability being established, would be: first defenders - 26.19%; second defenders - 38.10%; third defenders - 2.38%; fourth defenders - 1.79%; fifth defenders - 16.07%; sixth defenders - 8.03%; and seventh defenders - 7.44%. However, it was also agreed by the defenders that no formal decree for apportionment was required.
Pleadings and Issues
[3] The pursuer avers (statement of fact 5) that:
"In consequence of the exposure to asbestos the pursuer has contracted bilateral pleural plaques, pleural thickening and asbestosis...In about 2004...[he] was found to have pleural plaques with calcification, pleural thickening and asbestosis. The pursuer is breathless and lacking in energy. He finds difficulty in walking and climbing stairs. He is also anxious about the potential implications of asbestos related disease and for his future health. He is at an increased risk of serious deterioration of his condition by contraction of asbestos related lung cancer, diffuse bilateral pleural thickening and/or mesothelioma. The pursuer is a smoker and in conjunction with his asbestos exposure he is at high risk of lung cancer. It is likely that the asbestosis will progress such that he will become 30% disabled in his lifetime. He is also likely to lose 4 years of life expectancy (sic) by reason of his asbestos related conditions. The pursuer has and will suffer considerable pain..."
The defenders do not admit the nature, extent and consequences of any loss, injury or damage sustained by the pursuer. The first and fifth defenders make positive averments about the pursuer being a smoker and continue:
"The pursuer suffers from emphysema, connective tissue disease, Raynaud's phenomenon, transitional cell carcinoma of the bladder, hypertension and had an aortic heart murmur. He has suffered from pericarditis and pleurisy".
The remaining defenders aver that pleural plaques are harmless, presumably thereby accepting their existence, but otherwise make similar averments to those of the other defenders concerning the pursuer's various conditions.
[4] The primary issues are first whether the pursuer has pleural thickening as a result of exposure to asbestos and asbestosis itself, in the form of pulmonary fibrosis. Secondly, it is whether the pursuer's physical problems such as breathlessness, which were not disputed at the proof, are caused by asbestos related disease as distinct from other conditions, notably connective tissue disease (CTD) and emphysema. It was not suggested that the pursuer's bladder cancer, heart problems or hypertension had any relevance to the problems complained of. A CTD is a chronic inflammatory autoimmune disorder which can affect all "connective tissue" (joints, skin, muscle, blood etc.). Rheumatoid arthritis (inflammation of the joints) is an obvious example of this, although it mainly affects the joints. CTDs are not "organ specific". They can affect different organs.
Medical Notes - 1985-93
[5] There
was considerable focus on the content of selected passages in the voluminous
notes made by the pursuer's general medical practitioners (7/2) and various
other doctors, whom he attended at the
[6] The
various medical witnesses were presented with extracts from the GP
records. These in turn included records
from the hospitals attended. Because much of the evidence of the experts was
based upon their interpretation of entries in the records, it is necessary to
set out at some length just what entries were referred to, although the weight
to be given to the content of these entries may be another issue (infra). The earliest record referred to
(7/2 p 215) is dated
[7] On
[8] In
December 1987, the pursuer was back in the
[9] The
pursuer attended his GP on
[10] Back at his GP's surgery on
[11] On
[12] At the end of the year, the pursuer was suffering pain in his left chest, with some on the right side too. The GP entry was "Pain on deep inspiration" (p 219). Back for a review at the Hospital in January 1989, Dr Logie wrote "Presumed SLE" and once more recorded the pursuer's chest as "clinically clear". The pursuer was still on 5 mgs of Prednisolone at this time. Lung function tests carried out in November 1989 produced:
|
FEV1 |
VC |
FEV/VC |
FRC |
RV |
VC |
TLC |
RV/TLC |
TCO |
KCO |
|
3.0 |
3.75 |
80 |
2.86 |
1.66 |
|
5.64 |
29 |
6.80 |
1.49 |
[13] In May 1990, the pursuer was noted as having "some intermittent left lateral chest ache which is neither ischaemic nor pleuritic in character" (p 22). In November 1990, Dr Logie's registrar recorded (p 20) the pursuer's chest as "clear, no rub, no creps". A year later, a further "chest clear" was recorded (p 17). In October 1992, a different registrar wrote (p 13) "Chest is clear, although there were a few scattered coarse crepitations". Lung function tests carried out in November 1993 were:
|
FEV1 |
VC |
FEV/VC |
FRC |
RV |
VC |
TLC |
RV/TLC |
TCO |
KCO |
|
3.30 |
4.19 |
79 |
3.15 |
1.34 |
|
5.61 |
24 |
7.46 |
1.61 |
Some time passed before the next series of significant entries.
Medical Notes - 1997-2007
[14] Dr
Peter Leslie, consultant general physician at the
"Recently he describes a feeling as if he is "walking on stones" and there is certainly evidence of peripheral sock type neuropathy (nerve disturbance). His joint pains have mainly involved his ankles but they are of no problem at present. He has an intermittent purpuric type rash involving his legs and possibly a photosensitive rash on his face. When he has symptoms of fever he increases his steroid from the maintenance dose of 2.5 mgs with quick resolution of his symptoms..."
Dr Leslie's diagnoses were: "1
Probable SLE; 2 Raynaud's Phenomenon
? Overlap syndrome; 3 Peripheral neuropathy; 4 Purpuric
rash...".
Something appears to have gone amiss with the review at the
"I still think the question arises whether [the pursuer] should commence Hydroxychloroquine for management of possible lupus (SLE) and I think this requires a definitive rheumatological opinion".
On
[15] Dr Richmond is subsequently described as a rheumatology
registrar and later as a consultant rheumatologist. Her involvement appears to have been the
first by a specialist in rheumatology.
On
"I note original history with polyarthralgia, and later developing pericarditis and pleuritic chest pain. I note he has always had a raised ANA and rheumatoid factor, though double stranded DNA titres have been very low titre (sic) and as far as I can see extractable nuclear antigens have been negative when checked...
It certainly sounds as though he has a connective tissue disease...."
Dr Richmond referred him to the rheumatology clinic, where she would see him again. Her formal diagnoses in the letter to the pursuer's GP (quoted above) did not include CTD.
[16] On
"Currently his Raynaud's is very troublesome...He has an itchy rash over the lower half of his legs which has been present for years, but does not tend to fluctuate, and does seem to be photosensitivity...He has a photosensitive facial rash.
...He has never had joint symptoms since his original onset. He denies pleuritic chest pain, breathlessness or coughs...He does have intermittent fever and sweats which has also been a longstanding feature of his illness, and responds to a slight increase in dose of steroids...
...He has a mild malar rash...He is clubbed and I note this has been documented for a long time. He also has scattered nail fold infarcts and obvious Raynaud's.
...Chest is clear in particular with no evidence fine respiratory creps...
I note features predominantly consistent with SLE. He has been ENA (?ANA) positive over a long period of time, although he doesn't have an elevated double stranded DNA..."
Her diagnoses this time included: "Undifferentiated connective tissue disease; ANA positive; Rheumatoid factor positive; Photosensitivity; Raynaud's phenomenon...". "Undifferentiated" CTD (UCTD) is, by definition, not the same as SLE. Lung function tests carried out in June 1998 produced:
|
FEV1 |
VC |
FEV/VC |
FRC |
RV |
VC |
TLC |
RV/TLC |
TCO |
KCO |
|
3.05 |
4.00 |
76 |
3.64 |
1.68 |
4.38 |
6.06 |
28 |
6.90 |
1.34 |
[17] On
"the lung markings are diffusely increased possibly due to a degree of COPD (chronic obstructive pulmonary disease). No focal lung abnormality. Comparison was made with previous chest radiograph from 1998. There has been no significant change since that time".
On
[18] On
[19] At the rheumatology clinic in June 2002, the pursuer's CTD was
noted as being "in remission". He had no
skin rash, had no photosensitivity when on holiday in
[20] On
"I felt that mostly his features were entirely consistent with SLE, he is positive for ANA, though his double stranded DNA has never been elevated".
Dr Richmond referred to bi-basal crepitations being found in June 2004, suggestive of possible early fibrosis. Of substantial significance, she referred to the results of the CT (computerised tomography) scan taken the previous month which showed calcified pleural plaques "which the radiologist felt were more consistent with asbestos exposure". She also mentioned the various lung function tests, which she regarded as stable since 1989. Lung function test results in August 2004 were:
|
FEV1 |
VC |
FEV/VC |
FRC |
RV |
VC |
TLC |
RV/TLC |
TCO |
KCO |
|
2.70 |
3.60 |
75 |
3.67 |
1.99 |
3.69 |
5.68 |
35 |
7.48 |
1.59 |
[21] In August 2004, the pursuer was seen by a respiratory physician (Dr JF Faccenda) at the Borders General. He was noted "clubbed" but "Chest auscultation was entirely clear". At this time, the results of the CT scan and the existence of benefits for asbestos related disease were discussed with the pursuer. In October 2004 Dr Faccenda's specialist registrar added "pleural plaques" to the diagnoses (which still included UCTD). The pursuer was noted as having "no respiratory symptoms". It was observed that his claim for asbestos related disease was underway.
[22] In September 2007, the pursuer took an overdose of his co-drydamol pain killers (5/10 pp 2, 39). At that time he was noted as having recently
given up smoking 30 cigarettes a day. As late as
Radiology
[23] The radiologist who reached the conclusion concerning asbestos in 2004 did not give evidence. However, the CT scan, which was dated 28 June 2004, an x-ray dated slightly earlier on 15 June and another taken on 18 January 2002 were subjected to anxious scrutiny by the three eminent radiologists who gave evidence. All three were extremely well qualified and experienced in chest x-ray and CT scan interpretation. There was no reason to prefer one over the others by reason of their qualifications or experience. Ultimately, there was consensus on many aspects of the radiology. They all agreed that the pursuer had pleural plaques, with calcification, as a result of exposure to asbestos. They all agreed that the CT scan showed that he had pleural thickening.
[24] The radiologists did lock horns over whether this thickening was "diffuse". In that connection, all agreed that a formal radiological diagnosis of "diffuse" thickening requires a continuous area with dimensions: (i) at least 3 mm in thickness; (ii) at least 5 cms transversely (latitudinally, across the chest); and (iii) at least 8 cms longitudinally (vertically, up and down the chest). This test is stated in a standard text book called "Radiologic Diagnosis of Diseases of the Chest" (2001) by Nestor Muller et al., although it derives from an earlier medical paper in 1989. The more important dimension is the vertical one since the lungs expand more on that axis, as regulated by the diaphragm, than laterally, as determined by rib cage expansion. The figure of 8 cms is a random one, selected simply to distinguish persons likely and not likely to have a disability resulting from such thickening. Eight centimetres is about one quarter of the vertical length of the chest. People can have a disability even if they do not meet the formal criteria for this diagnosis.
[25] All the radiologists agreed that the vertical dimension of the thickening as seen on the CT scan was at least 6 cms. This could be measured physically by ruler on the four lowest slices of the eighteen CT images taken at 1.5 cm intervals during the scan. However, the images did not extend below the area of thickening; i.e. they did not capture the lowest point of the thickening. This presented a difficulty in determining whether the formal criteria for the diagnosis of "diffuse" thickening had been met.
[26] There was some discussion about whether the costophrenic angle had been "obliterated" when seen on a conventional (plain film) x-ray. This is another test for diffuse pleural thickening, deriving from the work of the International Labour Organisation in 2003. The costophrenic angle is at the bottom of the costophrenic sulcus; the lowest area of pleural cavity present on both sides of the body between the diaphragm and the chest wall. It is "obliterated" if the angle cannot be seen on the x-ray image. If it cannot be seen, that is because the thickening of the pleura renders the angle invisible on the image.
[27] At the proof, the pursuer's expert consultant radiologist was
Michael Sproule (42), based at the Western Infirmary
and
"There is loss of sharp definition of both costophrenic angles and pleural based shadowing extending up the lateral aspect of the right hemithorax. The appearance is...consistent with pleural thickening".
Comparing this with the later 2004 x-ray, he comments:
"...the left costophrenic angle is sharply defined. The appearance on the right side remains the same".
He found, therefore, that the x-rays showed some loss of clarity of the angle on the right side, but not "obliteration", indicating some pleural thickening in that area. Looking at the CT scan, he observes:
"In both hemithoraces there are focal areas of partially calcified pleural thickening which are characteristic of parietal pleural plaques due to previous asbestos exposure.
Posteriorly in the right lower zone there is smooth sheet like thickening which appears to extend into the costophrenic sulcus (the study does not quite cover the entire thorax). The pleural thickening is greater than 5 cm around the hemithorax, 3mm thick and is at least 6 cm in cranio-caudal (head to tail) dimensions. The CT appearance is therefore highly suggestive of diffuse pleural thickening due to a "fibro-thorax". A "fibro-thorax" usually results from a previous exudative effusion which may itself have a number of causes including infection (empyema), trauma (hemothorax), asbestos exposure (benign asbestos induced effusion) or in association with connective tissue disease. Given the presence of parietal pleural plaques due to previous asbestos exposure the appearance is suggestive of diffuse pleural thickening due to previous benign asbestos induced pleural effusions. However, I note that the patient also has a history of connective tissue disease. It is not possible on radiographic criteria to exclude this as a cause of the diffuse pleural thickening. In the absence of a history of infection or trauma, clearly empyema or hemothorax are less likely.
In the lower lung zones bilaterally there are fine dot like and short irregular linear subpleural opacities. These are not confined to the dependent lung or parenchyma adjacent to pleural plaques. The appearance is therefore consistent with mild pleural fibrosis. Given the presence of parietal pleural plaques due to previous asbestos exposure, the findings are suggestive of early asbestosis".
Dr Sproule then summarises (or rather repeats) his position thus:
"1. There are focal areas of partially calcified pleural thickening in both hemithoraces which are characteristic of parietal pleural plaques due to asbestos exposure.
2. Posteriorly, in the right hemothorax there is smooth, sheet like thickening which appears to extend in to the costophrenic sulcus. The CT appearance is suggestive of "fibro-thorax". As discussed above, the presence of parietal pleural plaques due to previous asbestos exposures raises the possibility of diffuse pleural thickening due to previous benign asbestos induced pleural effusions. However, it is not possible on radiographic grounds to exclude diffuse pleural thickening as a consequence of connective tissue disease associated pleural effusion.
3. There are fine sub pleural parenchymal opacities in the lower lung zones which are consistent with mild pulmonary fibrosis. Given the presence of parietal pleural plaques due to previous asbestos exposure, the appearance is suggestive of early asbestosis."
[28] Dr Sproule explained that, as the pursuer had a CTD and had been exposed to asbestos, it was not possible to say which had caused, what he regarded as, the diffuse pleural thickening or the mild pulmonary fibrosis, which he thought was at an early developmental stage. The fibrosis took a reticular or honeycomb like form. Dr Sproule accepted that, on any view, the pursuer was right down "at the margin" of the diagnosis of diffuse pleural thickening. The signs of fibrosis on CT were subtle, not gross or florid. If the thickening and fibrosis had been there since the late 1980s, they were less likely to have been caused by asbestos exposure because greater progression over that period might have been expected.
[29] The first and fifth defenders called Colin Turnbull (61) as their consultant radiologist. He is based at the Western General Infirmary, Edinburgh, and has a special interest in imaging of the lungs (CV 25/9). He "adhered" to his reports (25/2 and 3). In relation to the 2002 x-ray, Dr Turnbull considered it to be "underpenetrated" but thought that it might be showing pleural thickening in the lower third of the right lung. The 2004 x-ray was better and suggested such thickening. However, the costophrenic angles were well defined.
[30] Turning to the CT scan, Dr Turnbull was led through almost all eighteen images, starting with the soft tissue settings and moving onto the lung settings. He described the presence of bilateral pleural plaques with calcification. His main report states:
"...there is more diffuse pleural thickening in the right lower thorax posteriorly which is greater than 3mm thick and greater than 5 cm wide extending for a craniocaudal distance of over 8 cm, meeting radiological CT criteria for diffuse pleural thickening".
He was able to point to the areas of thickening, especially those shown on soft tissue images 12/18 to 16/18. He accepted that it was hard to say where the thickening ended on the images but he had "implied" that it had extended more than the required 8 cms vertically.
[31] On the lung settings, he was able to see reticulation in the lung itself in images 9 to 15/18; that is pulmonary fibrosis. He reports:
"There is bilateral, lower lobe, peripheral, wild ground glass opacification with intralobular interstitial thickening and mild peripheral honeycombing...".
Dr Turnbull concludes:
"The CT scan shows bilateral pleural plaques with associated calcification, parenchymal bands and right lower thoracic posterior diffuse pleural thickening, typical of previous asbestos exposure. There is mild centrilobular emphysema.
There is bilateral, lower lobe, basal, sub-pleural interstitial pulmonary fibrosis with associated minimal fine honeycombing, traction bronchiolectasis and ground glass opacification. These changes, in associated (sic) with the pleural plaques, diffuse pleural thickening, pleural calcification and parenchymal bands could be due to asbestosis.
[The pursuer] also has a diagnosis variously given in the clinical letters of "undifferentiated connective tissue disease" or systemic lupus erythematosus. The changes of insterstitial pulmonary fibrosis on CT scanning in these conditions are indistinguishable in their radiological appearance and extent from those of asbestosis.
It is therefore not possible, on radiological appearances alone, to determine whether the interstitial pulmonary fibrosis in this case is due to asbestosis or connective tissue disease. There are definite radiological signs of previous asbestos exposure and right posterior thoracic diffuse pleural thickening, as detailed above".
He agreed that the pursuer's pleural thickening was "down at the lower reaches", being mild in nature. It was not possible to say "with confidence" that it was interfering with his lung capacity.
[32] Dr Turnbull expressed the view that SLE was a syndrome with
specific serological and clinical symptoms and signs. "Undifferentiated" and "mixed" CTD were, in
his mind, used interchangeably in the GP records. With all the CTDs
there was an association with pleural and pulmonary changes, as there was with
asbestos exposure. The changes were
indistinguishable radiologically. Dr Turnbull referred to a textbook: "
"SLE is commonly associated with pleural and pulmonary abnormalities. Pleuritis or pleural fibrosis is present in up to 85% of cases at autopsy, and pleural effusion is often visible on chest radiographs in patients who have SLE".
He also quoted from a paper (6/20): "Idiopathic Nonspecific Interstitial Pneumonia - Lung Manifestation of Undifferentiated Connective Tissue Disease" by Kinder et al published in Volume 176 of the American Journal of Respiratory and Critical Care Medicine (p 691), (2007). This states ("At a Glance Commentary") (p 691):
"Undifferentiated connective tissue disease is a recognised disease entity, but the pulmonary manifestations are not described. Their relationship is unknown".
The paper (Table 4) describes a number of patients with UCTD as having reticulation (fibrosis), as the pursuer has. However, the paper is largely a study of non smoking young women.
[33] In a later report (25/3), Dr Turnbull reviewed x-rays of the pursuer taken in 2006 and 2007 and noted that there was little change since 2002 and 2004. He concludes:
"The lack of any progression of the fibrosis...would tend to favour asbestosis or stable, treated connective tissue disease rather than idiopathic pulmonary fibrosis".
[34] The remaining defenders' consultant radiologist was Arthur Wightman (65), who had been in that post at the Royal Infirmary, Edinburgh, since 1975. He gave evidence at a Commission (7/9) on 18 and 19 February, in advance of the proof, which commenced on 26 February and continued for eight days. It was at this Commission that these defenders attempted to lodge the extract from the Webb, Muller and Naidich book (7/8 supra) and a document called "Diagnosis and Initial Management of Nonmalignant Diseases Related to Asbestos", an official statement of the American Thoracic Society (2003). Although he gave his evidence before the other two consultants, Dr Wightman's testimony was usefully taken as a commentary on the reports of the other two radiologists, as if he had given his evidence last (as would normally have been the case).
[35] Dr Wightman agreed with Dr Turnbull on the presence of pleural thickening, other than the use of the adjective "diffuse". Dr Wightman considered that it was unlikely that the length of the thickening was as much as 8 cms. He too had measured 6 cms, but considered that the next scan (had it existed), being 1.5 cms lower, would have been below the lung, indeed below the diaphragm. He could not say that the thickening did not extend as far as 8 cms, simply that he would not have expected it to do so. He agreed with Dr Turnbull on emphysema as a minor disability. He agreed generally with Dr Turnbull's conclusions but thought that the pleural thickening "might be caused by" rather than being "typical of" previous asbestos exposure. Essentially, like Dr Turnbull, as both asbestosis and CTD were well known causes of interstitial fibrosis, he thought that it was impossible to say which one was the cause. He regarded the "probabilities" as "absolutely equally balanced". Dr Wightman agreed that the more recent x-rays showed no significant change. It followed that he agreed with much of what Dr Sproule had reported, but he considered that CTD was equally likely to have caused the thickening rather than it simply being a cause which could not be excluded. He understood that all the commoner CTDs produced pleural effusions leading to pleural thickening and interstitial fibrosis. Whether the thickening was diffuse or not made no difference. So far as the costophrenic angle was concerned, Dr Wightman did not consider that the x-rays showed any blunting of the angle. Dr Wightman accepted that, were there to be a competition of diagnoses between asbestos exposure and an idiopathic condition, pleural plaques would point towards asbestos. But, he remarked, SLE was a known condition which the pursuer had.
Objection
[36] The only objection insisted upon at the end of the proof was that raised first by the pursuer during the Commission to take the evidence of Dr Wightman concerning the use of passages from the Webb, Muller and Naidich textbook ((supra) lodged provisionally as 7/8) to demonstrate that SLE was commonly associated with pleural and pulmonary abnormalities. The pursuer's complaint was that he had had insufficient time to consider this work and to research its references. The objection was to its late lodging and its incomplete nature. However, the Commission took place a week before the proof. The reference had been intimated on the Friday before the Commission, which had taken place on the following Monday. There had been and was, ultimately, plenty of time to consider and respond to the use of this reference, even if it required to be formally lodged (which is doubtful). The pursuer had subsequently lodged further references in the form of the Kinder paper (supra) and a textbook by Professor Rudd et al (infra). The objection is accordingly repelled.
Physicians
(a) Dr Reid
[37] Peter Reid (44), consultant physician, specialising in
respiratory medicine, at the Western General Infirmary,
[38] Dr Reid detected fine crackles at the bases of both the pursuer's lungs, a sign of possible pulmonary fibrosis. Spirometry produced figures of FEV1 at 2.8 (predicted (average) 3.71), FVC (forced ventilatory capacity) 3.63 (4.76) and FEV1/FVC at 77%. These demonstrated a restrictive ventilatory defect; that is a defect affecting the bellows capacity of the lungs caused by pulmonary fibrosis or thickening of the pleura. The defect was not an obstructive one, i.e. one causing a narrowing of the airways such as asthma or CPOD. Looking at the earlier spirometry, FEV1 had fallen from 3.05 (in 1988) and FVC had dropped from 4.19. Although spirometry tests showed an apparent improvement in 1993, Dr Reid thought that this could have been for a number of reasons, including the pursuer simply feeling better on the day of the tests. If there had been an obstructive disease, lung volumes would have increased. That had not occurred. Spirometry also tested the ability of the lung to absorb the gasses in the air (gas transfer). In fibrosis cases, the transfer figures (KCO and TCO) would be expected to drop. That had not happened here, suggesting that something else was occurring such as pleural thickening, which would cause an increase in transfer, effectively cancelling out any predicted drop as a result of fibrosis. Emphysema would also cause a drop in the gas exchange figures, but the CT scans showed the emphysema to be minor. The CT scan showed both pulmonary fibrosis and pleural thickening, thus, Dr Reid reasoned, their interaction was the most probable explanation for the spirometry figures produced over the years. But, he argued, the spirometry ought not be looked at in isolation, as it had its limitations.
[39] At the time of his report (
"Calcified pleural plaques...anteriorly in both hemithoraces, with some more diffuse pleural thickening in the right posterior hemithorax, with a small fleck of calcification".
He had reported that there was "no evidence of diffuse pleural thickening". He explained that he had underestimated the extent of the thickening because he had not, by then, seen the soft tissue CT images. He had subsequently done so and agreed with his colleague, Dr Turnbull, that they showed:
"...bilateral pleural plaques with associated calcification, parenchymal bands and right lower thoracic posterior diffuse pleural thickening" (report from Dr Turnbull 25/2 (supra)).
Dr Reid described pleural plaques as benign scarring, usually well circumscribed, being a discreet area of thickening up to 2 cm2 made up of fibrous tissue. They were strongly associated with asbestos exposure and no other cause was known. The exact pathogenesis of pleural thickening, in this case of the visceral pleura, was not known. It was generally caused by recurrent pleural effusions (exudates containing inflammatory cells) which had healed by scarring the tissue.
[40] Dr Reid agreed with Dr Turnbull that:
"There is bilateral, lower lobe, basal, sub-pleural interstitial pulmonary fibrosis with associated minimal fine honeycombing, traction bronchiolectasis and ground glass opacification. These changes, in associated (sic) with the pleural plaques, diffuse pleural thickening, pleural calcification and parenchymal bands could be due to asbestosis" (25/2 quoted (supra),
except that he would have used the
phrase "probably due to" asbestosis rather than the weaker "could be".
[41] Dr Reid
said that there were a number of different CTDs. SLE was one in which a particular pattern of
symptoms occurred, but there was a whole range of these diseases. The
determination of which type a person suffered from was the field of the
consultant rheumatologist. The pursuer
had originally been seen by a non-specialist and later by a specialist
rheumatologist, who had changed the diagnosis from SLE to UCTD. UCTD tended to occur in women and young
patients. Furthermore, as the Kinder paper (6/20 (supra)) explained, the pulmonary
manifestations of UCTD had not been described in medical literature. But those of asbestos related pleural
thickening and pulmonary fibrosis had been so described. These conditions were
known to result from asbestos exposure and that, on balance, favoured it as the
cause rather than a disease whose effects on the lungs and pleura had not been
described in any particular detail.
[42] Passages
from a chapter termed Pulmonary Manifestations of Systemic Disease written by
Professor Anthony Seaton (chapter 53 of Crofton & Douglas's Respiratory
Diseases, 5th edition (ed Seaton, Seaton
& Leitch) (2000)) were put to Dr Reid. These
included the following (p 1384):
"Acquired disorders
Connective tissue diseases
Pulmonary manifestations occur frequently in connective tissue
diseases. There is considerable overlap between the different diseases, between
the associated pulmonary manifestations and between the same pulmonary
conditions in the absence of obvious collaged disease. Thus classification of
the disorders is rather arbitrary and is likely to remain so until their
aetiology is better understood. Those
considered in this chapter are summarized in Table 53.1
Table 53.1 Respiratory
manifestations of connective tissue diseases
...
Systemic
lupus erythematosus
Pleurisy/pleural effusion
...
Interstitial fibrosis
...
Mixed connective tissue disease
Pleurisy/effusion
Interstitial fibrosis
..."
These, it was put to Dr Reid, pointed to fibrosis being a manifestation of CTD. However, although Dr Reid conceded Professor Seaton's academic credentials in relation to respiratory diseases, he would have deferred to the opinion of a rheumatologist in this field rather than to that of Professor Seaton. It was not legitimate to lump all CTDs together and to look at possible manifestations of CTDs in general. Simply saying that a person has a CTD is like saying he has a heart or liver disease. Unless the type can be specified, it is not possible to describe the expected manifestations. If the pursuer had UCTD, then it was the manifestations described as applicable to that CTD that had to be looked at, not those for SLE or "Mixed" CTD. He did accept that pulmonary fibrosis was a common manifestation in SLE patients.
[43] In relation to the paper by Kinder (6/20 (supra)),
Dr Reid acknowledged the expertise of Professor Talmage
King, the most distinguished of the authors, and described the understanding of
interstitial lung disease as evolving.
The American use of UCTD was as an umbrella term, different from "Mixed"
CTD. All the persons selected in the Kinder study had
pulmonary lung disorders. They were selected because of that and not because
they had CTDs.
The Court could not derive from this paper any information on how many
patients with UCTD had pulmonary fibrosis similar to that of the pursuer.
[44] Dr
Reid was referred to the report of Dr Graham Crompton
(25/1) (infra), his predecessor at
the Western General. He agreed with much
of its content as regards the pursuer's history, complaints and
examination. However, in relation to the
interstitial pulmonary fibrosis, Dr Crompton wrote
that "This could be asbestosis or a manifestation of connective tissue
disease". Dr Reid commented that, although it was possibly a manifestation of
CTD, it was more probably a manifestation of asbestos related disease having
regard to the high prevalence of that condition in those with a history of
asbestos exposure (perhaps 40%), as distinct from patients with CTD (perhaps
only 10%). Furthermore, there was
diffuse pleural thickening and this was a particular feature of asbestosis which
had not been observed with CTDs, especially
UCTD. Part of the Webb textbook (7/8 supra) was put to Dr Reid. This tabulated (Table 4-5) "Pleural
thickening or effusion" as well as "fibrosis" as CT findings in SLE
patients. Dr Reid had not seen this
before. He queried the lack of any references for the authors' statement that:
"SLE
is commonly associated with pleural and pulmonary abnormalities. Pleuritis or pleural fibrosis is present in up to 85% of
cases at autopsy, and pleural effusion is often visible on chest radiographs in
patients who have SLE".
There was no literature suggesting that diffuse
pleural thickening occurred as a consequence of SLE. Professor Seaton had
written (25/10 p 1389) that:
"SLE
is associated with a wide range of pleuropulmonary
complications... Pleurisy or pleural effusion is the most common, occurring in
about half of all patients".
But, commented Dr Reid, Professor Seaton had not
said that it caused diffuse pleural thickening.
Professor Seaton had written (p 1390), but had not referenced, that
infection and infarction both occurred frequently in SLE. Dr Reid accepted that infection could cause
thickening. However, Dr Reid's response was that the pursuer did not have SLE
and, even if he had, there was no evidence of infection or infarction. He stressed that, apart from substantive
asbestosis, there was nothing in the medical records which might have caused
diffuse pleural thickening. He would not
concede, other than from a rheumatologist, that the CTD, which the pursuer had,
was associated with diffuse pleural thickening. The information about SLE
causing such thickening came from autopsy results and not radiology. The Webb textbook entries were not
referenced. It was Dr Reid's day to day
experience as a clinician that chronic pleural thickening was not seen in SLE
patients. If Dr Turnbull were able to advise him that it was of a certain prevalence in CTD patients, then he might change
his view, if it were greater than for persons with asbestos exposure. But
radiology only provided one part of the puzzle.
[45] A
printout of the 1982 Revised Criteria for Classification of SLE from the
[46] Dr Reid
did not agree with Dr Crompton that, in the absence
of pleural plaques, it would have to be assumed that the pulmonary changes were
due to CTD. There had, after all, been a
history of asbestos exposure. He did
agree with Dr Crompton that, in the absence of
CTD, there would be no doubt that the fibrosis was asbestos related. Finger clubbing had also been noted in
1988. He disputed that the presence of
long-standing finger clubbing indicated that it was unlikely to be related to
asbestosis. Clubbing was not caused by
CTD as such, but in connection with pulmonary fibrosis. That fibrosis may have been long-standing.
[47] Dr Reid
did not consider that the absence of crackles in 1998 (supra) meant that asbestosis was unlikely. Crackles could be caused by pulmonary fibrosis.
The fibrosis might be caused by asbestosis or CTD. Crackles could also
be present simply as a result of the presence of fluid or inflammation of the
lung. Dr Reid accepted
that with asbestosis, once crackles were heard, they would not be expected to
go away again. If the crackles were associated with CTD, whether they would go
away would depend on the type of CTD and its treatment. Dr Richmond had noted in June 1998 that there
was "no evidence fine respiratory creps" (supra 7/2 p 79). It appeared that she
had been looking specifically for them. They had been recorded by others in
1987 and 1988 (supra). This was
consistent with the presence of fibrosis in the late 1980s, even if the
radiology were clear. Their later absence would, conceded Dr Reid, possibly be
a pointer away from asbestosis. However,
he explained that there were lots of explanations as to why the crackles were
not heard. Perhaps the crackles had been missed because of external noises
interfering with the auscultation during a busy rheumatology clinic. There was
no way of knowing.
[48] It was
put firmly to Dr Reid that the appearance and disappearance of crackles was
more consistent with the pursuer suffering not from asbestos but an "SLE
related condition" and he agreed that he would "go some way with" the cross
examiner on that issue. He agreed that
disappearing crackles were not consistent with fibrosis caused by asbestos
exposure. He did, however, consider it
was consistent with benign asbestos pleurisy, resolving itself. At this point
he was asked a general question about whether the diagnoses of SLE and
asbestosis were equally balanced. His answer to that was that if there was SLE
then "it is equally balanced". He was interrupted and prevented from going
further by an unfounded objection, indicative of the objector being concerned
with that answer, if it had been a general one.
Dr Reid appeared somewhat confused about what he had said. He was then asked a very long question with
several sub-clauses about whether: "standing back and looking at the history,
noting that the physicians from the 1980s onwards, looking at the constellation
of facts at that stage, did not consider that the pursuer's condition was
asbestosis but SLE or CTD, that on balance it is more likely than not that the
pursuer's condition is caused by some form of CTD", or words to that
effect. His answer was that "I would
contend that they are equally balanced".
In re-examination, and in response to somewhat leading questions, Dr
Reid explained that he was referring to the findings in the period of the late
1980s, a time when he was unaware of whether asbestosis had been
considered. He thought that there was an
equal balance then, but not for "the current state of affairs".
[49] Dr Reid
accepted that the GP and hospital records revealed the existence of pleural
effusion on
[50] Dr Reid
also accepted that the medical records showed that the pursuer had chest,
possibly pleuritic, pain in 2000 (7/2 p 228 (supra)) and again in 2001 and 2002. He accepted that these could be consistent
with infections, but not that they would cause pleural thickening. The pursuer was a smoker and prone to chest
infections. But such infections do not
cause pleural thickening.
[51] Dr Reid
explained that it was difficult to predict how asbestos related pulmonary
fibrosis would develop. Asbestosis is slowly progressive. Dr Crompton had concluded (infra)
that it was impossible to state "on the balance of probabilities" whether the
pulmonary fibrosis was asbestosis or a manifestation of CTD (25/1 p 7). Dr Reid disagreed. In this case there was a very strong history
of asbestos exposure, which comfortably exceeded the threshold for causing
asbestosis. The prevalence of pulmonary fibrosis in UCTD was not known. Given the prevalence of pulmonary fibrosis in
persons with high levels of asbestos exposure, such as the pursuer, the fibrosis
in his case was likely to be asbestos related.
In addition, Dr Reid repeated, there were the pleural plaques and the
diffuse pleural thickening.
[52] Dr Reid
accepted the general epidemiology set out thus by Professor Rudd (6/17 supra p 708):
"The interval between the onset of exposure to asbestos and the
development of symptoms of asbestosis is commonly 20 years or longer...New lung
and pleural lesions continue to appear more than 40 years after first exposure.
Asbestos fibres remain in the lungs for long periods, many permanently, and disease
may appear and progress long after exposure has ceased.
...
The long latent period contributes to the difficulty in determining the
attack rate among exposed persons and its relation to the dose of asbestos
inhaled...
The frequency and severity of asbestosis
increases with increasing dose of asbestos."
Dr Reid was not able to say when the onset of
asbestosis had occurred. His best guess
was that it was "some time" before the formal diagnosis in 2004. The disease
was progressing, as the lung function tests demonstrated, even if appearances
on plain film x-ray were unchanged.
There were many factors affecting the progress of the disease and the
extent of the dose was only one of them. The time taken between exposure and
diagnosis had been longer than average.
There had been a long latency period, but not a lot of weight could be
put on this. He accepted that if there
had been a rapid decline in the pursuer's condition between his own and Dr Crompton's reports, that would
have been very rapid for asbestosis and made that diagnosis unlikely.
(b) Dr Crompton
[53] Graeme Crompton (73) gave evidence for the first and fifth
defenders. He was a consultant physician until 1999, when Dr Reid succeeded to
his post at the Western General. Dr Crompton had an impressive CV (25/8). His overall conclusion (report 25/1) had
been that:
"...it is impossible to state whether this man's pulmonary fibrosis is
asbestosis or a manifestation of connective tissue disease. I saw (sic) this because the number of
patients with pleural plaques who go on to develop asbestosis is similar to the
number of patients with a connective tissue disorder who develop pulmonary
manifestations. Since there is no way of
distinguishing the two disorders on radiological criteria, similarly there is
no way of differentiating the two on clinical grounds".
However, having seen all of the medical records, he
had changed his view. Having regard to his continuing problems from 1985, Dr Crompton considered that the pursuer had a multisystem disease. He had features of SLE, but no formal
diagnosis of this had been possible because of the lack of an elevated double
stranded DNA. Back in 1988, Dr Macrae had diagnosed "Mixed"
CTD (7/2 p 159 (supra)) because of
that, but there was no distinction at that time between "Mixed" and "Undifferentiated"
CTD (see eg Crofton & Douglas etc. ((supra) 25/10 p 1384). Indeed, Dr Crompton had, until recently, been unaware of any such
distinction. There was a connection between SLE, mixed CTD and pulmonary and
pleural disorders. It did not matter
which category of CTD the pursuer fitted into.
A rheumatologist would say "mixed" even although it was almost SLE. If a person had a CTD, it would not be
surprising for him to have a lung problem, although it was more often the pleura
and pericardium that were affected.
[54] Dr Crompton was not familiar with the views of Webb et al (7/8 supra) to the effect that SLE could cause pulmonary fibrosis as
this was a radiological reference, but he knew that such fibrosis was a
manifestation of CTD. Dr Crompton tended to "shy away from" American medical
literature, such as the Kinder paper (6/20 (supra)), as he felt that the authors had
an inordinate desire to make up new diseases all the time, full of acronyms and
synonyms. The paper
reads:
"Rheumatologic studies have estimated that up to 25% of patients with
features of a systemic autoimmune disease do not fulfil ACR classification
criteria for CTD. These patients are
considered to have diffuse or undifferentiated CTD. The majority of such
cases...after years of follow up do not develop into a "differentiated" CTD
(e.g., rheumatoid arthritis, systemic lupus erythematosus,
systemic sclerosis, mixed CTD).
Consequently, it has been proposed that UCTD represents a distinct
clinical entity with the following criteria: signs and systems suggestive of a
CTD, positive serological results, and disease duration of at least 1
year. The most common clinical
manifestations of UCTD include the following: Raynaud's
phenomenon. Arthritis/arthralgias, pleuritis/pericarditis, sicca
symptoms, cutaneous involvement (photosensitivity,
rash), esophageal involvement, fever, and myositis. The
specific pulmonary manifestations of UCTD have not been studied".
Dr Crompton
was quite happy with the content of this, although the whole paper was based on
only 28 patients, all of whom had lung disease.
The pursuer did not fulfil the criteria for UCTD used in the Kinder paper and Dr Crompton did
not think it relevant to look at its content.
The pursuer had four of the eleven criteria for SLE (3, 5, 6 and 11 in
25/11 (supra)). He had started out with SLE. "Mixed" CTD was the
same as SLE without the elevated double stranded DNA. If an SLE patient
presented with a non SLE manifestation (such as those in Crofton & Douglas
etc. (25/10 supra p 1384) then a
doctor would be entitled to question whether that manifestation was being
caused by the SLE or something else.
Crofton and
[55] In his
report, Dr Crompton sets out two "points in favour of
asbestosis", viz. the pursuer's history of asbestos exposure and the
radiological evidence of bilateral pleural plaques. He testified that he would have been
surprised if Dr Turnbull had considered that the pursuer's diffuse pleural
thickening was characteristic of previous asbestos exposure. But he had written earlier in his report that
Dr Turnbull had indeed said that the thickening was "typical" of such
exposure. Nevertheless, Dr Crompton would not initially, but did eventually, accept
that this was a third point in favour of asbestosis. He said that the pursuer
did not fulfil the criteria for diffuse pleural thickening, but did accept that
the pursuer having pleural plaques was a factor which could be taken into
account when deciding whether the thickening was asbestos related. If the
pursuer did have a restrictive defect shown in lung function tests then that
could be caused by pleural thickening even if that thickening had not shown up
on x-ray and would not otherwise be expected to cause symptoms. The persistence
of the gas transfer figures despite the presence of pulmonary fibrosis did
point to asbestosis as a cause.
[56] Dr Crompton did not consider that the pursuer had finger
"clubbing" as distinct from "beaking" (this term not
being explained), but, if he did, then it could equally be caused by pulmonary
fibrosis caused by CTD as it could by asbestos related fibrosis
[57] Dr Crompton sets out "points in favour of..." CTD (p 7) as
including the pleural disease and effusions recorded in 1988 (7/2 pp 158, 159 (supra)) and the pulmonary changes shown
on x ray in 1989 and 1992 (pp 104-106). The pursuer had had pleurisy. He had a
pleural effusion suggesting an inflammatory process which resolved upon
treatment with steroids. This had been
preceded by pericarditis. There is no effective
treatment for asbestos related pleural effusions. They would not respond to steroids as a CTD
related effusion would. The effusion
would not have been cured by a diagnostic aspiration. No attempt would be made
to drain all the fluid for fear of causing a pneumothorax.
Steroids do make people feel better generally but an effusion itself does not
cause pain. It is only on successful
treatment, when the pleural layers come back together again, that pain would
return. Dr Crompton
was "nearly 100% confident" that the cause was CTD as no other disease would
respond in the way the pursuer had responded to the treatment. The pursuer's
history suggested that he had relapsed after dropping the doses of steroids;
that the CTD was being barely controlled.
The pleuritic pain persisted for two months
and that would be sufficient to cause pleural thickening, even it there was no
evidence on the x-rays at the time that it did so.
[58] Crackles
were, according to Dr Crompton, characteristic
findings in asbestosis and all other cases of pulmonary fibrosis. If asbestos related, they did not disappear.
The pursuer had fine bi-basal crackles in December
1987 but these had disappeared by 1998 (7/2 pp 162-4, cf
79-80 (supra)) when Dr Richmond
specifically looked for crepitations. This would exclude asbestos related pulmonary
fibrosis as a cause. This, at least, was what Dr Crompton
said in evidence, even although the significance of the disappearing crackles
did not loom large in his report (25/1 p 7). The crackles were noted again in
2002. In August 2004, Dr Faccenda noted that the
"chest auscultation was entirely clear" (7/2 pp 130, 126) but Dr Reid had heard
crackles in March 2005 and Dr Crompton had no
difficulty hearing the crackles in April 2007.
The note in September 2007 (6/10 p 42) that the pursuer's chest was
clear was in the context of the pursuer being admitted for an overdose and it
would not have resulted from a detailed chest examination. The note "chest
clear" would be a throwaway line in an out patient clinic.
[59] The
first evidence of pulmonary fibrosis was on the CT scan in 2004, so it had
appeared some forty to forty five years after the first asbestos exposure and
thirty years after the last exposure. The pursuer had a high enough exposure to
asbestos to cause problems, so Dr Crompton would have
expected the pursuer to have developed fibrosis long before 2004. A longer
period of latency after a heavy exposure pointed away from asbestosis, but
individuals responded in different ways. Dr Crompton
accepted that it was not possible to say how long the fibrosis had existed
before the CT scan. It remained
invisible on x-ray. Dr Crompton did not consider that it could have existed as far
back as 1998, when Dr Richmond had not detected any crackles. But he did accept
the idiosyncratic nature of the development of asbestosis described by
Professor Rudd (6/17 p 708 (supra)).
[60] If the
fibrosis had stemmed from asbestosis then some time would have had to have
elapsed for the appearance of the "honey-combing" or "ground glass" opacities,
which the pursuer had. If it had stemmed
from CTD, a more rapid development could occur than with asbestosis related
fibrosis, but the effect of the steroid suppressive therapy was not known. Professor Seaton (supra 1391) did write that "anecdotal reports suggest that [chronic
interstitial fibrosis in SLE patients] does not usually respond" to steroids,
but Dr Crompton had more experience of CTD
patients than Professor Seaton and that experience was that CTD related lung
disorders did respond to steroids.
[61] The
pursuer had told Dr Crompton in May 2007 that he was
short of breath after walking 60-70 yards (25/1 p4). This showed a rapid decline since Dr Reid had
seen him in March 2005. This was not typical of asbestosis, which is
very slowly progressive. The lung function tests did not support such a
change. Although initially stating that
there was nothing in the tests to suggest a restriction caused by pleural
thickening, Dr Crompton did accept, after some
prompting, that the lung function tests did suggest a restrictive ventilatory defect in the late 1980s, 1993 and 1998. Dr Crompton would not initially accept that, in the absence of
evidence of pleural thickening, this indicated the existence of pulmonary
fibrosis. He did eventually agree that, if there were a genuine restrictive
defect, it had to be due to pulmonary fibrosis and/or pleural thickening, if the
pursuer only had mild airways obstruction.
[62] Dr Crompton would laugh at the prospect of a mixed diagnosis.
It would, in his view, be ridiculous.
Doctors were taught not to give two diagnoses when everything could be
explained by one. However, Dr Crompton accepted that if the pursuer did not have CTD, he
would have no difficulty in saying that his condition was asbestosis. Dr Crompton's mixed diagnosis view seemed to be contradicted
by his view that in early 2002, the pursuer was complaining of right basal pleuritic pain and being tender over the right lower rib.
Scattered rhonchi, suggesting an obstructive airways
disease, were present (7/2 pp 229-230 (supra). Pulmonary problems did not cause rhonchi so, Dr Crompton reasoned,
there were two different pathologies.
(c) Dr Winter
[63] John
Winter (57), consultant physician with a special interest in respiratory
disease at
[64] In a
long, but clear, answer to a general question on fibrotic
changes to the lungs, Dr Winter explained that the CT scan revealed bi-basal
fibrosis and pleural thickening, although he had not seen all of the images.
The problem with these two changes was that they could be caused by both
asbestosis and SLE. There were certain
radiological conditions which could lead to a diagnosis of asbestosis, but
these were not present. A good history of asbestos exposure was needed, but, if
the changes were occurring more than fifteen to twenty years after exposure had
ceased, there was some authority for the proposition that they were unlikely to
be caused by asbestosis. Here there was
an alternative explanation for the pulmonary fibrosis, namely SLE. In his report he had been unable to form a
view on which was more likely but, having seen the records, SLE was more
likely. In particular, the pursuer had
active arthritis in 1985. He had then
developed chest pains. An ECG suggested pericarditis.
Crackles detected indicated an active inflammatory process in the
lung. Thereafter, the pursuer had
developed an effusion around the lung, which responded rapidly to steroid treatment. This made SLE more likely than
asbestosis. He continued to complain of
chest pain. He had skin problems in the
1990s. But his skin and joint problems
settled down on treatment. The crackles came and went, also suggesting acute
inflammatory problems which had been treated, leaving fibrosis. The cause of that was more likely to be SLE,
as it provided a single unifying diagnosis for all the symptoms. If it were possible to explain all the
symptoms in this manner, that diagnosis is the most likely. There could be both SLE and asbestosis but,
on the "balance of probabilities", SLE was the only cause, although it would
not surprise Dr Winter if a lung biopsy showed that it was asbestosis.
[65] Dr
Winter considered it significant that the pursuer had a pleural effusion in
March 1988 but this had gone by the following May (7/2 p 157), after the
prescription of steroids. It was more
likely that the steroids had cured the problem, rather than a diagnostic
quantity of fluid aspiration. There
required to be a lot of fluid, perhaps about half a litre, to show up on x-ray
and it was not likely, although it was possible, that this amount had been
aspirated.
[66] Dr
Winter thought that the latency period between the exposure to asbestos and the
discovery of pulmonary fibrosis pointed away from asbestosis. His basis for
this was that Parkes (Occupational Lung Disorders, 3rd
ed 1994 p 520, 6/22) states that if fibrosis occurs more than twenty years
after exposure, it is less likely to be asbestos related. This was so even if
Professor Rudd was of the view that the interval between exposure and symptoms
was "commonly 20 years or longer" and "New lung and pleural lesions continue to
appear more than 40 years after first exposure". It was not easy to say when
the pursuer's fibrosis had started, but it was very minor at the time of the CT
scan in 2004. If honeycombing were visible then, the fibrosis could have been
there for a few months or even decades.
[67] With
asbestosis, crackles in the chest should not go away, as they had done.
Crackles indicated something was going on in the lung tissue and not the
pleura. Although there could be differences of opinion on whether crackles
could be heard at a given time, there were many records stating that the chest
was clear, including one from a respiratory physician (Dr Faccenda). Dr Winter had heard
crackles, but on
[68] In relation to the pleural thickening, this could be a consequence of both SLE and asbestos exposure. There was no "blunting" of the costophrenic angle as would be expected with asbestosis. It was not possible to say whether the thickening was caused by asbestosis or SLE. Dr Winter had recently considered the Kinder paper (6/20), which had referred to a very rare group of patients with UCTD. The pursuer would not have fitted into this group. Dr Winter agreed with Webb et al (7/8 supra) that SLE could cause pleural fibrosis. He had looked up the references for the propositions in Webb. These were not produced, but Dr Winter was able to describe one of them as demonstrating that a certain proportion of SLE patients had interstitial lung disease (9 out of 34) and another as showing that some had pulmonary fibrosis (3 out of 38). Dr Winter was of the view that there was plenty of literature showing that lung and pleural disease were frequently encountered with SLE patients. He accepted that Crofton and Douglas ((supra) 6/21) did not mention pleural thickening in connection with SLE, but did in relation to asbestosis.
Conclusions of
Fact
[69] The pursuer has developed asbestosis,
in the form of pulmonary fibrosis, and diffuse pleural thickening as a result
of exposure to asbestos during his employment with the defenders.
[70] Although the pursuer initially submitted, somewhat peculiarly, that the radiology should be regarded as "largely neutral", he proceeded, correctly, to found upon it as evidence of the presence of both asbestosis (fibrosis) and diffuse pleural thickening caused by asbestos exposure. That is what the radiology points towards, even although there may be other possible explanations for the fibrosis and the thickening. The starting point when looking at the radiological findings is the undisputed presence of pleural plaques, with calcification, undoubtedly resulting from asbestos exposure. The second area of significance is the pleural thickening. The pursuer submitted that the differences between the radiologists over whether the pleural thickening was "diffuse" were of no significance. However, that is not the case. It is useful to determine whether the thickening is "diffuse" or not in radiological terms in order to assess its cause. It is "diffuse" or as close to that as makes no practical difference. It was not suggested that the plain film x-ray test of obliteration of the costophrenic angle had been entirely met, even if there was some loss of definition. In relation to the CT scan dimensional test, Dr Sproule referred to the thickening as "at least 6 cm" and thus being "highly suggestive" of it being "diffuse". Dr Turnbull reported that it was "over 8 cm", albeit that he said in evidence that he "implied" that, rather than measured it. It was only Dr Wightman who tentatively put forward a case for it not being "diffuse" because, he thought, the next (non existent) CT image would have been below where the pleura of the lungs ought to have been. Although that is no doubt a possibility, the evidence of Drs Sproule and Turnbull that the 8 cm dimension has been reached is preferable even if that achievement is to a degree uncertain. The significance of this dimensional achievement is not just its predictability to produce symptoms (infra) but, as Dr Turnbull concludes in his report, its existence, like the pleural plaques, as "typical of previous asbestos exposure". In this connection, Dr Turnbull was not simply saying, as Dr Wightman did, that the diffuse thickening might be caused by asbestos exposure as one of several options. He was expressing his opinion in writing that it is "typical" as such exposure. From a radiological point of view, the radiologists agreed that thickening might also be caused by a CTD, but none of the radiologists went as far as to express the view that it was typical in patients with a CTD.
[71] The third aspect of the radiology is the fibrosis, which, all agreed, is mild in nature. It is not disputed that fibrosis can be asbestos related or it can be caused by a number of other conditions. As Dr Sproule conceded, if the fibrosis were asbestos related then, if it had existed in the late 1980s, it ought to have progressed beyond its current subtle form. On the other hand, as Dr Turnbull wrote, the fact that it has not progressed at a rapid rate tends to favour asbestosis or a stable or treated CTD. It is impossible to say how long the fibrosis has been present but, as will be seen, it is likely that it was present in the late 1980s.
[72] Before leaving radiology, it should be noted that although it was submitted by the pursuer that Dr Turnbull disagreed with Dr Wightman on whether the vertical or circumferential dimensions were more important as regards causing lung restriction, their evidence seemed to be the same in regarding the vertical as more significant.
[73] Turning to the physicians, a number of difficulties presented themselves in the assessment of their evidence relative to the pursuer's condition. As a preface, the court would not wish to criticise any party for the use of economy in a litigation such as this one where the value of the case, in Court of Session terms, is very small. Keeping the number of medical witnesses to a minimum is sound policy. However, first, where a major issue is a competition of causes between asbestos exposure and a CTD, the absence of expertise in the causes, prevalence, symptoms and treatment of CTDs, especially in males of the pursuer's age, creates a significant evidential gap. It was far from clear that any of the medical witnesses was able to speak with any confidence on this subject, even if Dr Crompton attempted at times to do so. Although the respiratory physicians were able to stress that their departments tended to adjoin those of rheumatology and that they had close contacts with their neighbours, none purported to be especially skilled in CTDs. Secondly, although the parties were keen to focus on particular entries in the medical notes, many of these entries appeared to be being afforded a status well beyond their role as "notes" or as summaries and, in some cases, speculations and conjectures on possible diagnoses. Thirdly, this was compounded by the absence of any of the pursuer's treating physicians over the years, especially someone, such as Dr Richmond, from the rheumatology clinic or a general physician from the Borders General who might have spoken to a final diagnostic conclusion once pleural plaques had been discovered.
[74] It is not without importance to note that, throughout the examination and treatment of the pursuer over at least two decades, asbestos related disease does not appear to have been considered as a possible diagnosis. Once more, the absence of such treating physicians as witnesses should not be taken as a criticism of the parties, since they no doubt had their own good reasons for selecting the witnesses they called. But that absence still presents a gap which the Court has to take note of in reaching its conclusions on the evidence actually presented.
[75] Fourthly, in relation to the use of medical literature, such
literature is an entirely legitimate tool, which can be used to bolster or
undermine the opinions of the experts. In that connection, the pursuer referred to
"The function of the judge in a civil case is to decide where the truth lies or whether the case has been made out, on a balance of probabilities. One cannot entirely discount the risk that, by immersing himself in every detail and by looking deeply into the minds of the experts, a judge may be seduced into a position where he applies to the expert evidence the standards which the expert himself will apply to the question whether a particular thesis has been proved or disproved - instead of assessing, as a judge must do, where the balance of probabilities lies on a review of the whole evidence".
[76] The defenders founded strongly upon the approach of Lord Bridge in Wilsher v Essex Area Health Authority [1988] 1 AC 1074, where, in playing down the effect of the dicta in McGhee v National Coal Board 1973 SC (HL) 37, he stressed the need for a pursuer to prove the relevant cause of his condition as a matter of probability where multiple causes were postulated. It is, of course, accepted that such proof is required as a generality, although, in this case, on one view, the onus of proving that the pursuer had a CTD fell on the defenders as the parties averring that fact. Nevertheless, as has often been said, once the evidence in a case has all been heard, issues of onus seldom arise and the question for the Court is simply where the balance of probability has come to rest. It must be in the rarest of civil cases that it remains so finely and evenly balanced after a proper analysis of the evidence, that the Court is forced to hold a case not proved by reason of a failure by a party to discharge a burden of proof.
[77] There was nothing in the qualifications or experience of the respiratory physicians which suggested that the evidence of one of them should be preferred over that of another. They were all very well qualified and experienced and each of their opinions deserves respect. Each may be correct. Each of the physicians had difficulty in answering particular lines of questioning. For example, Dr Reid was undoubtedly floundering when attempting to deal with the "crackles" and Dr Crompton attempted for some time to avoid a direct answer to questions concerning the ventilatory defect shown up in the lung function tests from an early stage. The reason for their difficulties is, no doubt, because there are points clearly for and points plainly against the presence of asbestosis on the one hand and CTD on the other, especially when considered within a short diagnostic time frame.
[78] Overall the wider approach of Dr Reid to the history of the pursuer's condition and treatment and his open minded analysis of that has provided the more acceptable and likely diagnoses, notably his fundamental conclusion that the pursuer does have asbestos related disease in the form of pulmonary fibrosis (asbestosis) and diffuse pleural thickening, as well as a CTD. This is, of course, on the balance of probabilities on a review of the whole evidence. Dr Reid himself appeared to adopt this approach whereas the lasting impression from hearing Dr Crompton and Dr Winter is that they had both determined that it was not possible to say whether asbestos exposure or CTD had "probably" caused the pursuer's fibrosis and pleural thickening simply because both were theoretically capable of doing so as a matter of medical fact. The conclusion that the pursuer has some form of CTD has to be reached primarily because none of the physicians was prepared to dispute its existence, deferring to the rheumatology reports in the records in that regard. However, as Dr Reid did comment, the foundation for that diagnosis is far from being a firm one. But for the lack of challenge on the existence of a CTD, it might have been difficult to accept that existence in the absence of expert rheumatological testimony. The pursuer's CTD is not capable of definitive categorisation. It is not SLE, since the pursuer does not have the necessary elevated double stranded DNA. It is not UCTD, in the American sense, as the pursuer has the necessary elements for American SLE. It may be some form of "Mixed" CTD or UCTD in the British sense.
[79] One of the planks upon which the opinions of Dr Crompton and Dr Winter are based is the notion that if all symptoms can be explained by one diagnosis then that diagnosis ought to be preferred over there being two diseases present. This somewhat fundamental proposition was not put to Dr Reid for his comment. However, it is no doubt a useful aphorism given to medical students and trainee doctors and one to be borne in mind as a generality. But, it cannot be an absolute axiom applicable in all circumstances. This pursuer may well have a CTD, for some reason. But it is accepted that for many years he was also exposed to significant levels of asbestos, sufficient to cause asbestos disease. He has calcified pleural plaques indicating the presence of asbestos particles in his lungs. He also has emphysema caused by smoking. There would appear to be no sound reason not to consider, with an open mind, the possibility of his suffering from two or more conditions at the same time. Dr Reid's approach in this regard is again preferable to those of his colleagues. In that regard, concerning his answer at one point that the diagnoses of SLE and asbestosis were "equally balanced", this was in the context of the evidence available to the physicians in the 1980s and was not a general concession about the position, now that a CT scan has been carried out.
[80] There was no persuasive evidence that diffuse pleural thickening visible on CT images is a common
manifestation of CTD. Dr Reid's view on that, subject as it was to persuasion
otherwise from a rheumatologist, is again accepted especially his pointing to
the absence of medical literature supporting such a proposition and having
regard to his reported clinical experience.
Dr Reid was the subject of some valid criticism in submissions in
relation to his refusal to respond meaningfully to questions about the likely
manifestations of the pursuer's CTD without being told what CTD he had.
Nevertheless, there is force in his view that, if the defenders are maintaining
that the pursuer has pleural thickening and pulmonary fibrosis as a result of a
CTD then, in order to demonstrate how that might arise, they ought to be able
to state what CTD the pursuer has and then be able to point to the known manifestations
of that type as including such thickening and fibrosis. They have not done so. In so far as there is a current categorisation
of the pursuer's CTD it is UCTD and, as the Kinder paper points out, the
pulmonary manifestations of that disease (at least in its American guise) are
not described in medical literature.
[81] All the
experts heard crackles from the pursuer's lungs. It was accepted that crackles
can be caused by pulmonary fibrosis. Fibrosis caused by asbestos exposure does
not necessarily produce crackles. But if there was fibrosis caused by
asbestosis then that fibrosis would be permanent. Therefore, once established, any crackles
caused by that fibrosis would not disappear and re-appear. It would be a strong point in favour of the defenders'
case if it were established that any crackles detected in the pursuer's lungs had
disappeared. If they had then they
could not have been caused by fibrosis induced by the permanent presence of
asbestos particles. Thus, the defenders founded heavily, for example, upon the
existence of crackles in December 1987 and both March and April 1988 (supra) and the records in January 1989
that the chest was "clinically clear". In June 1998 Dr Richmond expressly wrote
"no evidence fine respiratory creps".
[82] Throughout
the records there are references to "chest clear", usually referring to
radiological results but sometimes also to what seem to have been stethoscopic examinations. Although Dr Reid's speculation
about the surrounding noises of a busy rheumatology clinic is not at all convincing,
little weight can be attached to a record stating "no evidence fine respiratory
creps" where the author does not give evidence and
there is no obvious explanation for that. Even assuming that the record
actually means what the defenders maintained it did, namely that there was no
evidence of fine respiratory crepitations (which is by no means certain), it has to be
borne in mind that this was a chest examination preceding any consideration of
asbestos related disease, when such crepitations
might have been more carefully looked for.
It was an examination by a rheumatologist and not a respiratory
physician. The entry is not therefore to be regarded, as the second etc.
defenders submitted, as "high quality hearsay" (whatever that may be).
[83] As the
defenders conceded in submissions, even although the CT scan showed there to be
fibrosis present in the lungs in 2004 and all the experts detected crackles
relative to that fibrosis, respiratory physicians (Dr Faccenda
and her registrar) had separately failed to detect crackles in 2007, even
although the presence of established fibrosis was by then well established.
That would seem to suggest, if it were not obvious, that mistakes in the
detection of crackles can be made. No doubt they may be more evident at some
times than others. At all events, the fact that at some points in the medical
records crackles have been noted by some doctors and at others they have not,
goes little way towards establishing a pattern of disappearance and
re-appearance in clinical terms. In that regard, relative to the medical use of
the phrase "chest clear", it is not without significance that the registrar
examining the pursuer's chest in October 1992 regarded it as "clear" despite
the presence of "a few scattered crepitations". Crackles are detected at various times from
1987 through to 2007. It is likely that
they were always detectable upon a careful and detailed examination but that
they were not always detected in the context of, in particular, a primary
diagnosis of CTD rather than respiratory disease.
[84] The
defenders founded upon the apparent resolution of the pursuer's pleuritic pain and the disappearance of the effusion. This,
it was argued, was illustrative of a CTD resolved by steroids. Dr Reid
struggled under effective cross examination in relation to the disappearance of
the effusion and his explanation that the aspiration might have removed it was
not convincing. However, so far as pain is concerned, that is, of course, highly
subjective. The pursuer was being given doses of steroids which would, no
doubt, make him feel better intermittently. He was also taking pain killers.
The pursuer was not a particularly good historian, as was illustrated by his
surprising inability to recollect past episodes of a variety of pains requiring
visits to his local surgery (see (infra)
on damages). His reports of pain, the lack of it and its degree may not be very
reliable. He was a heavy smoker, prone to chest infections. He may have had an effusion, and indeed pleuritic pain, caused by something other than asbestos
exposure, including as a result of whatever CTD he might have. That may well
have resolved to some degree upon treatment with steroids. However, that does
not lead to a conclusion that the pulmonary fibrosis and pleuritic
thickening detected on the CT scan are caused by CTD as distinct from
being asbestos related.
[85] Overall,
the general picture of the pursuer's history is one of intermittent complaints
of pain and of discomfort in his chest.
From time to time, he seems to have considered it sufficiently symptom
free to avoid calling in at his GP surgery.
Given his intake of steroids and painkillers, he may have felt that
whatever symptoms he had were resolving to an acceptable level. But the impression from the notes is that the
pain and discomfort is seldom reported as disappearing altogether for any
prolonged period. It seems to be always there in the background, albeit that,
on occasion, the pursuer may have considered it absent on a given date. The lung function tests show that in the late
1980s, he did suffer from a mild restrictive defect. That restriction has continued, and slowly
become worse, over the three decades since then. It is not without significance
that, over that period too, he was reported as having clubbed fingers; a known
consequence of pulmonary fibrosis. Like
the crackles, sometimes the clubbing was not detected by some of the doctors
over the years, but a sufficient number did find it. It has almost certainly always
been present in some degree and is, despite Dr Crompton's
view in evidence that it might only be "beaking",
present now. This also suggests a continuing pulmonary defect. Dr Crompton, it
should be noted, did not state that it was "beaking"
in his report. Rather, he said that it
was "Clubbing/beaking of fingers (known to be
longstanding)". In so far as he maintained that there was no clubbing, his
evidence is rejected.
[86] If the
pursuer has had fibrosis over this time, then the pursuer's gas transfer
figures would have been expected to drop, but they have not done so. There must be a reason for this. Dr Reid's explanation that something else has
been happening is a convincing one. It fits in with his persuasive view that
the pleural thickening, which has now been confirmed on the CT scan, has been
the cause. There has, as Dr Reid stated,
been an interaction over the years of the two conditions which, it is now
established, the pursuer has, namely pleural thickening and pulmonary fibrosis. In this connection, the lung function tests
do not reveal a sharp deterioration in the pursuer's condition between seeing
Dr Reid and Dr Crompton. The pursuer has not
deteriorated rapidly over this time. He exaggerated his difficulties, as caused
by his breathlessness, when seen by Dr Crompton, and
to a degree also when giving evidence.
[87] The
significance of the latency period depends upon when it is thought that the
pursuer developed symptoms of asbestos related disease. If it were thought that
these had only occurred when the diagnosis was made in 2004, then clearly the
time lapse from the commencement or the cessation of exposure until then might
be regarded as a significant pointer away from asbestosis. But, as concluded
above, the probability is that the pursuer had some fibrosis, albeit in a mild
and very slowly progressing form, from the late 1980s, causing a mild
restrictive ventilatory defect. If that is correct, and it is the conclusion
reached here, then the pursuer developed symptoms within about fifteen from the
cessation of exposure and within thirty years of his initial exposure. These appear to be well within the normal
latency periods to be expected for asbestos related disease.
Damages
[88] The
pursuer sought a final award of damages and did not insist upon his first
conclusion for a provisional sum.
(a) Evidence
[89] The
pursuer said that he was currently not well.
He suffered from shortness of breath during the day and at night,
causing broken sleep. He broke out in
sweats during the night. He had pains in
his left side. He was unable to walk
more than fifty yards or to go up hills, without becoming out of breath. He had been like that for five or six years,
but he had got worse in the last four to five years. He had grown "a good bit
worse" since seeing Dr Reid. He later said that he had suffered shortness of
breath since 1987. He would now use a car if he had to go more than two hundred
yards. He had many grandchildren but was
unable to engage with the younger ones as he once had with the older
children. He needed to take pain killers
six or seven times per week. He had
suffered from bladder and heart problems but, once treatment of these had been completed,
he was told by his GP that something else was wrong. His doctor had told him, he said, that he had
to put a label on it and that he would "just put it down as SLE". "They said"
there was something wrong with his connective tissue and asked him if he had
pains in his joints. He did not have any
pain in his joints but did have in his chest.
He also had Raynaud's and poor blood
circulation in his legs, from the calf down.
He was prescribed Prednisolone. He would break out in sweats and began
shaking if he withdrew from it. His symptoms recurred if he stopped taking the tablets.
He had no recollection of increasing his steroid dose in 1997-98 because of
skin or joint pain. He had no
recollection of having knee and ankle problems in 2000, or of any joint pain at
all. He did have chest problems, although he did not remember pain, in 1997-98
when his lung was drained. He could not
remember chest pain in 2000, 2001 or 2002, but he did accept that he had
visited his GP regarding chest problems. Finger clubbing had not been
mentioned. He used to smoke, latterly 50
grams per week before reducing this to 12.5 grams a week (4 or 5 cigarettes per
day) and eventually giving up last year.
[90] The
pursuer said that he had first been told that he had an asbestos related
condition after Dr Richmond had sent him for the CT scan. Dr Faccenda had
told him that he had asbestos in his lungs.
After a medical examination, had been told that, for
the purposes of industrial injuries disablement benefit, he was 15% disabled. He had received £6,789 in February 2005
(25/7) as benefit for asbestosis.
[91] The
pursuer told Dr Reid (30 March 2005) that he was short of breath on exertion
such that, although he could walk for about half a mile at his own pace on
level ground, he would be short of breath if he had to hurry or climb stairs or
inclines. On the Department of Work and
Pensions' COPD Disability Rating Scheme scale (25/6) Dr Reid considered that
the pursuer was 20% disabled, although he could qualify for 30% if the account
to Dr Graham Crompton on
[92] Dr Reid thought that the comments in his
report (6/6 p 7) required alteration in light of the finding of diffuse pleural
thickening on CT scanning. He "stuck"
with his comment that the asbestosis may be stable but is usually slowly progressive,
especially as the pursuer is a smoker.
He estimated that "respiratory disability due to asbestosis will
progress to a maximum of 30% of his total disability in his life time". He thought that this was unlikely to require
any additional care or support. Were he
to continue smoking, his emphysema would progress towards causing 15% of his
total disability.
[93] In his report, Dr Reid said that the pursuer was at a 5% risk of developing malignant mesothelioma. An assessment of 2% (infra) was too low and applied where a person only had pleural plaques. The pursuer's asbestos exposure had increased the likelihood of him developing lung cancer by fourfold. As he already had an 8% chance of developing lung cancer from his smoking, he had, Dr Reid reasoned, a 32% prospect of lung cancer. This risk would diminish if, as the pursuer said, he had ceased smoking. The pursuer's life expectancy, but for his condition, would be 20.69 years for a man aged 63. His various non asbestos related conditions, including CTD, reduced that by seven years. Dr Reid considered that it was reduced by four years as a result of the asbestos related risks of developing malignant disease. The asbestosis itself would not progress to a fatal degree. The view (infra) that there was no decrease in life expectancy was out of step with the chapter in Professor Rudd's book (6/17).
[94] Dr Crompton was of the view that the pursuer's disability was
between 10 and 20% on the scale (25/6 supra). That would be split "50-50" with the pursuer's
emphysema and bronchitis. If he had
asbestosis then he had a 2% risk of developing mesothelioma. It was not as high as 5%. He was at increased risk of developing lung
cancer too, although it was difficult to assess in percentage terms. The ordinary smoker had an 8% risk. Perhaps
20% was appropriate, but it was not as high as four times 8%.
[95] Dr Winter saw the pursuer in April 2007 (report 7/5), when he said he could walk long distances on the flat. If what he had said to Dr Crompton (supra) were correct, then the change was inexplicable. At the time he saw him, Dr Winter thought he was 20% disabled on the scale. On the basis of Dr Wightman's report of the CT scans, Dr Winter thought the emphysema, and COPD, caused half or perhaps three quarters of that with the balance being caused by the pulmonary fibrosis. Any pulmonary fibrosis was minor and it was not possible to say that it contributed to any restriction, although it might do so.
[96] Dr Winter considered that the pursuer was at greater risk of
developing lung cancer and mesothelioma as a result
of his asbestos exposure and smoking, perhaps at 3% risk for both. Dr Winter
would have been prepared to move 2% from this in either direction, and thus 5%
was not unreasonable. Professor Rudd's patients
(6/17 supra) had different diagnostic
criteria, based on chest x rays. Dr Winter dealt many cases of lung cancer in
Dundee and made a rough calculation in the witness box of a normal incidence of
11/2 % over a ten year period. Mesothelioma cases were
half those of lung cancer. The pursuer's life expectancy as a result of all his
various conditions was reduced by 5%; 3% as a result of malignancy.
(b)
Submissions
[97] The
pursuer sought only solatium
and interest. He submitted that a reasonable figure was £30,000, one half of
which was attributable to the past. He produced a useful table of various
Scottish cases with an up to date revision of the awards made in them. It was accepted that the first five of these
cases (Timms v
Barclay Curle 2007 CSOH 166, unreported, [2007]
CSOH 166; McKenzie v Barclay Curle
2002 SLT 649; Kerr v Newalls
Insulation Co 1997 SLT 723; Stanners v Graham Builders Merchants 1995 SLT 728;
and Myles v Glasgow District Council 1994 SCLR 1112) involved pursuers with
greater disabilities than the present pursuer.
However, the pursuer in McKenzie v Cape Building Products 1995 SLT 695,
who was aged 52, did have pleural plaques and thickening and sub-pleural fibrotic changes. He had late onset asthma as well,
contributing equally to his breathlessness. He was at risk of developing mesothelioma or lung cancer and had been assessed at 15%
disabled for Department of Social Security purposes. The award had been
£25,000, worth just over £37,500 now, and this had been sustained upon a reclaiming
motion (1995 SLT 701). In Lightbody v
Upper Clyde Shipbuilders 1998 SLT 884, the award had been £15,000 (over
£19,000 now) for a 59 year old with pleural plaques, minor pleural thickening
and a small chance of developing mesothelioma. He was described as having a moderate degree
of "exertional" breathlessness. The pursuer argued
that this award was low and "out of kilter" with other cases. Bateman v Newalls Insulation Co 1987 SCLR 445 was
a
[98] The
pursuer also founded upon the English Judicial Studies Board Guidelines which
advised £40,750 for "Injuries to Internal Organs" "(C) Asbestos-related
Disease" "(c) Asbestosis", involving "Respiratory disability of between 10 to
20 per cent". The "bottom" bracket was £28,830. "(d) Pleural thickening"
causing breathlessness carried a range of £23,000 upwards. The pursuer relied
upon the table in Kemp & Kemp: Quantum of Damage (K3. Respiratory Organs:
Asbestos-Related; p K0004), which incorporated an uplift following on from Heil v
Rankin [2001] QB 272, notably upon the English cases of: Seward v Corby Borough Council (2004) Kemp & Kemp K3-017.1 (£40,000 for
a 52 year old with similar problems as the pursuer); Snell v Newalls
Insulation (1998) Kemp & Kemp K3-018 ((£30,000 for a 72 year old);
and especially Ryan v BRB Residuary (2005) Kemp & Kemp
K3-019.1 (£20,000 for a 68 year old) and Urwin v Darlington Insulation
(1996) Kemp & Kemp K3-021, which was at the bottom end of the scale at
£15,000 for a 72 year old with 10% disability.
[99] Interest
ought to be at 4% on half of the total from the date of discovery of the
disease in June 2004.
[100] The first to fifth defenders submitted that solatium ought to be £20,000 with interest also on half of
that figure from the date of diagnosis. They reminded the Court that no damages
were available for pleural plaques on their own, or for the prospect of
developing a disease in the future or anxiety because of that (Rothwell v
Chemical and Insulating Co [2007] 3 WLR 876). On the scale (25/6) the
pursuer was 10 to 20% disabled. Half of the disability was smoking related, so
the award should reflect a disability level of about 7.5%, or less if Dr Winter
was preferred to Dr Crompton. The pursuer had been coy about his
breathlessness and the lung function tests did not support any rapid
deterioration in his condition. Age was an important factor in the damage assessment. All of the Scottish cases in the table were
examined. It was argued that the pursuer
in McKenzie v Cape Building Products (supra)
was much younger. Lightbody v
Upper Clyde Shipbuilders (supra)
was a good analogy involving again a younger pursuer but lesser malignancy
risks. Nicol v
Scottish Power (supra) was an
unusual case where a high award was made in respect of the anxiety
element. Cook v Wyvern Structures
2001 SLT 1212 was also useful, involving a potential award of £15,000 (£18,000)
for 35% disablement. Of the English cases, Ryan
v BRB Residuary (supra) was the most helpful. The £6,789 received by the pursuer (25/7) as
benefit for asbestosis required to be deducted (Ballantyne v Newalls
Insulation [2001] ICR 25).
[101] The remaining defenders adopted these submissions. They
submitted that the court should find in fact that: (1) the pursuer suffers from
mild breathlessness, causing 20% disablement of which 5% is attributable to
pulmonary fibrosis; (2) 15% is attributable to emphysema; (3) the fibrosis is
caused by CTD and the emphysema by cigarette smoking; (4) there is no
breathlessness caused by pleural thickening; and (5) there is no risk of the
pursuer developing malignant disease because of exposure to asbestos.
(c) Award
[102] As noted above, the lung function tests do not warrant the
conclusion that the pursuer's pulmonary difficulties have rapidly deteriorated
in recent years, although they have grown worse. The pursuer has not had his
troubles to seek and has a variety of health problems unrelated to his asbestos
exposure, notably significant heart and bladder disease. His asbestos related condition, as manifested
in symptoms, consists of a mild restrictive ventilatory
defect which causes him breathlessness on exertion. He is only slightly worse
than when Dr Reid saw him in March 2005 (see supra on exaggeration). He can walk without much difficulty on
level ground but will need to rest if he is required to hurry or climb. He may have occasional disturbed sleep.
[103] The pursuer might just manage to fit into the 20% disability
category on the scale produced (25/6 (supra);
the categories of which jump from 10% to 20%). Dr Crompton's
assessment of between 10% and 20% on the scale seems reasonable. The pursuer's
pulmonary disability is therefore assessed at 15%. The condition is very slowly
progressive and it may progress to the 20% level, but not to the 30%
category. It was accepted that only part
of this is caused by asbestos related disease because of the existence of
emphysema and, on Dr Reid's analysis, some form of CTD. There were various different proportions
attributed by the respiratory surgeons ranging from one quarter of his
condition to CTD, but none to his emphysema, from Dr Reid to Dr Winter's
[104] The pursuer is at increased risk of developing mesothelioma and lung cancer. Again, various percentage figures were
presented. The risk of mesothelioma is very low, and
5% will be taken. Lung cancer risk is
higher. Dr Crompton's 20% if the pursuer was still
smoking may be too high, and Dr Reid's arithmetical calculation does not seem
statistically valid. Perhaps something in the region of 15% may be about
right. There must be some reduction in
life expectancy, but this will be small. Two to four years seems reasonable
having regard to the various figures, ranging from nil to seven (including the
CTD element).
[105] Solatium is
reasonably assessed at £25,000. In that
regard, the submissions on behalf of the first to fifth defenders are accepted
as broadly accurate. The Court's task is
to award damages for a slowly progressive disabling condition currently
assessed as 7.5% attributable to asbestos related disease and carrying with it
relatively small risks of malignant disease and consequent possible reduction
in life expectancy. Although by no means on all fours with it, the case of Lightbody v
[106] It was agreed that the £6,789 awarded in February 2005 (25/7)
falls to be deducted from the solatium, leaving a principal sum of £18,211. Interest was only sought from the date of
diagnosis following upon the CT scan in June 2004. It was not disputed that it should run at 4% on
a past element of one half. On that basis, it would run on £12,500 to February 2005, and on the balance of £5,711 thereafter. The interest
amounts to about £900. Decree will accordingly be for £19,111.