Timms v Barclay Curle Ltd & Ors [2007] ScotCS CSOH

"He worked in engine rooms. He was exposed heavily to asbestos during this employment. Although even here he says that the exposure was intermittent. He says that asbestos was being used by others around him, particularly laggers, sometimes creating heavy exposure".

That account seems to involve substantially greater exposure than appeared from the pursuer's own evidence, where it was indicated that he only spent approximately ten days in ships' engine rooms. In relation to the pursuer's employment with the predecessors of the second defenders, Dr Henderson noted that when asbestos blankets were moved "the dust came off them". He also noted that when the pursuer worked for the third defenders at Braehead Power Station asbestos had been handled and the pursuer believed that asbestos dust was created. As mentioned above at paragraph [12], Dr Henderson initially thought that the pursuer had not received sufficient exposure to asbestos to develop asbestosis but changed his mind; he did so because he had become aware of cases where the levels of asbestos exposure were less than the classic cases but asbestosis developed. In cross-examination he stated (page 74) that, with passage of time, he had seen evidence that undermined his original opinion; he had seen cases similar to the present in which there had been an expert review of the likely fibre load which concluded that the asbestos level was enough to cause asbestosis. Although there had not been any such analysis in the present case, Dr Henderson stated "I am not certain that I would re-endorse my own earlier opinion that the exposure has not been sufficient enough". On that basis Dr Henderson thought that the pursuer had had a sufficient level of asbestos exposure, and would adhere to that view unless contradicted by an expert on the subject. The cases relied upon by Dr Henderson were not specified; by contrast, in the standard textbook, W.R. Parkes, Occupational Lung Disorders, 3rd edition, 1994, detailed studies of cases are discussed and thresholds of exposure are set out.

[18 ] In his report of October 2005 (No 26/17 of process) Dr Crompton recorded the occupational history that had been given to him by the pursuer. In relation to the period of employment with the first defenders, he noted

"During this period he worked in the engine rooms of ships which were being refitted. Frequent exposure to lagged pipes etc. Occasionally worked alongside laggers".

In relation to the period of employment with the predecessors of the second defenders, Dr Crompton noted that "Asbestos blankets were frequently frayed and shed dust". In relation to Braehead Power Station, Dr Crompton noted that asbestos was stored in drums, which frequently broke. It had been assumed that asbestos dust had been disturbed by pigeons in the building. In his diagnosis in the report, he noted the history of asbestos exposure as a point in favour of a diagnosis of asbestosis, but he thought that it was outweighed by other matters. When Dr Crompton gave evidence, however, the pursuer's evidence as to his occupational history was put to him (day 3, 2.11), and he concluded that the level of exposure was not sufficient to support a diagnosis of asbestosis. He stated (day 3, 2.52) that a person who had worked as a lagger, mixing asbestos paste all the time, could get asbestosis after one year's exposure. Someone working alongside a lagger would usually take at least five years of daily exposure. The pursuer, however, had experienced intermittent exposure, not heavy exposure. Dr Crompton would expect greater exposure than the pursuer had described if he were to get asbestosis. In his report he had assumed greater exposure than had been suggested by counsel on the basis of the pursuer's evidence. Dr Crompton further accepted that the severity of asbestosis generally depends on the amount of exposure; according to the literature there was a definite relationship between the cumulative dose of asbestos and the severity of the disease, and also a relationship between the level of exposure and the time taken to develop the disease. In general, I think that it is fair to say that Dr Crompton's views were in accordance with the standard literature.

[19 ] In cross-examination (day 4, 12.00) Dr Crompton adhered to the view that, given the pursuer's degree of exposure to asbestos, it was unlikely that he had asbestosis. The pursuer's exposure had not been anything like a person working alongside laggers, where five years' exposure could be enough to produce asbestosis. It was suggested that the asbestos given off by blankets when the pursuer was working for Stewarts & Lloyds and British Steel would produce exposure similar to a person working alongside laggers; Dr Crompton responded that that might be so if one can say that there was exposure to asbestos every time a blanket was used, but he had assumed that a new blanket was unlikely to give of much asbestos. It was then suggested that the blankets deteriorated rapidly, in periods ranging from days to a week or two; Dr Crompton responded that, if new asbestos blankets were hazardous as soon as they were used, the position would be similar to a person working with a lagger; if not, the positions were not comparable. In re-examination (day 4, 3.39) Dr Crompton was asked how often he envisaged frayed blankets being used. He replied that he had not envisaged that they had been used every day; exposure would occur when blankets were near the end of their lives. He was asked his view on exposure if the blankets were replaced once every one or two weeks, and he replied that he had assumed the blankets would be replaced every few weeks; in other cases that he knew about blankets had been used for months, and problems had arisen there.

[20 ] My opinion of the pursuer's evidence is that the exposure produced by the blankets was not the same as a person working alongside a lagger. The pursuer's description of his working conditions at Tollcross was significantly different from his description of conditions in the engine rooms of ships; while conditions were clearly trying at Tollcross, and there was some asbestos exposure, it was plainly not of the same level. Moreover, there was no suggestion in evidence that asbestos blankets were dangerous as soon as they were used; it seemed clear from the pursuer's evidence that it was when the blankets deteriorated that asbestos was given off. That accords with Dr Crompton's position in re-examination. Overall, I am of opinion that Dr Crompton's final position, that it was unlikely that the pursuer would have developed asbestosis on the degree of exposure described by him, was in accordance with the pursuer's evidence.

Radiological examination

[21 ] The pursuer was the subject of a number of x-rays and CT scans. Chest radiographs (x-rays) were taken at the Western Infirmary on 29 June 1999, 23 May 2002 and 6 April 2005. CT scans were performed on 22 August 2002 at Gartnavel General Hospital and on 23 May 2005 at the Golden Jubilee Hospital.

[22 ] The radiological evidence was reviewed by Dr Sproule. In a report dated 17 August 2005, relating to the two CT scans dated 22 August 2002 and 23 May 2005, he concluded that in both hemithoraces, particularly posteriorly and in the paravertebral regions, there were focal areas of pleural thickening which were entirely consistent with parietal pleural plaques due to previous asbestos exposure. In the sub-pleural parenchyma in the mid and lower zones there were opacities and a reticular abnormality, together with mild patchy ground-glass shadowing and honeycomb formation. Those findings were characteristic of lung fibrosis. Dr Sproule concluded that, given the presence of parietal pleural plaques due to previous asbestos exposure, those features were highly suggestive of asbestosis. He further concluded that there had been a modest progression in the severity of the lung fibrosis between 22 August 2002 and 23 May 2005. It is apparent that the existence of pleural plaques, which Dr Sproule thought indicative of asbestos exposure, was an important part of his reasoning. In evidence Dr Sproule stated (day 2, 11.38) that the distribution of abnormalities was predominantly in the subpleura, in the mid to lower zones of the lungs. That pattern was found in both asbestosis and CFA. There was an unequivocal fibrosis, but no reliable means of distinguishing asbestosis and CFA. The ground glass opacity was common in CFA but occurred "not infrequently" in asbestosis. The parenchymal bands were the opposite. His conclusion (11.46) was that the most useful indicator was the presence or absence of pleural plaques. Those indicated asbestosis. They were not conclusive, but they were strongly suggestive. So far as progression of the disease was concerned, Dr Sproule would describe the progression as "moderate". That did not help to discriminate between the two conditions; it was slow for CFA but fast for asbestosis. The scans did, however, show unequivocal evidence of the progression of the condition. In cross-examination (2.52) Dr Sproule adhered to the view that the most useful indicator for asbestosis in the pursuer's case was the existence of pleural plaques. Statistically, no other factor discriminated as well as pleural plaques. That was so even though asbestosis and pleural plaques involve different processes from each other.

[23 ] Dr Turnbull reviewed all of the material referred to in paragraph [21] above. In a report dated 26 May 2006 (No 26/14 of process) he indicated that the radiographs of 29 June 1999 and 23 May 2002 indicated that the lungs were clear and that there were no pleural abnormalities. The radiograph of 6 April 2005 indicated bilateral mid and lower zone reticular interstitial opacifications, more marked to the left. The CT scan of 22 August 2002 indicated patchy area as of "ground glass" opacification and bilateral mixed intralobular interstitial and interlobular septal thickening in a predominantly posterior subpleural distribution with bibasal fine honeycombing, most marked in the lower lobes but also involving the upper lobes. These changes were more extensive in the right lower lobes. There was associated mild bilateral posterior pleural thickening. There were no pleural plaques and no pleural calcification. The CT scan of 23 May 2005 also indicated patchy areas of "ground glass" opacification, together with septal thickening and honeycombing, most marked in the lower lobes but also involving the upper lobes. These changes were much more extensive than on the previous examination both in distribution and in depth. The associated mild bilateral posterior pleural thickening persisted unchanged from the previous scan but was less obvious. Once again, there were no pleural plaques and no pleural calcification. Dr Turnbull's opinion, as expressed in his report, was that on the balance of probabilities the changes that he noted were typical in their appearance, distribution and speed of progression with idiopathic pulmonary fibrosis (CFA). There was no radiological evidence of previous asbestos exposure, with no pleural plaques or pleural calcification. The rate of progression of the pulmonary fibrosis over three years from 2002 to 2005, with a normal chest radiograph in 1999, was not typical of asbestosis.

[24 ] In the course of his evidence in chief (day 3, 12.05-12.14), on being referred to the CT scans of 2005, Dr Turnbull pointed out that the abnormalities in the lung had moved higher than in previous scans. The fibrosis had become greater, extending over more of the pleural surface, and had a greater depth, especially on the left side. The "ground glass" phenomenon, which is typical of CFA, was apparent, and had progressed since 2002. Honeycombing was also apparent, and was more extensive latterly in the 2005 scan. Thus in both extent and appearance the fibrosis had progressed. Dr Turnbull went on (day 3, 12.24) to state that he remained of the opinion expressed in his report No 26/14 of process. Counsel them put to Dr Turnbull the possibility that he was wrong in his interpretation of the pleural thickening observed in the lungs, which he thought was not connected with asbestos related pleural plaques; on that basis Dr Turnbull was asked whether it would follow that the pulmonary fibrosis seen in the CT scans was asbestosis. Dr Turnbull replied in the negative. First, the progression of the pulmonary fibrosis was relatively rapid compared with asbestosis. Secondly, the ground glass appearance was uncommon with asbestosis. Thirdly, the distribution of the pulmonary fibrosis, especially in the upper lobes, was uncommon with asbestosis.

[25 ] Dr Turnbull's final view was that the pursuer displayed pleural thickening associated with pulmonary fibrosis, in such a way that the fibrosis caused the thickening. He pointed out irregularities in the lung that seemed close to the pleura (day 5, 2.12, 2.38). Dr Sproule had referred to images in the CT scans where there was not this sort of association (in particular at images D2 13 and 17 in the 2002 scan and image 83.15 in the 2005 scan); in these cases there was pleural thickening but the adjacent lung was normal. In these cases (day 2, 11.37) Dr Sproule thought that the pleural thickening was due to a true pleural disease rather than any problems within the lung itself. Dr Turnbull (day 3, 11.16, 12.23) thought that there was disturbance in the lung on a repeated basis close to the pleura. On this particular matter I find it difficult to prefer one witness to the other; both witnesses gave convincing explanations of their respective views, and I do not think it appropriate to form my own view based on examination of the scans. This does not, however, affect my view of the other evidence, discussed in the preceding paragraphs.

[26 ] Dr Crompton, although not a radiologist, commented on the radiological evidence. In my opinion he was well qualified to do so, because much of the work of a specialist in respiratory diseases involves an understanding of x-rays and CT scans; these form an important part of the primary material with which such a specialist must work. In his report of October 2005 (No 26/17 of process) Dr Crompton noted that a point in favour of a diagnosis of asbestosis was the CT scan evidence of subpleural interstitial pulmonary fibrosis in the lower lobes of the pursuer's lungs. In evidence (day 3, 3.06) he qualified this by pointing out that CFA usually starts in the lower zones of the lungs but nearly always progresses upwards to the higher lobes. Asbestosis, by contrast, starts in the lower zones but rarely progresses to the higher lobes. In the present case such progression to the higher part of the lungs was observable. In favour of a diagnosis of CFA, Dr Crompton relied on the presence of ground glass appearances in the CT scan of 2002. In evidence (day 3, 3.10) he stated that this feature was highly indicative of CFA rather than asbestosis. CFA involves inflammation and fibrosis of the interstitial parts of the lung and the air spaces. The ground glass feature is a measure of the degree of inflammation present. In evidence (day 3, 2.46) Dr Crompton referred to the fact that in the 2005 CT scan shadowing could be seen in the upper zones of the lungs. He described this as highly significant for clinicians; in Parkes on Occupational Lung Disorders (cited above) it was stated that if pulmonary shadowing of this type is found above the middle of the mid zone or in the upper zone of the lungs there was no asbestosis. That statement in Parkes was perhaps rather dogmatic. Nevertheless, shadowing could be seen in all zones by 2005, and that included parts of the lung that one would not expect asbestosis to affect. Dr Crompton also stated that the 2005 CT scan indicated a rapid deterioration from 2002; I deal with this part of his evidence at paragraphs [29]-[30] below.

Rate of progression of disease: radiological examination

[27 ] It was a matter of agreement among the expert that the progression of CFA is markedly faster than that of asbestosis. The progression of the disease can be observed in three respects: through the radiological examination of the patient's lungs; through lung function tests; and by observation of the patient's general condition.

[28 ] So far as radiological examination is concerned, Dr Turnbull considered that the speed of progression revealed by the CT scans of 2002 and 2005 was an indication of CFA rather than asbestosis. Dr Sproule accepted that the two scans showed unequivocal evidence of progression (day 2, 11.49), but would describe the progression as moderate. In distinguishing the two conditions this progression was unhelpful; it was slow for CFA but fast for asbestosis. He came down in favour of asbestosis because of the existence of pleural plaques. I found that Dr Turnbull was able to point out very clearly the areas where progression had occurred, and he impressed me as confident in his opinion. On this matter, accordingly, I am inclined to prefer his evidence.

[29 ] In his report of October 2005 (No 26/17 of process) Dr Crompton relied on the rapid progression of the interstitial pulmonary fibrosis as a point favouring a diagnosis of CFA. In evidence (day 3, 3.12) he gave a detailed explanation of the typical progression of the two diseases, CFA and asbestosis. Asbestosis generally progresses very slowly; in Parkes on Occupational Lung Disorders (cited above) it was indicated that in the past the disease had taken between 15 and 35 years to progress. The rapidity of progression could depend on the level of exposure. In this case the rate of progression was somewhere in the middle of the range. The x-rays taken in 2002 and 2005 indicated quite rapid development; that in 2002 was normal, whereas that in 2005 indicated that the mid zones of the lungs were affected. (It should be noted that the degree of detail in x-rays is different from that in CT scans; x-rays show gross abnormalities, and they cannot be directly compared with CT scans). The progression was not as rapid as some cases of CFA, but in Dr Crompton's opinion the progression was more rapid than any patient with asbestosis that he had seen. Dr Crompton also pointed out (day 3, 2.42) that the 2005 x-rays indicated shadowing in the mid as well as lower zones. This could be seen more extensively in the CT scans of comparable date. In 2002, by contrast, there was no evidence of gross abnormalities on the x-rays, and the CT's revealed abnormalities only in the lower zones of the lungs.

[30 ] This aspect of Dr Crompton's evidence was taken up in cross-examination (day 4, 3.19). Dr Crompton refused to accept the proposition that the pursuer had pleural plaques and had not shown any significant progression clinically or on lung function tests, and only moderate progression on CT scans. He stated that the x-rays were to the contrary; the x-rays in 2002 were normal, but they were grossly abnormal by 2005. Dr Crompton illustrated this by reference to the actual x-rays, in a manner that I found easy to follow.

[31 ] Dr Henderson agreed that the rate of progression of the disease is an important indicator as between asbestosis and CFA. On the interpretation of the CT scans, he indicated that he would defer to the views of radiologists (page 45). He accepted that there had been some progression between the two CT scans (pages 48, 65), but had difficulty in comparing them because the scans were of a different nature from each other. He did, however, indicate that on the basis of lung function tests the disease had not progressed greatly over a period of four years (page 49); this was one of the more crucial things in his analysis of the case. It is perhaps fair to say that Dr Henderson attached less importance to the rate of progress of the disease than Dr Crompton or Dr Turnbull. He dealt with this matter in cross-examination (pp 90-92), where he pointed out that the extent to which the condition progressed might depend upon the stage at which it was diagnosed; if diagnosis occurs early progression will be noticed, even with asbestosis. Consequently he did not accept a statement in Parkes on Occupational Lung Disorders that with asbestosis the progression is very slow or absent. I find Dr Henderson's point about the time of diagnosis understandable; if progression occurs, the amount of progression that is observed must depend on the stage at which diagnosis takes place. In this part of his evidence, however, it seemed to me that Dr Henderson was confusing the fact of progression with the speed of progression. The critical point made in Parkes, and emphasized by both Dr Crompton and Dr Turnbull, is that CFA progresses much more quickly than asbestosis. On assessing the expert evidence as a whole, I am bound to say that I prefer the views of Dr Crompton and Dr Turnbull on the significance of the speed of progression of the patient's condition in distinguishing between asbestosis and CFA. I found both of them to be clear and convincing witnesses who were obviously totally familiar with their areas of expertise, and both gave evidence in a very fair manner.

Rate of progression of disease: lung function tests and observation of patient

[32 ] A major part of the pursuer's complaints was breathlessness; this clearly caused him serious difficulty, and was the main reason for his being unable to continue working. His impression, as stated in cross-examination, was that the breathlessness was becoming worse (date 1, 3.14). Dr Crompton pointed out (day 3, 3.20) that it was difficult to assess the pursuer's respiratory functions because he had hyperventilation as a major cause of his breathing problems; this was anxiety-related over-breathing. That type of hyperventilation is usually associated with pins and needles and dizziness, as was reported in the pursuer's case. In addition, he had a history of anxiety. It seemed to me that Dr Crompton's views on this matter were justified.

[33 ] It was accordingly necessary to make use of lung function tests in order to assess the pursuer's ability to breathe. These took the forms described in paragraph [14] above. Such tests were carried out on the pursuer on a number of occasions. Dr Crompton, in a report dated 26 May 2006, commented on tests carried out between July 2002 and August 2005. These indicated that there was no evidence of airways obstruction. They did not confirm the deterioration that appeared to be clear on the CT scans. Dr Crompton was unable to explain this feature. He did, however, state (day 3, 3.42) that the lung function tests are a less sensitive measurement of pulmonary lung disease than CT scans. He also pointed out that, in relation to the principal lung function test that is used, spirometry, it is often difficult for patients to co-operate, in breathing out fully or breathing quickly. It had been noted that the pursuer had problems with the spirometer. In general, he thought that spirometry was of very limited value in the assessment of restrictive lung disease. Other tests were more useful. Dr Crompton had also examined the data from tests carried out in February 2004 and June 2006 (Nos 6/10, 26/15 (appended documents) and 26/18 of process). The comparison of these tests, in particular the plethysmography tests, showed a deterioration of 17% in total lung capacity and the deterioration of 25% in residual volume. Dr Crompton described that as "quick" (day 3, 3.49).

[34 ] Dr Crompton was also referred to a brief report by Dr Henderson dated 19 June 2006. In this report Dr Henderson noted that the pursuer had had full lung function tests on 1 June 2006, and stated that the results indicated that the pursuer had a significant physiological deficit, which was definitely a cause of disability. Dr Henderson assessed the disability at 25% due to interstitial lung disease, but pointed out that the actual disability was greater because of hyperventilation. This report was put to Dr Crompton, and he was asked about its significance, ignoring the evidence from CT scans. Dr Crompton stated that the pursuer had shown a marked physiological deterioration between late 2001 and June 2006. He thought that that was too rapid for asbestosis, but it fitted perfectly well with a diagnosis of CFA (day 3, 3.59). In my opinion that view is significant, because it is based on evidence independent of the radiographic evidence, but confirms the results that Dr Crompton derived from the x-rays and CT scans.

[35 ] Dr Henderson placed considerable emphasis on the fact that the measurements based on spirometry did not appear to have become worse (pp 29, 50, 92, 102). Dr Henderson did accept, however, that the pursuer had found it difficult to do the spirometry tests (page 32). In my opinion the spirometry evidence is of limited value in this case, both because of its inherent unreliability as described by Dr Crompton and because of the pursuer's failure to co-operate fully with the tests. Thus Dr Henderson's evidence is open to some degree of criticism because of his considerable reliance on the spirometric tests. In addition, it can be said of Dr Henderson that he did not fully address the apparent deterioration shown by the plethysmography tests carried out in June 2006 (pp 101-103, in cross-examination). In my opinion these tests are significant, for the reasons stated in the last paragraph.

Conclusions on diagnosis

[36 ] It is nearly always difficult to decide between the views of eminent medical experts. That is especially so where, as in the present case, they gave their evidence in a moderate and reasoned fashion, and appear to have a genuine disagreement as to the pursuer's diagnosis. I have nevertheless come to the conclusion that a diagnosis of CFA must be preferred to a diagnosis of asbestosis. I reach this conclusion for a number of reasons. In the first place, it seems to me that the pursuer's exposure to asbestosis was not particularly great, and was certainly not of the order that is typically associated with asbestosis. Dr Henderson's eventual diagnosis of asbestosis was based to a significant degree on the view that cases of asbestosis have been noted where the degree of exposure was less than in the classic cases: see his report of 20 March 2006, No 6/8 of process. I do not doubt that such cases have been observed, but it seems to me that there is a logical flaw in the reasoning at this point. The fact that some cases of asbestosis have been observed where the exposure was less than the classical cases does not mean that such cases are common. The evidence of Dr Crompton, which was amply supported by Parkes on Occupational Lung Disorders, was that the likelihood of asbestosis is normally proportionate to the level of exposure. The existence of exceptions does not invalidate this as a general proposition. Consequently I think that the levels of exposure to which the pursuer was subjected must inevitably be a factor tending against a diagnosis of asbestosis.

[37 ] In the second place, I consider that the radiological evidence, as spoken to by Dr Turnbull in particular, favours a diagnosis of CFA. Dr Turnbull was supported in this respect by Dr Crompton. The appearance of the x-rays and CT scans tended to support CFA, especially the appearance of "ground glass" opacification and the progression of the fibrosis into the upper zones of the lung. Dr Sproule relied in particular on the existence of pleural plaques and the appearance of calcification as supporting a diagnosis of asbestosis. For reasons discussed in the immediately following paragraphs, I am not persuaded that either of these features has been made out. In the third place, I am of opinion that the speed with which the fibrosis has progressed points rather strongly in favour of CFA. That is especially apparent on the radiological evidence, both x-rays and CT scans. This was spoken to very clearly by Dr Turnbull and, making allowance for the fact that he is not a radiologist, Dr Crompton. I accept their evidence on this matter, and I consider that evidence to be of critical importance. The speed of progression is less supported by the lung function tests, especially the spirometry tests. The evidence from the lung function tests was relied upon by Dr Henderson, who pointed out (page 49) that the spirometry had been virtually identical between 2002 and 2006; consequently the disease had not progressed a lot over a period of four years. Other evidence, however, especially that of Dr Crompton, tended to indicate that spirometry is not the most accurate of tests, and the pursuer had difficulty in carrying out the tests properly. By contrast, the plethysmography tests tended to indicate a substantial deterioration, which Dr Crompton considered pointed towards CFA. Moreover, on an assessment of the evidence as a whole, it seemed to me that the evidence available from x-rays and CT scans was likely to be more reliable than that derived from lung function tests; that was the view adopted by Dr Crompton, and I adopt his evidence on this point. Overall, I consider that the evidence on the speed of progression of fibrosis clearly favours a diagnosis of CFA.

Pleural plaques

[38 ] Dr Sproule relied on the existence of pleural plaques as an important marker of asbestosis. In addition, the pursuer has a separate claim in respect of pleural plaques. It is accordingly necessary to consider whether he does in fact have pleural plaques as a result of asbestos exposure during his periods of employment with the defenders. All of the expert witnesses accepted that the pursuer suffered from considerable pleural thickening. They disagreed, however, as to whether pleural plaques existed. Dr Sproule indicated what he considered to be pleural plaques in the scan carried out on 23 May 2005; these were found in images 83.15 and 118.15 (day 2, 12.12). Dr Henderson accepted that there was diffuse pleural thickening, but described it as "not classically that of a plaque" (page 68); he later stated that he did not say that these were classic textbook plaques, but he thought that there was asbestos-related thickening (page 84). Dr Turnbull, when referred to the high-resolution CT scan of 2005, disagreed that there was any pleural plaque visible (day 3, 12.04). In his report (No 26/14 of process) Dr Turnbull reviewed the CT scans of 2002 and 2005, and concluded that there was no radiological evidence of previous asbestos exposure, with no pleural plaques or pleural calcification visible in either scan. He maintained that view in cross-examination. He was referred (day 5, 3.00) to certain images in the 2002 CT scan (D2 12, 13, 14, 17), and asked whether they demonstrated a classic pleural plaque. He replied in the negative; he explained that a plaque has a rounded edge at its junction with the lung, whereas the feature shown in those images tapered off. In re-examination (day 5, 3.35) he developed his answers, he stated that pleural plaques are usually separate areas, rarely more than 3 cm in length or width; usually plaques are greater than 3 mm in depth into the lung, and the edges are usually rounded and smooth. Pleural thickening is different; it usually tapers rather than being rounded at the edge. In the present case the individual areas of pleural thickening did not have rounded edges, and were tapered. Dr Crompton stated (day 3, 2.40) that he could not see evidence of pleural plaques. He explained that pleural plaques are easily visible, rather like crazy paving on a lawn with grass in between. Pleural thickening is less defined. In the pursuer's case, he did not think that there were pleural plaques. I found Dr Turnbull's evidence convincing, both generally and on this matter. He is and extremely experienced radiologist, and I do not think that I can disagree with his evidence on the basis of my own inspection of the CT scans and other radiological evidence. Moreover, Dr Turnbull's opinion derives some support from Dr Henderson on this point, and considerable support from Dr Crompton. In the circumstances I conclude that it has not been proved that the pursuer has any pleural plaques, although he does have areas of diffuse pleural thickening; Dr Turnbull, Dr Crompton and Dr Henderson all accepted the latter point.

[39 ] Dr Sproule stated (day 2, 11.15) that the calcification of pleural plaques may be significant. He stated that, if multiple or focal areas of calcified pleural thickening are found, that is virtually pathognomic of parietal pleural plaques due to asbestos exposure. Dr Turnbull (day 3, 3.45) accepted that if calcification is found that tends to be associated with asbestos exposure, especially if the calcification is multiple or bilateral. He was then asked about the significance of the absence of pleural calcification. He stated that it is now possible, using scans, to pick up tiny bits of calcification; in persons with occupational exposure to asbestos who have pleural plaques it is very unusual not to pick up some of these. In the present case, however, he had detected no calcification. In re-examination (day 5, 2.40) Dr Turnbull stated that, where there had been significant occupational exposure to asbestos he would expect floral changes to show calcification of modern CT scans, at least in most cases. In the present case, however, calcification was not visible. As mentioned in the last paragraph, I have concluded that it is not been proved that the pursuer suffered from pleural plaques. Once again, I do not think that I can disagree with Dr Turnbull's evidence on the basis of my own inspection of the CT scans. Consequently I conclude that it has not been proved that calcification was visible on the pursuer's scans.

[40 ] The fact that the pursuer suffers from pleural thickening is not in my opinion significant. There was no evidence that pleural thickening to the extent visible on the pursuer causes symptoms; that was accepted by Dr Henderson (page 69) and by Dr Crompton.

Damages

[41 ] For the reasons stated above, in particular at paragraphs [36] and [37], I am of opinion that it has not been proved that the pursuer suffers from asbestosis. Similarly, for the reasons stated at paragraph [38], I am not persuaded that he suffers from pleural plaques. I must accordingly assoilzie the defenders. In case that is later held to be incorrect, however, I must now consider the level of damages that would have been awarded had the pursuer's case been made out.

[42 ] A number of matters relating to damages were agreed in a joint minute. It was agreed in particular that the pursuer retired on medical grounds on 8 February 2003. It was agreed that between 8 June 2002 and 1 February 2003 the pursuer lost earnings amounting to £1,400, and that between 1 February 2003 and 6 April 2005 he lost earnings amounting to £23,600, a total loss of £25,000. It was further agreed that the pursuer makes no claim for loss of pension rights.

[43 ] That leaves the question of solatium. The pursuer was clearly disabled. Dr Henderson suggested (page 99) that the pursuer was 25% disabled as a result of interstitial lung disease. Dr Crompton indicated (day 3, 3.58) that the pursuer's physiological deficit was at least 25%. It was not in dispute that there was a psychogenic component in the pursuer's disability. This resulted in his regarding himself as more disabled than he would otherwise be. It seemed to me, however, that this was a genuine response by the pursuer to the situation in which he found himself. The medical records indicated that he was anxious by nature. Moreover, it was clear both from the medical records and from the pursuer's own evidence that he was severely upset and depressed when he had to stop work. For this reason I am of opinion that there is a connection between the pursuer's physical condition, in particular his disablement, and his psychogenic problems. This is essentially a case of taking the victim as one finds him. Consequently I consider that the whole of the pursuer's disability must be taken into account.

[44 ] The solicitor for the pursuer submitted that an award of £45,000 would be appropriate by way of solatium. He referred to the guidelines issued in England by the Judicial Studies Board, which indicated arrange of figures between £26,500 and £58,000, with an indication that respiratory disability of between 10 and 20 per cent will probably attract an award in the region of £40,000. I was also referred to a number of cases, of which the following appear to me to be useful indicators of the appropriate level of award. In McKenzie v Barclay Curle Ltd, 2002 SLT 649, Lady Paton awarded solatium of £35,000 (worth £40,115 at the date of proof) to a man of 61 who suffered from asbestosis and other conditions. The pursuer was held to suffer from a 50 percent disability, half of which was attributable to asbestos-related conditions. In Kerr v Newalls Insulation Co Ltd, 1997 SLT 723, Lord Hamilton awarded solatium of £32,500 (worth £42,313 at the date of proof) to a man of 58 who suffered from asbestosis. His total disability from all causes was assessed at 50 per cent, of which 30 per cent was attributable to the asbestosis. The asbestos-related complaints consisted of breathlessness and a serious restriction of his range of abilities. The case is of interest for present purposes because the pursuer was of a nervous disposition, and that had exacerbated his symptoms; the psychological component was, however, regarded as part of the consequences of asbestosis. That is in accordance with the view that I have taken in the last paragraph. Reference was also made to Stanners v Graham Builders Merchants Ltd, 1995 SLT 728, where Lord Morton of Shuna would have awarded solatium of £30,000 (worth £40,931 at the date of proof) for lung fibrosis, had it been asbestosis; a fairly broad brush approach was taken in that case. In Myles v Glasgow District Council, 1994 SCLR 1112, Lord Abernethy awarded solatium of £27,000 (worth £37,169 at date of proof) for asbestosis causing a disability of approximately 25%. In McKenzie v Cape Building Products Ltd, 1995 SLT 695, affirmed 1995 SLT 701, Lord Penrose awarded solatium of £25,000 (£35,750 at the date of proof) for asbestosis which caused breathlessness. The breathlessness inhibited the pursuer's ability to work but did not amount to a material incapacity.

[45 ] Counsel for the pursuer submitted that an award in the range of £25,000 to £30,000 would be appropriate as solatium. He pointed out that in McKenzie v Barclay Curle Ltd the pursuer was younger than the present pursuer, and the Lord Ordinary pointed out that the degree of disability was particularly severe. In Kerr, the pursuer was younger, and had a relatively high (10%) risk of contracting lung cancer; in the present case that risk was assessed at 5 per cent. In Stanners the pursuer's life expectancy was only five years, and consequently the case seemed rather more serious than the present. In Myles the symptoms were, it was submitted, not dissimilar to the present case; if anything they were less severe. The pursuer was, however, younger. In McKenzie v Cape Building Products Ltd, the pursuer was younger than the present pursuer, and his risk of lung cancer was 10%. The fibrosis was progressive. In the Inner House the award of £25,000 was said not to the wholly unreasonable; I note that the Lord Justice Clerk stated that it fell comfortably within the range of awards cited.

[46 ] In all the circumstances I am of opinion that an appropriate award of solatium would be £38,000. The present case appears to me to be somewhat more serious than McKenzie v Cape Building Products Ltd, where the pursuer did not suffer from a material incapacity. I think that the awards made in McKenzie v Barclay Curle Ltd and Kerr provide a reasonably good guide. In the former case the disability attributable to asbestos-related conditions was assessed at 25 per cent, and in the latter case at 30 per cent. In the present case the level of disability is assessed at 25 per cent or slightly greater. The pursuer is, however, slightly older than the pursuers in those cases, and I have taken that into account. In the present case there is no loss of life expectancy. I would accordingly have attributed one-third of the solatium to the past, and would have awarded interest at 4 per cent per annum from 1 January 2002, the approximate date when the pursuer's problems started, to the date of the award, and interest at the rate of 8 per cent from the date of decree. So far as earnings loss is concerned, I would have awarded interest at the rate of 4 per cent per annum from 8 June 2002 on £1400 and the same rate from 1 February 2003 on £25,000. Those rates would have continued until 6 August 2005, immediately before the pursuer gave up work; interest of 8 per cent would have been awarded thereafter. Finally, I should note that it was agreed that, if any award were made, it should be divided among the defenders in the following proportions: 2.5 per cent against the first defenders, 82.5 per cent against the second defenders and 15 per cent against the third defenders.

[47 ] For the reasons stated above, however, I will assoilzie the defenders from the conclusions of the summons.

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	Scottish Court of Session Decisions
You are here: BAILII >> Databases >> Scottish Court of Session Decisions >> Timms v Barclay Curle Ltd & Ors [2007] ScotCS CSOH_166 (05 October 2007) URL: http://www.bailii.org/scot/cases/ScotCS/2007/CSOH_166.html Cite as: [2007] CSOH 166, [2007] ScotCS CSOH_166

Scottish Court of Session Decisions