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	Scottish Court of Session Decisions
You are here: BAILII >> Databases >> Scottish Court of Session Decisions >> McConnell v British Shipbuilders & Ors [2000] ScotCS 148 (6 June 2000) URL: http://www.bailii.org/scot/cases/ScotCS/2000/148.html Cite as: [2000] ScotCS 148

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[1] The pursuer, Mr McConnell, retired in May 1993 at the age of 60 after a lifetime of work as a marine engineer. He began his apprenticeship as a fitter in Scotts' shipyard in Greenock in 1949 when he was fifteen years of age. Thereafter he worked as a sea-going engineer for a number of merchant companies before joining the public service in the employment of the Ministry of Defence. Throughout his working life he was exposed to asbestos dust and fibres. British Shipbuilders, the first defenders, Cory Ship Towage (Clyde) Limited, in liquidation, and the company's official liquidator, the seventh defenders, and the Lord Advocate, representing the Ministry of Defence, the eighth defenders, admit that they were negligent in exposing Mr McConnell to asbestos dust and fibres during his periods of employment with them respectively. Mr McConnell developed serious lung disease. The main issue between the parties at proof was whether it had been established that he contracted asbestosis. The defenders contended that he suffered from emphysema.

[2] During his apprenticeship Mr McConnell worked beside other employees of Scotts who applied asbestos insulation during the assembly of marine engines. The insulation used varied in form. There were pre-formed sections for the insulation of pipe work and other components. Asbestos sheeting was used on flat surfaces. Asbestos paste, made from a mixture of fibre and water, was applied at joints and to certain irregular surfaces. Cutting of pre-formed sections, the repeated application and removal of sections, and the mixing of paste all produced quantities of particles which circulated in the space in which Mr McConnell had to work. As a sea-going engineer he required to carry out on board maintenance and repair work which often involved the removal and replacement of insulation. These operations produced air-borne particles. He often required to work in confined spaces where there was little airflow and consequently more prolonged exposure. In his employment with the seventh defenders he worked in the engine rooms of tugs where there was little space. In his employment with the Ministry of Defence he often worked in small compartments in the hulls of submarines. It was clear on the evidence, and it was not disputed by the defenders, that if Mr McConnell had contracted asbestosis that would have been consistent with the environmental conditions in which he worked. On the other hand, Mr McConnell was a heavy smoker from the age of sixteen. He stopped smoking in 1985. It was not disputed that the level of his smoking over that period could have caused emphysema which would not have been relieved by stopping smoking when he did.

[3] Mr McConnell was for most of his life an active man who enjoyed exercise in the open air. He kept fit. He began to notice shortness of breath early in 1990 when he was climbing ladders in the course of work or hill walking. But he had a complex history of chest problems that were investigated from time to time, apparently without definite diagnosis, and treated generally with antibiotics. He also had heart problems. He must have had tuberculosis in earlier life, from scarring identified on later x-ray examination. In 1952 he had pneumonia in the lower zone of his left lung. By 1953 he was aware of chest problems. In October 1953 he asked his General Practitioner to arrange for a chest x-ray. The x-ray was clear, as was a repeat x-ray in February 1954. He was examined again in April 1955. It was reported that there was no recent change and no evidence of significant disease in the lung fields. In August 1955 his chest was reported clear. In October 1966 it was reported following x-ray examination that there was evidence of some bronchitic changes only. In September 1975 he had heart problems. It was recorded at that time that there was a family history of early coronary deaths. In November 1977 he had further chest x-ray examination on the visit of an R.A.M.C. mass x-ray team. It was reported that there were opacities at the apices of both lungs. He was examined at Inverclyde Royal Hospital, Greenock. It was reported that his heart was not enlarged. There was some scarring in both upper lung zones, especially on the left, but there was no active lung disease. The report was interpreted as clear. In April 1980 he reported that he had been feeling tired for a year. In May he was referred to Dr Semple's chest clinic at Inverclyde. In January 1981 he reported night sweats and was again referred to the chest clinic. In December 1981 he complained of a dull ache in the right lower chest which was worse on deep breathing. A chest x-ray was instructed. On 15 December it was reported that the chest x-ray was "basically" clear, with little change over the last eighteen months.

[4] Until early 1983 there had been no reference to asbestosis and none of the clinical signs of asbestos related disease had been noted. On 2 February 1983 there was a record in the General Practitioner's notes: "looks like clubbing". A further chest x-ray was ordered. On 4 February it was reported that the basal lung markings were slightly coarse suggesting early chronic bronchitic change. There was a small adhesion at the right costophrenic angle. More localised old scarring was seen in both upper zones. There was no active lung disease. On 9 February his General Practitioner noted finger clubbing. In July 1985 he was again referred to Dr Semple for review. At that time he reported that he could walk ten miles comfortably. He saw Dr Semple on 23 July. It was reported that all was well. During 1985 he suffered two inferior myocardial infarctions. Night sweats were reported in January 1986. An x-ray report on 29 July 1987 commented on basal bronchitic change with more localised old scarring at the extreme left base. There was no active lung pathology. In March 1993 it was reported that there had been no identifiable major change in appearance since 1987. In February 1994 he reported increased breathlessness. The possibility of emphysema was raised. Chest x-ray examination on 11 February was interpreted by his General Practitioner as "ok". The radiologist reported that there was no recent change in appearances and no acute lesion. There appeared to be emphysema and old scarring at the lung bases. It was noted that he reported having been exposed to asbestos most of his working life. Asbestosis was diagnosed by the Benefits Agency Medical Services in 1994. Following the report of that diagnosis he was again referred to the chest clinic in December 1994 for further examination. The General Practitioner's reference letter referred to exposure to asbestos. It gave an account of increasing breathlessness. There was an account of the findings of the Benefits Agency Medical Services in November. In March 1995 he reported continuing intermittent night sweats. In 1995 and 1996 asbestosis is mentioned in the records with little explanation if any. Throughout the period there were numerous biology and haematology investigations and reports.

[5] Mr McConnell was seen by the Benefits Agency Medical Services on 27 September 1994 following a claim for Industrial Disablement Benefit which he had submitted on the ground that he had contracted asbestos related prescribed disease. The results of the examination were reported in November 1994. The medical adviser, Dr Barton, reported that on chest examination he had found bilateral fine basal inspiratory crackles. On the right these occurred postero-laterally. On the left they were circumferential. They were accentuated by coughing. Chest x-ray examination showed some interstitial fibrosis. There was no bilateral diffuse pleural thickening. Lung volumes were normal, but gas transfer was moderately impaired at 64% of the predicted value. On the balance of probabilities asbestosis was diagnosed. Mr McConnell was examined for reassessment in October 1997. No finger clubbing was identified. There was no cyanosis. There were a few moderate crackles. There were basal interstitial fibres on x-ray examination. There was some increase in clinical signs of asbestosis and his disability assessment was increased.

[6] Inverclyde Royal Hospital reports on Mr McConnell reflected a somewhat confused picture. On 9 March 1993 it was reported that there was no objective evidence of ongoing angina, following examination. On 16 February 1995 Dr Semple reported that chest x-ray, in his view, showed minor fibrotic changes. There were no other features to suggest asbestos exposure such as pleural thickening or calcification. Nor could he find fine inspirational basal crackles. Mr McConnell's pulmonary function was, in Dr Semple's view, consistent with a minor restrictive defect rather than airways obstruction. On 10 October 1995 deep vein thrombosis was diagnosed. On 19 February 1996 Dr Semple reported that Mr McConnell was a bit more breathless that on previous examination. On this occasion he did hear some basal crackles. Further review following CT scan was promised.

[7] Dr Semple's senior house officer, Dr Rawstron, reported on 16 May. The CT scan had shown no evidence of asbestos related disease. He said that the overall appearances were consistent with honeycombing secondary to end-stage chronic obstructive airways disease, which was surprising in view of the documented restrictive lung defect with basal crackles. Further examination was proposed. Following discussion with Dr Semple, Dr Rawstron added a footnote to his letter which disclosed a degree of perplexity about the results. Dr Semple reported further on 6 June 1996. The material observations were contained in a post-script to his letter:

"COAD" was an abbreviation for chronic obstructive airways disease. Following exercise tests, Dr Semple reported further on 13 June that Mr McConnell was moderately severely impaired by breathlessness on exertion.

[8] On 10 July 1996 Dr Semple reported to Mr McConnell's solicitors on completion of his assessment. He commented:

[9] In February 1998 Mr McConnell had pneumonia followed by a lung abscess. He was admitted to Inverclyde Royal Hospital for seven to ten days and thereafter was treated with antibiotics for a period.

[10] Against the background of this history it was not surprising to hear conflicting assessments of Mr McConnell's condition. The tone of the evidence was surprising, however, and some of the opposing views were expressed aggressively and in an uncompromising manner which one might not have expected of wholly objective experts. Dr Semple was not available as a witness. Professor Anthony Seaton, Professor of occupational and environmental medicine at Aberdeen University, was firmly of the view that Mr McConnell had asbestosis and did not have significant emphysema. He was dismissive of the opposing view. Dr Moran, a retired consultant physician with a specialist interest in respiratory disorders, and Dr Mary Stevenson, a consultant radiologist, expressed the view that Mr McConnell was suffering from severe emphysema and did not have any significant degree of diffuse fibrosis such as might characterise asbestosis. From their respective points of view they were dismissive of Professor Seaton's opinions. In the end it appeared that Mr McConnell's signs and symptoms did not fall squarely within the textbook definitions of either of the principal diseases in contention. He displayed some signs consistent with each, and his principal symptom of breathlessness was consistent with each. The evidence of the medical witnesses fell into three main chapters: clinical examination, lung function tests and radiological examination. Professor Seaton and Dr Moran were taken through the medical records in considerable detail. This was an inconclusive exercise, and I shall not comment further on it than I have in narrating the contents of the records above.

[11] Professor Seaton summarised the classical features of asbestosis and of severe emphysema. Clinically, asbestosis was characterised by persistent, fine crackles at the bases of the lungs, heard on auscultation, during inspiration. Finger clubbing appeared in advanced cases. Radiological evidence included fibrotic changes in alveoli walls, pleural plaque and pleural thickening. Lung function tests showed abnormal reduction in diffusing capacity, that is the capacity of the lungs to transfer oxygen from inhaled air into the blood, usually associated with a reduction in total lung volume. An adequate history of exposure to asbestos was required. In cases of severe emphysema one found on clinical examination an over-inflated chest which moved poorly, and sounded quiet on auscultation. There were no crackles, and there was no finger clubbing. Radiological evidence included dark lung fields, attenuated blood vessels and thin walled bullae, generally in the upper parts of the lungs. In terms of lung function, there was airflow obstruction, and reduced diffusing capacity. Diffusing capacity was reduced in proportion to the reduction in forced expiration. According to his evidence differentiation was simple applying these tests. Dr Moran's evidence covered substantially the same topics. Generally he took a less simplistic view of the differentiation of the two diseases. He emphasised in particular the need to have regard to changes as the conditions developed. There were material differences between the two in relation to the interpretation of the radiological evidence and the results of lung function tests.

[12] Professor Seaton explained the clinical approach to the diagnosis of asbestosis as the identification of pulmonary fibrosis, characteristically in the middle and lower levels of the lungs, and less frequently in the apices, taken with an appropriate history of exposure, and the presence of other physical signs including finger clubbing, inspirational crackles on auscultation, and dysfunction of the lungs in terms of volume and diffusing capacity. Typically there was no interference with airflow. Dr Moran's selection of features of significance was not materially different except in relation to the importance of a history of exposure to asbestos. Many of the differences between the two were of emphasis, and in relation to the significance to be attached to the presence or absence of individual signs. But a number of serious differences of opinion emerged.

[13] Professor Seaton examined Mr McConnell on 28 August 1995. Dr Moran examined him on 8 July 1996 and on 9 October 1998. Their findings in relation to crackles on auscultation were discussed at considerable length. Professor Seaton explained that persistent inspirational basal crackles, due to abnormal opening and closing of small air-ways, were a clinical feature of asbestosis, but not of emphysema. They were found in association with other conditions, but none of these could be relevant in this case. In cross-examination he rejected the suggestion that smoking related diseases caused Mr McConnell's crackles. For example, Mr McConnell did not suffer from obliterative bronchitis in which crackles could be a feature. The features of crackles which he highlighted in Mr McConnell's case were persistence, tone and timing. Transient crackles might have no pathological significance. Mr McConnell's persisted despite tests. In asbestosis crackles were fine in tone. That test was satisfied. Timing was important. In asbestosis they occurred in the middle to the end of inspiration. Crackles on expiration were not relevant. In cross-examination he distinguished crackles associated with smoking related diseases such as bronchitis. In that disease one found early high-pitched inspirational crackles, but they were different in pitch, and could be identified at the mouth. There would be other signs and symptoms of bronchitis. He rejected emphatically the suggestion that the crackles heard in the bases of Mr McConnell's lungs could be due to anything other than pulmonary fibrosis.

[14] In Dr Moran's view, crackles heard in the lungs were almost always associated with an abnormality. One of the classic signs of asbestosis was a specific pattern of audible crackles. Fine crackles were similar to the sound produced by rubbing one's head hair between one's fingers. Coarse crackles had a sound similar to that produced by pouring milk over rice crispies. Medium crackles were somewhere in-between. It was a matter of experience and clinical judgment how one characterised the crackles heard in any given case. The characteristics of importance in asbestosis were that the crackles were fine, heard towards the end of the inspiratory cycle, absent from the beginning of that phase, and absent on expiration with the exception of any period at the start of expiration when the lungs still exercised elastic pull. In cases of advanced asbestosis one might hear crackles on expiration because of concomitant conditions. Crackles indicative of diffuse pulmonary fibrosis persisted from breath to breath and week to week. And they did not disappear on deep breath testing. If the crackles were not fine or tended to spill over into expiration they were not likely to be due to asbestosis. Mr McConnell's medical history indicated varying patterns of crackles. There was no evidence of persistent crackles. The crackles reported and found by him were of the wrong pattern. On first examination he found crackles which were not fine, but medium, evenly distributed and persisted throughout inspiration and into expiration. On re-examination he found scattered, scanty medium crackles at both bases on inspiration and medium to coarse crackles throughout inspiration at the lateral aspect of the left base. The crackles found by him and others were not consistent. On one occasion Dr Semple had found no crackles. And they were first identified long after the expiry of what would have been a reasonable interval from first exposure to asbestos. Crackles could and did occur in association with emphysema. In a case of pure emphysema the chest sounds were quiet. Crackles were not diagnostic of emphysema. But complications such as infection occurred, and in combination the conditions produced crackles.

[15] In Mr McConnell's records the possibility that there was finger clubbing was noted in February 1983. Professor Seaton and Dr Moran both found signs of the condition, though they disagreed on the extent of it. They agreed that finger clubbing was not diagnostic of asbestosis, though it was a characteristic of the disease. Its significance depended on the coincidence of other signs and symptoms. As a matter of degree, Dr Moran considered that the condition was present on balance and was only slightly developed. The angle between the nail and the nail bed had changed from natural. But the developed form, of a drumstick appearance, had not developed. It used to be thought a significant feature, but was now known to be associated with a wide range of diseases of the heart liver and lungs. It was most commonly now associated with lung cancer. The next category of association was diffuse fibrosis, and within that group with cryptogenic fibrotic alveolitis rather than asbestosis. Finally it was found in conditions of chronic lung infection comprising any form of chronic suppurative disease. Clubbing was not always a later manifestation of pulmonary fibrosis. In a proportion of cases of cryptogenic fibrosis it was the first sign of developing disease. It would be unwise to draw inferences from finger clubbing. Professor Seaton considered that Mr McConnell's finger clubbing was "definite". His view was that finger clubbing was usually only seen in advanced cases of pulmonary fibrosis. In association with crackles it was almost always diagnostic of pulmonary fibrosis. It could be found associated with emphysema, but it was not a feature of that disease. One would always look for a cause of the finger clubbing other than the emphysema. In cross-examination, he agreed that there were numerous causes of the condition. Chronic lung conditions such as cystic fibrosis might cause the condition. So also might a number of other conditions, none of which applied in this case. He was dismissive of most of the hypothetical cases put to him as "silly argument".

[16] Dr Moran reported finding probable faint central cyanosis caused by lower than normal blood oxygen levels. The finding was consistent with the results of lung function tests.

[17] Each of Professor Seaton and Dr Moran instructed out a series of lung function tests. There was a great deal of technical evidence about these tests which it is unnecessary to rehearse. They measured airflow, lung capacity, and diffusing capacity. Contrary to the recorded findings of the physicians at Inverclyde Royal Hospital, Professor Seaton and Dr Moran agreed that Mr McConnell did not suffer from chronic obstructive airways disease. They detected no airways obstruction. Airflow was normal on testing for forced vital capacity. Dr Moran repeated the tests after Mr McConnell had inhaled a bronchial dilator and found a degree of "bronchial lability" in the form of a minor improvement in airflow. This might indicate that despite the normal readings there was some degree of obstruction that was relieved by the dilator. However he did not suggest that this was a material consideration in the present case, and his evidence on the point appeared somewhat tentative. The experts agreed that Dr Semple's finding of chronic obstructive airways disease was wrong.

[18] Professor Seaton found that Mr McConnell's lung volume achieved about 80% of the value predicted in his case. Despite the shortfall Professor Seaton considered that total volume was around the norm for Mr McConnell's age and physique. He distinguished fibrosis, in which there was a tendency for lung volume to diminish, from emphysema in which the lungs might be increased in volume up to 120% of predicted. Dr Moran found lung volume to be normal on his first examination and slightly increased on second examination.

[19] The most contentious of the elements of these tests were diffusing capacity and its relation to total lung volume, the transfer coefficient. Professor Seaton explained that the development of fibrosis in the alveolar walls inhibited the absorption of oxygen by the blood. In severe cases the lungs might lose their spongy texture altogether. He found in September 1995 that Mr McConnell's diffusing capacity was 48% of predicted value. The transfer coefficient was 47% of the predicted value. In his opinion that pattern was a result of fibrosis. Emphysema was not the cause of this degree of functional impairment having regard to the other values recorded. He was asked whether abscesses might cause a reduction in diffusing capacity. He thought they could, but not in Mr McConnell's case. He had been tested both before and after he suffered from abscesses in February 1998, and there was no change in the values measured.

[20] Dr Moran found that diffusing capacity and transfer coefficient were both significantly reduced. He said that by far the most common cause of reduced diffusing capacity was emphysema. Asbestosis was also a cause. The transfer coefficient helped distinguish. In emphysema lung volume might be larger than expected for a given reduction in diffusing capacity. One found a relatively low transfer coefficient. In cases of diffuse fibrosis, testing lung function over time, one would expect to find a reduction in total lung capacity and a reduction in diffusing capacity and that the reductions would be proportional. The reduction in diffusing capacity was related to shrinkage in the volume of the lung, and so the transfer coefficient was preserved. In this case diffusing capacity was 26% of predicted, on re-examination, well below the normal range. The diffusing coefficient was also very low at 30%. The coefficient was disproportionately depressed. The re-testing of lung function did not show large changes between 1997 and 1998. But they were significant. If Mr McConnell had had developing fibrosis total lung volume would have been expected to be smaller. It was not. With fibrosis one would expect residual volume to have fallen. On the contrary it had increased. These were the signs one would expect with developing emphysema. More pertinently, if diffusing capacity had fallen dramatically compared with lung volume due to fibrosis one would expect a proportionate change in the ratio of residual volume to total lung capacity. Total lung capacity had not fallen. There was an increase in residual volume. More of the inhaled air was being "trapped" in the lungs.

[21] The factor of airways obstruction took on considerable significance in relation to the diagnosis of emphysema. Professor Seaton said that the most common cause of breathlessness was obstruction of the airways. Emphysema was characterised by a reduction in respiratory flow. In cross-examination he contended that while many people with emphysema did not show signs of airways obstruction, those were cases of trivial disease. Even a low level of the disease would be associated with some increased resistance to airflow. In Mr McConnell's case there was no obstruction and accordingly he could not have significant emphysema. It was impossible for a person to have the degree of reduction in diffusing capacity found in this case due to emphysema without airways obstruction. No competent chest physician would take a different view. Dr Moran's view was quite different. He said that it was well recognised that a large percentage of people suffering from emphysema would have little or no airways obstruction. Mr McConnell's case was relatively unusual in an advanced case of the disease in that there was no obstruction even of the small airways. In developed pulmonary fibrosis one would not expect to find airways obstruction. In severe emphysema one would. But there was a wide spectrum. He estimated that people with Mr McConnell's signs might constitute 10-15% of those with emphysema. Dr Moran said that there was epidemiological evidence from American studies to support that view.

[22] Taking the test results together, Professor Seaton's view was that one had a typical pattern of alveolar damage caused by pulmonary fibrosis. The results were the opposite of what one would expect in emphysema. In emphysema, additional lung volume compensated for the reduction in diffusing capacity caused by destruction of the alveolar walls. In cross-examination he resisted the suggestion that the reduction in diffusing capacity in this case could be consistent with emphysema because the other results were normal. One could not express a view by reference to one value only. Dr Moran similarly had regard to the whole test results in stating his view that the results could not be consistent with diffuse fibrosis.

[23] The period during which Mr McConnell attended for investigation of his chest complaints had seen radiological science develop from the mass x-ray programmes of the post-war years through increasingly sophisticated x-ray technology into the era of the CT scan. Dr Stevenson explained that x-ray films and CT scan plates provided complementary information in current practice. The complexity of the information available had led to the development of sub-specialist interests. She had a major interest in chest radiography. Professor Seaton made extensive use of x-ray and CT materials in his clinical and research work. He was cross-examined extensively on the expertise of the radiologist as compared with the clinical physician in the interpretation of such materials. It would be invidious to attempt to resolve the general issues raised. But Professor Seaton was clearly correct in the emphasis he placed on the role of the radiologist as provider of one element only of the total information on which clinical judgment had to be reached. Dr Moran had a similar approach. But he emphasised the importance of expert radiological evidence given the limitations of physical examination of the patient.

[24] There was agreement that what one sought in investigating the possibility of a diagnosis of asbestosis was evidence of pleural plaques, especially calcified plaques, and pleural thickening, and evidence of fibrosis. In this as in other areas, Dr Moran emphasised that it was a matter of degree. In the least developed case there might be no radiological evidence at all. There were some standard patterns such as dot-like opacities a short distance in from the pleura, following the line of the pleura. At a late stage there would be more radio dense opacities. A network of fibrotic tissue could appear. The boundary lines might be thick or thin. Picturesquely, the radiological appearance might be described as honeycomb. There might be trans-pulmonary banding on CT scan. Ultimately there might be mesothelioma. According to Dr Moran, a characteristic of asbestosis was diffuse fibrosis. Apart from the extreme case, the physician would be interested in differentiating emphysema. Where there was emphysema one might find that the patterns of the lungs and of blood vessels within the lungs were altered. There was often attenuation of the broncho-vascular markings. However, the radiology of emphysema was extremely variable. In early stages the disease might not be resolvable on CT scan. At a later stage it might be observable without ever developing bullae. Bullae might not have detectable walls, or might have thin or walls of varying thickness. Dr Moran explained the process in the typical development of emphysema as a breakdown of the alveoli walls causing adjacent air sacs to coalesce forming enlarged air spaces. The classic appearance was of a dark area bounded by fine lines which did not follow normal anatomical features. The lines found in diffuse pulmonary fibrosis never had, overall, the appearance of emphysematous bullae.

[25] Dr Moran's view was that Mr McConnell's lungs showed gross emphysema throughout merging into very large thick-walled cavities at the lung bases. Asbestosis was characterised by diffuse fibrosis. He had never come across the two conditions simultaneously. If the patient started with emphysema fibrosis would not develop by absorption of asbestos fibres. If diffuse fibrosis was established before the tendency to emphysema it was impossible to see how emphysema could develop. The defining characteristic of emphysema, the loss of alveoli walls, would be impossible if they were fibrotic.

[26] Dr Stevenson's approach was generally similar to Dr Moran's. She characterised emphysematous bullae generally as large air spaces, over one centimetre in diameter, distributed mainly at the edges of the lungs, and having thin walls. She identified such bullae in the apices of both lungs. There, the large air filled spaces appearing as black areas in the films had ill-defined thin walls. The concentration of these bullae was less marked as one moved down into the middle areas of the lungs. She said that bullae were sometimes associated with the compression of tissue between the air spaces, caused by the enlargement of the spaces. In contrast to emphysema, one did not find large air spaces in cases of asbestosis. Cases of diffuse fibrosis were demonstrated by small air spaces, evenly distributed in a honeycomb fashion. That was not the appearance of the bases of Mr McConnell's lungs. She said that the appearances of the bases of the lungs was consistent with emphysema.

[27] Professor Seaton's view of the typical radiological picture of emphysema was the same as the other experts, namely large black areas defined by thin walls. But he placed more evidence on the thinness of the walls as defining characteristics of emphysema. He identified emphysematous changes in the apices of Mr McConnell's lungs. In the basal areas of Mr McConnell's lungs there were, on Professor Seaton's evidence, large black areas defined by easily identified walls indicative of fibrosis. He said that the radiology showed widespread fibrosis typical of asbestosis. It was put to him that the radiological evidence in this case was of non-uniform air spaces inconsistent with fibrosis. It was further suggested that in honeycombing the cysts were typically two to three millimetres in diameter. He rejected these suggestions absolutely. He had "sliced through many fibrotic lungs" and could speak from post mortem experience. He had found wide variation in shape and distribution of fibrotic conditions. Professor Seaton was not challenged on his post mortem experience, and there was no contrary evidence.

[28] Dr Moran considered that if the markings at the bases of the lungs were indicative of fibrosis, there was an alternative explanation to asbestosis. The fibrosis associated with asbestosis was characteristically diffuse. The process led to contraction of the walls of the alveoli, to tearing apart of the cells resulting in the development of spaces. The radiological signs were not consistent with that process. Almost every patient with emphysema had some fibrosis. There tended to be low-grade infection which scarred the cell walls. There was a history of infection. Mr McConnell had had pneumonia. He was often treated with antibiotics. He suffered from night sweats. He had once had tuberculosis. These factors would all have led to scarring, and fibrosis. Professor Seaton rejected the suggestion of low-grade infection of the alveoli. Infection of the alveoli was pneumonia. Bronchitis affected the airways, and might be a low-grade infection of which a person could be unaware. If one had pneumonia one would be aware of it.

[29] Dr Moran tendered an alternative explanation of the appearance of radio dense areas in the lung bases. In some cases of emphysema one had apparent thickening of cell walls because the expanding air spaces compressed the tissue between making it radiologically opaque. Professor Seaton dismissed this theory. Dr Moran suggested that as adjacent air spaces coalesced they lost efficiency so that on inhalation air entered but the bullae then collapsed. This did not happen on every cycle, but over time. Adjacent tissue appeared to be squeezed. Dr Moran could not provide a satisfactory explanation of the process generally or how it might have arisen in this case.

[30] Dr Stevenson identified pleural abnormalities in slices 6 and 16 of a series of CT scan films of 15 February 1996. These comprised pleural thickening posterio-laterally on the left side and a number of small calcified pleural plaques. In her opinion these signs represented minimal abnormalities. There was no evidence of diffuse pleural thickening. Professor Seaton placed considerable emphasis on these films. He also identified plaque or fibrous tissue in slices 2 and 3, plaque in slices 5 and 6, abnormal tissue in slice 7, a small area of calcification in slice 11 and abnormal tissue in slices 12 and 13. He found specs of calcification in an extensive plaque extending from the spinous process almost to the chest wall shown in CT slices 13 to 18. Dr Stevenson disagreed emphatically. She rejected the suggestion put to her that there was extensive plaque shown in CT slices 13 to 18. What one saw in slices 17 and 18 was the intercostal muscle. The areas identified in slices 11 to 15 showed the beginnings of the rib extending from the spine. In her view the signs were "absolutely not" indicative of plaque. Dr Stevenson was cross-examined at length on the interpretation of these slides. She demonstrated the basis for her views by reference to the films and by reasoned answers on the physiology of the chest.

[31] There was further controversy. It was put to Professor Seaton that with first exposure soon after 1949 asbestosis would have developed by the late 1960's. He rejected the suggestion. The timing of the development of asbestosis depended on the person, and the quantities of asbestos to which he was exposed and the period of exposure. The identification of first symptoms in the 1980's was wholly consistent with low dose exposure over many years. He calculated Mr McConnell's exposure using standard formulae. It is unnecessary to rehearse the arithmetic. Dr Moran's view, based on the literature of epidemiological studies, was that radiological evidence of asbestosis was likely to show within twenty years, and that there was likely to be clinical evidence at about the end of that period.

[32] With few exceptions, I have come to the conclusion that the main issues between Professor Seaton on the one hand and Dr Moran and Dr Stevenson on the other hand cannot be resolved on the evidence before me. I accepted that each was a truthful witness, and in particular that the evidence each gave about his own clinical experience was acceptable. One was therefore left with a number of irresolvable differences of opinion. Dr Stevenson's objectivity was challenged in cross-examination and in submission. Professor Seaton was critical of her reports. He said that if they had been presented to him in a clinical context he would have seriously questioned the competence of the writer. Alternatively the reports were biased. The terms of Dr Stevenson's reports were subjected to critical examination, and it was suggested that the opinions she expressed had been influenced by Dr Moran. There were undoubtedly deficiencies in the reports. In evidence she accepted that, and it was amply demonstrated. But there was no basis for the suggestion that she was less than objective in giving evidence before me. In my view she was a careful and helpful witness who sought honestly to make sense of the x-ray and CT films which otherwise might have been impenetrable mysteries. Subject to matters of interpretation on which the issue essentially turns on differences between Professor Seaton and Dr Moran, I accepted the positive interpretations she advanced, and, in some respects more significantly in resolving the dispute between Professor Seaton and Dr Moran, I accepted her evidence rejecting certain aspects of the interpretations on which Professor Seaton relied.

[33] It is possible, and in my view legitimate, to form definite conclusions on some of the issues which divided the experts in this case. For example, I found compelling Dr Stevenson's evidence (a) that what was shown in slices 17 and 18 of the CT scan was the intercostal muscle; and (b) that the areas identified in slices 11 to 15 showed the beginnings of the rib extending from the spine. I did not accept the interpretation advanced by Professor Seaton in relation to the signs found in scan slices 11 to 18. In my view it became clear that he had confused the representation of the intercostal muscle and the rib cage in identifying the critical areas as plaque. So far as pleural thickening and calcified plaques were concerned, I accepted as reliable Dr Stevenson's evidence. There were pleural plaques in slices 6 and 16, and pleural thickening in slices 13 15 and 16. These signs were consistent with and provided evidence of exposure to asbestos, but they were of minimal radiological significance.

[34] The experts were in substantial agreement about the upper areas of the lungs and about the mechanism by which the abnormalities would had developed there. There were large emphysematous bullae there, extending down to the middle of the lungs. In relation to the lower levels of the lungs, I did not accept Dr Moran's evidence that radio dense areas might reflect compressed tissue. Dr Stevenson said that emphysematous bullae were sometimes associated with the compression of tissue between bullae caused by the enlargement of the spaces. However, it was clear that the physiological process of compression of tissue which supported this view was information derived from Dr Moran rather than a matter of radiological science. There was ample evidence that in some cases of emphysema the chest is expanded overall, a barrel-chest being one of the classic signs of the disease. It might have been possible to envisage a build up of pressure on normal tissue in such a case. But Mr McConnell did not have that condition. In cases of airways obstruction it might have been possible to envisage local pressure being built up. The problem in this case was to envisage, in a normally expanded chest, differential pressure in cells that were interconnected by airways that were open and unobstructed so that tissue containing air and blood vessels could become compressed. Dr Moran accepted that he had no satisfactory explanation of the process generally, and offered none that related particularly to Mr McConnell's case or signs. I could not accept the suggestion made in the absence of an intelligible explanation of it. On this matter I accepted the evidence of Professor Seaton that what was shown in the CT scans in the case of Mr McConnell was fibrosis, not compressed normal tissue.

[35] Having accepted Professor Seaton's evidence as credible, it follows that diffuse fibrosis generally and asbestosis in particular can be associated with air spaces that are irregular in shape and distribution. In this respect one had an example of what was a common feature of this case. For every sign there was a body of conventional wisdom, found in standard textbooks, and a body or bodies of wisdom developed by experts with particular experience. Dr Stevenson's interpretation of the radiological evidence of the condition at the bases of Mr McConnell's lungs clearly reflected one level of accepted wisdom. But her evidence could not prevail against Professor Seaton's practical experience. I consider that it could not be taken as a necessary characteristic of fibrosis generally or asbestosis in particular that the radiological evidence was of relatively even distribution of small well defined air spaces with fibrotic walls typical of honeycomb sections.

[36] In these circumstances, I consider that it was proved that there was fibrosis in the bases of Mr McConnell's lungs. However, the question whether the fibrosis was indicative of asbestosis cannot be resolved on the radiological evidence. Mr McConnell had a history of chest trouble which, on Dr Moran's view, would cause fibrotic scar tissue and give rise to the appearance found in the CT scans. Professor Seaton could not say that the fibrosis shown was necessarily indicative of asbestosis. I am of the view that there was no conclusive radiological evidence whether the basal areas of the lungs did or did not show signs of asbestosis.

[37] The results of the experts' clinical examination of Mr McConnell reflected differences in relation to their factual findings and differences of interpretation. In particular, they differed significantly in relation to their clinical findings on auscultation. The characterisation of the tone of crackles as fine, medium or coarse necessarily involved a degree of subjective assessment of what was heard. But the difference was extreme, especially in respect of Dr Moran's finding of coarse crackles on re-examination. Timing of crackles was a matter of dispute. So far as one could rely on them without the testimony of the doctors who made them, the medical records supported Dr Moran's evidence that there had not been consistency over a period. Each witness was experienced and described a similar approach and similar values. Professor Seaton's findings fitted the paradigm. Dr Moran's did not. The basic factual issue of what they found and whether one or the other was more reliable could not be determined on their evidence alone. Negatively, there was no basis on cross-examination on which it would be appropriate to reject Dr Moran's evidence in favour of Professor Seaton. In these circumstances it would be impossible to find that Mr McConnell did show a pattern of crackles consistent with asbestosis.

[38] In relation to finger clubbing, it is proper to conclude that that condition was present. But its diagnostic significance is necessarily contentious in the absence of a finding of relevant crackles. Professor Seaton's evidence of his clinical findings depended on the association of finger clubbing and a relevant pattern of basal crackles. Since the issue of crackles cannot be resolved in Mr McConnell's favour, the clinical significance of finger clubbing cannot be determinative of whether or not Mr McConnell has asbestosis. The evidence of clinical examination therefore failed to establish that Mr McConnell did have asbestosis, and failed to support that diagnosis along with other signs.

[39] The critical issue on lung function tests was not measurement but interpretation. As set out above, Professor Seaton and Dr Moran disagreed on the significance of the values for and changes in the diffusing coefficient. They approached the definition of the problem differently. Essentially Professor Seaton's thesis seemed to me to depend on the proposition that with developed emphysema the inflated lung volume would offset the reduction in diffusing capacity. Dr Moran's approach was that with developed diffuse fibrosis, as in asbestosis, the diffusing coefficient would be maintained because of reduction in lung volume. I have found it impossible to resolve the differences of approach so as to reach a view on the positive tests applicable which would enable one to accept the opinion of one expert as against the other. There is no objective material other than their respective opinions to apply in weighing one body of evidence against the other. It must follow again that Professor Seaton cannot be preferred over Dr Moran, and that the results of the lung function tests cannot be used to support a diagnosis of asbestosis as opposed to emphysema.

[40] There was one aspect of this chapter of the evidence on which it appeared to me that Professor Seaton's evidence could not be taken as wholly reliable, namely the significance of the lack of airways obstruction. It was impossible on the evidence to resolve the issue conclusively. Dr Moran's physiological and clinical experience was extensive. Professor Seaton had vast experience as a chest physician. Each had an impressive academic history. The court has no independent expertise in such matters and any view must be qualified. Professor Seaton accepted that there was emphysema in the apices of Mr McConnell's lungs. The basis on which he dismissed it as insignificant was that there was no airways obstruction. His reasoning on this matter was circular and flawed, in my opinion. It was clearly shown that Mr McConnell had large emphysematous bullae at least in the upper zones of each lung. I was satisfied that it was in those areas that emphysema was typically found. There was nothing to suggest that the radiological signs were of trivial emphysema. It could not therefore be the case, on the evidence before me, that airways obstructive disease was always present except in cases of trivial emphysema. For present purposes, on the evidence, a diagnosis of emphysema in Mr McConnell's case could not be precluded by the absence of obstructive airways disease unless Dr Moran were shown to be wholly wrong in his evidence that there was epidemiological support for serious emphysema without airways obstruction. That was not demonstrated. It is sufficient for present purposes that on the evidence a diagnosis of emphysema in Mr McConnell's case could not be precluded by the absence of obstructive airways disease. In my view, that, at least, was established. But on this matter I incline to the view that Dr Moran's evidence was to be preferred.

[41] Radiologically there are signs of asbestos related changes in the lungs. Dr Stevenson identified these. As a lower common denominator what she found was established though Dr Moran perhaps was unconvinced. But it was not established that there was significant radiological evidence of advanced asbestosis as Professor Seaton contended. It is impossible to dismiss the evidence based on clinical experience of the two main protagonists, or otherwise distinguish between them on the characterisation of the opaque boundaries of the air spaces shown on CT scan, other than to say that they indicate fibrosis.

[42] In the result, I am of opinion that the pursuer has proved only that he has minor radiological evidence of asbestos related changes in his lungs. He has not established that his present condition is due to asbestos-related disease rather than emphysema. I shall therefore assoilzie the defenders.

[43] Had I found Mr McConnell entitled to damages, I would have fixed the amount of solatium at £25,000, of which one half would have related to the past and one half to the future. Had asbestosis been proved to be the condition causing Mr McConnell's breathlessness and consequent disability, the cases of Kerr v Newalls Insulation Co Ltd 1997 S.L.T. 723 and Lightbody v Upper Clyde Shipbuilders Ltd 1998 S.L.T. would have defined the bracket within which to select an appropriate sum.