Scottish Court of Session Decisions

OUTER HOUSE, COURT OF SESSION [2009] CSOH NUMBER102A
	OPINION OF MORAG WISE, QC Sitting as a Temporary Judge in the cause ANDREW YOUNG Pursuer; against (FIRST) THE ADVOCATE GENERAL FOR SCOTLAND, representing the Ministry of Defence in Scotland and (SECOND) THE ADVOCATE GENERAL FOR SCOTLAND representing the Department of Trade & Industry in Scotland Defender: ­­­­­­­­­­­­­­­­­________________

Pursuer: Hajducki QC, Marshall, Solicitor Advocate ; Thompsons

Defenders: McCormiack, ; Morton Fraser

14 July 2009

[1] The pursuer was born on 18 May 1949. He worked in the Rosyth Dockyard in the employment of the Ministry of Defence as an apprentice fitter and then a fitter from about 1968 until 1976. He worked on vessels undergoing refit and repair. He stripped asbestos lagging himself and he worked in the vicinity of laggers who were stripping and applying asbestos lagging. Subsequently, from 1976 until 1984, he worked for British Coal as a surface fitter. In that employment he worked on steam boilers and locomotives that were lagged with asbestos, on occasions removing asbestos lagging and using asbestos based packing material for valves.

[2] Mr Young now suffers from a lung condition, interstitial lung disease, which is a disease of the parenchyma, the part of the lung responsible for the exchange of oxygen and carbon dioxide. The contention made on his behalf at proof was that he suffers from asbestosis as a result of exposure to asbestos during the periods of employment referred to above. The contention for the defender on the other hand was that Mr Young suffers not from asbestosis but from an idiopathic lung condition unrelated to asbestos exposure, namely cryptogenic fibrolising alveolitis ( CFA), also known and referred to as idiopathic pulmonary disease (IPD). Put shortly, if the pursuer suffers from CFA the defender's would not be responsible for his condition.

[3] The parties entered into a Joint Minute (No 23 of Process) in relation to certain important matters. In particular, paragraphs 1 and 2 thereof are in the following terms;

"1. The pursuer was exposed to asbestos during his employment at Rosyth Dockyard (in the employment of the Ministry of Defence) and Comrie Colliery (in the employment of the National Coal Board) as a result of the negligence of his employers.

2. The pursuer has had sufficient cumulative exposure to asbestos to be at risk of developing asbestosis of the lungs."

[4] In the absence of controversy about the nature and length of his employment and relative exposure to asbestos, the pursuer did not give evidence. The level of damages in the event of a finding that he has developed asbestosis was also agreed in the Joint Minute. Each party led evidence only from an expert witness, Dr Robin Rudd for the pursuer and Professor Robin Stevenson for the defender.

Dr Rudd's evidence
[5] Dr Robin Rudd, BA MB BChir MA MRCP MD FRCP has been a consultant physician since 1983. He has pursued clinical and research interests in asbestos related disease for at least 25 years. He held the post of consultant physician and Honorary Senior Lecturer to St Bartholomew's and London Chest Hospitals from 1996 until 2006. He has published 35 peer reviewed papers on asbestos related diseases. He has prepared expert reports for litigation since 1983 and has given evidence as an expert witness in a number of cases involving asbestos related claims, including at the trial stage of Fairchild v Glenhaven Funeral Services Limited [2002] UKHL 22. Dr Rudd is also interested in the comparison between asbestosis and CFA. The subject of his MD thesis in 1982 was the physiological aspects of CFA and their relationship to prognosis. More recently he and two other colleagues carried out the largest single UK study that has investigated the change over time of lung function and chest radiographic findings in patients with asbestosis and in asbestos workers without asbestosis.

[6] In his evidence Dr Rudd explained that he had reviewed the medical records and reports relating to Mr Young and had produced his own report (No 6/15 of Process) to which he spoke. He had not found it necessary to meet Mr Young. He said that the records indicated that Mr Young had been subjected to classic shipyard heavy exposure to asbestos when lagging and then working in the vicinity of laggers at Rosyth. His subsequent work at British Coal was comparable to the shipyard work in terms of asbestos exposure. Dr Rudd contrasted the level of the pursuer's exposure with that of a plumber who occasionally came across asbestos sheeting, which he described as intermittent, light exposure to asbestos dust.

[7] Dr Rudd went on to explain that both asbestosis and CFA patients would experience lung fibrosis, where scar tissue is deposited in the alveolae (air sacs of the lung) and which has the effect of making the lungs stiffer and more difficult to expand, thus less oxygen is gained from each breath. Many cases of such lung fibrosis are cryptogenic, meaning of hidden origin or unknown cause. According to Dr Rudd, before a diagnosis of CFA can be made, one would require to exclude the known causes of pulmonary fibrosis such as asbestosis, so it is a diagnosis by exclusion.

[8] The condition asbestosis arises where the diffuse fibrosis of the lungs has been caused by the inhalation of asbestos dust. Asbestos excites an inflammatory reaction in the fibrous tissue. Dr Rudd said that a diagnosis of asbestosis required evidence of diffuse fibrosis of the lungs together with a history of sufficient exposure to asbestos. In some cases there will be pathological evidence of asbestosis where a lung biopsy is performed post mortem, but he said this does not tend to be carried out during a patient's life due to the risks involved and that clinical evidence is usually sufficient for diagnosis.

[9] One of the reasons why it was important to differentiate between asbestosis and CFA in diagnosis is that asbestosis is untreatable, whereas 30% of CFA sufferers have shown good results from steroid treatment. However, unfortunately the improvement through treatment tends to be short lived and the disease progresses. The rate of progression differs markedly as between asbestosis and CFA. Asbestosis progresses in time and may ultimately lead to respiratory failure and death. The rate of progression is relatively slow and in most cases it is rare to see it develop less than 20 years after exposure. The progression of CFA is "quicker and worse". Dr Rudd expressed views on the comparative rates of survival from the onset of symptoms between CFA and asbestosis sufferers. He said that the median survival for those with CFA was two and a half years, in contrast to an expected twenty to thirty year survival period for asbestosis sufferers, whose life expectancy may be reduced by only a few years.

[10] So far as the development of the pursuer's condition was concerned, it was clear from the records that he had had lung fibrosis at least since 2004 when he had reported increasing shortness of breath. When examined, he was found to have crackles over the lung bases indicating the presence of diffuse interstitial fibrosis. CT scans taken in August 2005 and May 2007 showed evidence of that interstitial fibrosis. There were no discrete pleural plaques. There was mild emphysema. There was little change between 2005 and 2007 with at most minor progression of the interstitial shadowing. Dr Rudd's assessment of these CT scans was that they were consistent with, although not specific for, asbestosis. He was asked about the absence of pleural plaques. He agreed that they are present in most cases of asbestosis but he said that their absence is not evidence against it. Overall the radiology was not determinative. He was asked to comment on a study by Copley et al entitled "Asbestosis and Idiopathic Pulmonary Fibrosis: Comparisons of Thin-Section CT Features" (No 6/18 of Process) which found that only five per cent of asbestosis sufferers do not have pleural disease. Dr Rudd confirmed that the five per cent without pleural disease were those known to have asbestosis - i.e where the diagnosis of asbestosis had been made notwithstanding the absence of pleural disease. He referred to a smaller study he had carried out where he had found twelve per cent of known asbestosis sufferers had no pleural disease. He maintained that the figure was really between four and twelve per cent taking all studies together. He contrasted these more recent studies, which were based on CT scans, with older studies which concluded that between thirty and forty per cent of asbestosis sufferers had no pleural disease because such disease couldn't really be detected on X ray alone. Dr Rudd recalled the first case he had been involved in as a consultant. His patient was a docker who was refused benefits that he would have received if suffering from an asbestos related condition. After he died the pathology showed clear asbestosis of the lungs but no pleural plaques. In summary Dr Rudd's position on this point was that the absence of signs of pleural disease doesn't constitute evidence against a diagnosis of asbestosis.

[11] The pursuer had undergone a series of lung function tests, about which Dr Rudd gave evidence. These tests measure both the pattern and severity of the impairment. Serial tests over time show the rate of deterioration, thus the rate at which the disease is progressing. The first lung function test was carried out on the pursuer on 6 May 2005 by his General Practitioner (No 6/1 of Process, page 50). This was a simple test using a spirometer, a device into which the patient blows and which then measures his capacity to breathe air in and out. The results were very close to average for a man of the pursuer's age and height. Further tests were carried out in June 2005 by a Dr Selby, Consultant in Respiratory Medicine. Dr Rudd examined the results (No 6/2 of Process, page 10). The further spirometry test was divided into FEV1, which is the amount that can be blown out by the patient in one second and FVC, the total amount that can be blown out. On these, Dr Selby's findings added nothing to the previous result from the General Practitioner. The additional lung volume and diffusion tests were of interest. A total lung capacity (TLC) test measures the total amount of gas in the lungs when full and is most informative when assessing disease. Diffusion tests are designed to test the ability of the lungs to take up carbon monoxide from inspired air. A test for the diffusing capacity of lungs for carbon monoxide (DLCO/ TLCO) measures the capacity of the lungs a whole. Diffusion tests measure function rather than simply volume. In June 2005 Dr Selby's results recorded an FVC reading of 4.2, a TLC reading of 5.99 and a DLCO/TLCO reading of 7.24. There is a margin of error in such test results and variables can include the different apparatus used in different laboratories. Erroneous readings can be obtained if the patient doesn't make the maximum effort when performing the tests, but there was no suggestion of that in June 2005.

[12] The pursuer was tested again in Glasgow on 4 October 2006, 17 October 21007 and 12 January 2009. The results of those three further tests are summarised in a document attached to a letter from Professor Stevenson (No 7/2 of Process) and both experts used that summary in their evidence. The relevant summary results were as follows ;-

04/10/2006: FVC - 4.4, TLC - 5.6, TLCO - 7.5

17/10/2007: FVC - 4.2, TLC - 5.6, TLCO - 7.1

12/01/2009: FVC - 4.4, TLC - 5.5, TLCO - 6.1

He was also tested in Edinburgh in November 2007 and May 2008, where the TLCO results were 6.45 and 5.38 respectively.

Dr Rudd was asked to analysed these, particularly the three Glasgow results. He explained that the 4 October 2006 results were broadly within the margin of error one might expect between readings, although there was some significance in the TLC reading which had dropped from the previous year. There was very little difference between these readings and the subsequent readings on 17 October 2007, where the TLCO was slightly down at 7.1 but not significantly so. The most recent results of 12 January 2009 showed no important drop in the FVC and TLC readingsTLC readings. There was a drop in the TLCO reading which would be indicative of a more significant decline if maintained in subsequent readings. It was noteworthy that the FVC reading hardly changed over the whole period of observation, as someone moving more quickly to total respiratory failure would have results showing a drop in FVC of 30 - 50%.

[13] Dr Rudd was referred also to a set of readings from 16 March 2007 (No 6/11 of Process) but he was clear that these were based on a sub-maximal performance by the patient and could be disregarded. Taking the whole period, Dr Rudd was of the opinion that the results displayed a small but probably significant decline in lung function and gas transfer, but not a great deal of worsening clinically. The rate of progression was more consistent with asbestosis than with CFA. He pointed out that the period during which the pursuer has been under observation is longer than the median life span for those with CFA. He had calculated that in statistical terms the rate of decline in gas transfer was 1.14 units over a period of 31/2 years which is a decline of approximately 0.33 units per year. He referred to a study of the rate of decline of lung function in asbestos workers with and without asbestosis where the mean rate of decline (on asbestosis sufferers) was found to be 0.18 units per year with a standard deviation of 0.15 (Al Jared et al, 1993, No 6/17 of Process). It followed from that statistic that the upper end of the range within which the rate of decline would lie in 95% of patients would be 0.48 units per year, being the mean plus two standard deviations. Mr Young's deterioration was accordingly within the range which is observed in patients with asbestosis. The point of the 1993 paper, Dr Rudd explained, was to consider two new techniques for looking at the progression of asbestosis and CFA. He referred to Table 1 on the paper which listed 30 patients with asbestosis of varying ages (the mean age being 60), consisting of current smokers, ex-smokers and non-smokers, with other variations being the duration of exposure to asbestos and the time since the first such exposure. Those patients were part of a larger group that included others who were not asbestosis sufferers. The table lists their lung function results and in particular the change per year in the TLCO. It illustrates that some asbestosis sufferers in the group had a greater rate of annual decline than Mr Young. Dr Rudd explained that a standard deviation is the statistical measure of the extent to which individuals vary from the mean. The study involved a smallish number of people and it was important to interpret the statistics in a biological context. It was the average and maximum rates of decline that were of interest. A cluster of patients in the study had results close to the 0.33 figure. Dr Rudd's conclusion was that Mr Young was within the parameters of decline that one would expect in an asbestosis sufferer, albeit that a diagnosis of asbestosis wouldn't have been excluded by a more rapid decline.

[14] On the issue of the median survival for both conditionsCFA Dr Rudd referred to a large study in which he had been involved of 588 patients with CFA where the median survival was found to be 2.43 years. The figure was not greatly influenced by age or sex. The study took place over a ten year period between the mid 1990's and 2005/6. The relevant papers were published in journals in 1997 and 2007 (British Thoracic Society Study on Cryptogenic Fibrosing Alveolitis, Nos 7/4 and 7/5 of process). Even allowing for other studies that might have found median survival to be four years, Dr Rudd pointed out that Mr Young had already survived longer than average for CFA sufferers. He noted that Mr Young had not received any treatment consistent with a diagnosis of CFA.

[15] Dr Rudd explained that in general terms the level of exposure to asbestos was not significant in diagnosis once a patient was over the minimum threshold dose to cause the condition. That threshold was measured in fibres per millimetre (ml) years, a combination of the product of mean airborne fibre concentration plus the duration of exposure in working years. Thus exposure of 5 fibres per millilitre of air for 5 years would give 25 fibres per ml year. The sort of exposure the pursuer had was well over the minimum threshold, perhaps into hundreds of fibres per ml year.

[16] In conclusion Dr Rudd's opinion was that in a case where radiological evidence and lung function tests are consistent with either condition, then the most important diagnostic feature is whether the patient has had sufficient exposure to asbestos to render him at risk of developing asbestosis. If there is a history of sufficient exposure then the patient cannot meet the diagnosis by exclusion for CFA. In light of the agreement that Mr Young had sufficient cumulative exposure to be at risk of developing asbestosis, then the information overall pointed, on a balance of probabilities, to his suffering from asbestosis. Insofar as the rate of progression was a factor, Mr Young's results illustrated a marginally faster progression than asbestosis but slower than CFA. He was still working and there was no indication as at the date of proof that he was likely to succumb in the near future.

[17] Under cross examination, Dr Rudd agreed that 25 fibres per millilitre year was regarded as the threshold of exposure for risk of asbestosis. He disagreed that Mr Young's exposure to asbestos could be described as "modest". On the statistic of only five per cent of asbestosis sufferers having no pleural disease Dr Rudd agreed that this was a factor to weigh in the balance, but explained that it had to be considered in context. Given the agreement that this pursuer had had sufficient exposure to asbestos to be at risk of asbestosis, the statistic was of much less weight. He was asked about the differences in recording of results between laboratories in Fife, Glasgow and Edinburgh. He confirmed that there are certain uniform standards and that for example all of the equipment requires to be calibrated. There can be minor differences of 1 or 2% by using different equipment in different laboratories. Given the choice all tests would be taken at one laboratory, but where a range of results from different laboratories was available it was better to look at them all, particularly if this meant there was data over a longer period. While Dr Rudd took no issue with the Glasgow results relied on by Professor Stevenson in isolation, he noted that these did not cover the whole period of available results. Dr Rudd was cross examined in some detail on his comments about the rate of decline in asbestosis sufferers and in particular his comments about the Al Jared 1993 paper (No 6/17 of process) and the statement that the upper end of the range within which the rate of decline would lie in 95% of patients with asbestosis would be 0.48 units per year, being the mean of 0.18 and two standard deviations. It was suggested to Dr Rudd that the results of the Al Jared study did not represent a normal distribution that would be represented by a symmetrical hump when drawn. The formula for standard deviation was put to him (7/7 of Process) and it was suggested that if the average decline is 0.18, then the first standard deviation would be only 0.03 to the left of the centre, thus the distribution was not " a symmetrical hump". Dr Rudd explained that he was not arguing that the results showed a perfect normal distribution and that he was using statistics only as a way of looking at the data. It was the measurements themselves that mattered. He had provided a useful descriptive statistic, but because of the fairly small number of patients he agreed that the results would not be reproduced as a perfect symmetrical hump. However, the Al Jared study was a peer reviewed paper and the real point was that most of the observations made within it fell within the range of Mr Young's results. When he had been told that the issue of the distribution of the results in the Al Jared paper might be raised in his evidence Dr Rudd had not checked the matter himself although he was sure that it would have been checked at the time the paper was written. Dr Rudd was one of the authors of the 1993 paper, Dr Al Jared having been one of his students with whom he had subsequently worked with on a number of papers. The consideration of the mean and standard deviations from the mean gives researchers a good idea of where the majority of patients will lie. Even with a small number of patients, the results bear some approximation to a normal distribution. The message he drew from the study was not dependent on whether or not the statistical approach was optimal.

[18] Under further cross examination on the point, Dr Rudd accepted that if Mr Young had been a current smoker, that would contribute to deterioration in lung function, but the information was that the pursuer was an ex- smoker. He was referred to the results of ex- smokers in the study and agreed that these appeared to indicate that the average decline in lung function for non- current smokers was about 0.07, with a standard deviation of 0.1135, which was notably below his figure of 0.33. The data thus indicated that the decline in Mr Young's case seemed well above average for a non--current smoker, although Dr Rudd noted that he didn't know when Mr Young gave up smoking. In any event, his opinion was that he would only give weight to the deterioration as a factor in the differential diagnosis if it was extremely rapid, which would then point clearly in favour of CFA. The statistics of non- current smokers was a valid point, but didn't affect the crucial diagnostic point of the exposure to asbestos at a level giving rise to a risk of asbestosis. Dr Rudd was also cross examined about the large study of 588 patients (Nos 7/4 and 7/5 of Process). He acknowledged that the study had started at a time when diagnosis of some of the patients will would have been made by plain radiograph. He said that the time lag between the condition showing up on radiograph compared with the more sophisticated CT scan was about a year. With reference to the question of excluding IPF where there has been exposure to asbestos, he, he explained that the intention in the study had been to exclude patients who had had sufficient exposure to be at risk of asbestosis, because the authors recognised that if there has been sufficient exposure to asbestos thatthen there there is a risk of asbestosis then that usually negates a diagnosis of CFA because there is a known cause: by definition CFA is a condition without a known cause. While he didn't suggest that those with asbestosis were immune from CFA, he was clear that on a balance of probabilities the pursuer had asbestosis because of the agreed exposure at a level giving rise to a risk of the condition developing and the clinical physiological features being consistent with that diagnosis. The extent of the pursuer's emphysema was mild and insufficient to be a factor in the diagnosis. Dr Rudd noted that he was unable to identify Professor Stevenson in any of the literature of asbestosis or CFA and didn't understand him to have a particular specialist interest in either condition.

Professor Stevenson's evidence

[19] Professor Robin Stevenson, MB ChB, MRCP,MD, MD, FRCP was as indicated the only witness called on behalf of the defender. He has been a consultant in the field of respiratory medicine since 1980 and is currently a consultant physician of General and Respiratory Medicine in Glasgow. He is a Fellow of the Royal College of Physicians of both Edinburgh and Glasgow. His chair involves teaching within the hospital. His clinical interests include interstitial lung disease and occupational lung disease and he has recently been President of the Scottish Thoracic Society. He heads a General Respiratory Unit in Glasgow the main work of which involves patients with airway disease caused by smoking. Typically he sees patients suffering from lung cancer or pneumonia. About a quarter of patients will present with interstitial lung disease and a minority of those patients would be classified as asbestosis sufferers. He sees patients from the whole of Strathclyde with some referrals from other parts of Scotland. The shipbuilding industry was initially the most common source of asbestos exposure in Strathclyde. Also the construction of power stations gave rise to many cases although the exposure was for shorter periods. Factories that prepared asbestos products in the 1950's and 1960's also gave rise to high levels of exposure. Professor Stevenson described his interstitial lung clinic as small. He sees about 20 patients there every Tuesday of which perhaps 3 or 4 will be new patients. He said that he now makes a diagnosis of asbestosis relatively infrequently. When he does, it tends to be where there has been sufficient exposure to asbestos and the existence of pleural plaques.

[20] On the central question of differential diagnosis as between asbestosis and CFA, Professor Stevenson agreed that the first task was to take an occupational history with particular emphasis on the level of exposure to asbestos. He expressed the general view that any exposure after the early 1970's tended to be light exposure given the heightened awareness of the risks of exposure by that time. The next stage was to exclude other causes, either occupational or otherwise. For example, sarcoidosis looks superficially like CFA . If the diagnosis narrows down to a choice between asbestosis or CFA then he said that the radiology is important, because about 95% of asbestosis patients will have pleural plaques and those with CFA will not, as CFA does not involve disease of the pleura. A lung biopsy would determine categorically which of the two conditions a patient suffered from. Where that was not done, as in Mr Young's case, lung function tests were of assistance. He confirmed, as Dr Rudd had, that the significant tests were the TLC and TLCO tests which measure the efficiency of gas exchange in the lungs. He agreed that the equipment used for gas transfer tests could differ between laboratories. One device used is a plethysmorgraph, a rigid box in which the patient sits and blows into a mouthpiece, another uses a sealed ventilatory system, with a transparent booth and a nose clip and mouth piece. He thought that the Glasgow laboratory used both types of devices and he couldn't say what was used in Fife or Edinburgh. According to Professor Stevenson, if such lung function tests showed no deterioration over time, then one would have to query a diagnosis of CFA.

[21] Professor Stevenson spoke to his first report (No 7/1 of Process), dated 12 December 2006. In relation to the pursuer's exposure to asbestos, he noted that the material period of employment was clearly 1968-74 when Mr Young worked in close proximity to laggers and also had to remove old asbestos lagging from pipe work and valves himself. He recorded the medical history already set out by Dr Rudd. He did comment on an apparent discrepancy about when the pursuer had given up smoking, as the medical records had different entries about this. It seemed to have been sometime between late 2001 and late 2002 (see GP records, 6/12 of Process, pages 59, 61 and 62). In October 2006 Professor Stevenson had interviewed and examined the pursuer and pulmonary function tests were carried out. He had reviewed the chest radiographs. On the basis of the information available to him at that time, Professor Stevenson said he had been prepared to accept that the pursuer could have an asbestos related disease. However, he said that he regarded the pursuer's exposure to asbestos as "mostly indirect with a bit of direct exposure" and noted that the total exposure was only over an eight year period. He said that there was no doubt that the risk of asbestosis is related to the cumulative exposure to asbestos. While he considered (in 2006) that Mr Young was likely to have had significant exposure to asbestos, the absence of pleural disease was even then the factor against asbestosis. He referred to the Copley paper (No 6/18 of process) and the statistic that of 87 patients with asbestosis only 4 had no pleural disease. He calculated that that meant a patient was twenty times less likely to have asbestosis where he had no pleural disease. However, at that time, because of the remaining chance that asbestosis might still exist he felt he couldn't exclude it as a diagnosis without either a lung biopsy or further monitoring of the progression of the disease. If it did not progress within four to five years, he stated, it would point to the condition being asbestosis. Thus he concluded in December 2006 that he was not clear whether the pursuer's interstitial lung disease was due to asbestosis or CFA.

[22] Professor Stevenson also analysed the Glasgow lung function test results summarised in No 7/2 of process, together with a summary of the TCO (or TLCO) test results only (No 7/9 of Process). He agreed with Dr Rudd that the Fife results of March 2007 could be excluded as a "rogue result" due to lack of effort. Taking only the three Glasgow results into account, the latest of which were from January 2009, his opinion was now that the drop in the gas transfer factor from 7.5 to 7.1 and now to 6.1 could only mean progressive interstitial lung disease which was "......much more likely to represent cryptogenic fibrosing alveolitis or UIP than asbestosis". He accepted that he did not know why there was a discrepancy between the fall in gas exchange and with the lung volume tests, i.e. why the two were not deteriorating in concert, but he said it was not an uncommon picture.

[23] In terms of the specific reasons for his disagreeing with Dr Rudd's opinion, Professor Stevenson reiterated that he considered the absence of pleural disease to be significant, primarily because he didn't understand the pursuer to have suffered exceptionally heavy asbestos exposure. He considered that the absence of pleural disease fed directly into the probability issue of the diagnosis and he felt that Dr Rudd had refused to accept the implications of the Copley study on which he (Dr Rudd) had been personally involved. Professor Stevenson also disputed the validity of looking at different results from different laboratories to calculate the extent to which the rate and pattern of the pursuer's decline accorded with other asbestosis sufferers. He was surprised that someone of Dr Rudd's eminence had thought fit to do so. He thought that there was no point in taking a single result from a single lab and so, the second Fife results having been disregarded by agreement, it followed that the first Fife results should also be ignored. Looking at both the Glasgow and the Edinburgh results, Professor Stevenson concluded that it was hard to conclude anything other than that there is a progression of the disease. He asserted that the pattern seemed to be consistent between those two laboratories, although that pattern may he said be "bumpy" rather than a straight line progression. That would account for the apparent improvement in function between the Edinburgh results of 19 May 2008 and those in Glasgow in January 2009 ( results summary at No 7/9 of Process).

[24]

On the Al Jared study into the rate of decline in asbestosis sufferers ( No 6/17 of Process) Professor Stevenson spoke to a graph that had been prepared plotting the results of that study (No 7/8 of process). His view was that as the pursuer was an ex- smoker he should be in the left hand end of the graph. If one plotted the results of the pursuer's Glasgow tests alone, his rate of decline was 0.62, which was a greater progression that any of the patients in the Al Jared study. He said that meant this pursuer was not behaving like a typical patient with asbestosis. He agreed that from the medical records it looked as if the process had started by 2004. He did not accept that the median survival of 2.43 years in the British Thoracic Society Study ( No's 7/4 and 7/5 of Process) was accurate, given that the study started when plain radiograph was still in common use for diagnosis. There could, he said, be a long time lag between a disease showing on a CT scan and one showing on X ray. He was surprised that Dr Rudd had said the time lag was about a year. He had a lot of patients who had been diagnosed with CFA and had been attending his clinic " for years". He concluded that his feeling on median survival was five years from the time of diagnosis. In Mr Young's case he would not mark the date of diagnosis with the time that crackles were heard on chest examination. Diagnosis usually comes at the time of a complaint of breathlessness by the patient. He contended that diagnosis in this case should be taken as 2005, three to four years prior to proof, which he argued was lower than the median survival. He was critical of what he saw as Dr Rudd's approach of taking the facts of exposure to asbestos and pulmonary fibrosis and concluding that these amounted to a diagnosis of asbestosis.

[2425] In conclusion Professor Stevenson's view, expressed in his letter of 16 February 2009 (No 7/3 of Process) was that he was now more confident that Mr Young has IPF instead of asbestosis for the following reasons ;-

(a) He had modest exposure to asbestos

(b) There are no pleural plaques on CT scanning

(c) The rate of decline in lung function from measurements in one laboratory is greater than normally occurs in asbestosis

(c) His survival over the period of observation is not uncommon in patients with CFA.

He was clear that he could state his opinion no higher than on a balance of probabilities and that the issue was not "black and white".

[2526] Under cross-examination Professor Stevphenson maintained his position that, notwithstanding the agreement that the pursuer had had sufficient cumulative exposure to be at risk of developing asbestosis, the level of exposure was relevant to diagnosis. He said that if the exposure was moderate to light, that counted in diagnosis. When it was put to him that Dr Rudd had estimated that the pursuer would be well above the threshold of 25 fibres per ml years, he accepted that his knowledge of the fibre counts involved was insufficient to comment and that Dr Rudd's knowledge of the literature on that would be more extensive. He also accepted, fairly and without hesitation, that Dr Rudd was a recognised expert on asbestosis and CFA.

[2627] In relation to the readings used to monitor whether Mr Young's disease was progressing, Professor Stevphenson was asked why he had not regarded the lack of deterioration in the FVC or TLC readings as significant. He said that he accepted they probably were significant but that the reason for the difference in readings was not understood. He made the point that one cannot distinguish between asbestosis and CFA on the basis of lung volume tests. The gas transfer tests were significant because they showed deterioration. He accepted that the existence of emphysema would be a factor in that, although he noted that the emphysema was mild. Where emphysema was more predominant in a patient, it was difficult to interpret TLCO readings. While with Mr Young's mild emphysema it was not so much of a confounding variable, it did have to be taken into account.

[2728] When asked about what variation, in terms of margin of error, for results from the same laboratory would be acceptable, Professor Stevphenson indicated that a variation in the TLCO reading of 0.5 would fall within that margin. He accepted that there was a danger of placing too much emphasis on these readings, but pointed out that these were all he had to work with. So far as excluding the first Fife lLaboratory test results from June 2005 was concerned, he felt that it was inappropriate to compare results from different laboratories. He commented that if the lack of quality control in the Fife laboratory meant that the March 2007 results had to be excluded then so should the 2005 results form the same laboratory, although he accepted that it was Dr Rudd rather than he who had spotted the discrepancy with the 2007 results. When it was pointed out that the Edinburgh test results were also out of line with the Glasgow ones he commented "Yes, it's an imperfect world, we try to do our best."

[2829] Further cross-examination concerned the 2008 interstitial lung disease guideline from the British Thoracic Society (in collaboration with others), (No 6/16 of Process). At paragraph 5.2 of the paper the following view is expressed:-

"Change in FVC has emerged as the serial lung function measurement most consistently predictive of mortality. In part this may reflect the good reproducibility of FVC; thus, a change in FVC of only 10% is needed to identify a true change in disease severity (as opposed to measurement variation). By contrast, a minimum change of 15% is required in TLCO, a less reproducible variable. Thus, serial FVC is likely to be more sensitive to change than serial TLCO."

Professor Stevphenson accepted that such a view was valid when looking at mortality, but emphasised that the change in gas transfer measurement that he had placed reliance on in this case he interpreted as " just"just telling you that there's a problem, not that it is leading to death." He accepted that any conclusion from the TLCO readings was not clear cut and that while the figures pointed in a certain direction ".....they don't scream at you".

[2930] When cross-examined on the median survival of CFA patients issue, Professor Stevphenson clarified that his doubts related to whether the study relied upon by Dr Rudd (Nos 7/4 and 7/5 of Process) was applicable to the present day, given the change from using plain radiographs to CT scans to detect disease. He said that current suggestions were that median survival is longer than Dr Rudd suggested. He agreed that it could be presumed that the authors of No 7/5 of Process had taken other studies into account in writing their paper as some at least were referred to in their footnotes. He maintained that the survival rate for CFA was "...longer than the literature would have us believe". Four to five years was the norm, so far as he was concerned. If that was correct, then the pursuer was currently at about the time of median survival and was currently in work, not at the advanced stage of the disease and no imminent danger of demise. If the pursuer has idiopathic pulmonary fibrosis, he said, he has an indolent and low grade form of that disease. But his decline in lung function was greater than in the average population, which tended to militate against a diagnosis of asbestosis.

[3031] On the issue of the statistical approach to the test results, Professor Stevphenson agreed that he used the same method as Dr Rudd but came to a higher figure because he used only the first and last Glasgow results, as opposed to the first and last of a total of 7 results. He agreed that if one took the mean figure of 0.18 from the control group in the study (No 6/17 of Process), then Mr Young, at 0.33 was within one standard deviation from that using Dr Rudd's approach.

[3132] In re- examination it was suggested to Professor Stevphenson that if one took only the first and last Glasgow results, the TLCO readings had dropped by 18.67%, which was more than the 15% minimum required to identify a true change in the disease according to the paper at 6/16 of Process. He agreed with that proposition. Taking the Edinburgh results only, the drop was 16.59%.

Submissions for Pursuer

[3233] In submissions for the pursuer, Mr Hadjucki contended that as there was effectively no dispute about the facts in the case, the matter must turn solely on the expert evidence. Both consultants were very experienced in the field of respiratory medicine, but Dr Rudd had the advantage of having both academic and clinical experience in asbestosis and CFA. Professor Stevenson was a general lung consultant whose main workload was seeing patients with chronic airways disease caused by smoking. He properly deferred, properly, to Dr Rudd's expertise on some matters in his evidence. One criticism that could be made was that Professor Stevenson seemed reluctant to diagnose anyone as having asbestosis rather than CFA.

[3334] Mr Hadjucki submitted that it was clear that the pursuer's condition was either caused by (i) the admitted level of exposure to asbestos or (ii) an unknown cause. In support of his contention that the cause was exposure to asbestos, he argued that the pursuer's exposure to asbestos was well over the minimum exposure of 25 fibres per millilitre year. Dr Rudd was clear that the level of exposure was sufficient for diagnosis and Professor Stevphenson's reservations should be disregarded. Once one is over the minimum threshold it is simply a question of how badly one might suffer from the condition as distinct from being relevant to diagnosis.

[3435] So far as the radiological evidence was concerned, it showed the fibrosis itself, but it was neutral so far as diagnosis between the two conditions was concerned. It was accepted that it was unusual for asbestosis sufferers not to have any pleural disease. The number of asbestosis sufferers without such disease had been found to be between 5% (Copley ) and 12% (Rudd). The issue was whether either of those statistics militated against a diagnosis of asbestosis. Dr Rudd said that they did not. At its highest it was a factor, but it was the exposure that favoured a diagnosis of asbestosis on a balance of probabilities. In this context it was noted that Professor Stevphenson always referred to pleural plaques in evidence rather than pleural disease. He used a lack of pleural disease as a diagnostic tool, which would inevitably preclude a diagnosis of asbestosis in a proportion of asbestosis sufferers. His approach, contended Mr Hadjucki, was less analytical than that of Dr Rudd, the latter expert having seen considerably more patients and studied the differential diagnosis in greater detail. So far as lung biopsy was concerned, while Professor Stevphenson had described it as the "gold standard" of diagnosis, Dr Rudd had given good reasons, which were unchallenged, why it would have been inappropriate to carry out that invasive procedure in Mr Young's case.

[3536] It was pointed out that no diagnosis of CFA had ever been clearly made by those treating Mr Young. Whilst in a letter to the pursuer's GP ( No 6/12 of Process), Dr Selby had suggested that he was considering treatment in light of an apparent diagnosis of IPF/CFA, but that letter followed from what both experts agreed was a " rogue result" in March 2007,. Nno treatment consistent with a diagnosis of CFA had ever taken place.

[3637] So far as the lung function tests were concerned, Mr Hadjucki submitted that all of the tests should be taken into consideration, otherwise the length of observation would be cut by 36%. The defenders wanted to cherry pick the results by excluding the first results from the Fife laboratory. It was pointed out that if the TCO results of only the first and last of all the readings were taken, the overall decline in lung function was 15.75%. If the first result from Fife was excluded, the three Glasgow results showed a decline of 18.7%. Taking the Edinburgh results only the decline was 16.6%. Reading these statistics in conjunction with the 2008 Guidelines of the British Thoracic Society (No 6/16 of Process) two points were made. At page vii the Guidelines note that a change of 10% in FVC readings was required in CFA cases. In contrast, Mr Young's FVC readings have shown remarkable consistency, as have the TLC readings. Only Mr Young's TLCO readings had shown a deterioration. Dr Rudd had said in evidence that the TLCO figures shouldn't be taken in isolation and that the TLC figure was most important, while Professor Stevphenson seemed to have dismissed all but the TLCO readings. The pursuer's position was that the lung function test readings were of limited value but that if they were to be taken into account they were more consistent with a diagnosis of asbestosis than CFA.

[3738] Mr Hadjucki submitted that the most interesting figures were the mortality figures in the extensive study the results of which are produced at Nos 7/4 and 7/5 of Process. That was a study where patients were to be excluded if they had sufficient occupational exposure to asbestos to be accepted as a basis for pneumoconiosis. The overall median survival from entry to the study was 2.43 years. While Professor Stevphenson said he and other colleagues disagreed with this study, even he accepted a median survival of 5 years. Mr Hadjucki suggested that the pursuer's mortality is going to be atypical of CFA, even if that longer period was taken. He noted that Mr Young had been accepted as suffering from occupational pneumoconiosis resulting from his working with asbestos for the purpose of the Social Security (Industrial Injuries) (Prescribed Diseases) Regulations 1985.

[3839] In summary, Mr Hadjucki submitted that the admission of sufficient exposure to put him at risk, the predicted mortality being inconsistent with CFA, the radiological signs being neutral and the lung function tests overall suggesting a relatively slow progression, all pointed in favour of the pursuer's condition being asbestosis.

Submissions for Defender

[3940] For the defender, Mr McCormick began by submitting that although it was admitted that the pursuer had had sufficient exposure to put him at risk of developing asbestosis, the magnitude of that risk was not admitted. Given that the only issue for the court was whether the pursuer has developed asbestosis, the defender should be assoilzied, either because Professor Stevenson's evidence should be preferred, or if I was unable to prefer the evidence of either expert witness, in which case the pursuer would be unable to discharge the burden of proof on him.

[4041] Mr McCormick put forward a number of criticisms of Dr Rudd's evidence. There was an error of transcription in his report in relation to the date of the first FVC test, which fed through to what was recorded in the report about the length of time during which the pursuer had suffered from luing fibrosis. It was accepted, however, that in his evidence Dr Rudd had clarified the period as five years, from 2004. An attack of Dr Rudd's treatment of statistics in the Al Jared study (No 6/17 of Process) was made. He accepted in cross examination that the statistical rule which he purported to apply (mean plus or minus two standard deviations covers 95%) required a symmetrical, normal type distribution. It was contended that he had failed to give evidence that this requirement was satisfied, or that he had attempted to check it. It was contended that the graph (Nno 7/8 of Process) and the evidence of Professor Stevenson were sufficient to show that the requirement was not satisfied. Mr McCormick went so far as to contend that Dr Rudd was evasive when pressed on the matter. Dr Rudd had said that the paper concerned had been peer reviewed and that the focus on his treatment of statistics was " making a mountain out of a molehill", but he had used the statistic to classify the decline in Mr Young's TLFCO results as normal.

[4142] Mr McCormick said it was significant that Dr Rudd had stated that there was "little published on the rate of decline" in asbestosis. The only paper he cited was the Al Jared study. Even the pursuer's annual decline in TCO was 0.33, that was clearly above the highest figure for ex or non smokers and well above the overall average of 0.07. The pursuer had been a smoker but was thought to have given up in late 2002.

[4243] I was invited to accept Professor Stevenson's evidence on the dangers of comparing results between different laboratories. The Glasgow rate of 0.62 or the Edinburgh rate of 2.14 were even further above the results in the Al Jared paper. It was suggested that Dr Rudd's refusal to accept that CFA was more likely when only these results were considered contrasted with what was described as the more open-minded approach of Professor Stevenson. Mr McCormick also criticised Dr Rudd's disregard for the fact that only 5% of asbestosis sufferers do not have pleural disease. It was argued that it was reasonable to weigh different probabilities such as lack of plaques, rate of decline, survival time and so on when reaching an overall view as to the balance of probabilities.

[4344] Dr Rudd's evidence about survivorship had been based principally on the studies Nos 7/4 and 7/5 of Process which were based on patients recruited in 1990 to 1992 at a time when they already had abnormal radiographs and were accordingly much further down the road of CFA. Mr McCormick criticised Dr Rudd's suggestion that there would be less than a year's delay between CT scans showing fibrosis and radiographs showing fibrosis as not being "backed by evidence." He invited me to rely on Professor Stevenson's estimate of a five year median survivorship based on his clinical practice and those of his colleagues. It was suggested that the pursuer is now at about the median survival for CFA, thus roughly one half of other CFA patients would have survived this long.

[4445] It was suggested that the difference between Dr Rudd and Professor Stevenson as to whether the pursuer's exposure had been moderate or heavy was not particularly important, although I was invited to accept Professor Stevenson's contrast between this case and the very heavy exposure of the past.

[4546] In conclusions, Mr McCormick argued that Dr Rudd's approach came close to saying that if there was sufficient exposure to create a risk of asbestosis and there is fibrosis of the lungs, then the fibrosis is asbestosis and should be rejected. He contended that Professor Stevenson's approach was to weigh the factors jointly and should be preferred.

Discussion

[4647] It seems to me that the starting point in considering the issue of whether Mr Young suffers from asbestosis or CFA is the agreed evidence about his exposure. It is accepted (i) that the pursuer was exposed to asbestos during his employment at Rosyth Dockyard (in the employment of the Ministry of Defence) and Comrie Colliery (in the employment of the National Coal Board) as a result of the negligence of his employers and (ii) that he has had sufficient cumulative exposure to asbestos to be at risk of developing asbestosis of the lungs. Accordingly, this is not a case where the length and severity of exposure to asbestos fibres must be considered in assessing the likelihood of the pursuer suffering from the condition. The risk factor for it is indisputably present.

[4748] A number of other undisputed factsfindings should be noted at this stage. The pursuer has suffered from fibrosis of the lungs since 2004, when he had reported shortness of breath and was found to have crackles over the lung bases which indicated the presence of diffuse interstitial fibrosis. The first relevant lung function tests carried out thereafter were in June 2005 in Fife. A series of lung function tests hasve taken place since then, the most recent results being in Glasgow in January 2009. The results of those tests are as recorded in paragraphs (insert nos)
[11] and [12] above. The pursuer has continued in employment between 2004 and the date of proof.

[4849] Taking the evidence of both expert witnesses together, it seems to me that there are four main areas of contention to be examined. These can be summarised by posing the following questions;

(1) How important to the differential diagnosis is the agreed cumulative exposure to asbestos at a level sufficient to be at a risk of developing asbestosis?

(2) How important to the differential diagnosis is the absence of pleural disease?

(3) Lung Function Tests. (a) Should all tests carried out be taken into account or only the series from a single laboratory? (b) What significance if any should be attributed to the results of theof the lung function tests that are taken into account?

(4) What are the relative median survival rates for the two conditions? Where does the pursuer currently sit within those? What significance if any should be attached to that?

[4950}] Before addressing each of these questions in turn, I have the following general conclusions to make on the two expert witnesses. While both experts gave their evidence in a reasonably measured and helpful manner, I have no little hesitation in preferring the evidence of Dr Rudd to that of Professor Stevenson on the material issues in the case. Dr Rudd was an impressive witness. He is far more experienced than Professor Stevenson in the particular skill of differential diagnosis between asbestosis and CFA. It has formed a reasonably significant part of both his clinical and research activities. As already indicated, Professor Stevenson quite properly deferred to Dr Rudd on some of the more technical aspects, such as the detail of the calculation of asbestos fibres per millilitre year. Further, contrary to the submissions made for the Defender, it seemed to me that Dr Rudd was the expert who was willing to look at all the available material in reaching his conclusion, while Professor Stevenson had a tendency to "to " cherry pick" the results that fitted better with his conclusion, for example by excluding the original results of the Fife laboratory and by effectively ignoring the lack of deterioration in the serial FVC and TLC results. I noted also that on matters that where he disagreed with Dr Rudd he was unable to point to any specific research in his favour, maintaining for example that the survival rate for CFA was " ...longer than the literature would have us believe." At times his view appeared to be more of a " gut reaction "reaction" than a considered opinion based on the available material. I will now elaborate on this general comparison of the two experts in addressing the specific questions I have identified.

[4951] On the first question, there was a clear difference in approach between the two experts. Dr Rudd was clear that, as CFA is a diagnosis by exclusion, agreed exposure to asbestos at a level that gave rise to risk of that condition, was a crucial diagnostic factor. Professor Stevenson, although noting the importance of the occupational history appeared to regard it as no more than one of the factors to weigh in the balance. It seems to me that Dr Rudd is correct in his approach to this issue. One can readily envisage situations where a patient has had some exposure to asbestos, but there is a question about whether it was at a level sufficient to give rise to a risk of developing the disease. There the exposure would be no more than an adminicle of fact to be weighed in the balance of the differential diagnosis. But in this case Dr Dr Rudd said that the Pursuer pursuer had exposure well over the minimum threshold of 25 25 fibres per millilitre years and Professor Stevenson deferred to Dr Rudd's greater knowledge on fibre counts. In any event, I accept Dr Rudd's evidence that once over the minimum threshold, the level of exposure is not relevant to diagnosis, only to severity of the condition. For these reasons I accept that the agreed exposure sufficient to give rise to the risk of asbestosis is a crucially important starting point on the issue of differential diagnosis.

[5052] In relation to the second question, the absence of pleural disease requires to be considered. The statistics highlighted in the evidence (Copley et al, No. 6/18 of Process) relate to asbestosis sufferers, not a comparison of those with asbestosis and those with CFA. Thus it could be misleading to express the likelihood of the Pursuer pursuer suffering from asbestosis by reference to those statistics. The issue is whether it feeds into the balance of probabilities on the differential diagnosis at all. Dr Rudd concluded that while it may be factor, it should be given far less weight than other issues, such as the agreed exposure to asbestos and the rate of decline. I agree with that conclusion. Professor Stevenson's approach of attributing such importance to the absence of pleural disease would inevitablye result in his wrongly excluding that minority of asbestosis sufferers without pleural disease from diagnosis. Dr Rudd was able to point to a specific example form from his own clinical experience of a patient who had died without being correctly diagnosed as suffering from asbestosis because of the absence of pleural disease. It was not suggested to Dr Rudd that he was too influenced by that one unfortunate experience and I did not form the impression that he was. The example simply highlighted that it would be wrong to use the absence of pleural disease as a central diagnostic feature.

[5153] So far as the lung function tests are concerned, a range of results was were available, spanning the period April 2005 to January 2009. The two experts agreed that the results of the Fife laboratory in 2007 should be ignored as " rogue" results where the patient had not performed properly, perhaps due to suffering form a cold or similar virus. The sole basis of excluding the 2005 Fife results put forward by Professor Stevenson was that they came form from a different laboratory. But reference was made to results from an Edinburgh laboratory, which were of some interest, albeit that they had to be treated with caution given the discrepancies that can exist. On balance, it seems to me that it is more helpful to consider all of the available material, including results from different laboratories, unless there is a specific reason to reject a particular set of results as unreliable. Here, there is no such reason and where the task is to assess the results to see whether there has been an overall deterioration in lung function, it would be artificial to exclude the first set of properly obtained results. To do so, as suggested above, effectively amounts to selecting the results that best suit the conclusion of the party who seeks to ignore themone set.

[5254] The question of the significance, if any, to attach to the lung functions test results overall is a more difficult one. Dr Rudd's view was that they showed that Mr Mr Young's condition was behaving more like asbestosis than CFA, although he accepted that one particular result, the drop in TLCO between 2008 and 2009 from 7.1 to 6.1 would be significant if the decline continued in future results. Professor Stevenson considered that the drop was significant enough to help tip the balance in favour of the diagnosis of CFA. He concluded that the rate of decline ( using only the Glasgow results) was greater than occurs in asbestosis. In my view, the results must be taken together, not just by comparing the results of the different laboratories, but also by considering all results taken on each occasion. I accept Dr Rudd's evidence that one must look at both the volume (TLC) and the function of the lungs (TLCO) to get a picture of the disease. Of all the test readings only one result - the drop in TCLO was probably significant. The FVC and TLC readings showed very little decline. All of the readings were subject to a margin of error that could be as much as 0.5 for the TLCO reading in question. Both experts agreed that the results were not so marked as to point very clearly in favour of one diagnosis or the other. However, Dr Dr Rudd expressed the view that on balance the rate of progression was more consistent with asbestosis than CFA. Much was made in cross examination of Dr Dr Rudd of his reference to statistics to illustrate that Mr Young's decline was consistent with that of other asbestosis sufferers as found by Al Jared et al in the study published at No 6/17 of Process. I gained the impression that Dr Rudd was knowledgeable about statistics and well understood the contention that was being made, namely that the results of the Al Jared study did not represent a normal distribution that would be represented by a symmetrical hump and that the standard deviation suggested by him might accordingly be overstated. His response was that he was not attempting to suggest that the results showed a perfect normal distribution and that he had used the statistic only as a way of looking at the data, rather than as a diagnostic test. As the Al Jared paper ( in which Dr Rudd had been involved) was peer reviewed it remained of some importance, as most of the observations within it fell within the range of Mr Young's results. Insofar as he was asked about this, Professor Stevenson did not profess to be an expert in statistical analysis. His point was that, if one plotted the results of the Pursuer's pursuer's Glasgow tests alone, the Pursuer's pursuer's rate of decline was 0.62 units per year, which was greater than any of the patients in the Al Jared study. In light of the view I have taken about looking at all of the available material, I do not consider that evidence to be of as much assistance as the figure of the average decline of 0.33 units per year using the whole period of test results. That decline falls within the range found in the Al Jared paper. In summary, the test results span a four year period. Nothing in them is illustrative of the type of rapid decline that seems to be typical of CFA, where one would expect Mr Young's symptoms also to have materially worsened. Accordingly, I accept that, while it is quite finely balanced, the test results support rather than detract from a diagnosis of asbestosis.

[5355] The two experts also differed over the issue of the relative survival rates for the two conditions. They agreed that CFA tended to progress quicker than asbestosis, but Professor Stevenson said that he had patients who had been diagnosed with CFA and who had been attending his clinic for some years. Even leaving to one side the possibility that some of those patients could have been incorrectly diagnosed, such anecdotal information is less helpful than the published results of a large UK study ( NosNo's 7/4 and 7/5 of Process), where median survival was found to be 2.43 years. It is certainly possible that the very low median survival of patients in that study is explicable in part by the stage that their disease had reached by the time of entry. Other studies, albeit smaller ones, have found median survival of four to five years. I cannot prefer Professor Stevenson's suggestion that various medical professionals might disagree with the published literature to the evidence of Dr Rudd who was involved in the major study concerned. Taking all of the evidence led on this aspect together, I can conclude only that average survival from diagnosis for CFA sufferers is somewhere between 2.43 and 4.5 years. Mr Young has now survived longer than average for a CFA sufferer. That is another factor that points, on balance, to him being an asbestosis sufferer. . It is again noteworthy in this context that the Pursuer pursuer has continued to work and that there are no physical signs of the rapid decline that is, sadly, an inevitable feature of CFA.

Decision

[5456] In summary, I have reached the view that all of the important diagnostic factors in this case militate in favour of a diagnosis of asbestosis and I find that that is the condition from which the Pursuer pursuer suffers. Accordingly, the defender is liable to him in damages.

[5557] While the parties have agreed damages in the total sum of £50,000, ( representing £34,208 for solatium, £7,514 for past wage loss and £8,278 for future earnings) interest to date will require to be added to that and I will have the case brought out By Order so that parties can address me on the specific sum to be awarded in the final decree.