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Cite as: [1999] ScotCS 218

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OUTER HOUSE, COURT OF SESSION

0724/5/97

OPINION OF LORD BONOMY

in the cause

LINDA ROSE SMITH AND OTHERS,

Pursuers;

against

UPPER CLYDE SHIPBUILDERS LIMITED (IN LIQUIDATION) AND ANOTHER,

Defenders:

________________

Pursuers: D. I. Mackay, Q.C.; Thompsons

Defenders: R. W. J. Anderson; Biggart Baillie

8 September 1999

William Nairn Smith died on 13 October 1997. Prior to his death he raised this action for damages. The action has been continued by his executors and family. There is no doubt that Mr Smith died of a form of cancer which affected the pleura, the outer lining, of the right lung. The defenders are the successors of his employers, John Brown Shipbuilders Ltd, for whom he worked for between four and five years between 1959 and 1969. While working there as a coppersmith's assistant he was exposed to asbestos dust and its adverse effects. The defenders accept that they are liable to compensate his estate and his relatives, if that exposure caused the cancer from which he died. However Mr Smith was a heavy smoker who drank to excess and was always an anxious individual. The defenders maintain that it has not been proved that the cancer from which he died was caused by his exposure to asbestos in the employment of John Brown Shipbuilders Ltd. The other possible cause is a particular form of cancer of the lung which arises in the lung or adjacent respiratory tract.

The cancer caused by exposure to asbestos dust is mesothelioma. Counsel and the expert witnesses were agreed that during life it is difficult to make a firm diagnosis of mesothelioma. Indeed it can even be difficult at post mortem. Before Mr Smith died mesothelioma had been diagnosed by those responsible for his care. Their opinion was firm enough to convince the procurator fiscal, to whom the death was reported, to decide that a post mortem was unnecessary. If there had been a post mortem, it is unlikely that a proof would have been necessary. The post mortem would probably have been conclusive. I was not addressed on the normal role of the procurator fiscal in such circumstances, nor on any guidance that there may be to fiscals from Crown Office. However it is clear that in a case such as this the procurator fiscal should be slow to accept the diagnosis made in life and decide that there should be no post mortem. If it is important for any purpose to know whether or not a deceased contracted mesothelioma, then a post mortem is necessary. Relatives are often anxious that there should be no post mortem. Fiscals may well want to respect that wish wherever possible. However, relatives may not be aware of the difficulties of diagnosis that should be known to fiscals. It would be of assistance in any case where mesothelioma is suspected if fiscals were to advise relatives that a post mortem would be appropriate if a firm diagnosis of mesothelioma was likely to be required for any purpose.

It is plain from the evidence of the deceased and that of John Stewart, an independent Health and Safety Consultant, who had personal experience of visiting all the important shipyards in the West of Scotland in the 60's in his role as factory inspector, that the deceased was exposed to many times the quantity of airborne asbestos that was recognised in the early 1960's as the level above which exposed employees were at risk of contracting disease. In the end there was no dispute between the parties but that the deceased was exposed in a way that could readily cause mesothelioma. The medical experts were agreed that the most likely time for such a condition to manifest itself was thirty to forty years after the exposure. Mr Smith fell comfortably into the category of those exposed to asbestos in the late 1950's and 1960's who might be expected to contract mesothelioma.

Medical opinion was, however, divided on the question whether asbestos did in fact kill Mr Smith. The pursuers were able to rely on the opinion of Dr John Borthwick MacDonald, Consultant Physician at Crosshouse Hospital, Kilmarnock, who treated the deceased and diagnosed his condition as mesothelioma, and the expert evidence of Dr James Wright Kerr, Consultant Physician, Dr Brian Moule, Consultant Radiologist, and Professor George Peter Thomas Barclay, Consultant Pathologist, who each considered that asbestos killed Mr Smith. The defenders relied on the expert evidence of Dr Allen Robert Gibbs, Consultant Histopathologist, and Dr Francis Moran, Consultant Physician, each of whom considered that on balance the cause of death was adenocarcinoma, a form of lung cancer probably caused by smoking. The choice for me is between these two. A number of these witnesses acknowledged that their diagnosis was marginal, and all were agreed that the diagnosis was a difficult one to make, particularly in the absence of a post mortem examination. While both parties invited me to determine the balance of probabilities in their favour, it was an important part of the defenders' submission that I might find the issues so evenly balanced that I could not make a determination either way. As a result, their submission encapsulating both positions was that the pursuers had failed to prove on a balance of probabilities that the deceased died as a result of mesothelioma caused by his exposure to asbestos.

Counsel were agreed that the court was a far from ideal forum to determine this difficult issue. That might be true if what they sought was the "true" diagnosis of the deceased's condition. However it is not the function of the court to provide the definitive answer to a question such as that. What the court has to decide is whether the case advanced for the pursuers has been established on a balance of probabilities. Applying that test to this case the question is whether it has been proved that it is more probable than not that the deceased died because of exposure to asbestos. If that is not established the defenders succeed.

The doctors in the case arrived at their opinions of the cause of death by applying their knowledge and experience to the diagnosis of the deceased's condition from their consideration of material provided from various sources, which differed from doctor to doctor, but which included the results of the use of diagnostic tools, histories taken in interview, examination of the deceased (in two cases only) and clinical assessment of the overall picture presented. As a result of considering the material available to them the doctors have reached different conclusions. In that situation it would be presumptuous of me to think that the court can analyse the material available to provide a definitive answer. I have come to the conclusion that, in light of the evidence presented and the submissions made in this case, the appropriate way for me to determine the question is to evaluate the opinions by considering the relevance and importance of the material founded upon by each witness, the weight the witness gave to the various factors identified as material to the issue of differential diagnosis, the process by which the diagnosis was made, and any change in emphasis on particular factors and indeed any change in opinion along the way. In the end, I consider the question for me is whether I am sufficiently confident in the opinions, or any of them, expressed in favour of the diagnosis of mesothelioma to say that that opinion is probably correct.

There were three issues over the admissibility of evidence. The first of these related to the extent to which regard might be paid to the whole terms of a publication or an expert report which was spoken to in part in evidence. For the pursuers, Mr D I Mackay, Q.C., submitted that, once part of a publication or report had been referred to, then the rest of it could be taken into account. Mr R W J Anderson, for the defenders, submitted that I could take account of parts of publications and reports not spoken to, but that I must do so with caution quite simply because they were not the subject of cross-examination. At one stage there was an issue about reference to reports produced and agreed in terms of a joint minute to be "reports prepared by the persons by whom they bear to have been prepared", which had not been spoken to at all but, in the end, no such report was relied upon. On the question of reports and publications spoken to in part, I do not consider it appropriate to have regard to the remainder thereof. For example, reference was made in the evidence of Dr Gibbs to a publication by Hartmann & Schütze, which eventually became No.54 of process. That reference was to the total number of mesothelioma and mesothelioma-like tumours found on post mortem examination in 33,500 autopsy cases. Within that publication, and indeed within a paragraph that was partly spoken to by Dr Gibbs, there is a statement that there is no correlation between the origin of a mesothelioma-like tumour (in this case adenocarcinoma) and smoking or exposure to asbestos. That conclusion depends on quite separate material from the results of the post mortems carried out. No witness spoke to that conclusion. Indeed the only witness who was asked, Dr Moran, stated firmly that it was wrong. In that situation the only evidence I can take account of is that of Dr Moran. Apart from that specific example, both counsel referred in only fairly general terms to parts of that publication not specifically spoken to in evidence. I did not find that any of these references would have been of any assistance to me had I considered it appropriate to refer to them. As it is I have left out of account any reference that was made to the contents of any publication or report not spoken to or adopted in evidence.

The second issue related to the way in which the defence case was conducted. The pursuers contended that they had been prejudiced in the presentation of their case and that that should be reflected in the way in which I treated certain evidence.

As I indicated above, the issue in the case is one of differential diagnosis between mesothelioma and adenocarcinoma. The alternative of adenocarcinoma is a refined version of the defenders' case on Record in Answer 6 that the deceased's symptoms were "suggestive of cancer of the lung". Adenocarcinoma is a form of cancer of the lung. Dr Moran considered that 40% to 50% of lung cancers are now adenocarcinomas. However it is only a small proportion of these adenocarcinomas that mimic the classic appearance of mesothelioma. That the issue was as finely tuned as that only began to emerge in cross-examination of the pursuers' first medical witness Dr Kerr.

Mesothelioma is a tumour of the pleura. The adenocarcinoma which Drs Gibbs and Moran had in mind is a tumour which originates in the lung, probably the lung substance where the interchange of air takes place, or in a fairly remote part of the bronchial tree, which may be beyond the sight of a doctor looking through a bronchoscope inserted through the respiratory tract into the lungs. The tumour spreads from there to the pleura. The appearance of the tumour on the pleura, certainly on x-ray and CT scan, is identical to that of mesothelioma. The mechanism of death is the same: the tumour spreads over the pleura to encase the lung and squeeze it and restrict the function of the lung.

The fact that the differential diagnosis was between these two conditions was not heralded in the Record or the reports lodged on behalf of the defenders and spoken to in evidence. In his report, No. 31/1 of process, Dr Gibbs referred throughout to "lung cancer". In Dr Moran's reports 32/1 and 32/2 there is no indication of the specific nature of the suggested alternative to mesothelioma, and in concluding the latter report Dr Moran said "...it is a reasonable conclusion that the balance of probabilities marginally favours the diagnosis of bronchial carcinoma." Bronchial carcinoma is an expression covering a whole range of forms of lung cancer. Indeed Dr Moran agreed that his opinion expressed in court was much more refined than that in the reports and that the reasons for arriving at his conclusion were either not mentioned or not clearly highlighted in his reports.

Mr Mackay submitted that the pursuers had been prejudiced in the presentation of their case by the defenders' failure to disclose their case prior to the proof and by the progressive development of the defenders' case in the course of the proof. He relied particularly on the fact that it was not put to any of the pursuers' witnesses in clear terms that the choice was a stark one between these two conditions with the result that particular points relied upon by the defenders had not been presented to the pursuers' witnesses for comment.

Mr Mackay also founded upon the circumstances which led to there being no post mortem. The action was raised by the deceased in life. By the time Dr Moran was instructed to examine the deceased the Record had been closed. He carried out the examination on 25 June 1998. A proof was assigned for November 1998. Dr Moran's report following his examination was not written until 5 November 1998, after the deceased had died. As at his death the diagnosis of mesothelioma, which had already been made at Crosshouse Hospital at the end of 1997 and the beginning of 1998, had not been challenged by the defenders and there was not seen to be any need to do a post mortem. While Dr Moran explained that he considered his first report to be very much a preliminary one since he anticipated being able to take account of post mortem findings before writing his final report, it is plain that the objective of the deceased was to have the case heard in life.

Taking both points together Mr Mackay submitted that, because of the prejudice caused by the failure to challenge the diagnosis prior to the death and the way in which the case developed in the course of the proof, where the evidence on any matter was evenly balanced or there were two possible inferences which might be drawn from evidence, I should make the finding or draw the inference that was favourable to the pursuers.

While I find force in that submission, I have not found it necessary to approach the evidence in that way. On the other hand, had I found the evidence to be so finely balanced that I could not make a determination on the balance of probabilities in favour of the pursuers or the defenders, I would have found for the pursuers on the strength of this point, since I regarded the prejudice as material and caused by the overall conduct of the case by the defenders.

The third issue related to two pieces of evidence given by Professor Barclay. He had seen medical notes kept by the hospice where the deceased spent the last three days of his life. That was his second admission. In his report of 23 January 1998, 38/9 of process, confirmed in his evidence, Professor Barclay recorded a note on re-admission to the hospice of "an enlarged cervical node mass" being seen. He also recorded from his study of these notes reference to haemoptysis during these last three days. Haemoptysis is blood staining of the sputum from a bleeding lesion in the lung or possibly some part of the respiratory tract. Professor Barclay found that the late stage at which both these features were identified supported his diagnosis of mesothelioma. Pursuers' counsel, however, submitted that evidence from the hospice records, which were not produced, was inadmissible. He submitted that the admissibility of hearsay evidence in written form in terms of section 2(1) of the Civil Evidence (Scotland) Act 1988 depended upon the application of Rule of Court 36.8 requiring a party wishing to rely on such evidence to make application to the court to receive the written statement. No application had been made under the Rule and so the written statement was inadmissible. Apart from that, the best evidence rule required that the hospice records should be produced before they could be relied upon. In my opinion neither of these arguments is a basis for declaring this evidence to be inadmissible. Rule 36.8 applies to the situation where a party seeks to rely on a statement or a report without that being spoken to by any witness. In the present case Dr Barclay spoke to the statement which is relied upon. That statement was just as much the evidence of the examining doctor at the hospital as his oral evidence would have been since it was simply his record of what he found. The examining doctor could easily have been led to speak to what he found without reference to that statement. Equally, he could have been invited to refer to it as an aide memoire. In terms of section 2(1)(b) of the 1988 Act, such a statement, spoken to by a witness in oral evidence in the course of the proof, is admissible as evidence of any matter contained in the statement of which direct oral evidence by the person making it would be admissible. In terms of section 2(1)(a), evidence shall not be excluded solely on the ground that it is hearsay. Professor Barclay gave hearsay evidence of the statement made by the examining doctor at the hospice. The present circumstances are not bedevilled by any problems relating to the distinction between original documents and copies such as occurred in Japan Leasing (Europe) plc v Weir's Trustee (No.2) 1998 S.C. 543. In my opinion Professor Barclay gave straightforward hearsay evidence admissible in terms of section 2.

On the other hand, in relation to hearsay evidence of this kind there is always a question over the weight, if any, to be attached to it. For reasons which I shall explain, I found the evidence of Professor Barclay an unsatisfactory basis for arriving at a conclusion as to diagnosis. I am not prepared to rely on his evidence except where it is supported by other evidence which I accept. That does not apply to his recollection of what was in the hospice records.

There is a further reason for disregarding Professor Barclay's recollection of these records. I am satisfied from other evidence in the case that what may have been recorded as a cervical lymph node mass was in fact a multi-node goitre which had been noted when the deceased was a patient at Crosshouse Hospital and also by Dr Moran when he examined him. That condition was accepted as unrelated to whatever caused the deceased's death. So far as haemoptysis is concerned, I am satisfied from other evidence that at the distressing terminal stages of the deceased's illness it is entirely possible that an infection affecting the lung, combined with the stress caused by the deceased's gasping for breath, might well have given rise to a bleeding lesion. The earlier presence of haemoptysis would be a factor against diagnosis of mesothelioma. At the stage at which it may have appeared, it was in my opinion a factor of no significance.

Before I deal with the opinions of the medical witnesses, it is appropriate that I should record the relevant clinical history.

In early Summer 1996 the deceased began to suffer from increasing breathlessness. Although he indicated in his evidence at commission and at examination by Dr Moran that the onset was earlier, that is inconsistent with the evidence of his wife, and the medical records, which parties accepted as accurate. It is plain that the deceased had a bad memory affected by medication. When he attended Crosshouse Hospital on 25 and 26 July he had been suffering 4 to 6 weeks of increasing breathlessness. His chest was x-rayed then. The radiologist reported as follows:

"No previous chest films available for comparison. There is extensive opacification in the right lung field with pleural shadowing along the lateral aspect of the lung and fluid in the fissure. Following aspiration there has been slight reduction in the pleural shadowing over the right lung. Extensive pleural shadowing, which is most probably due to fluid rather than pleural thickening, persists. Underlying intrapulmonary pathology particularly around the right hilum cannot be excluded. The trachea is displaced towards the right side of the level of the thoracic inlet, presumably by an enlarged left lobe of thyroid.... Appearances are suggestive of multinodular goitre."

Dr MacDonald, the responsible consultant physician, was on holiday when this was done. In his absence his registrar prepared the report for the deceased's general practitioner, and this was seen by Dr Macdonald before it was sent out on 1 August. In it he reported as follows:

"Chest x-ray was reported as showing partial collapse of the right lung with a probable pleural effusion. There was also a central opacity highly suspicious of a bronchial neoplasm... Obviously we are suspecting a pulmonary neoplasm (and ? mesothelioma) but this remains unconfirmed."

In fact, as can be seen above, the chest x-ray was not reported as showing partial collapse of the right lung.

A further x-ray instructed by Dr MacDonald on 19 August showed little change.

The deceased was then admitted to Crosshouse Hospital on 9 November 1996 for bronchoscopy, which was carried out under general anaesthetic by Dr Glynne R Jones, consultant physician. He reported as follows:

"Using the fibrescope, the right upper lobe segmental orifices were all patent. Reddish tissue bulged into the posterior segmental bronchus right upper lobe more distally. The area was biopsied but histology showed a fragment of lung tissue without any significant disease. No evidence of malignancy was seen."

Dr Jones further recorded that the bulging tissue looked more inflammatory than malignant and was possibly a slowly clearing right upper lobe pneumonia, although he could not rule out the presence of an underlying malignant lesion. During the proof a letter dated 19 January 1998, which Dr Jones wrote to Professor Barclay, was produced. In that letter he said the following:

"I cannot now recall for certain whether the lesion did extend distally from that point, but reading the notes suggests to me that I could not see the distal extent of the lesion. I cannot say whether the reddish tissue I saw was more in keeping with inflammatory than malignant disease. I accept your view that mesothelioma tissue can look like granulation tissue at times. It seemed probable that the lesion which I identified was responsible for the partial collapse of right lung. I did suspect that the tissue had arisen in lung parenchyma with subsequent infiltration of the bronchus from outside, but that is purely a subjective opinion."

Following a further x-ray in November, the deceased attended again at Crosshouse Hospital on 18 December for CT scan. The report says this:

"Circumferential pleural thickening extends from the right lung apex to base. This is associated with generalised loss of volume within the right lung. No apparent hilar or mediastinal lymphadenopathy. The left lung field is clear... These appearances are in keeping with a mesothelioma. A 21 gauge needle was used in an attempt to aspirate any fluid component at the right lung base. No fluid was obtained....".

When Dr MacDonald saw the deceased on 9 January 1997 he reported episodes of exceptionally severe stabbing right chest pain lasting two to three minutes occurring roughly once a week. A chest x-ray taken then showed the progression of the tumour and a reduction in right lung volume.

At that stage it was plain to Dr MacDonald that the condition was terminal. There is no satisfactory evidence of the results of any examination of Mr Smith between then and his death in October.

In their reports, and in their evidence, the medical witnesses dealt with a number of clinical features identified by diagnostic tools, such as CT scans and bronchoscopy, by examination, and by taking a history from the deceased, which could be relevant to the diagnostic conundrum "is it mesothelioma or lung cancer?" However, as the defenders' case became more refined, first of all in the evidence of Dr Gibbs, and then in the evidence of Dr Moran, it became clear that many of the features which often help to distinguish one from the other were largely immaterial to the differential diagnosis in this case because of the similarity in nature of the two tumours in issue and in the mechanism by which they affected the patient and ultimately killed him. Much time was spent on the question whether shadows on x-ray film were indicative of pleural fluid or pleural thickening. If they represented pleural thickening at an early stage in the progression of the disease, then that would favour mesothelioma. In the end, Dr Moran's position was that the shadows could be either or a mixture of both and were consistent with either diagnosis. The complaint of 4 to 6 weeks increasing breathlessness on presentation was consistent with both conditions. One diagnostic feature that is normally particularly helpful as identifying mesothelioma is the development of severe pain because the tumour erodes ribs and penetrates the chest wall. However, the type of adenocarcinomatous tumour postulated in this case can do exactly that. The very late development of mestastases, i.e. secondary tumours, and the absence or very late occurrence of haemoptysis are indicators of mesothelioma. However, these are features consistent with the form of adenocarcinoma advanced here. The same is true of the absence of finger clubbing and of the period of survival from diagnosis. In any event, there was a dearth of material in relation to a number of these factors because there was no evidence of the results of any examinations of the deceased after 9 January 1997.

The expert medical witnesses fell into three categories, two pathologists, two chest physicians and one radiologist. Each was able to express an opinion as to the appropriate diagnosis of the deceased's condition, albeit that meant entering, to some extent, into the area of the specific expertise of others. Each of the witnesses was, in my opinion, qualified to express such an opinion.

Having said that, I consider it to be important that a medical witness should exercise some caution in reaching conclusions where the conclusions depend to a large extent on material falling within the particular expertise of another. In view of the difficulties of diagnosis recognised by each of the other witnesses, I found Professor Barclay's conclusion that the material available was "overwhelmingly in favour of the diagnosis of malignant mesothelioma" rather surprising. I note that in January 1997, Dr MacDonald used the word "overwhelmingly" in relation to that diagnosis, but in the context of advising the deceased and his wife his opinion on his condition at a stage when a decision had to be taken on how to handle the terminal balance of the deceased's life. In writing to the deceased's general practitioner on 13 January 1997, he expressed his conclusion much more cautiously and said quite simply that he felt that Mr Smith had a mesothelioma. The material available for a pathologist to work on in this case was extremely limited in the absence of post mortem findings. The bronchoscopy findings of Dr Jones were the main piece of pathology evidence available to Professor Barclay. He considered that the failure to remove any malignant tissue suggested that the targeted reddish area must have been bony hard. That suggested to him that the reddish tissue was likely to be mesothelioma of a particular granulated type. No other witness considered that the evidence relating to the reddish tissue was suggestive of a mesotheliomatous tumour at that location. I considered his conclusion about the nature of the reddish area to be entirely speculative. He proceeded on the basis that Dr Glynne Jones did not remove any part of the area he targeted. The same assumption was made, but leading to a different conclusion, by Dr Moran. However, the written record made by Dr Jones, and the letter quoted above, do not indicate that he thought he had failed to remove a piece of the tissue he targeted. He stated that there was no significant disease and no evidence of malignancy. He did not state that he had failed to remove some of the reddish tissue. I am not prepared to read any more into these documents than the facts specifically recorded. The subjective opinion of a consultant physician not called to give evidence, qualified in the way it is in Dr Jones's letter, is, in my opinion, of no value as evidence. If either party had intended to rely to any significant extent on the findings, or lack of findings, made by Dr Jones or on the nature of the material he saw and biopsied or failed to biopsy, then that party ought to have led him as a witness. In their evidence, the defenders' witnesses relied on certain interpretations of what was stated by Dr Jones, which I did not find convincing. I shall deal with that in due course. The pursuers' counsel, on the other hand, did not invite me to rely on the evidence of Professor Barclay and thus did not invite me to rely on his interpretation of this pathological material. In my opinion, that was a wise decision.

While Professor Barclay is plainly eminent in the field of pathology in which he has been a consultant since 1965, and while he had a close involvement in the developing study of the relationship between asbestos and mesothelioma during his time in Rhodesia, later Zimbabwe, where he was Professor of Pathology at the Medical School in Salsbury for 20 years from 1971, there was no attempt made in the presentation of his evidence to relate his experience there to the issue that arises in this case. His position was made difficult by his having a certain view of the history of the deceased, which was not borne out by the evidence. He understood him to have had a three year history of chest illness from 1994, and throughout his evidence he appeared to proceed on the basis that by December 1996 the mesothelioma was of long standing and had been developing insidiously for a lengthy period. In deciding that the material was overwhelmingly in favour of the diagnosis of malignant mesothelioma, he relied on his interpretation of the work of Dr Jones, with which I have already dealt, the views largely of others rather than himself on the interpretation of x-rays and CT scans, and the developing clinical course of the disease which he had misunderstood. When it came to listing the factors that he considered supported his diagnosis, he did so under reference to an out-dated edition of the leading textbook on Occupational Lung Disorders by Parkes. I found his evidence unconvincing and I am not prepared to rely on his opinion.

Dr Gibbs, led by the defenders, is a very distinguished histopathologist, who has published extensively on chest diseases, including bronchial carcinoma, occupational lung diseases in general, and mesothelioma and other asbestos related diseases in particular. The pathology of the lung, including the diagnosis of lung cancer or mesothelioma, is his particular area of expertise. He recognised the handicap of the absence of post mortem. In his report, No.31/1, it is not possible to identify why he concluded that there were slightly more factors in favour of a diagnosis of lung cancer than mesothelioma. He identified a number of items which are neutral. He referred to chest pain and breathlessness and considered that, if they went back to 1994, that would favour lung cancer. However, the evidence did not support that. He acknowledged that the CT scan appearances on their own favoured a diagnosis of mesothelioma. In mentioning haemoptysis he did not suggest that that occurring or not was of any real significance. I have already indicated my reasons for leaving haemoptysis out of account. He relied on what he perceived to be the greater risk of developing lung cancer if you are a smoker than of developing mesothelioma if you are exposed to asbestos. Counsel were agreed that the statistical evidence in the case was largely unsatisfactory, with the one exception of the material contained in the study by Hartmann & Schütze, referred to earlier, to which I shall return. I agree with counsel that the rest of the statistical evidence presented was too vague to provide a basis for reaching any conclusions on the question of differential diagnosis. All that was proved from the witnesses' knowledge of statistics was that Mr Smith was at risk of contracting mesothelioma and at risk of contracting lung cancer.

The one material factor Dr Gibbs appeared to rely on in his report as favouring lung cancer was evidence of the collapse of the upper lobe of the right lung. In cross-examination he appeared to concede that he may have made an assumption about upper lobe collapse from what he had read in the medical records to which I have already referred. He conceded that he might not have seen any satisfactory evidence of a lung collapse, but maintained that that was not what mattered. A partial collapse of the lung would point towards lung cancer, since it was likely to be the result of a blockage in the bronchial tree caused by a tumour. However, in the present case the important thing was that "something was going on in the lung". He considered that there was some abnormality. He had seen slides of the tissue obtained by Dr Jones. That looked like normal lung tissue and did not appear inflamed to him. In re-examination he repeated the point saying: "What matters is that there is something going on within the lung substance." I found it very difficult to understand what he meant. He explained in his evidence that the fact that the reddish tissue was bulging was of no significance in pointing to a differential diagnosis. He made no mention of the tissue bulging in his report, and that is why. Indeed he said that, because the biopsy was negative, he took no account of it. It was a relatively normal lung that he saw on the slides, but there was "an abnormality". He thought that perhaps Dr Jones's forceps had slipped off the material. However, of more importance to him was that he thought Dr Jones had seen something abnormal. He suggested three possible explanations: (1) a tumour which was out of reach and growing away further out of reach; (2) a tumour arising outside the bronchus but growing to involve the wall of the bronchus; or (3) inflamed tissue at the centre of which was a small tumour. All of these suggestions depended upon the observation and impression of Dr Jones. In the absence of evidence from him, I am not prepared to draw any conclusion about the nature of what he saw as indicative of "something happening" that is consistent with any specific diagnosis, in this instance lung cancer or more particularly adenocarcinoma. Mr Anderson, in his submissions, pointed to the evidence of Dr Gibbs that he had reached the conclusion that the evidence narrowly favoured a diagnosis of adenocarcinoma from a consideration of all the relevant factors. However, in his submission he identified no factor on which there is satisfactory evidence which points to that diagnosis.

In the course of cross-examination, Dr Gibbs volunteered evidence from his recollection of a published study by Hartmann & Schütze entitled "Mesothelioma-like Tumours of the Pleura: A Review of 72 Autopsy Cases". This document (No.54 of process) was one of a number of documents which the defenders sought to lodge at the bar when the case called for proof. They were all articles from journals that Dr Gibbs would refer to. It was conceded that they were, on the face of it, intimidating. It was acknowledged that the pursuers had had no opportunity to consider them. It was suggested that they might assist the clearer comprehension of what was not a straightforward matter. In opposing the lodging of these, Mr Mackay explained that he had just received them and was not in a position to judge the significance of them, and that it was far too late for these to be allowed to be lodged. I refused the motion because the pursuers had been given no opportunity to consider these prior to the proof. After Dr Gibbs had given evidence Mr Mackay sought to lodge the Hartmann & Schütze paper. Since the initial reference to the material therein was one made spontaneously by Dr Gibbs, and since the figures he had referred to were thereafter the subject of re-examination and further cross-examination, and in the interests of accuracy in relation to a matter on which evidence had been led without objection, I allowed the study to be lodged, on the understanding that I would consider any motion made by the defenders, for example for adjournment or to recall Dr Gibbs, in the event that they felt prejudiced by any use made of the material in the report. In the event, no additional evidence emerged under reference to the report and no motion was made for the defenders.

The evidence given by Dr Gibbs, which can be cross-checked against the publication, was that out of 33,500 miscellaneous autopsy cases collected over more than 30 years, between 1957 and 1987, there were 219 diffuse pleural tumours, that is tumours like that suffered by the deceased. In the study diagnosis was done by histological testing. Because that was not possible in 41 cases they were left out of account. Of the remaining 178 cases, 106 were primary pleural mesotheliomas. Of the other 72 cases the vast majority, viz. 63, had obvious primary lung adenocarcinomas. Indeed in 27 cases the appearance had been misinterpreted as mesothelioma at first examination at post mortem. The point Dr Gibbs sought to make from this evidence was that there has generally been an over-diagnosis of mesothelioma in the absence of adequate histological tests. In keeping with that it was possible that endeavouring to diagnose mesothelioma without either histological tests or any post mortem examination could lead to mis-diagnosis in favour of mesothelioma. Thus an adenocarcinoma bearing the appearance of a mesothelioma on CT scan might be misdiagnosed. I take account of that. However, Dr Gibbs, like Drs Moran, Kerr, Moule and MacDonald expressed the view that the CT scan appearances in this case pointed towards mesothelioma. The only value of the statistical material from the study is that it tends to support the view that most diffuse pleural tumours which look like mesotheliomas are mesotheliomas.

Dr Francis Moran is a familiar expert witness in cases involving asbestos related disease. That is so because he has an unrivalled experience in examining and treating patients suspected of suffering from asbestos related complaints. He has spent a working lifetime as a clinician in that field. He has seen hundreds of patients with a view to giving evidence in court and, although retired now from his clinical post at Glasgow Royal Infirmary, close to the shipyards and other industrial concerns where asbestos was prominently used, he continues to examine patients with a view to giving expert evidence. His work has been in respiratory medicine in general and as a result he has enormous experience of diagnosing and treating lung cancer. He was the final witness. He heard most of the earlier evidence. He had the benefit, therefore, of making a judgement and diagnosis having heard the views of the other witnesses on the material facts. Against that background I must obviously be slow to reject his opinion. His opinion in evidence was the same as that expressed in his letter of 3 February 1998, No.32/2 of process:

"...it is a reasonable conclusion that the balance of probabilities marginally favours the diagnosis of bronchial carcinoma."

Mr Anderson in his submissions invited me to accept Dr Moran's evidence because he had made his diagnosis after considering all the evidence. He contrasted that with the approach of Drs Kerr and Moule, which he characterised as starting from a presumption in favour of mesothelioma because of the x-rays and CT scans. I was surprised to hear Mr Anderson contrast the respective approaches in this way. I was not conscious of such an approach in the evidence of Drs Kerr and Moule. On the contrary I formed the impression that Dr Moran had reached a preliminary view on scanty material and had tended to view any additional material that emerged in the context of how that might be seen to fit in with the view he had formed. I found it unsatisfactory that in the letter I have referred to and in his original report of 5 November 1997, No.32/1 of process, Dr Moran made no reference to adenocarcinoma nor the particular appearance thereof that mimics mesothelioma. I quite appreciate that it might be said that mesothelioma mimics the appearance of that particular form of adenocarcinoma. However, that approach would be inconsistent with the general view I have recorded above that the appearance on CT scan was the classic appearance of mesothelioma and the acknowledgement by Dr Moran and Dr Gibbs that that is the diagnosis towards which the CT scans point. In view of the failure to obtain biopsy material, the CT scans have remained the best diagnostic tools available. It was a noticeable feature of cross-examination of the pursuers' witnesses that the clear-cut choice between mesothelioma and adenocarcinoma giving the appearance of mesothelioma was not specifically put as the defenders' case. My impression was that the case, largely founded on the evidence of Dr Moran, was developing as the proof progressed. In the end, his position was that the most important pieces of material leading him to the conclusion that the balance favoured adenocarcinoma were the findings by Dr Jones at bronchoscopy. He interpreted Dr Jones's report and letter as indicating that he had not managed to biopsy his target bulging red tissue. I have already explained why I am not prepared to draw such a conclusion in the absence of evidence from Dr Jones. Dr Moran drew from the bronchoscopy result the conclusion that a primary adenocarcinoma was developing distally in the bronchus. When the evidence of Dr Kerr and Dr Moule to the effect that there was no sign of a primary tumour in the lung or bronchial tree which could account for the spread of tumour to the pleura and ultimately to envelope the lung was put to him, he responded that the shadow on the right upper lobe on x-ray and the appearances of pleural effusion or thickening shown on CT scan included the primary tumour at its source. In the face of the very clear evidence of both Dr Kerr and Dr Moule about the absence of any sign of a primary tumour and its significance to their conclusions, the possibility that the very shadow and features they were regarding as pleural tumours might in fact be partially within the lung was never put to them. I found that unsatisfactory. When I suggested to Dr Moran that it was unsatisfactory that a point as important as that had not been put to either of these witnesses, he agreed. This point emerged fairly late in his evidence. One might be forgiven for viewing it as an afterthought. I confine myself to regarding it as another example of the unsatisfactory way in which the defenders' case appeared to develop as the proof progressed.

Dr Moran also relied on evidence that there was at least a partial collapse of the upper lobe of the right lung. That was important to his opinion since one obvious explanation for that would be blockage of a bronchus caused by a tumour. He could not recollect whether he had simply relied on the letter which inaccurately recorded the x-ray report as indicating a partial collapse, or whether there was some other source for that information. Since the report of the x-ray which was supposed to show the partial right collapse does not refer to it, and since Dr Moran had no clear recollection of any other source than inaccurate reference to that report, there was no acceptable evidence from Dr Moran of a partial collapse of the lung. I have accordingly come to the conclusion that the material on which he relied principally to decide narrowly in favour of lung cancer did not provide a sound factual basis for his conclusion.

It is plain from Dr Moran's report of 5 November 1997 that he formed a poor impression of the deceased when he saw him on 25 June 1997. He may well have been entitled to do so. When it came to expressing his opinion on his condition, he recognised that Mr Smith had malignancy in his right chest, which almost certainly involved the pleura. However, Dr Moran's opinion was that it could not be said that the CT scan was diagnostic of mesothelioma. He then went on to express reservations about whether Mr Smith had worked continuously enough in employment exposed to asbestos to have contracted mesothelioma. He referred to his life long and continuing heavy smoking, up to 40 cigarettes per day. He then concluded:

"For all these reasons and despite the fact that he appears to have a malignant tumour involving the pleura, it cannot be said that the balance of probabilities favours a diagnosis of mesothelioma at this stage."

Although in the earlier review of medical records and history he did refer to the letter which mentioned partial collapse of the right lung and to the initial diagnosis as bronchial carcinoma and recorded the bronchoscopy result in one sentence, I find it surprising that none of these are mentioned in the "opinion" section of the report in view of the importance of these factors in his evidence.

He was later asked to comment on a report by Professor Barclay and responded to instructing agents on 3 February 1998 in 32/2. He reviewed a number of factual matters and stated that he had already addressed the question of appearance at bronchoscopy (presumably in the report), and then concluded as follows:

"If one were to date the onset of Mr Smith's illness to 1994 then I believe the balance of probabilities would fairly strongly favour the diagnosis of bronchial carcinoma. Dating the onset to or near mid-1996, the features favouring bronchial carcinoma are the very heavy and prolonged smoking history, the collapse or partial collapse of the right upper lobe, the eventual appearance of haemoptysis, the appearance of a probable large malignant node mass in the neck and the absence of markers of asbestos exposure. The features in favour of mesothelioma are the history of exposure to asbestos (which may have been minimal) and the appearances on the CT scan which although consistent with mesothelioma could also occur in bronchial carcinoma. Having regard to the clinical course of Mr Smith's illness and to the available evidence, lacking as it is in important detail, it is a reasonable conclusion that the balance of probabilities marginally favours the diagnosis of bronchial carcinoma."

Apart from the reliance on factors for which I do not consider there is a sound factual basis or which are neutral, the absence of reference there to the bronchoscopy results as of any significance on the narrow diagnosis is surprising. For these various reasons I do not have confidence that Dr Moran's diagnosis is soundly based in this particular case. I am not prepared to make a finding on a balance of probabilities on the strength of his opinion. My decision not to rely on the opinion of Dr Moran is fortified by the view I have formed of the evidence of the other witnesses to which I now turn.

One factor which made the evidence of Dr Moran particularly important was that he was one of only two medical witnesses who examined the deceased in life. The other was Dr MacDonald, the consultant in charge of his case at Crosshouse Hospital, Kilmarnock. I have already made reference to his ultimate diagnosis in January 1997. He was described by both counsel as a witness who left a favourable impression because of the straightforward and clear way in which he gave his evidence. At the conclusion of his evidence I particularly noted my impression that he dealt confidently with the questions, was comfortable in his knowledge of the case, was at ease in the witness box, and had a particular facility to make complex matters clear. When the deceased was first admitted to hospital in July, Dr MacDonald was on holiday. He later took charge of his case. Initially Dr MacDonald had suspected lung cancer. He knew the deceased was a fairly heavy smoker. He had chronic bronchitis and he had some wheezing. Thereafter as the investigation progressed, no clear evidence emerged to support that suspected diagnosis. The x-rays in July showed either pleural effusion or pleural thickening. An attempt was made to withdraw fluid by aspiration, but none was withdrawn. The presence of fluid rather than pleural thickening would have been an indicator pointing towards lung cancer, since fluid was a more common feature of lung cancer than mesothelioma, although it was agreed in the end that the latter could produce both fluid and thickening. Dr MacDonald did not regard the bronchoscopy as providing evidence of the presence of a malignant tumour within the lung. None of the other indicators of lung cancer, such as haemoptysis or enlarged lymph nodes in the mediastinum, appeared. There was no evidence of any change within the lung itself during the period the deceased was in his care. It was in his opinion unusual for there to be no sign on x-ray or scan of some changes in the lung as the primary lung cancer tumour developed. As with so many other things it was possible for a tumour to remain occult, but very unusual. Although his assistant, Dr Byrne, had reported an earlier x-ray as showing a partial collapse of the lung, that was a mistake. The x-ray report disclosed no such finding. The CT scans taken on 17 December showed the classic features of a mesotheliomatous tumour encasing the lung. Shortly thereafter, when he saw the deceased in January, he complained of periodic severe stabbing pains. When he consulted with the deceased and his wife in January he felt that the correct diagnosis was mesothelioma. Unfortunately the alternative of adenocarcinoma spreading over the pleura to encase the lung was not put to Dr MacDonald. The possibility that a sub-pleural tumour could do so was put, but what exactly was meant by a sub-pleural tumour and the relevance of such a condition to the case did not become clear since the matter was explored no further.

While Dr MacDonald remained firmly of the view that the correct diagnosis was mesothelioma, I would not have been prepared to make a finding that the deceased died from mesothelioma on the strength of his evidence alone. He had seen fewer cases of mesothelioma than the other medical witnesses - 30 to 40 - and based his diagnosis largely on one positive piece of information, viz. the CT scan results, which were not explored with him in any detail in evidence, and on other largely negative or neutral findings. While I had confidence in his approach and in his diagnosis, I would not have been prepared to make a finding on a balance of probability in the absence of reliable support for this conclusion. The important thing for me is that Dr MacDonald was the consultant physician responsible for the investigation and treatment, as far as that was possible, of Mr Smith's condition. Dr Moran acknowledged that in making a difficult diagnosis, where a number of factors have to be taken into account and evaluated together, the treating physician who has seen the patient has an advantage over others because he has seen for himself the overall presentation of the illness in the patient.

The expert consultant physician led by the pursuers was James Wright Kerr. He has been retired from clinical practice for over 9 years. While that is of some importance in assessing his evidence, Mr Anderson for the defenders did not identify any specific part of his evidence that was affected by that fact. While Dr Moran is more recently retired from clinical practice and is more widely involved in the examination of patients for medico-legal purposes, Dr Kerr has a wealth of knowledge and experience gained over many years of active clinical practice in the heartland of asbestos related complaints. He was consultant physician at Glasgow's Western Infirmary throughout his career from the 1950s. He was in practice there in the late 1960s and 1970s when the effects of exposure to asbestos emerged. Countless patients suffering from asbestos related complaints have been examined and treated by him and his colleagues. Since he was first instructed after Mr Smith's death, he did not have the benefit that Dr Moran and Dr MacDonald had of seeing the deceased in life. He is nevertheless very well qualified to express an expert opinion on the appropriate diagnosis in this case.

An important element in his conclusion was his finding that there was no evidence of partial collapse of the right upper lobe caused by obstruction of an airway. He placed material reliance on his interpretation of the x-ray films and CT scans taken at various stages. The starting point was an x-ray of 17 August 1989 which showed clear lung fields and a normal and undisturbed trachea. The deceased had attended for that x-ray because of the goitre in front of his trachea. In x-rays taken on 25 and 26 July 1996 the trachea was seen to be deviated towards the right and there was considerable shadowing over the right lung. While the goitre might partially explain the deviation of the trachea, the main reason for that was the constriction of the upper part of the lung by tumour causing the trachea to deviate towards that lung. Had there been a blockage causing partial collapse of the lung, then the deviation would have been greater. Dr Kerr was convinced that the shadow over the lung was pleural thickening rather than fluid and therefore solid pleural tumour. An unsuccessful attempt had been made to remove fluid. That, along with the configuration of the shadow, convinced Dr Kerr that the shadow was thickening and thus a tumour. Dr Kerr had looked for signs of "intrapulmonary pathology" as against "pleural pathology", in other words signs of changes within the lung that might indicate the development of a tumour. He could find none. He considered the findings of Dr Jones on bronchoscopy to be consistent with his findings on x-ray. In his opinion the pink tissue seen by Dr Jones was consistent with a reaction in the lung to the constriction by the pleural tumour. A lateral x-ray film of 19 August and further x-ray film of 28 November were consistent with his view.

The CT scans of 8 December 1996 confirmed the position for him. They showed the development of the tumour which now encircled the lung and the trachea. The involvement of the trachea explained its continued deviation. The picture presented was a classic picture of mesothelioma. Further support for the view that exposure to asbestos had affected the right lung was to be found in the presence of pleural plaques, a feature caused by the effects of asbestos, on a CT scan of the left lung. The final x-ray was on 9 January 1997 and showed the progression of the tumour with the lung volume decreasing generally.

A number of other features of the case noted by Dr Kerr were consistent with the condition being mesothelioma. Dr Kerr was examined and cross-examined at length on these features, such as breathlessness, pain, finger clubbing, etc. I have already indicated that in view of the similar nature of mesothelioma and the adenocarcinomatous tumour advanced as an alternative by Dr Moran these do not materially assist a differential diagnosis. When the possibility of adenocarcinoma, along with a number of other possibilities, was put to Dr Kerr, he acknowledged that it could account for the appearances on x-ray and CT scan. However, the important thing to observe is that the various features that could be significant for diagnostic purposes were put to Dr Kerr, he considered them carefully, and in the light of all of them be confirmed his view that the appropriate diagnosis was mesothelioma. In the end, there was no dispute but that the other features were not in themselves diagnostic either way and were consistent with either diagnosis.

The only radiologist to give evidence was Dr Brian Moule. He supported the diagnosis of Drs MacDonald and Kerr. As a consultant radiologist for 33 years at Glasgow Royal Infirmary and Ross Hall Hospital he has a wide experience of considering x-ray films and, for the last 15 years since scanners were introduced, CT scans disclosing asbestos related lung damage, including mesothelioma. In the x-ray film of 25 July 1996 he identified a number of shadows as pleural thickening, in particular a grey line along the right lateral chest wall, linear opacities across the ribs towards the mid-line and the elevation of the right dome of the diaphragm. The linear opacities were particularly helpful diagnostic indicators because they were lines which did not correspond with fissures and could be said with certainty to be the result of pleural thickening. The film of 26 July showed virtually the same features, and that of 19 August showed the elevated right dome of the diaphragm and pleural thickening of the lung posteriorly. The further development of the pleural thickening to virtually encase the right lung could be seen in the CT scans of 18 December. All of these various films showed deviation of the trachea towards the right. In the area of the neck he considered that to be the result of the goitre. Lower down both trachea and oesophagus were slightly displaced, which he considered to be the result of the contraction of the lung caused by the surrounding pleural thickening occupying the chest area. He considered that if there had been a significant lung collapse the trachea would be displaced further to the right. He could see on film and scan no evidence of a localised collapse of the right lung. Indeed, he considered it significant that the spacing of the ribs and the dimensions of the rib cage appeared to be similar on the right and left sides of the chest, whereas if the right lung had collapsed to any material extent the rib space would appear smaller on the right side of the chest. What could be seen was general reduction of lung volume caused by the constricting effect of the widespread pleural thickening. The scans also showed the extension of the pleural thickening through the chest wall eating into rib. He also identified nodular bulges. All of these features were characteristic of mesothelioma. He also found support for this diagnosis in the fact that the scans showed pleural calcification on the left lower chest postero-medially. The overall appearance of the CT scans was of a classic presentation of mesothelioma as a primary tumour encasing the lung. He acknowledged that these characteristics can occur in lung cancer. However he, and as far as he was aware everyone else who had studied the films and scans, had been unable to identify the site within the lung of any tumour which could have spread from there to the pleura.

At various stages in his evidence Dr Moule acknowledged that individual features on the scans could be said to be consistent with lung cancer, albeit that would be unusual. For example, he did acknowledge that nodular pleural thickening can occur in lung cancer and he also acknowledged that the tumour encasing the lung, which was so characteristic of mesothelioma, can occur in lung cancer. It was plain that he had considered the possibility of these features being indicative of lung cancer rather than mesothelioma. However, having done so, he came to the conclusion that the picture was one of mesothelioma, because he could not find any feature such as collapse of the lung that was particularly indicative of lung cancer, and what he did find was a picture that was the classic presentation of mesothelioma.

In my opinion, both Dr Kerr and Dr Moule approached the task of diagnosis objectively. They considered all material factors. In the light of their knowledge and experience they concluded that the condition suffered by the deceased was mesothelioma. I reject Mr Anderson's submission that Dr Kerr was unduly influenced in his consideration of the matter by the CT scans. In my opinion they were the best diagnostic tools available in this case. I did not understand Dr Moran to disagree. It was for Dr Kerr to give appropriate weight to these in the light of his acknowledge and experience when considered against all the other relevant material. In my opinion that is what he did. Dr Moule's knowledge and experience in interpreting x-rays and CT scans confirmed the conclusions which Dr Kerr drew from them. Both Dr Kerr and Dr Moule gave sound reasons for concluding that there was no evidence of a tumour developing in the lung or bronchial tree. Of particular importance in arriving at a final diagnosis was the view formed by both independently that there was no evidence of lung collapse consistent with obstruction of airways by a tumour and that any contraction of the lung was entirely explained by the developing tumour encasing the lung and trachea. That evidence is inconsistent with Dr Moran's view that there was partial collapse of the lung for which there must be some explanation other than the pleural tumour. I have already explained why I consider no positive finding pointing towards lung cancer can be drawn from the bronchoscopy results. I can find no reason for considering the conclusions reached by Drs Kerr and Moule to be other than sound. I have confidence in their respective diagnosis. For what little weight it has, the study by Hartmann & Schütze supports their diagnosis.

Mr Mackay, for the pursuers, invited me to rely upon the very fact that mesothelioma was the certified cause of death in the deceased's death certificate as a fact in support of that diagnosis. While a death certificate may in itself be acceptable evidence of the fact of death, I do not consider the certificate on its own to bear any weight on the question of the cause of death.

Accordingly, on the strength of the combined evidence of Drs MacDonald, Kerr and Moule, I am satisfied that the condition from which the deceased died was probably mesothelioma. I accordingly find that the defenders are liable to make reparation to the pursuers for their resultant loss.

Parties have agreed damages in terms of their joint minute.

I shall accordingly repel the defenders' pleas and sustain the first and second pleas-in-law for the pursuers and pronounce decree in favour of the first named pursuers as executors of the deceased in the sum of £57,410.26 in terms of the first conclusion, decree in favour of the deceased's widow, the second named pursuer, in the sum of £28,500 in terms of the second conclusion, and decree in favour of the third, fourth and fifth named pursuers in the sums of £2,000, £5,000 and £5,000 respectively in terms of the third, fourth and fifth conclusions. Interest will run on each of these awards from the date of decree.