Durie Or Cook v Wyvern Structures Ltd [2000] ScotCS 233 (22 August 2000)

BAILII is celebrating 24 years of free online access to the law! Would you consider making a contribution?
No donation is too small. If every visitor before 31 December gives just Â£5, it will have a significant impact on BAILII's ability to continue providing free access to the law.
Thank you very much for your support!

[1] The pursuer in this action of reparation is the daughter of Charles Durie ("Mr Durie") and his wife Janet ("Mrs Durie"), who both resided at 34 Rylees Road, Glasgow. Mr Durie was born on 7 May 1917 and died at the age of 75 on 26 August 1992. Mrs Durie survived him by only two days, dying on 28 August 1992. The pursuer was confirmed as Mr Durie's executrix on 20 September 1993 and as Mrs Durie's executrix on 19 May 1993. She sues as an individual and as executrix of each of her parents. The action was originally raised by Mr Durie on about 6 July 1992 against the first defenders. By interlocutor dated 16 December 1994 the pursuer was sisted as pursuer in place of Mr Durie. Her children were also sisted as pursuers at the same time, but by a subsequent amendment they left the process, and I am no longer concerned with any claim by them. The second defenders were brought into the action by virtue of an interlocutor dated 13 September 1995. The second defenders departed at the proof from a plea-in-law tabled by them to the effect that the action so far as directed against them is time barred. I am accordingly concerned only with issues relating to the merits of the action and to the quantum of damages.

[2] The cause of Mr Durie's death was certified as "i(a) Metastatic Disease (b) Bronchial Carcinoma". The pursuer's case is that as a result of negligent exposure to asbestos while in the employment of both defenders Mr Durie contracted bilateral pleural thickening and pulmonary fibrosis (asbestosis) and that he died of metastatic disease and bronchial carcinoma as a direct result thereof.

[3] Neither of the defenders admit that Mr Durie was employed by them, so the first issue I have to consider is whether the pursuer has succeeded in proving that he was employed by each of them. The pursuer was born on 15 December 1954 and could give no direct evidence about Mr Durie's employment before she was born or whilst she was very young. She did, however, say that he told her that he had worked on ships in various places and mentioned particular employers by name. These were the first defenders, who were then called Munro & Miller Limited, and the second defenders, Shaw Petrie Limited. He did not mention any dates to her, but said that he had been with each of them for various periods. The main evidence on this issue came from Francis Maguire, a partner in the firm of Thompsons, the solicitors instructed by Mr Durie and thereafter by the pursuer. He spoke to documents contained in the file relating to Mr Durie, and also to more general information held by his firm relating to employers and to employees who had been exposed to asbestos in the course of their employment with them. One source of information is the Contributions Agency, who can provide details of a person's employers from 1961 onwards. Mr Maguire obtained such a history relating to Mr Durie, which showed him to have been in continuous employment from 1961 to 1980 with a number of employers. Neither of the defenders appeared in the list. There was no evidence that Mr Durie was exposed to asbestos in the course of his employment with any of these employers.

[4] This history requires to be related to that taken from Mr Durie by a Special Medical Board when he attended a Medical Boarding Centre in Glasgow on 20 August 1990. According to this history, Mr Durie worked, among other occupations, for seven years as a boilermaker's helper and for seven years as a plumber's helper, a period of 14 years in all. As related to the remainder of this history, this led the Board to conclude that he had been exposed to asbestos for about 14 years from 1958 to 1972. It seems clear from information provided by Mr Durie to Mr Maguire that in giving this history he was referring to his employment with the defenders. In this case, the dates which the Board arrived at cannot be correct, because they are inconsistent both with the information provided to Mr Maguire and with the employment history from 1961 onwards which I have already referred to. I am not disposed to place reliance on the dates which the Board arrived at.

[5] By contrast, I was impressed by the care with which Mr Maguire had gone about the task of establishing Mr Durie's employment history on the basis of information provided by him and with the help of former fellow employees. Employment histories collated by the solicitors assisted in tracing some of these. Mr Maguire's file contained a number of hand-written letters by Mr Durie and a legal aid application signed by him on 12 March 1992. A former fellow employee, Robert Milligan, who had died by the date of the proof, provided a hand-written statement confirming the employment of Mr Durie by the first defenders "during 1946". The legal aid application, which at that stage related to proposed proceedings against the first defenders only, contained the statement that he was employed by them from about 1942 to about 1946. Mr Durie did, however, state in correspondence with Mr Maguire that he had been employed by the second defenders, and indicated that he had been in touch with named persons who confirmed this. These persons were not called as witnesses, but reference to them in the correspondence lends credence to Mr Durie's statement that he was employed by the second defenders.

[6] On the basis of this information it is averred in the pursuer's pleadings that from about 1942 until about 1946 Mr Durie was employed by the first defenders, and in about 1946 and again between about 1956 and 1962 and again in about 1965 he was employed by the second defenders. The history provided by the Contributions Agency would exclude any employment with the second defenders from 1961 onwards, but otherwise I am prepared to accept that Mr Durie was employed by each of the defenders for periods of several years prior to 1961, and on balance I am prepared to treat the periods prior to 1961 referred to in the pleadings as being reasonably accurate. There is no suggestion that Mr Durie would not have done his best to give a truthful account of his employment history and while, as can be seen from the history in the Medical Boarding Centre records, vagueness or faulty recollection may give rise to the attribution of incorrect dates, I am satisfied that Mr Maguire took sufficient care to establish a history for the purposes of litigation for me to be entitled to place reliance upon it. Neither of the defenders was in a position to challenge the information provided by Mr Durie that he was employed by each of them, and this issue was not strongly contested by either of them. For the reasons I have discussed I am prepared to accept that Mr Durie was employed as averred by the pursuer, except for the period from 1961 onwards.

[7] Mr Durie told Mr Maguire that he was employed as a plumber's mate. The pursuer avers that he worked at various shipyards and that while on board ship he worked in confined spaces alongside and in close proximity to the plumbers in the boiler rooms, engine rooms and cabins. The plumbers worked with asbestos and he assisted them. In addition, insulators and joiners worked in and around the places where he worked and they worked with asbestos. He and his fellow workers were involved in the mixing of asbestos powder with water to form paste and cement (colloquially known as "monkey dung") and in cutting boards and sheeting with knives and saws. These averments are based on information provided by Mr Durie. There is support for them in the statement provided by Robert Milligan to Mr Maguire. He said that during 1946 there was a large backlog of ships waiting to be converted from coal to oil burning, so the majority of the work was carried out in the engine room and boiler room. He continued:

This appears to me to be a graphic account of conditions which were no doubt typical in the industry at the time. There is no similarly detailed account of conditions that Mr Durie would have experienced while he was employed by the second defenders, but the information he gave was to the effect that they were similar to those with the first defenders, which is why the pleadings do not distinguish between them. The pursuer said that he complained in her hearing of dirty working conditions with both defenders. There would be asbestos dust in his hair, clothes, mouth, sandwiches and so on.

[8] I am satisfied that there is sufficient information to allow me to conclude not only that Mr Durie was employed by each of the defenders for the periods I have mentioned, but also that during these periods he experienced significant exposure to asbestos, sufficient to cause or materially contribute to any asbestos-related disease from which he subsequently suffered.

[9] By joint minute the parties have agreed that, subject to proof of employment, Mr Durie's exposure to asbestos while in the employment of the defenders was negligent.

[10] Both of the defenders have tabled pleas seeking apportionment between them of any liability to make reparation to the pursuer, in terms of section 3 of the Law Reform (Miscellaneous Provisions) (Scotland) Act 1940. This issue was more strongly contested between the defenders than was the question whether Mr Durie had been employed by either of them. In a case where there was sufficiently detailed evidence about the duration and intensity of exposure to asbestos in the course of the pursuer's (or deceased's) employment with each of the defenders, it would be possible to apportion liability between them on a basis related to that evidence. In the present case such evidence is lacking. I have already referred to such of it as is available. Reference was made to a passage in the evidence of Dr James Kerr, an expert witness for the pursuer, in which he said that Mr Durie told him that the bulk of his exposure to asbestos was during the war years. This might point to greater exposure while in the employment of the first defenders than in that of the second defenders. I am not, however, disposed to place much weight on Dr Kerr's report of what Mr Durie said to him, as compared with what Mr Durie told Mr Maguire. Mr Maguire was concerned, as Dr Kerr was not, to establish periods of employment with different employers and the degree of exposure during each period of employment, and the information provided by Mr Durie for this purpose did not place the same emphasis on the war years. I have come to the view that there is no material evidence upon which I could base a distinction between the two defenders. While in the course of his employment with each of them Mr Durie was negligently exposed to asbestos for a period and to a degree sufficient for each of the defenders to have made a material contribution to any asbestos-related disease from which he suffered in later life. In the circumstances I propose to regard their contributions as being equal to each other because I am unable to find any basis for distinguishing between them. This being so, I would apportion any liability to make reparation to the pursuer equally between the defenders.

[11] There was ample evidence that throughout his adult life Mr Durie was an habitual smoker of cigarettes. Figures which he gave for his consumption varied from time to time and, as is common with smokers, may in any event have been understated. He also professed at times to have reduced his consumption or to have given up smoking entirely (as doctors repeatedly advised him to do), but his claims were belied by the nicotine stains on his fingers. It is not necessary for me to arrive at any accurate figure for his consumption of cigarettes, but on the evidence I would estimate it at no less than ten a day except towards the very end of his life. It was not in dispute in any event that his consumption of tobacco was quite sufficient to cause or materially contribute to smoking-related diseases. There was also ample evidence, and it was not in dispute, that for many years Mr Durie suffered from obstructive airways disease, chronic bronchitis, emphysema, and pneumonic and other chest infections.

[12] It was a matter of concession that, if it was proved that Mr Durie suffered from asbestosis and that he died from bronchial carcinoma, then his exposure to asbestos made a material contribution to the bronchial carcinoma. The evidence on the questions whether Mr Durie suffered from asbestosis during his lifetime and, if so, whether he died as a result thereof came from five expert witnesses: Dr James Kerr, a consultant physician, and Dr Brian Moule, a consultant radiologist, who were called as witnesses for the pursuer; Dr Francis Moran, a consultant physician, who was called for the first defenders; and Dr Colin Turnbull, a consultant radiologist, and Dr Graham Crompton, a consultant physician, who were called for the second defenders. Each of these witnesses prepared one or more reports, which were lodged as productions. Also lodged as productions were the records of the Southern General Hospital, Glasgow, relating to Mr Durie and part of a form completed by the Special Medical Board also relating to him. Also lodged were a number of radiographs (commonly called x-rays), which I shall describe more fully in due course. By Joint Minute it is agreed that the records of the Southern General Hospital relate to Mr Durie; but it is not agreed that they are accurate. No medical witness was called apart from the experts I have mentioned, from which it follows that no-one from the general practice attended by Mr Durie, the hospital staff or the Special Medical Board was called as a witness.

[13] Before I turn to the evidence of the expert witnesses, I propose to set out the terms of the hospital and other records which were referred to in the evidence. It is to be understood that at this stage I am merely repeating what is stated therein without making any finding as to its accuracy.

[14] The hospital records to which reference was made start with a request dated 28 April 1969 by Mr Durie's GP asking for a chest x-ray to be carried out and stating that the patient complained of weight loss, cough and bilateral chest pain. By letter dated 5 May 1969 Dr K R Urquhart, an assistant chest physician, reported that x-ray examination of Mr Durie showed no evidence of any active intra-pulmonary disease. This radiograph was not lodged as a production. On 12 February 1980 Mr Durie's GP requested that he be seen as he was complaining of cough and anterior chest pain. By letter dated 25 February 1980 Dr Urquhart reported that he was seen on 21 February and that he was not "chesty" as a rule. He had a flu-like illness in December 1979 and had heavy blood-staining of his sputum for several days. This improved after antibiotic treatment but he had recurrence of chest symptoms about six weeks previously. This had now settled but he did get a bit short of breath on effort and had an angina-like discomfort in the chest. The chest was clinically clear. X-ray examination of it showed emphysema. The lung fields were otherwise clear. The previously reported consolidations had completely resolved. It appears from this letter that there had been a number of x-ray examinations, but none of the radiographs was lodged. Dr Urquhart concluded by stating that further follow-up at the chest clinic was not required. By letter dated 20 August 1980, however, Mr Durie's GP again referred him to the hospital, stating that he complained of persistent chest pain and breathlessness. By letter dated 28 August 1980 Dr D Giannini, an assistant chest physician, reported that Mr Durie was seen on that date. He had had no recurrence of the haemoptysis, but had still been having attacks of upper chest pain, particularly when he became breathless. He was a heavy smoker and occasionally had a productive cough. His general condition was good and there was no lymphadenopathy or clubbing of the fingers. Clinically the chest was quiet. x-ray showed changes of emphysema as before and lung function studies on the vitalograph confirmed the presence of obstructive airways disease. The radiograph was not lodged.

[15] On 17 November 1981 Mr Durie's GP again referred him to the hospital, stating that he continued to complain of atypical chest pain, but there had been recent coughing of blood. By letter dated 25 November 1981 Dr Giannini reported that Mr Durie was seen on the previous day. His main complaint was of sternal pain which he felt was superficial and had been present on and off for some years. He tended to have a productive cough and on one occasion some weeks previously he had slight bloodstaining of his sputum. He became a bit breathless on exertion and lung function studies on the vitalograph showed some obstructive airways disease. Clinically the chest was quiet. There was some local tenderness over the sternum. He said that he had a possible injury to his sternum some years previously. Chest x-ray again showed changes of emphysema, but x-ray of the sternum did not show any bony abnormality. Again, this radiograph was not produced.

[16] On 27 June 1986, Mr Durie's GP again referred him to the hospital, stating that he had recently had some chest pain and some blood-tinged sputum. Mr Durie attended on 22 July 1986. X-ray examination of his chest was carried out and Dr W B James, a consultant radiologist, reported that there were appearances compatible with chronic bronchitis and emphysema, which he described as marked. He stated that no other abnormality was demonstrated. This radiograph, which was a postero-anterior (PA) view, taken with the patient standing, was produced. Mr Durie was examined by Dr Jean Black, a senior house officer, who by letter dated 23 July 1986 reported that he told her that four weeks previously he developed worsening of long-standing sternal pain which was sharp and diffuse with no precipitating or relieving factors, and at the same time developed a cough and had three to four days of sputum with dark red haemoptysis. This had now settled. The past history included three or four episodes of haemoptysis over the previous seven years, investigations proving negative. On examination his chest was clear. Chest x-ray showed no active changes. As yet, no sinister cause had been found for his haemoptysis, but Dr Black intended to see him back at the clinic in three months' time.

[17] He was seen again on 22 October 1986, when further x-ray examination of his chest was carried out. In a report dated 23 October 1986 Dr H Dobson, a senior resident, reported on the radiograph that there were changes compatible with chronic bronchitis and emphysema. There was a slight increase in size but not density of the left hilum with a suggestion of increased lung markings in the adjacent lung in the lower zone. These changes seemed to progress somewhat from the previous examination of 23 July 1986 and in view of the history the possibility of a central neoplasm was raised and follow-up was advised. This radiograph, also PA, was produced. Notwithstanding the terms of this report, Dr L Prasad, a chest physician, by letter dated 23 October 1986, reported that Mr Durie was reviewed in the clinic as a follow-up. He was keeping reasonably well apart from aches and pains. Clinically his chest was clear. X-ray did not show any change. On 3 November 1986, however, Dr R D H Monie, a consultant physician, wrote to Mr Durie stating that following his recent x-ray Dr Monie would like to organise for a further view to be taken, and telling him to expect an appointment. On 10 November 1986 fluoroscopy was carried out on Mr Durie's chest. Dr D A R Robertson, a consultant radiologist, reported that the left hilum appeared composed of normal vascular markings and that there was no fluoroscopic evidence of lymphadenopathy. Dr Monie wrote to Mr Durie's GP on 12 November 1986 in similar terms.

[18] On 5 December 1986 Mr Durie's GP again referred him to the hospital stating that he had suddenly become unwell that day with abdominal pain and vomiting up blood which was red in colour. He also had diarrhoea. The GP asked if he could be admitted for investigation for this because there was no past history of any gastro-intestinal symptoms. Mr Durie was admitted to hospital. X-ray examination was carried out. Dr Robertson reported on a radiograph of his chest that there had been no change since the examination of 22 October 1986. This radiograph, also PA, was produced. He also reported on a radiograph of the abdomen that a small area of fluid level behind the heart shadow suggested hiatus hernia but he advised that another radiograph be carried out following a barium meal. On 10 October 1986 Dr James reported on a radiograph following such a meal that there was a large partially reducible direct hiatus hernia with marked gastro-oesophageal reflux, and that no other abnormality was demonstrated. By letter dated 18 December 1986 to Mr Durie's GP, Dr Monie reported that he had been discharged home. The diagnosis was an upper gastro-intestinal bleed due to a Mallery Weiss tear and hiatus hernia.

[19] On 12 April 1990 Mr Durie's GP referred him to the hospital stating that he had been complaining of pain over the left side of his chest wall which was pleuritic in nature together with impaired appetite and weight loss of greater than one stone in the previous one to two months. He stated that Mr Durie gave no history of previous asbestos exposure. He had arranged a chest x-ray for him on 4 April 1990 and the changes were compatible with chronic bronchitis and emphysema but in addition there appeared to be a mass at the left hilum. He was therefore concerned that Mr Durie had bronchial carcinoma and he asked for an urgent appointment. A radiograph taken on 4 April 1990 was produced. This was a left lateral view. It was not clear if a PA view was taken.

[20] Mr Durie was seen by Dr A G Fennerty, a consultant physician, on 30 April 1990. X-ray examination of his chest was carried out, but the radiograph was not produced. Counsel for the second defenders objected to the leading in evidence of the contents of Dr Fennerty's letter on the ground that his opinion depended on the radiograph which was not produced. I allowed this evidence to be led under reservation. Dr Fennerty reported that on examination there were "bilateral coarse end expiratory creps [crackles], loud from the left" but there were no other abnormalities. Chest x-ray confirmed bilateral basal fibrosis with some probably pleural thickening on the left. The left hilum was enlarged. Dr Fennerty stated that he would review the x-rays to see if there had been any change. He was unsure of the cause of the chest pain. Mr Durie might have had a significant asbestos exposure to account for the pleural thickening and mild basal fibrosis. The pain might be secondary to some benign pleurisy. His weight loss was more worrying, however. He intended to review Mr Durie in three weeks' time.

[21] Dr Fennerty saw Mr Durie again on 21 May 1990 and by letter dated 22 May reported to the GP that there had been some reduction in the left-sided pleuritic pain and an increase in weight. In view of his asbestos exposure and basal fibrotic changes he suggested that it might be worthwhile applying for industrial compensation. He said that he would review him again in two months' time with a repeat chest x-ray. At the same time Dr Fennerty made a request for full lung function tests to be performed on Mr Durie at Glasgow Royal Infirmary. Some tests had been carried out on him at the pulmonary function laboratory at the Southern General Hospital on 22 October 1986, 21 May 1990 and 23 July 1990, and were subsequently carried out on 21 January 1991 and 16 September 1991, but the tests which were carried out at Glasgow Royal Infirmary on 13 June 1990 were more extensive. These were for body plethysmography and flow volume, with results for spirometry, diffusing capacity and plethysmography. On one version of these, consisting of one page only, it was reported that body plethysmography revealed mild airways obstruction, bronchodilator produced no significant response, and the diffusing capacity and transfer co-efficient were reduced. In another version, with the same results for spirometry, diffusing capacity and plethysmography, and with additional results on subsequent pages for flow volume and flow volume loop, it was reported that the diffusing capacity and transfer co-efficient were reduced. The flow volume loop values were near the lower end of the predicted range and were in keeping with obstruction in the smaller airways. With the diffusing capacity and plethysmography, overall the results were consistent with emphysema.

[22] On 23 July 1990 Dr Fennerty saw Mr Durie again. By a letter dated 24 July to the GP he reported that Mr Durie's symptoms were much the same with intermittent back pain and shortness of breath. He could walk about a mile on the flat but one flight of stairs and hoovering the house could make him quite breathless. His auto-antibodies were negative but his full pulmonary function tests show "a marked increase" (by which he meant, parties were agreed, "decrease") in his transfer factor and transfer co-efficient. Dr Fennerty stated: "On the balance of probabilities, I think it likely that this man has asbestosis." He noted that he was proceeding with a claim. There was little that he felt able to do for him at that time but he said that he would keep him under review and see him again in six months' time.

[23] On 20 August 1990 Mr Durie was examined by the Special Medical Board in connection with a claim he had made for industrial disablement benefit. An x-ray examination of his chest was carried out and the form completed by the Board included a report on the radiograph. This radiograph was not lodged. Objection was taken by counsel for the second defenders to the line of evidence relating to the Board's diagnosis because it depended on this radiograph. Again, I allowed this evidence to be led under reservation. The Board concluded that, on the balance of probabilities, asbestosis was present. Mr Durie had had fourteen years of asbestos exposure. Chest x-ray showed lower zone interstitial fibrosis and bilateral inspiratory crackles were audible in the chest. He also suffered from emphysema. In a letter to Mr Durie's GP dated 20 August 1990 Dr Deborah Yates, the senior medical officer, reported on the Board's conclusions in rather more detail. She wrote that on examination there was no clubbing or cyanosis. Auscultation of the chest revealed bilateral inspiratory crackles, louder on the left than on the right. These were diminished but not abolished by coughing. Heart sounds were normal. Chest x-ray showed lower zone interstitial shadowing, greater on the left than the right, compatible with asbestosis. There was some left hilar enlargement but she understood that this had been previously investigated and that the shadowing was thought to be vascular in origin. The Board had reviewed the hospital case notes and chest x-rays (she did not say which). They had also seen the hospital lung function tests.

[24] On 16 October 1990 Mr Durie's solicitors (the present pursuer's solicitors) wrote to Dr Kerr asking him to conduct an examination on Mr Durie and report to them on any injury sustained as a result of his industrial exposure to asbestos. Dr Kerr arranged to examine Mr Durie at Ross Hall AMI Hospital on 7 November 1990, where a chest x-ray was carried out. This radiograph, a PA view, was produced. It appears that Dr Kerr and Dr Moule conferred about it at the time. By letter dated 14 November 1990 Dr Kerr reported to the solicitors. He noted Mr Durie's exposure to asbestos. He went on to state that about eight years previously Mr Durie had developed haemoptysis and was investigated at the Southern General Hospital where he was kept under observation. Nevertheless, he only learnt about a possible hazard due to his asbestos exposure in July 1990 (i.e. as a result of Dr Fennerty's opinion). He went on to write:

[25] On 15 January 1991 Dr Kerr wrote again to the solicitors stating that he had had the opportunity to examine the notes from the Southern General Hospital regarding Mr Durie, including the pulmonary function tests carried out at Glasgow Royal Infirmary and correspondence from the DHSS. He referred briefly to the hospital notes from 1969 to 1986, commenting that there was no mention of asbestos or that the lung condition might be related to industrial exposure to asbestos. He referred at more length to the opinion expressed by Dr Fennerty and to the views of the Special Medical Board. He concluded by stating that the reports and the medical records were consistent with his own findings when he examined Mr Durie on 7 November 1990. He stated that further there was no evidence in the records that Mr Durie was aware that he had industrial lung damage due to asbestos before the early months of 1990.

[26] On 21 January 1991 Mr Durie was reviewed in the chest clinic. In a letter written on that date to his GP Dr S Cooper, a senior house officer, described Mr Durie as "this gentleman with asbestosis". The letter stated that he remained breathless on exertion but otherwise appeared quite well. He had no cough or spit. He had been suffering from shingles. He was to be reviewed again in six months' time. He was seen again at the chest clinic on 17 June 1991, with no record beyond the fact of his attendance, and then again on 16 September 1991. On the latter date Dr Monie wrote to Mr Durie's GP that he had seen this "man with asbestosis" and that on the whole he was fairly well from the chest point of view. He was still having trouble with post-herpetic neuralgia. He arranged to review him back in the chest clinic in a year's time.

[27] In the event, Mr Durie required to be admitted to hospital as an emergency case on 24 August 1992. By letter of that date his GP wrote that he had been seen on 21 August 1992 with severe lower back pain which had worsened as he moved in a chair. There were no focal signs but the pain was of such intensity as to require diamorphine and valium. He was seen the next day and was more settled. On 24 August 1992 the pain was less severe but he was markedly anaemic. The doctor felt that he required in-patient investigation of his anaemia and back pain.

[28] What happened thereafter can be taken from a letter by Professor F I Caird to the GP dated 1 September 1992. In this letter Dr Caird stated that Mr Durie was admitted to the Professorial Geriatric Unit on 24 August and died there on 26 August. He complained of three months of low back pain following a fall and also of weight loss, poor appetite and exertional dyspnoea. On examination he was very dyspnoeic and pale. There was finger clubbing. There were some crackles at the right base, and a smooth enlargement of the liver to two fingers breadths. There was some increase in tone and reflexes on the left side, with a flexor left and an equivocal right plantar. Investigations showed an anaemia, leucocytosis, a very high ESR, renal failure, and hypernatraemia. Chest x-rays showed extensive consolidation in the right lobe and possibly in the left posterior basal segment, with probable prominence of the right hilum. Ultra-sound of the liver showed areas of reduced reflectivity, very suspicious of metastases. A working diagnosis of bronchial carcinoma with widespread metastases was made, and he was begun on analgesics. He died suddenly two days later. In a postscript, the professor wrote that x-ray of the lumbar spine showed wedging of L1, but no definite evidence of metastases.

[29] Following Mr Durie's admission two radiographs were taken, one on 25 August 1992 and the other on 26 August 1992. Both of these were produced. The first was an anterio-posterior (AP) view and the second was a right lateral view, both taken with the patient sitting and with the use of portable equipment. In relation to the first of them Dr J Wardlaw, a radiologist, reported that there was consolidation in the right lower zone with bulkiness of the right hilum which even allowing for the amount of patient rotation would be suggestive of an underlying tumour mass. There were bilateral upper zone fibrotic appearances in keeping with tuberculosis. There was a general background increase in the lung markings in keeping with previous occupational exposure or possibly chronic obstructive airways disease. It is clear from the report that the radiologist had not had access to previous films for comparison. In relation to the radiograph of 26 August 1992 Dr K Fowler, a radiologist, reported that the heart size could not be assessed accurately on the projection. There was extensive consolidation in the right lower lobe. There also appeared to be some collapsed consolidation in the left posterior basal segment. The patient was markedly rotated and this, combined with the consolidation, was causing prominence of the right hilum. A follow up film was advised. In addition to the radiographs, ultrasound examination of Mr Durie was carried out. On 25 August 1992 a consultant radiologist, Dr C Campbell, reported inter alia that the liver was slightly enlarged and there were several small areas of reduced reflectivity in the right lobe, very suspicious of metastatic deposits. There was some dilatation of the IVC and hepatic veins consistent with cardiac failure or fluid overload.

[30] After Mr Durie's death his family refused to give consent for a post mortem examination of his body to be carried out, and it was cremated.

[31] As I have said, of the medical witnesses who gave evidence only Dr Kerr had had the opportunity of examining Mr Durie. Apart from this examination, Dr Kerr's report of which I have quoted, the medical witnesses, including Dr Kerr, had to base their opinions on the records I have referred to and on the seven radiographs which were lodged. It would be convenient to summarise what these were. Each of the radiographs taken at the Southern General Hospital on 22 July 1986, 22 October 1986 and 5 December 1986 was a postero-anterior (PA) view taken with the patient standing. The radiograph taken for the GP on 4 April 1990 was a left lateral view. The radiograph taken at Ross Hall Hospital on 7 November 1990 was another PA view taken with the patient standing. The radiograph taken at the Southern General Hospital on 25 August 1992 was an antero-posterior (AP) view taken with the patient sitting and using portable equipment. The radiograph taken at the Southern General Hospital on 26 August 1992 was a right lateral view taken in similar conditions. I do not regard it as my function to say what, if anything, I make of these radiographs on my own observation. It was abundantly clear throughout the proof that the use of such radiographs as a diagnostic aid requires keen powers of observation and considerable training and expertise. It was striking to what extent during the proof the expert witnesses disagreed about what could actually be seen on each of the radiographs, let alone how they were to be interpreted and what conclusions could be drawn from them. I therefore confined my role to sitting or standing beside each of the expert witnesses as he gave an account of what he could see on the radiographs and what conclusions he drew. The radiographs were viewed in Court with the aid of portable viewers. In the earlier stages, and particularly during Dr Kerr's evidence, only one viewer was available, but by the end of the proof there were three. These did not all provide the same intensity of illumination, but they assisted some of the witnesses to make side-by-side comparisons. It was not feasible to reduce the general level of lighting in either of the courtrooms which was used during the proof. Viewing conditions were thus far from ideal. Some, though not all, of the expert witnesses had viewed some or all of the radiographs before giving evidence. I shall comment on this in due course. To assist me in taking notes of their evidence, and to enable what an earlier witness had said to be put to later witnesses, the witnesses made a number of sketches of the main features which they claimed to identify.

[32] Before summarising the evidence of the expert witnesses, I think that I should make further reference to reports prepared by them which were lodged as productions, because it can be seen from these reports that the battle-lines had been drawn up well in advance of the proof.

[33] I have already referred to Dr Kerr's first two reports. In a third report to the pursuer's solicitors dated 11 February 1994 he said that he had now had the opportunity to examine the case records of the Southern General Hospital including Mr Durie's final admission on 28 April 1992 and records from Glasgow Royal Infirmary which were entirely pulmonary function data. After referring to certain passages in the records he stated that they confirmed that Mr Durie had asbestosis and that his death was due to bronchial carcinoma with metastases. He stated that it was accepted that individuals with asbestosis had a significantly greater risk of dying from bronchial carcinoma than a similar cigarette smoker who had never been exposed to asbestos. Asbestosis was therefore a significant factor in Mr Durie's development of his fatal illness, bronchial carcinoma.

[34] Dr Crompton's first report, to the second defenders' solicitors, was dated 6 November 1997. It was prepared after detailed examination of the medical records. Dr Crompton said that it was apparent from the medical records that Mr Durie had respiratory problems for a considerable time prior to his death. He then quoted various passages which supported this. He also referred to reports on chest radiographs and said that no mention of pleural abnormality was made in any of the x-ray reports he examined. He said that it appeared that the diagnosis of asbestosis had been made because of the history of exposure to asbestos, bilateral basal shadowing on the chest x-ray on which the Special Medical Board based their opinion, and the presence of inspiratory crackles on auscultation of the chest. It appeared that the cause of death was bronchial carcinoma with multiple metastatic spread but there was no proof of this diagnosis. Dr Crompton continued by stating that there could be no doubt that Mr Durie had severe chronic obstructive airways disease and that it was possible that he developed asbestosis which was first detected in 1990. However, the majority of patients who developed asbestosis (in the region of 80%) had obvious asbestos-related pleural abnormalities on the chest radiograph and in this case these abnormalities had not been mentioned by any radiologist or clinician. Dr Fennerty had described a unilateral pleural abnormality. Unilateral pleural abnormalities were common in patients with chronic obstructive airways disease. It was possible that Mr Durie had gross bullous emphysema of the upper lobes which caused compression of the perhaps more normal lower lobes and that this led to the appearances described by Dr Fennerty. In this situation crackles were not unusual. Although there was no histological or cytological proof of the diagnosis of bronchial carcinoma with metastatic spread, the reports of the chest x-rays and ultrasonography of the liver were compatible with this diagnosis. However, Mr Durie was a heavy smoker and this caused him to have chronic bronchitis and emphysema and could also be entirely responsible for his developing bronchial carcinoma. From the information obtained from the medical reports Dr Crompton stated that it was difficult to give an opinion about whether or not he had asbestosis. He said that he would be in a much better position to express an opinion if he was able to scrutinise the chest x-rays.

[35] Dr Crompton thereafter made a second report (undated) following his examination of chest x-rays. He reported that the chest radiographs dated 22 July 1986 and 22 October 1986 showed evidence of pleural thickening or possibly plaques on the left but there was no evidence of pleural abnormality on the right. The 22 October 1986 radiograph showed some pulmonary shadowing in the left lower and mid zones and also in the right lower zone. However, the left sided pulmonary abnormalities were not present on the radiographs dated 22 July 1986 and 5 December 1986, indicating that the pulmonary abnormality on that dated 22 October 1986 was transient and, therefore, likely to be inflammatory (possibly bronchopneumonia). The right sided pulmonary abnormality visible in the right lower zone on the radiographs dated 22 July 1986 and 22 October 1986 was much less evident than on that dated 5 December 1986 and, therefore, this pulmonary shadowing was also unlikely to be permanent fibrosis. The radiograph dated 5 December 1986 was not of excellent quality as the extreme right costo-phrenic angle was not visible and there was a linear artefact in the right lower zone. The lateral radiograph dated 4 April 1990 was normal except for some flattening of the hemi-diaphragms indicating obstructive airways disease. He stressed, however, that a lateral film was rarely of any value in the assessment of pulmonary or even pleural shadowing. The AP sitting radiograph dated 25 August 1992 showed quite extensive patchy shadowing in the right lower zone compatible with pneumonia. The pleural changes on the left were not visible and on this radiograph there was no evidence of interstitial shadowing which could be interpreted as fibrosis (asbestosis). The left costo-phrenic angle was not clear but there were no interstitial changes above the left hemi-diaphragm. The right lateral radiograph dated 26 August 1992, which Dr Crompton assumed to have been taken while the patient was sitting, confirmed the changes in the right lower lobe. These changes looked like pneumonia. Dr Crompton continued by stating that the chest radiographs taken in 1986 showed left sided pleural abnormality but none on the right. The pulmonary changes were not present on all the chest x-rays and were unlikely, therefore, to be evidence of any form of fibrosis. The radiograph dated 25 August 1992 was a poor film to assess pleuropulmonary disorders which might be caused by asbestos since it was a film taken in the AP sitting position, while conventional chest x-rays in fit individuals were taken in the PA standing position. The 1992 chest x-rays showed right lower lobe pneumonia but no evidence of any other pathology. On the balance of probabilities it was Dr Crompton's opinion that the chest x-rays he examined did not support a diagnosis of asbestosis. It can be seen that Dr Crompton had not had the opportunity of reporting on the radiograph taken at Ross Hall Hospital on 7 November 1994.

[36] Dr Turnbull, in his first report dated 16 January 1998, reported on the same six radiographs as had been seen by Dr Crompton. He reported that the older radiographs from the Southern General Hospital showed evidence of dichroic fogging which slightly obscured lung parenchymal details. There was no evidence on any of them of any consistent abnormality in the pleura or pulmonary parenchyma to suggest either the presence of pleural plaques or interstitial pulmonary fibrosis. There was no evidence of pleural calcification. The heart, mediastinum and pulmonary vascularity appeared normal. The radiographs dated 25and 26 August 1992 showed extensive mixed interstitial and alveolar shadowing in the right lower zone shown to lie posteriorily in the right lateral view and consistent with inflammatory change in the right lower lobe. The heart, mediastinum and hila appeared normal even though the patient was rotated to the left and in an AP sitting position. The pulmonary vascularity also appeared normal. There was no evidence of any pleural thickening, pleural plaques or pleural calcification and, apart from the inflammatory changes in the right lower lobe, no evidence of any interstitial shadowing to suggest pulmonary fibrosis. Dr Turnbull concluded by saying that there was no evidence on the radiographs examined by him to suggest the presence of pleural plaques, pleural calcification or interstitial fibrosis. He agreed with Dr Crompton's examination of the chest x-rays and also concluded that in his opinion the chest radiographs he had examined did not support the diagnosis of asbestosis.

[37] Dr Moule reported by letter dated 20 January 1998 to the pursuer's solicitors on the radiograph taken at Ross Hall Hospital on 7 November 1990. This appears to have been his first written report on it, and it was the only radiograph on which he reported prior to the proof. He reported that there was a little pleural thickening laterally in the mid and lower zones and on the domes of the diaphragm. A curvilinear opacity was seen through the left side of the heart shadow apparently separate from the descending thoracic aorta and this could be due to some calcification of the mediastinal pleura. Some pulmonary fibrosis might also be present in the mid parts of both lungs but there was no convincing evidence of pleural plaques as such. There was also some pleuro-pericardial thickening obliterating the right cardio-phrenic angle. There was some prominence of the aortic knuckle but the heart was not transversely enlarged. The rather coarse background pattern of parts of both lungs could be consistent with some COPD (chronic obstructive pulmonary disease). Dr Moule concluded by saying that the distribution of the pulmonary fibrosis suggested that it might be due to asbestosis. The left hilum was also enlarged. This could be due to vascular causes but underlying neoplasm could not be excluded on this film.

[38] The radiograph dated 7 November 1990 was sent to Dr Turnbull, who reported on it on 25 February 1998. He said that the heart was not enlarged but there was prominence of the pulmonary arteries with diminished peripheral pulmonary vascularity in keeping with pulmonary hypertension. There were no skeletal abnormalities. There was coarse reticular-nodular shadowing in both lower zones, particularly in the costo-phrenic angles and the left cardio-phrenic angle, with peripheral fine pleural thickening on the left. There was associated loss of definition of the outer third of the right hemi-diaphragm, the left hemi-diaphragm and the left heart border. There was no pleural calcification. The appearances were non-specific and could be due to interstitial fibrosis, mild interstitial pulmonary oedema or resolving bilaterial bronchopneumonia. In the context of previous exposure to asbestos, the combination of pleural thickening and basal interstitial shadowing, even in the absence of pleural calcification, could be due to asbestosis.

[39] Dr Moran wrote a report dated 15 July 1998 to the first defenders' solicitors. He had available to him all the material I have so far mentioned, except for the reports by Dr Moule and Dr Turnbull on the radiograph dated 7 November 1990. He did however have this radiograph. He reviewed the records of the Southern General Hospital together with the radiographs. In respect of the radiograph dated 22 July 1986 he said that he agreed that it showed evidence of emphysema in that the right hemi-diaphragm was depressed. The lung markings were generally coarse as was commonly found in smoking-related lung disease and there were patchy infiltrates at both lung bases in keeping with pneumonic infection or possibly pulmonary infarction (in view of the haemoptysis). The radiograph dated 22 October 1986 again showed depression of the right diaphragm and widespread coarse lung markings but probably some reduction of the infiltrates at the lung bases. This and the previous film showed a probable small patch of pleural thickening on the left lateral chest wall but the costo-phrenic angle was sharp indicating that there was no diffuse pleural thickening. The pulmonary blood vessels were rather prominent on both films and the left lung root (hilar) vessels were particularly so on the film of 22 October 1986. This evidently raised the question of whether there might be a tumour at the left hilum but fluoroscopy (on 10 November 1986) later showed that the appearances were of normal vascular markings. The radiograph dated 5 December 1986 was poorly centred so that the right costo-phrenic angle was a little obscured. Comparing this with the previous two films showed that there was a further reduction in the infiltrates in the lower zones. The diaphragmatic contours were smooth and there was no evidence of interstitial fibrosis. There was a small vertical linear artefact overlying the right lower zone laterally. There was again minimal evidence of a possible patch of pleural thickening over the left lateral chest wall. This was less than in the film of 22 October 1986. The Ross Hall Hospital film dated 7 November 1990 was slightly rotated making the left hilar blood vessels rather prominent. As compared with the film of 5 December 1986 there were some increased bronchovascular markings particularly in the left lower zone together with some slight fluffy infiltrate, all suggesting pulmonary infection. The heart was probably enlarged in this film. The lung function test results dated 13 June 1990 showed the total lung capacity of 8.04 litres to be nearer the upper limit of the normal range. This was associated with mild airways obstruction and a severely reduced diffusing capacity and transfer co-efficient. The tests used for the report measured mainly obstruction in the large airways. Dr Moran had been in touch with the Department of Respiratory Medicine at Glasgow Royal Infirmary, where the tests had been carried out, to ascertain the results of the flow-volume study which was carried out at the same time. This showed results strongly suggestive of additional obstruction in the smaller airways. Taken together these tests did not support a diagnosis of pulmonary fibrosis but were entirely consistent with smoking-related emphysema. The lateral radiograph dated 4 April 1990 showed that both hemi-diaphragms were depressed and that there was an abnormally large area of lung anterior to the mediastinum (the heart and great blood vessels) and also posteriorly between the heart and the spine. All of these features were in keeping with severe emphysema. Turning to the radiographs taken following Mr Durie's terminal admission to hospital, Dr Moran reported that the radiograph dated 25 August 1992 showed widespread pneumonic change on the right side. The film was grossly rotated and no useful comment could be made about the presence or abs

[40] Dr Moran concluded by expressing the opinion that it was clear that Mr Durie had advanced chronic obstructive airways disease with emphysema, largely or entirely due to his smoking habit. He had evidence of recurring, sometimes severe, episodes of chest infection including several episodes of pneumonia. He might have had recurrent pulmonary thrombo-embolic disease accounting for his recurring haemoptysis and possibly some radiological changes on the chest x-ray from time to time. He appeared to have died of pneumonia complicating his chronic lung disease and accompanied by kidney failure, anaemia and liver enlargement. Although the working diagnosis on his final admission was lung cancer with spread, particularly to the liver, the ultrasound description of possible metastatic liver disease was quite tentative and did not appear to account for the clinically described liver enlargement. The chest x-ray taken on the final admission neither excluded nor particularly supported the diagnosis of lung cancer. There was no evidence of pleural plaque formation, diffuse or bilateral pleural thickening or of any definite interstitial fibrosis on any of the chest x-ray films available. Radiological and clinical signs which had been interpreted as suggesting basal fibrosis had been variable rather than constant as would be required for that diagnosis. The variations in the chest x-ray appearances had a high probability of being due to inflammatory change (chest infection and/or chemical inflammation due to aspiration of stomach contents into the lung caused by his hiatus-hernia-related oesophageal reflux) and/or episodes of pulmonary thrombo-embolism. If it was true that Mr Durie was first exposed to asbestos in 1958 (the date Dr Moran took from the records of the Medical Boarding Centre), had he developed asbestosis it would have been expected to be clinically and radiologically manifest by about 1978 and not to have appeared for the first time in the late 1980s. In any event, although asbestosis had been described as occurring in the absence of pleural plaques or diffuse pleural thickening, this was extremely unusual. Mr Durie was described as having developed finger clubbing between about late 1990 and the time of his death in 1992. Finger clubbing was unlikely to occur in asbestosis in the absence of radiologically obvious disease. There were many other causes of finger clubbing, including liver disease. It seemed unlikely that his clubbing would be accounted for by a bronchial carcinoma already present in 1990 and only coming to light in the latter part of 1992. Also, one would expect that a bronchial tumour which had been present from 1990 and causing death in August 1992 would have been very obvious on the chest x-rays. In Dr Moran's opinion there was no evidence in the material available to him that Mr Durie had any asbestos-related condition. It was also by no means certain that he died of a bronchial carcinoma. Dr Moran noted that there were considerable and possibly significant gaps in his medical history, in particular there was little information available on his chest condition between 1990 and 1992. He suggested that the solicitors might wish to consider trying to retrieve the general practitioner's records. As has been seen, these records were not in fact produced.

[41] The last written report was one addressed by Dr Kerr to the pursuer's solicitors and dated 19 October 1998. He had available to him the reports by Dr Crompton and Dr Moran and had the opportunity to examine the chest x-rays from the Southern General Hospital in addition to the radiograph taken at Ross Hall Hospital on 7 November 1990. He dealt first with the diagnosis of the asbestosis. He said that it depended on the individual having an industrial history of exposure to the inhalation of asbestos fibres. The clinical examination gave supporting evidence that the diagnosis always rested on the interpretation of the chest x-rays. It had long been recognised that the early changes of fibrosis due to asbestosis could be similar to changes in the x-ray related to ageing and to smoking and this frequently gave rise to conflicting reports in those interpreting the chest films. To deal with this problem the I.L.O. (International Labour Organisation) had introduced standardised techniques for the examination of shadows in the lung fields. This involved measurement of the diameter of width of these shadows. In category 1, the earliest, these were up to 1.5mm in length or diameter. As the asbestosis became more defined, the size of the shadows increased to 2mm or 3mm. Shadows of this category did not occur due to ageing or smoking. The radiographs dated 22 July 1986, 22 October 1986 and 5 December 1986 all showed shadowing of a reticular-nodular pattern in the costo-phrenic angles. These shadows measured 2mm to 3mm in diameter and were present bilaterally. In addition, in the film of 5 December 1986 there was some reticular-nodular shadowing in the mid zones and all these films showed evidence of some pleural thickening or pleural plaque on the right side. In addition, there was probably a pleural plaque in the right mid zone in the film of 5 December 1986. Dr Kerr noted that Dr Crompton in his report on the films of 22 July 1986 and 22 October 1986 agreed that there might be pleural plaque on the left side. The film of 7 November 1990 showed reticular-nodular shadowing at both lung bases involving the costo-phrenic angles and mid zones. Many of the shadows were greater than 1.5mm in diameter. In addition there was definitely pleural thickening on the left mid and lower zone. In this film it was not certain that there was evidence of pleural plaque on the right lower zone. Finally, Dr Kerr pointed out that comparative studies of chest physicians and radiologists in interpreting chest films had consistently shown that radiologists gave more consistent reports than the clinicians. He stated that it was important that in a dispute the solicitors should have a report or reports from a consultant radiologist.

[42] Turning to the diagnosis of chronic bronchitis and emphysema, Dr Kerr noted that Mr Durie gave a long history of cigarette smoking associated with productive cough and recurring bronchial infections. There was no doubt that clinically he had chronic bronchitis, which was frequently associated with the development of emphysema, which was an increase in the total lung volume due to destruction of air cells beyond the terminal bronchi. Confirmatory evidence of severe emphysema came from the measurements of flow volume. Moderate or severe emphysema was associated with ventilory flow rates of less than one third of the predicted value: this was a quotation from a textbook and was consistent with his own observation. Looking at Mr Durie's flow volumes, he had several FEV 1 (forced expiratory volume in one second) readings which had invariably been close to 3 litres, about 100% of his predicted value. In his opinion, this finding was not consistent with Mr Durie's having severe emphysema. Further, although the total lung volume was increased, it remained at the upper level of the normal range for Mr Durie. Dr Moran had stressed the evidence for impairment of the air flow in the small airways. Dr Kerr said that there was certain theoretical evidence to suggest that this type of change could occur in fibrosis due to asbestosis where studies with computer scanning had showed marked evidence of small emphysematous bullae associated with the pulmonary fibrosis. These changes would be consistent with air flow obstruction in the smallest airways. The gas transfer was 50% of predicted and this of course was a characteristic finding of asbestosis even in its early stages. Dr Kerr could not accept that the low gas transfer was solely due to emphysema when the FEV 1 was consistently at 3 litres and close to the predicted value. His conclusion was that Mr Durie had bronchitis but this did not give rise to the degree of air flow obstruction that one would expect with severe emphysema, and his breathlessness from 1986 onwards was largely due to his development of pulmonary fibrosis, the basis of which was asbestosis. In support of this he did have pleural plaques particularly on the left side and it was now accepted that there were occasions when with asbestos damage the plaques could be unilateral. The major cause of Mr Durie's breathlessness when Dr Kerr examined him was pulmonary fibrosis based on asbestosis.

[43] Dealing with Mr Durie's final illness, Dr Kerr said that review of the radiologist's report of the ultrasound examination of the liver and of the chest x-rays was consistent with the diagnosis of bronchial carcinoma with metastases but it was not conclusive and there certainly was not definite evidence of a neoplastic mass involving the right lower lobe. Nevertheless, bronchial carcinoma could present as acute pneumonia and, bearing in mind Mr Durie's clinical condition and marked clubbing of his fingers, on the balance of probabilities, Dr Kerr accepted the diagnosis that his death was due to a bronchial carcinoma with metastases.

[44] The proof took place in two instalments, in October 1998 and November 1999. Dr Kerr was the only expert witness to give evidence during the first of these instalments. In the second instalment, Dr Moule gave evidence. He was followed by Dr Moran, whose evidence was interrupted after he had given evidence in chief and had been cross-examined on behalf of the second defenders. Thereafter Dr Turnbull and Dr Crompton gave evidence. The proof concluded with the resumption of Dr Moran's evidence, when he was cross-examined on behalf of the pursuer and re-examined. I propose now to attempt to summarise the main points in each witness's evidence, with particular reference, given their importance, to what they said about the radiographs.

[45] Dr Kerr gave evidence that he was aged 74 and was a consultant physician at Ross Hall Hospital. During his career he had been consultant physician in respiratory diseases to the Western Infirmary, Glasgow, where he established the respiratory unit including the pulmonary function laboratory and the intensive care unit. This unit with four consultants was responsible for respiratory diseases in the Western District of Glasgow, including Clydebank and Dumbarton, a population of approximately 300,000. The department had been closely involved in the diagnosis of occupational lung diseases, particularly in the industrial workers on Clydeside, and had publications on various aspects of asbestos damage to the lungs including mesothelioma and lung cancer. Shortly before he retired in 1989 he was chairman of the Management Committee for Glasgow Western District Hospitals. He said that he had a special interest in asbestos damage. He had seen many patients with asbestos-related disease. His patients had suffered damage from industrial exposure to asbestos, principally in the Clydeside shipyards. It was his practice to take an occupational history and make an assessment of the degree of exposure. Modifying factors included the age of the patient and the time since his first exposure to asbestos, which was critically twenty to forty years. Many had been cigarette smokers with chronic bronchitis and air flow obstruction. They suffered from breathlessness and restriction in their ability to expand their chests. Sometimes they had beaking of their nails indicative of finger clubbing. They had chest crackles, usually at the lung bases. Most diagnoses were made from x-rays. Macrophages took asbestos fibres into the lung tissues and there was a tissue reaction in the form of fibrosis. This produced shadows in the lung fields, which tended to be at the base. The I.L.O., an organisation based in the USA, had drawn up a method of examining the lungs and categorised the fibrosis. The critical level was category 1, in which the round or linear shadows were no more than 1.5mm in size. Smoking or ageing did not tend to produce larger shadows. Reticular-nodular shadowing of 2mm to 3mm fell into category 2, and that was accepted as being true pulmonary fibrosis. There was then the question of causation, and this was where a history of industrial exposure to asbestos was of great assistance. There could also be pleural plaques and pleural thickening. The plaques were sometimes calcified, and this greatly assisted the diagnosis of asbestosis. Pleural thickening could be diffuse or bilateral. Lesser degrees of pleural plaques were said not to interfere with respiratory function. Mesothelioma virtually always in the United Kingdom was due to exposure to asbestos fibres, independently of cigarette smoking. Numerous studies showed that if there was asbestos damage to the lungs in a patient who was a cigarette smoker, there was an enhanced risk, certainly about ten times, of his developing lung cancer. Thus it had been accepted that a cigarette smoker who had asbestos damage to his lungs in the form of asbestosis or diffuse bilateral pleural thickening had a highly significant risk of developing lung cancer compared with a similar smoker who had never been exposed to asbestos.

[46] Dr Kerr was then taken over the terms of his reports, which I have already quoted, and the records he had seen. He said that he understood from what Mr Durie had told him that he had had quite heavy exposure to asbestos. He was not convinced that the results of the lung function tests were due to emphysema produced by cigarette smoking. He said that they were consistent with the diagnosis of asbestosis. He accepted that Mr Durie had chronic bronchitis with a persistent productive cough. The occasional haemoptysis was consistent with this. While Mr Durie had made no major complaint of back pain to him, Dr Kerr said that the recorded back pain could be related to pleurisy. It was possible for there to be benign asbestos-related pleurisy which was an additional clinical presentation. Counsel for the first defenders objected to the line of evidence on the ground that there was no record for pleurisy. I allowed the line to proceed under reservation, but it was not pursued.

[47] Dr Kerr said that when he saw Mr Durie originally breathlessness was his principal complaint. Chest pain was not a major factor. At his age he was quite liable to low back pain, which was not necessarily related to asbestos damage to the lungs. His interpretation of the circumstances of Mr Durie's emergency admission to hospital in 1992 was that there had been a significant deterioration in his health at that time. There had been a fresh event. Asbestosis gave increased morbidity but did not shorten life expectation. As he read the notes, there had been greater deterioration than would be expected from a history of asbestosis without a complicating factor. Mr Durie had an infection and consolidation with retraction of the right lower lobe at the point of death, he had clubbing of the fingers, he had what seemed like metastases in the liver, and on the balance of probabilities in Dr Kerr's opinion Mr Durie died from bronchial carcinoma. The immediate cause of death was that he became anuric and had renal failure. In his opinion his exposure to asbestos had made a contribution to this lung cancer, as had his smoking. A smoker who suffered from asbestosis was much more likely to get bronchial cancer.

[48] Dr Kerr was then asked to look at the radiographs which had been produced. He said that on the radiograph dated 22 July 1986 he could see vascular marking with additional mottling in the bases. There was reticular nodular mottling but this was likely to be due to smoking. There was pleural thickening on both sides at the seventh ribs. On the radiograph dated 22 October 1986 there were little mottled marks and horizontal marks on the right in the costo-phrenic angle and at the eighth rib, and on the left in the costo-phrenic angle with horizontal lines at the ninth rib. There was pleural thickening which was much easier to see on the left side at the seventh to eight ribs. On the right it was much less obvious, though he thought that it was still there. There was also reticular nodulation greater than 1.5mm in size. On the radiograph dated 5 December 1986 there was an obvious artefact. There were still little nodules on the right and left with pleural thickening. There might just be a plaque sitting on the face of the seventh rib on the right. There was an objection at this point because there was no record for pleural plaques and I allowed the line to proceed under reservation. Dr Kerr said that it was a matter of quantity: calcification in plaques could be helpful. There might just be a plaque sitting on the face of the seventh rib on the right. By and large he thought it was just pleural thickening on the left side. He was unable to make any decision about what appeared on the right side, and said that there was a big question mark over this radiograph, which might have been affected by foreign bodies.

[49] Dr Kerr said that the radiograph dated 7 November 1990 was taken at his request. He had discussed it with Dr Moule. There were mottling and lines in the right costo-phrenic angle at the level of the seventh rib, and on the left side, more marked than previously, in the costo-phrenic angle at the eighth and ninth ribs. There was quite evident pleural thickening on the left side between the ninth and tenth ribs and on the right at the seventh rib, with mottling between the sixth and seventh ribs on the right side. There was pleural thickening also at the level of the first and second and the sixth ribs on the left side.

[50] In relation to the radiograph dated 25 August 1992, Dr Kerr said that he saw degenerative changes in the spine, which would explain Mr Durie's back pain. He said that the blood vessels were somewhat congested in the upper part of the lungs: this was apical congestion. There was a lot of greying and mottling on the right side from the ninth rib downwards to the base. This was in a fine honeycomb pattern, which was consolidation. The big change was this area of consolidation. He also saw mottling around the ninth rib on the left side. He added that there was a faint line at the seventh rib on the right which could be a horizontal fissure. He was unable to make any comment on the pleural shadows on this film.

[51] In relation to the lateral radiograph taken on 26 August 1992 Dr Kerr said that it showed that all the mottling of consolidation was in the lower and posterior part of the right lung, with some collapse.

[52] Dr Kerr said that the diagnosis of asbestosis was made particularly on the radiograph dated 7 November 1990. There was some evidence of the changes in the previous radiographs. The cardinal changes were that on the right side there was significant evidence of pleural thickening and on the left side there were two small areas which were consistent with pleural thickening. At the lung bases there were reticular nodular shadows, a number of which were greater than 1.5mms either in length or in diameter. So the radiographs of 1986 were consistent with the findings in the radiograph dated 7 November 1990. Dr Kerr's conclusion was that Mr Durie had pleural thickening, marked on the left side, patchy but on the balance of probabilities present on the right side. Based on these observations, together with the industrial history, his clinical examination and the detailed pulmonary function tests, his conclusion was that the pulmonary fibrosis was due to asbestosis. In his final illness in August 1992, the radiographs showed that he had a right lower lobe consolidation with some associated collapse of the lung. Dr Kerr could not identify any mass in the lung in this area. His clinical examination showed evidence to support his having pneumonia with infection, but this did not exclude an underlying bronchial carcinoma. Clinically he had marked clubbing of the fingers and the ultrasound examination of the liver was reported as showing multiple areas consistent with tumour deposits in the liver. Therefore, on the balance of probabilities, he accepted the hospital diagnosis that he died of lung cancer. Had there been a post mortem examination that would have solved all the problems: there would have been histological evidence of asbestosis, if it was present, and tumour cells would have been identified in the lung and in the liver. Dr Kerr did not regard his diagnosis of asbestosis as being controversial.

[53] Dr Kerr estimated Mr Durie's disability as a result of asbestosis in 1990, after allowing for his smoking history, obstructive airways disease and emphysema, at 35%. By 1992, when he was admitted to hospital, he was 100% disabled. He expected that there would have been a fairly slow deterioration in his condition to early 1992.

[54] Somewhat later in Dr Kerr's evidence he was shown the radiograph dated 4 April 1990. He said that on the mid zone anteriorly there was some evidence of pleural thickening which was consistent with the pleural thickening he could see in the P.A. views. There was also thickening at the costo-phrenic angle of the left lung. There were appearances consistent with emphysema, but there was some ageing component to the shape of the chest.

[55] Summing up, Dr Kerr said that from the radiographs there were clear signs of pleural thickening and asbestosis and that there were other clinical signs.

[56] During cross examination, Dr Kerr made very few concessions. A passage in the opinion of Temporary Judge Coutts in McCance v Newalls Insulation Ltd, 12 May 1995 (reported as a note at 1996 S.L.T. 80), was put to him and he agreed that what he said there about the possible causes of basal fibrosis, which included smoking, chronic obstructive airways disease and emphysema was not the same as what he was now saying. He now had the benefit of using the I.L.O. categories. He agreed, however, that the I.L.O. study involved the use of standard films for purposes of comparison not only of the size, but also the shape and other characteristics of the appearances on the radiographs. He had not made such a comparison. He agreed that overall the absence of crackles was inconsistent with the presence of asbestosis. He also accepted that the presence of coarse crackles was consistent with chronic bronchitis. Pressed on his interpretation of the lung function tests, he said that emphysema accounted for part of the disability in pulmonary function, but not all. He said that there was new information that emphysematous bullae could be present in early asbestosis.

[57] Cross examined about his report dated 14 November 1990, Dr Kerr said that he did not mention emphysema, chronic bronchitis or obstructive airways disease because he thought the dominant factor was fibrosis and asbestosis. He agreed that it was reasonable to note what crackles he heard, but doubted the value of stressing that aspect and did not record this detail routinely. His diagnosis depended partly but not entirely on examination of the radiographs. Without them he could not have expressed an opinion even on the balance of probabilities. He accepted that radiologists were much more consistent than chest physicians in the interpretation of radiographs. If no plaque or calcification were present in the radiographs, a diagnosis of asbestosis was less likely.

[58] Dr Moule was aged 65 and had retired shortly before the proof. From 1966 to 1995 he was a consultant radiologist at both Glasgow Royal Infirmary and Ross Hall Hospital, and from 1995 until retirement he was at Ross Hall Hospital only. He said that he had considerable experience of persons exposed to asbestos. He saw them both at Glasgow Royal Infirmary and at Canniesburn Hospital, which he also covered. Later, with Dr Kerr, he saw many cases which had been referred to Ross Hall Hospital.

[59] He said that he saw in the radiograph dated 22 July 1986 probably emphysema and mottled markings in the mid zones and extending through the lower zones on both sides. Taken on their own these were suggestive of interstitial pulmonary fibrosis. There was pleuro-pericardial thickening on the right side and pleuro-diaphragmatic thickening on both sides. The aortic knuckle was prominent, suggesting hypertension.

[60] In respect of the radiograph dated 22 October 1986, he said that he did not think there was any significant difference from the earlier one and that he saw the same features. The exposure features of the film were not exactly the same, but his interpretation was the same.

[61] The only difference in the radiograph dated 5 December 1986 was that the transverse diameter of the heart seemed to have increased slightly. This was probably due to the patient's hypertension. On all these radiographs the enlarged left hilum did not really change, which suggested enlargement due to a vascular cause. He made a drawing indicating that he saw a possible pleural plaque below the right eighth rib.

[62] The radiograph dated 4 April 1990 showed thickening of the interlobar fissure, large pulmonary vessels, a wedge deformity of the dorsal vertebrae, and pleural thickening anteriorly and posteriorly in the region of the right hemi-diaphragm.

[63] The radiograph dated 7 November 1990 taken at Ross Hall Hospital had several features. On either chest wall there were faint lines which were due to pleural thickening. The right cardio-phrenic angle was obliterated due to pleuro-pericardial thickening. In both mid and lower zones, especially at both bases, there was a mottled appearance due to pulmonary fibrosis. There were two lines, which were not easy to see, which were almost certainly due to thickening of the mediastinal pleura with some calcification. The left hilar shadow looked even larger than previously. This was still likely to be due to enlargement of the pulmonary vessels rather than an underlying tumour. The aortic knuckle was more obvious, suggesting that hypertension was increasing.

[64] The radiograph dated 25 August 1992, which was very different from the other films, showed pneumonic consolidation in the right lower zone. This shadow had concealed underlying changes. He could still see fibrosis in the left lower zone. The cardiac size seemed to have increased. There was hilar enlargement on both sides, suggestive of enlargement of the main pulmonary vessels.

[65] The radiograph taken on 26 August 1992 showed diffuse opacity in the posterior part of the right lower zone where pneumonic consolidation had occurred. There were also features of pleural thickening. There were large hilar shadows which were either vascular or tumorous.

[66] Dr Moule explained that he had first become involved at Dr Kerr's request. Dr Kerr had given him background information about Mr Durie's employment history and said that there were crackles at both of the bases. He had discussed the radiograph dated 7 November 1990 with Dr Kerr. This was the film most likely to show the changes of asbestos-related lung disease and asbestosis. He had discussed this radiograph with Dr Kerr and said that on the balance of probabilities there was asbestosis. Relating this to the 1986 radiographs, he said that there was not any marked progress in the period from 1986 to 1990. The diagnostic quality of the three 1986 radiographs was quite adequate. There were abnormalities present, and he disagreed with what Dr Turnbull had reported about them. In conclusion, he said that there was no more than mild to moderate emphysema and it was certainly not bullous emphysema. The asbestosis which was present would have caused some restriction in the range of respiratory movements. In a person who had asbestosis to this degree there would be some limitation in his pulmonary functions and he would probably be more prone to respiratory infections.

[67] In cross examination Dr Moule said that he had a CT scanner at Ross Hall Hospital. While he was at Ross Hall Hospital Dr Kerr had referred all his asbestos cases to him. Dr Kerr told him that Mr Durie had had asbestos exposure and crackles. He asked Dr Moule if he saw signs of asbestos-related disease. He had not seen the records of the Southern General Hospital before coming to Court. When shown them, he did not agree with what had been written about the 1986 radiographs. He accepted that one of the classic signs of pleural thickening was a blunting of the costo-phrenic angle, which Mr Durie did not have. The distribution of fibrosis in the middle and lower parts of the lungs was somewhat suggestive of asbestosis. Dr Moule did not use the I.L.O. films.

[68] Taken over the radiographs, he accepted that there were fewer markings in the one dated 5 December 1986 than in the one dated 22 July 1986. He accepted that there were no features in the radiographs which could not be explained by reference to Mr Durie's known medical history, but in light also of his history of exposure to asbestos he said that Mr Durie had both bronchitis and changes consistent with asbestosis. He said that it was a matter of balance, deciding between one thing and another, and one could never be certain except by carrying out a lung biopsy. The only features in the radiographs which could not be explained by reference to Mr Durie's medical history were the linear shadows on the radiograph dated 7 November 1990 which looked very like mediastinal pleural thickening and calcification.

[69] Later in his cross examination, on behalf of the second defenders, Dr Moule explained not only that he had not seen the records of the Southern General Hospital before giving evidence, he had not seen any of the radiographs except that dated 7 November 1990 and he had not seen the reports by Dr Turnbull and Dr Crompton. He agreed that the circumstances of viewing the radiographs for the first time in court were less than ideal. Shown Dr Turnbull's report on the radiograph of 7 November 1990, he said that he disagreed that there was no pleural calcification. He said that the interpretation of radiographs was subjective. He had seen this radiograph in a medico-legal context. If he had been treating Mr Durie he would have ordered a CT scan. This could have been done at Ross Hall Hospital in 1990.

[70] In re-examination Dr Moule said that on the balance of probabilities the changes which he saw on the radiograph dated 7 November 1990 were at least partly due to asbestosis. It provided reasonable evidence of asbestos-related changes and in fact asbestosis.

[71] Dr Moran was aged 69 and was a retired consultant physician. He had been a consultant at Glasgow Royal Infirmary from 1966 to 1994. He had considerable experience of occupational lung disease, of which asbestos-related lung disease was the most common. He had done medico-legal work to some extent before retirement and a great deal since. He had reviewed the records of the Southern General Hospital. He said that by 1980 the picture was that Mr Durie suffered from chronic smoking-related lung infections and emphysema. By that date he pretty certainly had obstructive airways disease.

[72] Dr Moran had seen the radiographs. He said that he was familiar with the I.L.O. system of grading, but that it was to be used in a specific context. It was not possible to use the method without the standard set of films for purposes of comparison. He said that the radiograph dated 22 July 1986 showed irregular opacities which he would describe as small infiltrates in the lower zones, possibly caused by infection or pulmonary infarction. There were coarse broncho-vascular markings in the mid zones. There was a possible slight patch of pleural thickening on the left side. There were not the appearances of pleural thickening which would be expected in the case of asbestosis. He disagreed with Dr Kerr and Dr Moule about the presence of pleural thickening.

[73] The radiograph dated 22 October 1986, which was slightly more penetrative, might be expected to show infiltrates more clearly, but he could see nothing but coarse broncho-vascular markings. The appearances of the upper parts of the lungs were compatible with emphysema. There was no pleural thickening at the diaphragms. The appearance was consistent with a reduction in chronic bronchitis and the presence of emphysema.

[74] The radiograph dated 5 December 1986 contained no sign of infiltrates. The dot-like markings were obviously blood vessels seen on end. He could see nothing that corresponded to a plaque on the right side. He could see only the inner margin of a rib.

[75] Dr Moran said that the only kind of crackles which were relevant to the diagnosis of asbestosis were those which were relatively well defined, bilateral, fine and end inspiratory. If there were coarse, end expiratory crackles, these would be attributable to chronic bronchitis and obstructive airways disease. The crackles described by Dr Fennerty were not consistent with a diagnosis of asbestosis.

[76] Dr Moran said that the lung function tests including the flow volume loop test, supported his diagnosis. The diffusing capacity excluded pleural thickening and therefore excluded asbestosis. The tests suggested that Mr Durie had centrilobular emphysema.

[77] Dr Moran said that it was very difficult to rely on the Medical Boarding Centre's finding of asbestosis in the absence of the radiograph taken there. There was a feeling that this centre based its decisions on less evidence than doctors would do.

[78] Accordingly, nothing in the radiographs or the records relating to the period prior to 7 November 1990 was supportive of the diagnosis of asbestosis. Turning to the radiograph dated 7 November 1990, Dr Moran said that he could see emphysema in the upper zones of both lungs. On the right side the mediastinal edge had a normal appearance. No pleural thickening was seen. There were coarse broncho-vascular markings in the lower zone and a slightly flattened diaphragm. On the left there was a probable patch of pleural thickening in the mid zone. There were coarse broncho-vascular markings in the lower zone and a probable pericardial fat pad. The mediastinal edge was probably displaced by a tortuous aorta. He could see no evidence of pleural thickening on the diaphragm. Markings seen by Dr Kerr and Dr Moule were rib shadows or broncho-vascular markings.

[79] Shown Dr Kerr's report dated 14 November 1990, Dr Moran commented on the absence of information about the kind of crepitations heard by Dr Kerr, and whether they were on inspiration or expiration. He also commented on the absence of any mention of emphysema or bronchitis.

[80] Turning to the hospital records and radiographs relating to Mr Durie's last admission in 1992, Dr Moran expressed the opinion that he had pneumonia, which accounted for the consolidations seen in the radiograph dated 25 August 1992. The available information suggested consideration of cancer in the gastrointestinal tract.

[81] In cross examination, Dr Moran said that he had not heard of any theory about the relationship between early asbestosis and emphysema. He did not agree with Dr Kerr about the conclusions to be drawn from the F.E.V. 1 results in the lung function tests. The fluctuation in the figures suggested a variable degree of airways obstruction, which pointed to chronic obstructive airways disease. At one point, he said that he would say frankly that Dr Kerr's reports started off in a very tentative way about important clinical findings, but once the ball had started rolling people were sometimes led to over-interpret what they found.

[82] Dr Turnbull, who was aged 53, was a consultant radiologist at the Western General Hospital in Edinburgh. He had been a consultant since 1979 and became clinical director of radiology at the Western General Hospital in August 1997. Shortly before giving evidence he became director of radiological services throughout Lothian. He was honorary senior lecturer in radiology at Edinburgh University, having been a senior lecturer from 1982 to 1995. He said that he had particular expertise in cardiac and respiratory imaging throughout his career. He was only instructed in about one or two medico-legal cases a year.

[83] Referred to his reports, he said that he had viewed the radiographs on three occasions: once for the purpose of preparing his reports (when, as has been seen, he did not view them all together), and subsequently on two occasions to prepare himself to give evidence. The first of these was before the first instalment of the proof, and the second was more recently, in order to consider what he had been told about Dr Kerr's evidence. The viewing conditions in court were not optimal. What were needed were a darkened room and consistent box illumination. He had studied the radiographs at the Western General Hospital in a suitable room with multi-viewing boxes which had even illumination. He had also looked at the radiographs individually, using a large magnifying glass to look at areas of lung in more detail. He said that comparisons were better done side by side on a single viewer. As a matter of course he would look at a whole range side by side.

[84] Dr Turnbull said that he believed that there was no consistent evidence on the radiographs that Mr Durie had asbestosis, and on the balance of probabilities he thought that he did not. Asked about his report on the radiograph dated 7 November 1990, he said that if he had only this radiograph and was aware that Mr Durie was a smoker with a history of chronic bronchitis, emphysema and exposure to asbestos, he could not have excluded the possibility of asbestosis, but would require further tests. The signs on the radiograph were so non-specific that they could be due to chronic bronchitis, repeated chest infections, mild heart failure or asbestosis. This was what he meant by the second paragraph of his report dated 25 February 1998. The further investigation he would have recommended would have taken the form of CT scanning, specifically high-resolution CT scanning. This would have been his position as at November 1990. This produced very fine detail and could pick up changes which were invisible on radiographs.

[85] Asked to look at the series of radiographs, Dr Turnbull said that there were a number of minor abnormalities which were not consistent across the series. If the patient had asbestosis and pulmonary fibrosis he would have expected that these changes would be permanent and thus visible across the series. He explained how dichroic fogging (in which there was deterioration over time of silver halide crystals which remained unfixed) could obscure finer detail because it affected the emulsion over the whole of a film. The radiographs from 1986 had dichroic fogging.

[86] In respect of the radiograph dated 7 November 1990, Dr Turnbull adhered to the views he had expressed in his report about this radiograph. He said that he could see no pleural thickening. Where Dr Moule had indicated that he saw pleural thickening on the right side, Dr Turnbull said that he could see the inner aspect of the cortex of the rib at that side, but he did not think it was pleural thickening. He thought that Dr Moule was referring to the diaphragmatic contour which was very poorly defined and irregular, especially if there were interstitial changes in the lung because of pneumonia. He could see no mediastinal pleural thickening. On the right there was a normal para-vertebral stripe, and on the left he could see the outer aspect of the descending thoracic aorta within the cardiac border extending from the left hilum inferiorly to the cardio-phrenic angle. Accordingly all he could see was coarse reticular-nodular shadowing in both lower zones with some pleural opacification suggestive of thickening on the left side. There was poor definition of the outer one-third of the left hemi-diaphragm. History could explain all the appearances in the radiograph dated 7 November 1990. The pleural opacification could be due to illness or fluid, as could the reticular nodules, although these were also consistent with asbestosis.

[87] The radiograph dated 25 August 1992 was much less penetrative. Dr Turnbull said that he could see the edge of the aorta very clearly and the para-vertebral area reasonably clearly. He said that there was no evidence of mediastinal thickening. It would be difficult to exclude this because of the technical shortcomings of this radiograph, which was an AP sitting one with the patient markedly rotated to the left. If there was calcification, however, it should have been visible in a radiograph of this quality.

[88] Looking at the series of three radiographs taken in 1986 together, Dr Turnbull said that there were signs in both lower zones which were not constant. These did not suggest a progression of the condition. Nothing he saw made him depart from what he had previously written in his report dated 16 January 1998. Reticular nodules could be seen in each of these radiographs but varied from one to the next. The definition of the hemi-diaphragms also varied. These changes were not consistent with asbestosis. They were consistent with chronic bronchitis and emphysema. If the patient suffered from asbestosis you would have expected these features either to remain constant or to progress. He disagreed with Dr Moule about the presence of pleural diaphragmatic thickening. He also disagreed about the presence of probable fibrosis, thinking that they represented small areas of infection or resolving infection. Some of the features seen by Dr Kerr were, in Dr Turnbull's opinion, normal anatomical structures in a relatively obese patient. In the radiograph dated 22 October 1986 he pointed to some slight shadowing on the left side running parallel with the ribs which he concluded were muscles. He thought that what Dr Kerr had identified as a plaque was an anatomical feature at the costo-chondral junction. He said that Dr Kerr's drawings did not show consistent features which suggested a progressive disease. Given the history of Mr Durie's exposure to asbestos, he would not have expected asbestosis to appear for the first time between 1986 and 1990. Viewing the radiographs from 1986 onwards, he did not find the consistency necessary for a diagnosis of asbestosis.

[89] Dr Turnbull said that the radiograph dated 25 August 1992 showed an area of pneumonia in the lower right side. Markings in the left lung which were present in the radiograph dated 7 November 1990 were absent in the later radiograph. There was an increase in vascularity between 1990 and 1992, which obscured the fine detail. The appearances suggested a degree of oedema probably associated with heart failure. The radiograph dated 26 August 1992 was of no assistance for diagnostic purposes.

[90] Dr Turnbull said that he could not exclude the tentative diagnosis of bronchial carcinoma by reference to the August 1992 radiographs, nor could it be confirmed.

[91] In conclusion, after reviewing the drawings made by the preceding witnesses, Dr Turnbull said that he felt that the abnormalities described on the chest radiographs over a period of time were not progressive; they were inconsistent from radiograph to radiograph and therefore unlikely to represent a permanent progressive disorder such as asbestosis. Also, in a patient with a history of smoking, chronic bronchitis and chest infections, small abnormalities such as reticular nodular shadowing of the bases and lack of definition of the hemi-diaphragms could occur due to chest infections and their effects in the lungs. Irregular pleural opacification could occur with chest infections, pulmonary fibrosis and pneumonia. If there was asbestosis, it was usually progressive. There was no evidence from these radiographs that the changes were progressive or permanent. While the radiograph dated 25 August 1992 was difficult to interpret, there was no evidence in it of pleural abnormality. Dr Turnbull felt unable to make any firm diagnosis of emphysema, stating that the hyper-inflated lungs seen in the radiographs could be caused by this or by chronic obstructive airways disease. The I.L.O. standard relied upon by Dr Kerr had been adopted in the USA, but not to a large extent. Dr Turnbull did not use the I.L.O. films for his own work or for teaching, and had never seen a set. A suspected bronchial carcinoma would normally be investigated by bronchoscopy and biopsy.

[92] Dr Crompton, who was aged 64, was a recently retired consultant chest physician. He had been a consultant since 1969 and had worked solely as a respiratory physician. His fields of research had been mainly in airways disease and asthma. Referred to his reports, he said that he had examined the hospital records in great detail. Looking at the radiograph dated 7 November 1990, he said that its features, in isolation, could be due to asbestosis. But the changes in the lower zones could be due to interstitial pulmonary fibrosis or asbestosis. He was aware of Mr Durie's history of smoking, chronic bronchitis, emphysema and associated infections. He said that with knowledge of these factors, and of Mr Durie's exposure to asbestos, under no circumstances would he diagnose asbestosis on the basis of this radiograph. He would have included it in a differential diagnosis. If the patient had been prescribed antibiotics and had returned in two weeks and the abnormalities persisted, a CT scan would have been carried out. It was perhaps less likely that this would have been done in 1990.

[93] Reviewing the series of radiographs, Dr Crompton said that on the balance of probabilities in his opinion they did not support the diagnosis of asbestosis. The series in 1986 showed changes in the lower zones which varied considerably from radiograph to radiograph. These could not be pulmonary fibrosis. He therefore concluded that the shadows on the radiograph dated 7 November 1990 could not be fibrosis. If Mr Durie suffered from asbestosis, this should have been present in 1986 and it was not. He thought, on the balance of probabilities, that Mr Durie was suffering from infection in both lower lobes. Mr Durie also had a hiatus hernia with marked reflux. Dr Crompton thought that he had recurrent aspiration pneumonia caused by aspiration of gastric contents. He had been admitted to hospital in 1986 vomiting blood which was assumed to be due to a tear at the lower end of the oesophagus. The barium meal disclosed marked reflux.

[94] If Mr Durie had first been exposed to asbestos in 1942, it was extremely unlikely that he could have developed asbestosis between 1986 and 1990. This just did not happen. It was highly unlikely that asbestosis would develop more than 15 years after the last exposure. If he was suffering from asbestosis at all, Dr Crompton expected that he would have been suffering from it in 1986. Looking at the 1990 radiograph in isolation, asbestosis had to be considered, but if it was present he would have expected physical manifestations in the form of end inspiratory crackles, which were never coarse. Dr Kerr's description was not what would be expected of crackles in the case of interstitial fibrosis. He did not describe whether they were fine, medium or coarse. The coarse crackles described by Dr Fennerty were inconsistent with asbestosis. No crackles had been described in 1986, when they would have been expected to be present if Mr Durie was suffering from asbestosis. The 1992 radiographs showed pneumonia.

[95] At the hearing on evidence, counsel for the pursuer said that he appreciated that this was a difficult case for her. The onus rested on her to prove her case. In order to prove that Mr Durie suffered from asbestosis it was necessary to establish both that he had a significant occupational exposure to asbestos (which I have already discussed) and that he had suffered fibrosis which was consistent with that found in cases of asbestosis. The diagnosis of asbestosis could be established in a number of ways, i.e. by radiological evidence, by clinical findings and by a relevant work history. It was usually a combination of all of these which would establish a proper diagnosis. Counsel made it clear (at a later stage) that he was not arguing for a separate finding of pleural thickening if asbestosis was not proved.

[96] Counsel went on to say that in many ways the radiological findings were perhaps the most perplexing aspect of the case. Some radiographs appeared to have been lost. There was, unfortunately, a widespread divergence both in the radiological findings, i.e. in the actual signs or marks which those reviewing the radiographs claimed to be able to see, and in the interpretation of such findings. It was difficult to attribute such a divergence of views to the skill or experience, or lack thereof, of any of the expert witnesses. It did appear clear that such a divergence of views, although unusual, was by no means unheard of. Dr Moran had hinted that perhaps it might be something to do with attempting to find further radiological evidence to support a view which the interpreter had already formed of the existence, or otherwise, of the presence of asbestosis. The various drawings made by the witnesses illustrated vividly their varying interpretations and findings. What was worth noting was that the position was far from straightforward and that there were a number of complicating factors present, i.e. some emphysema, chronic bronchitis and infections, although the exact degree of these other conditions and how they were manifested upon the radiographs was not a matter upon which the witnesses appeared to agree. There was some agreement, however, in relation to the fact that the 1986 radiographs were not particularly good in quality and that they suffered from subsequent fogging. The lateral films of 1990 and 1992 were not of any great diagnostic assistance, while the film of 25 August 1992 was complicated by the extensive areas of consolidation in the right lower zone area and in any event was an AP sitting film. There was general agreement that the AP film of 7 November 1990 was, in quality, the best of the films in that it was well positioned and well exposed. However, it had not been suggested by any of the witnesses that one could merely look at one film in isolation without considering the other films, however defective in quality they might have been. What was interesting was that Dr Kerr and Dr Moule adhered to the view that there was a consistency of radiological signs consistent with asbestosis. In particular they both claimed to have seen fibrotic markings and bilateral pleural thickening consistent with a diagnosis of asbestosis and both made such a diagnosis on the basis of the series of radiographs insofar as these provided clear evidence. Although Dr Moule had not had the benefit of previously studying the radiographs other than that dated 7 November 1990, he examined them carefully in Court and gave a careful and reasoned view of both his findings and his interpretations. It seemed to have been accepted that a diagnosis could not be made on the basis solely of radiographs and indeed it was suggested that they were not a particularly good diagnostic tool compared with CT and high resolution scans. According to Dr Crompton CT scans were not widely used in the earlier 1990s, but it had to be accepted that had Mr Durie not died when he did it was possible and indeed probable that a CT scan would have been carried out and that the radiological evidence would thereby have been less controversial.

[97] Counsel submitted that the most important clinical findings appeared to be the presence of basal crackles and the lung function tests. Dr Kerr said that both of these were consistent with the diagnosis of asbestosis. Much had been made of the fact that Dr Kerr did not appear to have given a very full description of the crackles which he heard, but it was conceded by Dr Moran that Dr Kerr was a man of considerable experience in the field and that he, therefore, must have been satisfied that the sounds which he heard were consistent with his diagnosis. The descriptions given by Dr Fennerty and by the Special Medical Board appeared to be consistent with asbestosis and indeed must have been of such a nature that they were satisfied that asbestosis had been established on the balance of probabilities. Counsel submitted that the evidence in relation to the lung function tests appeared to be somewhat confused and at times contradictory and one would have to wonder how much weight could be placed on these findings when there were the complicating factors relating to emphysema and airways obstruction caused by bronchitis and infections. Dr Kerr had given a careful explanation of the findings and their interpretation, but it had to be conceded that a contrary explanation was given by Dr Moran.

[98] Counsel submitted that the history of Mr Durie's exposure to asbestos became a crucial factor. If there was lower-zone interstitial fibrosis and a history of exposure to asbestos, then he was probably suffering from asbestosis.

[99] Counsel accepted that where there was a divergence between the views expressed by the expert witnesses then the Court was faced with a difficult decision and it was incumbent upon the pursuer to convince the Court that the evidence given by her witnesses should be preferred to those called by the defenders. In the present case this was particularly difficult given that all of the witnesses appeared to have impressive credentials and to give evidence which was based on the same factual criteria. Very little had been conceded by any of them in cross examination and they hardly departed from their previously stated positions in examination in chief and in the various reports which they had prepared. If consistency of evidence was the sole determinant then it would be difficult to make any strong recommendation to the Court as to which witnesses or evidence should be preferred. Given the nature of the evidence itself it was also difficult to say categorically that one particular witness had misunderstood the medical issues and indeed in view of their various professional qualifications and experience it would perhaps be presumptuous so to do. At the end of the day, the Court would have to determine the matter on the basis of what impression was formed of the way in which the witnesses gave their evidence and in particular as to whether I found their evidence to be satisfactory, and consistent both with such other evidence as was found to be acceptable and in accordance with the understanding which I formed of the various matters spoken to. There were, however, a number of observations which could be made. Dr Kerr had extensive experience of seeing patients with asbestosis. He had an advantage over all the other witnesses in having examined Mr Durie and carried out certain tests. His diagnosis, therefore, could not be easily dismissed. Others who had been responsible for the care of Mr Durie either made a similar diagnosis, in the case of Dr Fennerty, or confirmed it, in the case of Dr Monie. Dr Fennerty would have had considerable experience of dealing with patients with a history of exposure to asbestos. The Special Medical Board had made their own independent assessment and although it was suggested that they were sometimes more inclined towards claimants than were other panels it could not be denied that they reached their conclusion on the basis of a series of x-rays and the basal crackles. Both Dr Fennerty and the Board had the benefit of the hospital notes and appeared to have taken these into account when making their diagnosis.

[100] Counsel submitted that Dr Kerr appeared to be willing to defer to the views expressed by radiologists in relation to the radiological findings and, on the whole, gave the impression of being relatively undogmatic and willing to consider other points of view insofar as they were put to him in cross examination. Dr Moule, who had many years of experience as a consultant radiologist and had a special area of experience in examination of radiographs of persons who had been exposed to asbestos was a careful witness who was not afraid to disagree in detail with Dr Kerr and was independent enough to disagree with the probability that the cause of death was a carcinoma, notwithstanding the fact that this would obviously weaken the pursuer's case on this second limb. Dr Moran appeared to be somewhat dogmatic and unwilling to concede even that there were any fibrotic markings present irrespective of whether or not they could be attributable to asbestos exposure. Dr Crompton had prepared his reports without the benefit of having seen the radiograph dated 7 November 1990. He did seem prepared to concede that the changes in the lower zone could be due to interstitial pulmonary fibrosis arising out of asbestos exposure. Dr Crompton appeared at times to be somewhat hesitant and to change his views when matters were raised again in re-examination, for example in relation to the importance of the lung function tests where there were the complicating factors of other conditions such as emphysema, bronchitis and infection. It had to be said that of all the defenders' witnesses Dr Turnbull was arguably the most impressive. It was worthy of note that he was prepared to say that on the basis of the radiograph dated 7 November 1990 there were features consistent with asbestosis notwithstanding the fact that he did not agree that such a diagnosis was correct when the whole series of films were viewed. Perhaps some emphasis could be placed on the fact that he could not distinguish certain of the features which Dr Moule pointed out as existing on various of the radiographs. Counsel submitted that I should be able to accept the diagnosis that on the balance of probabilities Mr Durie did suffer from asbestosis and that this condition, which was clearly manifest in 1990, would have been in existence since at least 1986 when, according to Dr Kerr and Dr Moule, signs of it were in evidence.

[101] On the question of bronchial carcinoma, counsel accepted that in order to make the diagnosis of cancer due to asbestos exposure, asbestosis must be present. Thus it had to be accepted that if the first limb of the case failed and the pursuer failed to prove that Mr Durie had asbestosis, then the second limb also failed. There had been a working diagnosis of bronchial carcinoma when Mr Durie was admitted to the Southern General Hospital in August 1992. The ultrasound report reported that there were several areas of reduced reflectivity in the right lobe very suspicious of metastatic deposits. The neuroradiology report reported findings suggestive of an underlying tumour mass. Unfortunately Mr Durie died before any further investigation could be arranged and no post mortem examination was carried out. Nevertheless the diagnosis was felt to be sufficiently accurate to be given on the death certificate. Dr Kerr expressed the view that on the balance of probabilities the death was due to bronchial carcinoma caused by the exposure to asbestos. Dr Crompton did not rule it out, despite lack of histological and cytological proof, and Dr Turnbull could not rule it out or confirm it either. On all of the evidence, counsel submitted, it would be open to the Court to find that, on the balance of probabilities, Mr Durie died from asbestos-related bronchial carcinoma.

[102] Counsel for the first defenders submitted that the pursuer had not proved that Mr Durie suffered from either bilateral pleural thickening or asbestosis. Nor had she proved that he died of bronchial carcinoma, and indeed the evidence suggested that he died of another condition. The only evidence that there was a bronchial carcinoma came from the working diagnosis mentioned in the hospital records. The provisional nature of such a diagnosis was spoken to by Dr Moran and not disputed. Had Mr Durie lived longer, more extensive tests would have been carried out on him. Dr Moule expressed the view that on the balance of probabilities Mr Durie did not have a bronchial carcinoma, but the chest radiographs taken in August 1992 suggested a vascular explanation for the appearances. That explanation, in relation to the right hilum in 1992, was consistent with the appearance of the left hilum in earlier years. No evidence was given which supported diagnosis of bronchial carcinoma other than by Dr Kerr, who to a large extent relied upon the contents of the hospital records and in any event deferred to the expertise of consultant radiologists in interpreting radiographs. Further, he accepted that those treating Mr Durie at the time considered that the radiograph dated 26 August 1992 tended to exclude bronchial carcinoma at the right hilum. Dr Crompton could not say whether bronchial carcinoma was present or not. His neutral position could not support the contention that it was likely on the balance of probabilities that Mr Durie died of this condition. Finger clubbing could be present where there was bronchial carcinoma but might be present in a large number of conditions. Dr Kerr said that he saw only finger clubbing when he examined Mr Durie in December 1990. While in his evidence in chief he said that this was quite relevant to the final illness, in cross-examination he excluded it as being caused by bronchial neoplasm, so its presence in 1992 did not imply presence of bronchial carcinoma; this negated his evidence in chief. While the ultrasound scan of the liver produced findings suggestive of metastases, these could have resulted from a primary tumour anywhere in the body. The unchallenged evidence of Dr Moran was that the most likely location for any such tumour was in the gastro-intestinal tract. His reason for this was that Mr Durie was found to be anaemic shortly prior to his death. Tests were suggestive of his having suffered a bleed. As there was no report of his coughing up blood during that period, it was likely that the bleed occurred not in the lungs but elsewhere. This gave a likely indication of the location of any neoplasm. In any event, counsel submitted, it was not proved that there was any primary tumour anywhere in the body. No biopsy was carried out on the liver to establish the presence of metastases. The clear evidence was that Mr Durie suffered a back injury several months prior to his final illness which rendered him largely immobile. He had a long history of smoking, obstructive airways disease, chronic bronchitis, emphysema, and pneumonic and other chest infections. A combination of these conditions could easily have caused his final pneumonia and his death, and this was the most likely cause of death.

[103] Accordingly, counsel submitted that the pursuer had failed to prove that she had any case for damages under the Damages (Scotland) Act 1976 and that similarly the death claim made in her capacity as her mother's executrix failed. The remaining issues were whether the deceased suffered during life any loss, injury or damage as a result of any asbestos-related condition, whether any services were rendered to him in respect thereof, and whether any person was deprived of services from the deceased as a result thereof.

[104] Counsel then advanced a submission on the question, esto bronchial carcinoma did cause Mr Durie's death, what was the cause thereof. Counsel submitted that mere exposure to asbestos did not cause or materially contribute to the onset of bronchial carcinoma. Dr Kerr had accepted this, saying that only if a patient suffered from either asbestosis or diffuse bilateral pleural thickening could it be said that there had been any increase in the risk of developing bronchial carcinoma. The pursuer did not claim on record that the deceased suffered from diffuse bilateral pleural thickening. Not even Dr Kerr suggested this. For reasons which would be discussed, the pursuer had failed to prove that Mr Durie suffered from asbestosis. Accordingly, even if he did suffer from a bronchial carcinoma, the defenders did not cause or materially contribute to the onset of this condition. There was ample evidence that a bronchial carcinoma could develop in the absence of asbestosis or bilateral pleural thickening and that cigarette smoking markedly increased the risk of development of a bronchial carcinoma. Dr Kerr accepted this. Indeed, cigarette smoking increased the risk substantially more than did asbestosis or diffuse bilateral pleural thickening, though the combination of factors was synergistic. There was ample evidence that the deceased was a heavy cigarette smoker throughout all of his adult life. In summary, the pursuer had failed to prove that he died of bronchial carcinoma and had also failed to prove that Mr Durie suffered from either asbestosis or bilateral pleural thickening. Esto she had proved bronchial carcinoma, bilateral pleural thickening did not cause or materially contribute to the onset of bronchial carcinoma unless it was diffuse. There was no evidence suggesting that any pleural thickening was diffuse in this case. Accordingly in order to prove causation the pursuer must prove the existence of asbestosis, and had failed to do so.

[105] Counsel referred to the smoking-related respiratory conditions from which Mr Durie suffered. There was evidence that he suffered numerous lung infections throughout his life and certainly since before 1980, and had suffered previous bouts of pneumonia, of unknown number but more than two prior to 1980. In addition to the smoking-related conditions, there was evidence that Mr Durie had a history of oesophageal reflux and that this could cause fibrosis. Dr Crompton spoke to this. Dr Kerr accepted it as a possibility, though he felt the location of the alleged fibrosis meant that this explanation was unlikely. There was also evidence that the deceased might have suffered from several pulmonary infarctions. While being at pains to minimise the effects of all these conditions, Dr Kerr accepted that such a medical history would account for significant breathlessness and could account for Mr Durie's final illness. All the other medical witnesses freely accepted that the symptoms suffered by Mr Durie were easily explained by his known and undisputed medical history. In relation to his final illness the evidence was that his substantial breathlessness shortly prior to death was easily explained by his long-standing respiratory conditions together with pneumonia and, to a lesser extent, anaemia and possibly hypertension.

[106] Counsel submitted that the pursuer's case on asbestosis and pleural thickening was based on the evidence of Dr Kerr and Dr Moule. Dr Kerr was not an impressive witness. It was plain from his initial report and the evidence of Dr Moule that he was concerned simply to ascertain whether or not there was evidence of asbestosis or pleural thickening and not to make a balanced assessment of Mr Durie's lung condition. His first report minimised Mr Durie's smoking history and did not mention either chronic bronchitis or emphysema. His later report, when the records were seen to disclose these conditions, simply indicated that the records were not inconsistent with his own views. Dr Kerr's explanation for not mentioning in his original report all the other conditions from which the deceased was suffering, that he considered the dominant factor in his illness to be asbestosis, was a wholly inappropriate reason for omitting such information. Counsel submitted that in the witness box Dr Kerr appeared somewhat evasive at times and was prone to suggest spurious explanations for facts which were anomalous to his position, for example in what he said about the radiograph dated 5 December 1986, his explanation for alleged pleurisy at the apex of the lung being caused by asbestos exposure, his evidence that the location of the alleged fibrosis at the bases of the lungs was indicative of asbestosis because smoking-related appearances were not found in that position being contrary to what he said in McCance v Newalls Insulation Ltd, and his explanation for not noting the quality and nature of the crackles which he said he heard upon examination of Mr Durie. More fundamentally, Dr Kerr's whole thesis was based upon the proposition that the radiological appearance of asbestosis could be distinguished from that of smoking-related damage by measuring the size of the markings on the radiograph. He purportedly based this upon the ILO study. In cross-examination he conceded that the study required close comparison with the standard films and that it was not merely the size, but also the shape and other characteristics of the appearances that were relevant. In short, his method was one of his own devising which had no sound basis and which was contrary to the method prescribed by the study and described in standard textbooks. It was apparent from all the other medical witnesses that use of the ILO films was not standard practice among consultant radiologists or chest physicians, even where properly used, and was not regarded as being useful in the differential diagnosis of asbestosis. It was surprising that Dr Kerr felt able to justify his position by suggesting he had used a standard method of diagnosis when he knew that he was operating contrary to the instructions and guidance written by the compilers of the materials upon which the study was based. Throughout his cross-examination Dr Kerr was forced to make concessions that there were numerous aspects of the case which were contra-indications to the presence of asbestosis and, to a lesser extent, bilateral pleural thickening. Reference was made to the absence of pleural plaques, the large lung volumes, the comparatively late alleged onset, the absence of crackles in 1986, the presence of coarse expiratory crackles in 1990, the unilateral crackles in 1992, the lack of fine, persistent, late inspiration, basal crackles at any time, and several other examples. On the basis of one theoretical study Dr Kerr had claimed that there was a causal link between asbestosis and emphysema. No other witness supported this view. The study was not produced. It was apparent that this alleged phenomenon only produced bullous emphysema. The process had been explained by Dr Moran; it was noteworthy that it was only possible when asbestosis was sufficiently advanced markedly to shrink the lungs, causing tearing of the lung tissue. For as

[107] Counsel submitted that while Dr Moule gave his evidence in a straightforward manner, the quality of his evidence on the issues of asbestosis and pleural thickening was poor. The general impression was of inadequate consideration to his evidence in chief, leading to exaggeration, followed by concessions in cross-examination. His starting position appeared to be due to the limited information with which he was provided and the limited remit which he was initially given. Even at proof he had a limited opportunity to view the radiographs and had not seen the medical records or the reports of the other expert witnesses. It was striking that his evidence in court suggested much more widespread pleural thickening than he seemed to have reported to Dr Kerr originally. Dr Kerr indicated that Dr Moule had found a little pleural thickening on the right side, but in evidence Dr Moule indicated widespread pleural thickening bilaterally, especially over the diaphragms. This was inconsistent with his original findings and also with those of every other radiologist or consultant physician who viewed the radiographs either at the time they were taken or in the context of the litigation. Counsel submitted that the reasoning upon which Dr Moule's conclusions was based did not stand up to scrutiny. He was of the view that asbestosis could not be identified by the appearance of the individual marks on the radiograph, but that it was the location of the marks which allowed a diagnosis of asbestosis. He conceded, however, that smoking-related causes could give rise to similar marks in the same position. Given Mr Durie's medical history, the justification for the conclusion that the markings were caused by asbestosis evaporated. Dr Moule indicated in several drawings that asbestosis was present throughout the mid and lower parts of the lungs, and that pleural thickening was present bilaterally over the whole of both hemi-diaphragms. Not even Dr Kerr had suggested that either condition was so widespread. He did not suggest that there was any pleural thickening on the diaphragms at all. The overwhelming evidence was that the shape of the diaphragms, on which Dr Moule had based his opinion about pleural thickening, was a feature of the emphysema from which Mr Durie undoubtedly suffered. Dr Moule accepted that the usual pattern for the onset of asbestos-related pleural thickening was that the costo-phrenic angles were obliterated first, but that this had not happened in Mr Durie's case.

[108] Counsel continued by submitting that Dr Kerr accepted that, apart from Dr Moule, no other doctor had ever, at any time, opined that there was bilateral pleural thickening and even Dr Kerr suggested that the thickening on the right side was less evidence. He did not suggest that it was evident at all in the 1986 radiographs, and was prepared to concede that it might not be present in the right side in subsequent radiographs. Counsel submitted that in the absence of proved bilateral thickening, it could not reasonably be argued that unilateral pleural thickening was caused by asbestos exposure, particularly where there was a clear and likely alternative explanation. Dr Kerr admitted that pleural thickening could be caused by past episodes of pneumonia, and accepted that the medical records suggested that Mr Durie had suffered from such episodes. He accepted that the radiological appearances were consistent with thickening caused by infection. Dr Moule accepted that pleural thickening, especially on the chest walls, could be caused by chest infections consistent with Mr Durie's known history.

[109] Counsel submitted that there was little in the clinical history and findings to support the proposition that Mr Durie suffered from asbestosis. The audible clinical sign indicative of asbestosis was the presence of crackles which were persistent, fine, basal, and late inspiration: Dr Moran and Dr Crompton had both stated this. There was no mention of crackles of any description in the hospital records until Dr Fennerty recorded coarse expiratory ones, which Dr Kerr conceded were consistent with chronic bronchitis. Dr Moran's evidence, which was to be preferred, showed that such crackles were more consistent with bronchitis than with asbestosis. The quality of the crackles heard by the Special Medical Board was not recorded. They were not truly persistent, they were not noted as being basal and they were not indicative of asbestosis. They were not consistent with what Dr Fennerty had heard or with what was heard in 1992. Accordingly, the crackles were not persistent over time in any manner consistent with the presence of asbestosis. Dr Kerr did not record the quality of the crackles which he heard, and against the background of his experience it was likely that if the crackles has been fine or late inspiration he would have recorded this. At the time of Mr Durie's death unilateral crackles were recorded. This was consistent with chronic bronchitis, infection and obstructive airways disease. In short, such crackles as were heard in Mr Durie's chest during his life were not indicative of the presence of asbestosis.

[110] On the question of finger clubbing, Dr Kerr had accepted that it could be caused by a large number of pulmonary and cardiac conditions. Dr Moran indicated that it was only associated with asbestosis when this was severe. Counsel invited me to accept Dr Moran's evidence.

[111] In summary, counsel submitted, the evidence of Dr Kerr and Dr Moule did not present any coherent or consistent justification for the proposition that the deceased suffered either from asbestosis or from bilateral (non-diffuse) pleural thickening. Their evidence was generally based upon incomplete information, inappropriate methodology and flawed logic. Except in the most general of their conclusions, they did not corroborate or support one another. In contrast, Dr Moran, Dr Turnbull and Dr Crompton presented careful, fair, balanced, consistent and coherent evidence to the effect that Mr Durie suffered neither from asbestosis nor from bilateral pleural thickening caused by asbestos exposure. Dr Moran and Dr Turnbull in particular were impressive witnesses whose reliability was not seriously challenged.

[112] Dr Kerr and Dr Moule had argued that there was no significant difference between the three 1986 radiographs. They accepted in principle that improvement in radiological appearances was inconsistent with asbestosis but consistent with smoking-related disease. The three expert witnesses for the defenders were however remarkable consistent in describing the changes in the lungs over the period in question and the explanation for these changes. The burden of the evidence clearly showed that the markings relied upon by the expert witnesses for the pursuer were variable over time and that they were largely infiltrates caused by current infection. To the extent that there might have been some permanent markings, these were isolated fibrotic changes caused by past infection, reflux, smoking and chronic bronchitis. Certain markings relied on by Dr Kerr and Dr Moule were blood vessels and rib irregularities. Of all the radiographs, that dated 7 November 1990 contained appearances which most resembled asbestosis, but seen in context these could be recognised for what they were. Counsel submitted that Dr Kerr and Dr Moule, who had started with sight of this radiograph alone, were swayed by this and did not appropriately revise their opinions once further radiographs and information were available.

[113] Counsel referred to the evidence of Dr Moran and Dr Crompton that there were numerous clinical contra-indications to the suggestion that Mr Durie had asbestosis. There was no consistent pattern of crackles. There was plainly a significant history of past serious respiratory disease. Nobody had suggested that Mr Durie had asbestosis and apart from the opinions of Dr Kerr and Dr Moule radiographs taken up to and including April 1990 did not reveal signs suggesting asbestosis. The documents relating to Mr Durie's final admission to hospital were not supportive of asbestos-related disease. The evidence of Dr Moran on the lung function tests was detailed and compelling. These showed clearly that Mr Durie suffered from emphysema and obstructive airways disease, particularly in the smaller airways, which accounted for such breathlessness as he suffered from. As a whole the results indicated centrilobular emphysema. Dr Kerr's point about the FEV 1 was ill-founded. Dr Crompton supported Dr Moran in connection with the lung function tests. The simple tests carried out at the Southern General Hospital between 1986 and 1991 showed substantial variation in result over time. As explained by Dr Moran, supported by Dr Crompton, this suggested a significant changeable element in the condition of Mr Durie, which was consistent with chronic bronchitis and infection and not with asbestosis. Dr Kerr's explanations for the variation in the figures were not convincing.

[114] Counsel submitted that all symptoms of breathlessness were explained by Mr Durie's known respiratory history. There was little evidence, apart from that of the pursuer, which counsel invited me not to accept because it was coloured by her feelings about the perceived cause of her father's death, that Mr Durie was substantially disabled by breathlessness until very shortly before his death. The weight of evidence was that his complaints of chest pain were inconsistent with asbestosis. His back pain was not caused by any asbestos-related condition. In conclusion, counsel submitted, the pursuer had failed to prove asbestosis or pleural thickening and in any event any breathlessness and pain which the deceased suffered was not attributable, at least significantly, to either condition.

[115] Counsel for the second defenders submitted that even if Mr Durie had asbestosis the pursuer had failed to prove that death was caused by lung cancer. Dr Moule expressed the opinion that the likely cause of death was pneumonia secondary to the effects of a back injury sustained in a fall on a bus in May 1992. Dr Turnbull and Dr Crompton were agreed that the presence of lung cancer, which could have been attributable to smoking, could neither be excluded nor confirmed. Had Mr Durie lived longer this would have been the subject of further investigation. At worst for the second defenders Dr Crompton was correct in concluding that there was no proof of bronchial carcinoma. At best for them Dr Moule was correct and an alternative cause of death had been proved. Counsel invited me to reject Dr Kerr's evidence that death was due to bronchial carcinoma. Had the pursuer intended to rely on the evidence of Dr Kerr that death was attributable to asbestos-related lung cancer, Dr Moule's opinion should have been challenged and this was not done; on the contrary the line of questioning in re-examination, which merely sought a reaffirmation of the evidence given by him in cross-examination, amounted to a concession that this evidence was correct. It mattered not to the defenders whether the Court went only so far as to conclude that the cause of death had not been proved or went further and held that a non-industrial cause had been proved. On either view the pursuer had failed to prove the essential fact that death was caused by lung cancer and this was what the Court was invited to conclude. This was sufficient to dispose of the pursuer's claims as an individual and as executrix of Mrs Durie.

[116] Counsel then turned to the pursuer's claim as executrix of Mr Durie, which depended on the answer to the question whether it had been proved that Mr Durie suffered from asbestosis. As a preliminary point, under reference to Lord Bonomy's comments in Smith v Upper Clyde Shipbuilders Ltd, 8 September 1999, at p.2, counsel submitted that plainly in the present case further investigations while Mr Durie was alive or a post mortem examination could have greatly assisted the resolution of the present dispute, if not settled it conclusively. Having regard to the history of the claim and the action as related to the possibility of further investigations or in any event a post mortem examination, the Court should look critically at the available evidence. Both Dr Kerr and Dr Moule had expressed their opinions by reference to the radiograph dated 7 November 1990, but accepted that had they seen Mr Durie in a treatment context they would have carried out further enquiries including a CT scan. Dr Crompton had been cautious in saying that CT scans might not have been as commonly used in 1990 as now, but Dr Moule had said in re-examination that CT scans were available then. There was ample opportunity to carry out further investigations and yet it was not done. Dr Moule had not even asked to see the other radiographs before giving evidence. This was not a case where death had come so quickly that there was no adequate opportunity to conduct investigations while the claimant was alive. It had not been explained why Dr Kerr and Dr Moule had failed to take advantage of the opportunity to carry out the normal investigations that they would ordinarily have carried out. It was unfortunate that the family had declined the offer of a post mortem examination. They may have been convinced of the cause of death, but they knew that by then there was a contested legal action.

[117] Turning to the available evidence, particularly the series of radiographs, counsel referred to a passage in the cross-examination of Dr Kerr when he accepted that he could not have expressed the opinion, even on the balance of probabilities, that Mr Durie had asbestosis without the radiographs. Counsel submitted that the radiological evidence refuted a diagnosis of asbestosis. Counsel had thirteen points to make on the interpretation of the radiographs. (1) Dr Turnbull and Dr Crompton agreed that the radiograph dated 7 November 1990 viewed in isolation could be consistent with asbestosis but could also be consistent with a number of other conditions, notably a combination of chronic bronchitis and emphysema with associated infection. This was what Dr Crompton termed a differential diagnosis. (2) All witnesses agreed that ordinarily a diagnosis of asbestosis would not be made on that one radiograph in isolation. (3) The difference between the pursuer's witnesses and the second defenders' witnesses was that the latter viewed the radiograph of 7 November 1990 in the context of the remaining films and expressed an opinion based on the series as a whole. Dr Moule's letter of 20 January 1998 was based on an examination of that radiograph alone and he did not see the others until he came to give evidence. In court he remained prepared to express an opinion based on that radiograph alone, apparently even without reference to the history. (4) It was quite extraordinary that Dr Moule had not seen the other radiographs before giving evidence, particularly given the terms of the second defenders' reports from Dr Crompton and Dr Turnbull. Equally it was inexplicable that he had not even seen those reports until they were handed to him in the course of his evidence in chief. In cross-examination on behalf of the second defenders he readily conceded that he was not viewing the films in ideal circumstances. He might be contrasted with Dr Turnbull, who viewed the whole series side by side in ideal conditions on one occasion prior to giving evidence, as well as having seen them all, though not together, on other occasions and having viewed them in Court. (5) When Dr Moule came to review the whole series for the first time in Court he plainly had no knowledge of Mr Durie's medical history. He did not see the medical records until he was cross-examined on behalf of the first defenders, and while giving evidence in chief he did not even know that Mr Durie was a smoker. The reliability of Dr Moule's evidence that the series as a whole supported a diagnosis of asbestosis on the balance of probabilities was undermined by the fact that he was not then alive to extensive material requiring equal consideration of the non-industrial respiratory conditions of chronic bronchitis, emphysema and associated infections. (6) When he first saw the radiograph dated 7 November 1990 Dr Moule's opinion was simply that it was "consistent with asbestosis". Even as late as January 1998 he was reporting only that the distribution of the pulmonary fibrosis suggested that it might be due to asbestosis. Dr Turnbull and Dr Crompton would not dispute that. This was not the answer to the case, however: the question was whether on the balance of probabilities asbestosis was the correct diagnosis, not whether the signs were consistent with it or suggested it. (7) What Dr Moule did not explain in evidence was how he could move from what was no more than a differential diagnosis to the opinion that asbestosis was the correct diagnosis on the balance of probabilities. The only piece of additional evidence that he cited as reinforcing his opinion was his observation of mediastinal calcification in the radiograph of 7 November 1990. Not even Dr Kerr observed thickening or calcification in that area and in cross-examination on behalf of the second defender

[118] Counsel for the second defenders accordingly submitted that the pursuer had failed to prove that Mr Durie was suffering from asbestosis. This was their primary position.

[119] The pursuer can only succeed in establishing liability against the defenders if she can prove that on the balance of probabilities Mr Durie contracted bilateral pleural thickening and pulmonary fibrosis (asbestosis) and that he died of metastatic disease and bronchial carcinoma as a direct result thereof. There are two branches to this, and counsel for the pursuer recognised that it might be proved that Mr Durie had asbestosis and that this resulted in his death from metastatic disease and bronchial carcinoma, or that it might be proved that he had asbestosis but not that his death was a direct result thereof. In approaching the evidence and counsel's submissions thereon I bear in mind what was said in Dingley v The Chief Constable, Strathclyde Police 1998 S.C. 548, 2000 S.C. (H.L.) 77, about the function of a Lord Ordinary in considering expert evidence.

[120] I propose to refer at this stage to the demeanour of the expert witnesses when they gave their evidence. As might be expected from consultants who were eminent in their respective fields, each of them gave evidence with authority. Counsel for the pursuer submitted that much would depend on my impression of the witnesses. Of the impressions which I recorded at the time, and which have remained with me, I would mention particularly that of Dr Turnbull in the first place. I found him to be a most impressive witness, and my summary of his evidence does scant justice to the impression he made on me at the time. Of all the witnesses who gave evidence about the radiographs, he was the one who had taken the most care to examine them before giving evidence and indeed who showed the most care in explaining during his evidence what features he could see in them and how he interpreted them. Counsel for the pursuer described Dr Turnbull as being tentative. I did not regard him as being anything of the sort. When asked a question or when explaining features in the radiographs he was at pains to think about what he wanted to say and then to say it as clearly as possible. I would describe him as thoughtful rather than tentative. Moreover, he appeared to me to adopt what I would regard as a proper scientific approach, which is to examine the evidence against as well as the evidence for a hypothesis before deciding whether to accept the hypothesis as proved.

[121] Dr Turnbull contrasted sharply with Dr Moule. Dr Moule had written for the first time in 1998 about the radiograph dated 7 November 1990. Given the limited amount of information available to him, it is not surprising that he wrote that the distribution of the pulmonary fibrosis suggested that it might be due to asbestosis. What appears to me to be astonishing, however, especially when the issues had been so fully explored when Dr Kerr gave evidence in the first instalment of the proof, was that Dr Moule had not considered the hospital records, the other radiographs or the reports of other witnesses thereon until he came to give his own evidence. Looking back over his evidence, once this had become apparent, I could see that he had put himself in the position of attempting to defend an initial hypothesis by seizing, with little opportunity for consideration, on items of evidence (or supposed evidence) which might support that hypothesis. As a result of this, his manner appeared defensive, particularly under cross-examination, and did not inspire confidence.

[122] Dr Kerr appeared to me, to an even greater extent, to adopt what I would regard as an unscientific approach. Having expressed a view in his report dated 14 November 1990 (the defects in which I shall mention later), he appeared to me thereafter to be willing only to dwell on items of evidence which might serve to support his original opinion. His unwillingness to accept alternative interpretations of this evidence, or to consider evidence which pointed in a different direction, became particularly apparent during cross-examination, when I formed a clear impression from his manner as well as the content of what he said that he was concerned to argue a case rather than to consider the facts with the degree of detachment that I would regard as appropriate in an expert witness. I was considerably more impressed by Dr Moran than by Dr Kerr. He gave his evidence in a more reflective manner and was clearly prepared to consider all relevant material before expressing a view on it. My impression, as I recorded it at the time, was that he really knew what he was talking about. Dr Crompton made a similar impression on me, although he was in the witness box for a shorter time than were the other expert witnesses.

[123] The expert witnesses referred in the course of their evidence to the records of the Southern General Hospital and the Medical Boarding Centre and to the radiographs. It was quite clear that not all the radiographs which had been taken of Mr Durie's chest were lodged as productions. In particular, those commented on by Dr Fennerty and the Special Medical Board in 1990 were not produced. In light of this, objection was taken to the admission of the records containing their opinions. I do not propose formally to sustain these objections, but I am disposed to place very little weight on the opinions expressed in these documents by comparison with those expressed by expert witnesses who gave evidence and the basis for whose opinions could be subjected to scrutiny in court. Dr Fennerty was not called as a witness for the pursuer, which might have been expected, if he was available, because it was he who first raised the question of the significance of Mr Durie's exposure to asbestos. As it is, the "bilateral coarse end expiratory creps", i.e. crackles, which he reported are, for the reasons given by Dr Moran, inconsistent with a diagnosis of asbestosis. I also attach some significance to Dr Moran's comments about the tendency of the Special Medical Board to favour applicants for benefit. What is reported in the form which has been produced may well be regarded as affording a slender basis for a diagnosis of asbestosis.

[124] When considering the material available to the expert witnesses, I bear in mind that investigation of his condition was confined to clinical examination, x-ray examination and pulmonary function tests. No CT scan or biopsy was carried out during his lifetime, and no post mortem examination was carried out. Dr Kerr was the only witness who examined Mr Durie clinically. He made no mention of the chronic bronchitis, obstructive airways disease and emphysema from which Mr Durie suffered from no later than 1980, notwithstanding having noted a history of cigarette smoking. He gave no description of the crepitations which he heard at the bases, so it is not possible to tell whether or not they were consistent with a diagnosis of asbestosis. He said no more to Dr Moule about these sounds than appears in the report. At best, therefore, in my opinion what Dr Kerr found on clinical examination went no further than to raise the possibility of asbestosis in light of the history of exposure to asbestos and the radiograph dated 7 November 1990, which all the witnesses were agreed when viewed in isolation could be consistent with asbestosis (but also of course with a number of other conditions).

[125] All the witnesses were agreed that, of the available evidence, the radiographs were the most important. I have attempted to record the main points that each of the witnesses made about these radiographs. The divergence between the witnesses both about what features could be seen in the radiographs and what interpretation to place upon them was remarkable. It was, I think, recognised by all the experts that in order to support a diagnosis of asbestosis it would be necessary to find features consistent with a condition which might remain constant or might deteriorate, but would not improve. I am not satisfied that, on proper examination, there is any evidence which would satisfy this requirement, let alone a sufficiently congruent body of professional opinion to persuade me on the balance of probabilities that the presence of asbestosis can be demonstrated on the radiographs or supported by reference to the hospital records. Dr Kerr's reliance on the I.L.O. categories appears to me to be flawed, for the reason given by Dr Moran, which was that if reliance is to be placed on the I.L.O. material comparison has to be made between their films and the film under examination. Dr Kerr did not do this. I also have strong reservations about what Dr Kerr said about information relating to the presence of emphysema in the early stages of asbestosis, since Dr Moran had never heard of this. Obviously, a history of exposure to asbestos raises the possibility that a patient with impaired respiratory function may be suffering from asbestosis, but given the history of Mr Durie's smoking and his undisputed chronic bronchitis, obstructive airways disease and emphysema, there is in my opinion no persuasive evidence that there is anything in the radiographs or hospital records which cannot be explained by reference to factors other than asbestosis. The results of the lung function tests were discussed at some length in the evidence of both Dr Kerr and Dr Moran. One of the reports on them, dated 13 June 1990, stated that overall the results were consistent with emphysema. Dr Moran accepted that this was the correct interpretation, and I am not persuaded that Dr Kerr advanced any sound reason for thinking otherwise.

[126] This appears to me to be a sufficient indication of my reasons for preferring the defenders' witnesses to those of the pursuer and for holding that the pursuer has failed to prove, on the balance of probabilities, that Mr Durie suffered from asbestosis. While I have given these as my main reasons, I would add that I accept the various criticisms of the pursuer's case which were advanced by counsel for the defenders and which I have previously recorded.

[127] It is not suggested that in the absence of proof that Mr Durie suffered from asbestosis during his lifetime, it is open to me to hold it proved that he died of an asbestos-related cancer. This branch of the pursuer's case must therefore also fail. I should however express a view about the evidence relating to the cause of his death. He died before the cause of his illness could be fully investigated, and no firm diagnosis of bronchial carcinoma was made. There were some signs which suggested this as a possibility, but no more. Of the expert witnesses, only Dr Kerr appeared to be prepared to treat this possibility seriously. The preponderance of the expert evidence was that he died of pneumonia, which was consistent with his previous medical history. There is no substantial body of evidence which would entitle me to hold it proved on the balance of probabilities that Mr Durie suffered from bronchial carcinoma. In any event, if he did, the most obvious cause of it was his smoking habit. Accordingly, even if I were satisfied that he did suffer from bronchial carcinoma, I would not have regarded that as a reason to hold that he suffered from any asbestos-related disease.

[129] I turn finally to the damages which I would have awarded had the pursuer succeeded on the first or both branches of her case on liability. I propose to deal with this matter comparatively briefly. Counsel for the pursuer addressed me first on the assumption that Mr Durie suffered from asbestosis but that his death was not a direct result thereof. He submitted that in consequence of suffering from asbestosis from at least 1986 onwards Mr Durie had a degree of pain and suffering which was attributable thereto in the form of breathlessness, distress and anxiety and that he was rendered more susceptible to infections and had an increased morbidity, over and above his other medical conditions. Counsel referred to the awards of solatium which had been made in McCance v Newalls Insulation Ltd 1996 S.L.T. 80, Kerr v Newalls Insulation Ltd 1997 S.L.T. 723, Stanners v Graham Builders Merchants Ltd 1995 S.L.T. 728, Myles v City of Glasgow District Council 1994 S.C.L.R. 1112, McKenzie v Cape Building Products Ltd 1995 S.L.T. 695, Bateman v Newalls Insulation Ltd 1987 S.C.L.R. 445, Lightbody v Upper Clyde Shipbuilders Ltd 1998 S.L.T. 884, Campbell v Campbell & Isherwood Ltd 1993 S.L.T. 1095 and Nicol v Scottish Power plc 1998 S.L.T. 822. Counsel submitted that but for the fact that Mr Durie's death came five years earlier than his normal life expectancy, an award in the range of £14,000 to £20,000 would be expected, given his age, general health and degree of disability. His period of suffering was reduced by about 50% due to his death and counsel suggested that a discount of, say, 25% from the total might be appropriate given the anxiety element which would be at its greatest in the period following diagnosis. Taking a mean figure of £17,000 and reducing it by 25% would give £12,750.

[130] Counsel for the defenders both submitted that, if it had been proved that the pursuer suffered from asbestosis, nevertheless this had a limited effect on him. Little weight was to be attached to evidence given by the pursuer about the extent of her father's disability. Dr Kerr's assessment was more reliable. On the view that the asbestosis had set in by 1986 he had suffered its effects for about six years and, had it not been for the terminal illness, he might otherwise have had a life expectancy of a further five years. Taking these factors into account, it was submitted that it would be reasonable to award 50% of the solatium that would have been awarded to a living pursuer. Solatium must also reflect his age. Had he been a living pursuer the range of solatium would have been from £14,000 to £18,500. In addition to some of the cases referred to by counsel for the pursuer, counsel for the second defenders referred to Brown v Saunders Valve Co Ltd [1998] C.L.Y. 1626 and Little v VSEL Birkenhead Ltd [1998] C.L.Y. 1627. He submitted that £8,000 was an appropriate sum for solatium.

[131] I approach the question of solatium on the assumption that I would have accepted the evidence of the pursuer's witnesses, particularly that of Dr Kerr. For that reason I proceed on Dr Kerr's assessment of Mr Durie as being 35% disabled by asbestosis, and I take the period for which he suffered that disability as starting in 1986. Obviously some adjustment needs to be made to take account of Mr Durie's premature death from an unrelated cause. Looking at the matter as best I can, in my opinion an appropriate award for solatium to the date of Mr Durie's death would have been £10,000 (i.e. £15,000, less one third to take account of the premature death). I would have thought it appropriate to award interest at half the then judicial rate of 15% for the period of approximately six years from 1986 to the date of Mr Durie's death in 1992, thereafter at 15% to 31 March 1993, and at the current legal rate of 8% from the latter date to the present. Had I made this award of solatium and interest, it would have been to the pursuer in her capacity as Mr Durie's executrix.

[132] Counsel for the pursuer then addressed me on the assumption that Mr Durie had asbestosis and this resulted in his death from metastatic disease and bronchial carcinoma. He submitted that an award for solatium on this assumption would be similar to that for mesothelioma. He referred to McManus's Executrix v Babcock Energy Ltd 1999 S.C. 569 and Mulgrew v Upper Clyde Shipbuilders Ltd, Kemp & Kemp, The Quantum of Damages, para. F2-018, and suggested that given Mr Durie's age and the relatively short period of his actual suffering, the sum of £40,000 was appropriate. He suggested that I award interest at 7.5% for the period of six months to the date of Mr Durie's death, at 15% thereafter to 31 March 1993, and at 8% from the latter date to the present. Counsel for the defenders did not advance any contrary submission on this head, and accordingly this is the award I would have made on this assumption. Again, this would have transmitted to the pursuer as executrix of Mr Durie.

[133] There is a claim under section 8 of the Administration of Justice Act 1982 in respect of services rendered by the pursuer and her family to Mr Durie. As counsel for the defenders pointed out, there was no clear evidence that services were required and if so to what extent they were required by reason of Mr Durie's asbestos-related conditions rather than his other conditions. There was however some evidence from the pursuer about the provision of services, and on the assumption which I must make, which involves the acceptance of Dr Kerr's evidence about the degree of disability attributable to asbestosis, I am prepared to accept the invitation by counsel for the pursuer to award £2,500 under this head, with interest at the rates suggested by him, i.e. 7.5% for six months to the date of Mr Durie's death, at 15% for the period from then to 31 March 1993, and at 8% from the period from the latter date to the present. This award also would have transmitted to the pursuer as Mr Durie's executrix.

[134] There is an uncontested claim for funeral expenses amounting to £1,200.50, with interest at 15% from the date of Mr Durie's death to 31 March 1993 and at 8% from the latter date until the present. I would have made this award also.

[135] The transmission of these awards, had I made them, would have been by virtue of section 2(1) of the Damages (Scotland) Act 1976, as substituted by section 3 of the Damages (Scotland) Act 1993: see section 6(6) of the 1993 Act, which gave effect to the substituted section in the case of the death on or after 16 July 1992 of a person in whom was vested immediately before his death a right to damages in respect of personal injuries.

[136] Although he had prepared a contrary submission, counsel for the pursuer conceded that section 1(4) of the 1976 Act was not replaced by the provisions of the 1993 Act until the latter came into force on 18 April 1993. In these circumstances he moved me to make a loss of society award in respect of Mrs Durie in the nominal sum of £500, to cover the period of only two days by which she survived Mr Durie. This was not opposed by counsel for the defenders, and I would have made this award, with interest at the same rates as previously. This would have transmitted to the pursuer as Mrs Durie's executrix.

[137] There is a claim under section 9 of the Administration of Justice Act 1982, which counsel submitted was for helping with the care of Mrs Durie during her fatal illness and which would be payable to the pursuer as Mrs Durie's executrix, but despite counsel's suggestion of a nominal figure of £1,000, there was insufficient evidence upon which I would have felt able to make any such award.

[138] This leaves the pursuer's own claim for loss of society. Having regard to the concession counsel for the pursuer had made, he moved me to make an award under this head of £3,000. This figure was not contested by counsel for the defenders, and I would have made this award. As suggested by counsel for the pursuer, I would have attributed 75% of this figure to the past, and would have awarded interest on that proportion at the rate of 7.5% from the date of Mr Durie's death to 31 March 1993 and at 4% from the latter date to the present.

[139] Having regard to the conclusion which I have reached on the merits however I shall, of consent, repel the third plea-in-law for the second defenders, and quoad ultra I shall sustain the third and fourth pleas-in-law for the first defenders and the fourth and fifth pleas-in-law for the second defenders, and assoilzie both defenders.

	[Home] [Databases] [World Law] [Multidatabase Search] [Help] [Feedback]
	Scottish Court of Session Decisions
You are here: BAILII >> Databases >> Scottish Court of Session Decisions >> Durie Or Cook v Wyvern Structures Ltd [2000] ScotCS 233 (22 August 2000) URL: http://www.bailii.org/scot/cases/ScotCS/2000/233.html Cite as: [2000] ScotCS 233

Scottish Court of Session Decisions