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Cite as: [2007] ScotCS CSOH_166, [2007] CSOH 166

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OUTER HOUSE, COURT OF SESSION

[2007] CSOH 166

PD1341/05

OPINION OF LORD DRUMMOND YOUNG

in the cause

THOMAS TIMMS

Pursuer;

against

(FIRST) BARCLAY CURLE LIMITED; (SECOND) CORUS UK LIMITED AND (3) REFRACTORY SERVICES LIMITED

Defenders:

Pursuer: Marshall, Solicitor; Thompsons

Defenders: Smith, QC, Balfour; Simpson & Marwick WS

5 October 2007

[1] The pursuer was born on 6 April 1940. He is a retired welder. During his career he worked for, among others, the three defenders or their predecessors. He now suffers from a serious condition of the lung, in the form of interstitial lung disease. Interstitial lung disease (a disease of the parenchyma, or spongy part of the lung, responsible for the exchange of oxygen and carbon dioxide) can take a number of forms. The pursuer contends that he suffers from asbestosis as a result of exposure to asbestos during his employment with the defenders. He also claims that he suffers from pleural plaques. The defenders, by contrast, contend that the pursuer suffers from cryptogenic fibrolising alveolitis (CFA), which is also known as ideopathic pulmonary disease (IPD) or usual interstitial pneumonia (UIP). Such a condition would not be related to asbestos exposure; consequently the defenders submit that they are not responsible for the pursuer's condition. The critical issue is accordingly whether the pursuer suffers from asbestosis or CFA. I should add that, in the event that it is found that the pursuer has contracted asbestosis and was exposed to asbestos during the course of his employment with any of the defenders, each defender admits that such exposure was caused through its fault and negligence.

History of employment; exposure to asbestos

[2 ] The risk of contracting asbestosis is directly related to the length and severity of exposure to asbestos fibres. Consequently it is important to consider the length of exposure to asbestos suffered by the pursuer in the course of his employment and the degree of exposure to which he was subjected. Evidence on this matter was given by the pursuer himself. Two other witnesses gave evidence on this part of the case. One of these was the pursuer's brother, Mr Robert Timms, who had worked with the pursuer at the premises of the second defenders' predecessors. The other was Mr John Paterson, who had worked for the third defenders at Braehead Power Station at the same time as the pursuer. I found all of these to be credible witnesses who were clearly trying to give an accurate account of conditions at the various premises. I accept their evidence, subject to one important qualification. No evidence was led from an occupational hygienist or any other person who could compare asbestos levels at the defenders' premises with those found in other forms of employment. As a result I found it necessary to take a fairly broad view of the evidence, and to reach conclusions on levels of exposure to asbestos by reference largely to the medical evidence.

[3 ] The pursuer began his apprenticeship as a welder in late 1955 with the Finnieston Engineering Co Ltd. He remained with them until 1961 or 1962, when he took up employment with the first defenders. He worked there for about six months. It was at this time that his first significant exposure to asbestos occurred. Most of this time was spent in the first defenders' workshops, but on occasion he required to work in the engine rooms of ships under construction. There he worked alongside laggers, who mixed asbestos and used it to lag pipes. He described the asbestos as "flying" around the engine rooms. It was accepted that working alongside laggers in a relatively confined space would result in heavy exposure to asbestos. In cross-examination, however, the pursuer stated that he only spent about ten days in total working in the engine rooms. Thus the duration of his exposure was limited.

[4 ] In about 1964 or 1965, after a further spell with the Finnieston Engineering Co Ltd, the pursuer took up employment with Stewarts and Lloyds Limited, who were subsequently taken over by the British Steel Corporation. The assets and liabilities of the British Steel Corporation were ultimately taken over by the second defenders. It is agreed that the pursuer was employed by the second defender's predecessors for periods totalling 165 months between the tax years 1964/1965 1979/1980. He was employed as a welder at premises in Tollcross, Glasgow. His work consisted of welding heavy pipework, including steam chests. This was clearly demanding work; it was both highly skilled and physically arduous. Because of the standards to which the welding had to be performed the steelwork that was to be welded had to be heated to very high temperatures; 400 degrees was common, and on occasion temperatures of 600 degrees were necessary. Asbestos blankets were used to keep the heat in the steelwork and to keep it away from the welder. These had to be placed by the welder. As they were used, they dried out and gave off asbestos dust. After use for some time they would break up, and they were replaced every day or two. Asbestos was also given off when a caulking gun was used near the asbestos blankets. The pursuer gave evidence of asbestos appearing at his feet and on his clothes. Sometimes, because of the length of the pipes, the welding had to be performed down pits that were 5, 10 or 15 feet deep. On occasion the pursuer spent three days welding a flange down such a pit. He described the asbestos in these conditions as "murder". After about 12 years working as a welder the pursuer became an inspector. At this point he was still exposed to some asbestos when he checked the welders, but it was clear that the level of exposure was very much less. In cross-examination the pursuer stated that, of his time as a welder with the second defenders' predecessors, approximately half, six years, had been spent on very high temperature work and another four years or so using asbestos blankets.

[5 ] It is clear that the pursuer was exposed to substantial amounts of asbestos, but this appeared generally to be when the blanket was old; in examination in chief the pursuer suggested that the blankets started to give off asbestos after four hours. Mr Robert Timms stated that dust was given off when he started using a blanket, but I think that the pursuer's account is likely to be more reliable. In addition, the pursuer stated that when he was working at especially high temperatures he would work half an hour on and half an hour off. That suggests that he was not exposed to asbestos to any substantial degree during the time when he was resting. At this point I am conscious of the lack of expert evidence, but on the basis of the pursuer's evidence and the evidence of Dr Crompton, one of the specialists in respiratory medicine who gave evidence, I do not think that his period of employment with Stewarts and Lloyds and British Steel can be described as a classic case of asbestos exposure. It is certainly not as intense as the degree of exposure experienced by laggers working in ships under construction. The pursuer's description of the latter situation was that the laggers were "flinging" asbestos about, and that is clearly well beyond what occurred with the asbestos blankets.

[6 ] The pursuer's third period of exposure to asbestos occurred when he was employed by the third defenders. It is agreed that he was employed by them for not less than periods totalling 36 months between the tax years 1986/1987 and 1989/1990. He was initially employed as a foreman process operator, responsible for the removal of materials from a disused power station at Braehead in Renfrewshire. When he started work there a hopper fall of asbestos was being demolished. Most of that material was picked up and packaged, ready for removal from the site. He was also responsible for supervising the stripping of cables, a task which sometimes required the removal of asbestos lagging. It seems clear, however, that during this period the pursuer's exposure to asbestos was not great. He described the atmosphere in the power station as "very dusty", but he stated that he could not say whether the material was dust or asbestos; it looked like ash. During his employment with the third defenders the pursuer worked at power stations other than Braehead, but his complaints of asbestos exposure were confined to that location, where he worked for two distinct periods.

[7 ] In summary, therefore, I conclude as follows. The pursuer was exposed to a high level of asbestos for a very short period, approximately ten days in total, when he worked for the first defenders. When he worked for the second defenders' predecessors, he was exposed to substantial amounts of asbestos dust, but not continuously. This was not a classic case of asbestos exposure. When the worked for the third defenders, his exposure to asbestos dust was fairly limited.

Development of medical condition.

[8 ] The pursuer gave evidence that, after leaving employment with the third defenders, he had worked principally for the City of Glasgow Council as a supervisor until 2003. He retired on medical grounds on 8 February 2003. At this point he was suffering from breathlessness. He had previously felt that he was getting slow at his work, but he gave up smoking and felt better after that. He found difficulty in climbing stairs, and was frequently tired, exhausted and fighting for air. It was clear that the pursuer was forced to give up work because of his medical condition; that was not in dispute. The pursuer had clearly been very upset by his inability to work, and had considerable difficulty in accepting that he was unable to continue working.

[9 ] Eventually the pursuer went to his doctor, who had noticed crackling in his back associated with his lungs. The pursuer stated that his problems had started three or four years before he first went to the doctor about the problem; that had occurred on 23 May 2002. In his medical records, however, it was indicated that he had suffered from breathlessness for six months before that visit to his doctor. The difference can, I suspect, be explained by the difference in the degree of breathlessness that is referred to, and I do not think that the difference is material. The pursuer's general practitioner had referred him to Professor Peacock at Gartnavel Hospital, where he had been x-rayed and diagnosed with pleural plaques. At first asbestos had not been mentioned, but eventually the pursuer had been diagnosed as suffering from asbestosis. The accuracy of that diagnosis is, of course, the critical matter that is in dispute; the defenders contend that the proper diagnosis is CFA, not asbestosis.

[10 ] The pursuer was examined in due course by Dr Allan Henderson, a consultant in respiratory medicine at Lorn & Islands District General Hospital, Oban, and Dr Michael Sproule, a consultant radiologist at the Western Infirmary and Gartnavel General Hospital, Glasgow. Both of these gave evidence as experts on the pursuer's behalf, in Dr Henderson's case on commission. The pursuer was also examined by Dr Graham Crompton, who was until 1999 a consultant in respiratory medicine at the Western General Hospital, Edinburgh, and Dr Colin Turnbull, a consultant radiologist in the same hospital; they both gave evidence on behalf of the defenders. All four experts agreed about certain of the general features of asbestosis and CFA, but they disagreed as to the pursuer's diagnosis. In addition, it is fair to say that some disagreement existed between Dr Henderson and Dr Crompton as to the details of the development of the two diseases. I will begin by describing the general features of asbestosis and CFA and the means of distinguishing between them. Thereafter I will consider the evidence given by the pursuer's and defenders' experts respectively as to the proper diagnosis in this case.

Features of asbestosis and CFA

[11 ] Asbestosis is condition involving fibrosis scarring of the parenchyma, the spongy part of the lung in which oxygen and carbon dioxide are exchanged. Asbestos which has passed into the parenchyma sets up inflammation which is followed by fibrosis scarring; that leads to distortion of the lung and reduction of its functional ability. CFA is similar to asbestosis in that it causes inflammation and then scarring of the parenchyma, but in this case the cause is not clearly identifiable. CFA is markedly commoner than asbestosis. Dr Henderson stated (page 72) that he saw a lot more patients with CFA. Dr Sproule agreed. Dr Crompton stated that CFA was twice as common as asbestosis in Scotland as a whole.

[12 ] Distinguishing between the two conditions is not always straightforward, but the expert witnesses agreed that certain established methods are used. First, because exposure to asbestos is required to give rise to asbestosis the patient's occupational history is relevant. Moreover, the likelihood of contracting asbestosis, the severity of the disease and the speed of progression of the disease all depend upon the amount of exposure to which the patient has been subjected (Dr Crompton, day 3, 2.55). Pleural plaques, by contrast, develop after a lower degree of exposure, and the vast majority of people with pleural plaques do not develop asbestosis. Dr Henderson seemed to agree generally with the proposition that the likelihood of asbestosis, and its severity and speed, are dose-related; that proposition is found in the standard textbooks and is vouched by the classic cases described in those textbooks. Nevertheless, a difference of opinion appeared to some extent between Dr Henderson and Dr Crompton. In his report on the pursuer (No 6/9 of process) Dr Henderson stated that he had become aware since 2003 of a number of cases of asbestosis where exposure been somewhat less than that seen in classic textbook cases. It was partly as a result of these cases that he changed his mind about the pursuer's condition. Dr Crompton, by contrast, adhered to a view similar to the standard textbook statements. I deal with this matter below at paragraphs [17]-[20].

[13 ] Secondly, differences can be seen in x-rays or CT scans. What is known as "ground glass" opacification is frequently observed. This is commoner in cases of CFA, although it can occur with asbestosis. All of the expert witnesses agreed that it was commoner with CFA, but was not exclusively found there. Dr Sproule pointed out that it is not a reliable discriminator (day 2, 2.37); Dr Turnbull stated that "ground glass" tended towards a diagnosis of CFA, but was not a predominant feature (day 3, 3.52). Both Dr Henderson and Dr Crompton were of a broadly similar opinion. With asbestosis a common feature is the presence of parenchymal bands, which are thick strands of fibrosis tissue that go into the lung from the pleural surface. Dr Sproule referred to this, without giving the feature much weight; Dr Turnbull (day 3, 11.26) thought that such bands were difficult to distinguish and were not necessarily a marker. A further marker, agreed on by all the experts, is the occurrence of pulmonary fibrosis in the upper areas of the lung; if that is observed, it tends towards a diagnosis of CFA; the feature is unusual with asbestosis. That view is supported by Parkes, Occupational Lung Disorders, 3rd ed, 1994, at page 512 (No 26/6 of process). Dr Sproule (day 2, 2.45) agreed that it indicated a tendency towards CFA, but he did not think that it was a reliable marker. Dr Henderson agreed (page 89). Dr Turnbull likewise agreed that this feature tended towards CFA. Dr Crompton (day 4, 2.46, 3.07) stated that development in the upper zones was highly significant for clinicians. He referred to Parkes; he thought that that work was somewhat dogmatic, but in the pursuer's case there was a very clear progression into the upper zones. Finally, Dr Sproule regarded the existence of pleural plaques as an important indicator of asbestosis rather than CFA; his evidence is discussed at paragraph [22] below. Dr Turnbull did not agree that there were any pleural plaques (day 3, 12.02), and Dr Henderson accepted that the pursuer did not have a classic pleural plaque (pp 82-84). I deal with this aspect of the evidence at paragraphs [38]-[40] below. Both asbestosis and CFA may result in their later stages in an appearance of honeycombing; this is relevant to the speed of progression of the disease.

[14 ] Thirdly, asbestosis progresses more slowly than CFA. The rate of progress can be observed in three ways. In the first place, the general observation of the patient's ability to function, and his own assessment of that, is relevant. In the second place, the rate of progress can be observed in x-rays and CT scans. There the general features described in the last paragraph can be seen to develop, and in the case of CFA progression can be seen into the upper part of the lung; that is less usual with asbestosis. In the third place, the rate of progress can be measured using various lung function tests. Three forms of tests are used. The first involves the patient's blowing into a device known as a spirometer, which measures the rate at which air can be expelled and the extent to which the lungs are emptied by the expulsion of air. The second involves the measurement of the capacity of the patient's lungs using what is known as the helium diffusion technique; the patient breathes in a small amount of helium and the level of dilution is measured, enabling the doctor to calculate the volume of the lungs. The third is known as plethysmography; this involves the patient's sitting in a rigid box and using a mouthpiece containing measuring devices, and enables the volume of air in the lungs to be calculated.

Diagnosis

[15 ] Dr Henderson examined the pursuer in 2003 and again in March 2006. Initially he thought that CFA was the more likely diagnosis. In his report dated 12 May 2003 he noted the existence of pleural plaques, which inevitably made one think of asbestosis, but he thought that the evidence did not clearly point in that direction. The CT evidence suggested that the appearance was not characteristic of asbestosis, and the pursuer's exposure to asbestos, while being sufficient to cause pleural plaques, was not of the sort of magnitude that was characteristically associated with asbestosis. Dr Henderson changed his mind at the time of the second examination, however, and came down in favour of asbestosis. His reasons for doing so were twofold. First, as noted in paragraph [11] above, Dr Henderson had become aware of cases where asbestosis had developed despite a lesser degree of occupational exposure than had been observed previously. Secondly, Dr Henderson reviewed the CT scans and concluded that they altered his opinion, with the result that on the balance of probabilities he thought that the diagnosis was asbestosis rather than CFA.

[16 ] Dr Crompton examined the pursuer on 24 October 2005 and carried out a review of the available reports of radiological examination and lung function tests. He came down in favour of a diagnosis of CFA. In his principal report (No 26/17 of process) he expressed the view that there could be no doubt about a diagnosis of diffuse interstitial pulmonary fibrosis, nor about the occupational history of asbestos exposure. In favour of asbestosis were the history of asbestos exposure and the CT scan evidence of subpleural interstitial pulmonary fibrosis in the lower lobes. In favour of CFA were the rapid progression of the interstitial pulmonary fibrosis and the presence of ground glass appearances on the CT scan of 2002. On a balance of probabilities Dr Crompton favoured CFA; he thought that the rapid progression of the disease process together with the absence of significant pleural changes on chest x-ray and CT made the diagnosis of asbestosis unlikely, despite the pursuer's history of occupational exposure to asbestos. I should add that, in his examination in chief, a summary of the pursuer's account of his exposure to asbestos was put to Dr Crompton, and he stated that the exposure described was less than he had assumed from the history given to him by the pursuer at the time of the examination. I deal with this below at paragraph [18].

Levels of exposure

[17 ] Dr Henderson noted the pursuer's employment history in his first report, dated 12 May 2003 (No 6/9 of process). In relation to the pursuer's employment with the first defenders, the report states:

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

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

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

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

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