Hynes v. Lobnitz & Ors [2008] ScotCS CSOH

OUTER HOUSE, COURT OF SESSION

[2008] CSOH 67

OPINION OF LORD CARLOWAY

in the cause

WILLIAM HYNES

Pursuer;

against

SIMON LOBNITZ and OTHERS

Defenders:

________________

Pursuer: TG Marshall, solicitor advocate of Thompsons

Defenders: (1^stand 5^th defenders): Smith QC; Simpson and Marwick WS

Defenders: (2^nd to 4^th, 6^th & 7th defenders): Summers; Biggart Baillie LLP

1 May 2008

Background

[1] The pursuer was born on 31 October 1941. He is a fitter to trade. He commenced work with the first defenders in November 1956; in part working on ships being constructed at their yard in Renfrew. He fitted pipes, engines and boilers. His work on the pipes involved him cutting lagging. He was also present when others applied asbestos sheet or paste lagging to pipes and boilers. The paste was made up on site by mixing asbestos powder with water. The yard appears to have changed ownership, but the pursuer continued to work in the industry until about 1959. He then left shipbuilding and was not exposed to asbestos again until his return to the Clyde in about 1965. Thereafter he worked with several other shipbuilding companies, notably the other defenders, doing the same type of work as he had with the first defenders, until about 1974.

[2] It is admitted (no 34 of process) by each defender that, during his employment with them, the pursuer experienced exposure to asbestos sufficient to cause asbestos disease. It is admitted by the first and fifth defenders (31 and 33) that they employed the pursuer for 44 and 27 months respectively and that his exposure to asbestos was as a result of their fault. It is admitted by the second, third, fourth, sixth and seventh defenders (32) that the pursuer's exposure during their employment of him was caused by their fault. These defenders also admit the periods of exposure as 64 months with the second defenders, 4 months with the third defenders, 3 months with the fourth defenders, 13.5 months with the sixth defenders and 12.5 months with the seventh defenders. The defenders accepted that, for pragmatic reasons, a joint and several decree could be made in the circumstances of this case; without prejudice to their position in other litigations. The defenders were all agreed that the appropriate apportionment, in the event of liability being established, would be: first defenders - 26.19%; second defenders - 38.10%; third defenders - 2.38%; fourth defenders - 1.79%; fifth defenders - 16.07%; sixth defenders - 8.03%; and seventh defenders - 7.44%. However, it was also agreed by the defenders that no formal decree for apportionment was required.

Pleadings and Issues

[3] The pursuer avers (statement of fact 5) that:

"In consequence of the exposure to asbestos the pursuer has contracted bilateral pleural plaques, pleural thickening and asbestosis...In about 2004...[he] was found to have pleural plaques with calcification, pleural thickening and asbestosis. The pursuer is breathless and lacking in energy. He finds difficulty in walking and climbing stairs. He is also anxious about the potential implications of asbestos related disease and for his future health. He is at an increased risk of serious deterioration of his condition by contraction of asbestos related lung cancer, diffuse bilateral pleural thickening and/or mesothelioma. The pursuer is a smoker and in conjunction with his asbestos exposure he is at high risk of lung cancer. It is likely that the asbestosis will progress such that he will become 30% disabled in his lifetime. He is also likely to lose 4 years of life expectancy (sic) by reason of his asbestos related conditions. The pursuer has and will suffer considerable pain..."

The defenders do not admit the nature, extent and consequences of any loss, injury or damage sustained by the pursuer. The first and fifth defenders make positive averments about the pursuer being a smoker and continue:

"The pursuer suffers from emphysema, connective tissue disease, Raynaud's phenomenon, transitional cell carcinoma of the bladder, hypertension and had an aortic heart murmur. He has suffered from pericarditis and pleurisy".

The remaining defenders aver that pleural plaques are harmless, presumably thereby accepting their existence, but otherwise make similar averments to those of the other defenders concerning the pursuer's various conditions.

[4] The primary issues are first whether the pursuer has pleural thickening as a result of exposure to asbestos and asbestosis itself, in the form of pulmonary fibrosis. Secondly, it is whether the pursuer's physical problems such as breathlessness, which were not disputed at the proof, are caused by asbestos related disease as distinct from other conditions, notably connective tissue disease (CTD) and emphysema. It was not suggested that the pursuer's bladder cancer, heart problems or hypertension had any relevance to the problems complained of. A CTD is a chronic inflammatory autoimmune disorder which can affect all "connective tissue" (joints, skin, muscle, blood etc.). Rheumatoid arthritis (inflammation of the joints) is an obvious example of this, although it mainly affects the joints. CTDs are not "organ specific". They can affect different organs.

Medical Notes - 1985-93

[5] There was considerable focus on the content of selected passages in the voluminous notes made by the pursuer's general medical practitioners (7/2) and various other doctors, whom he attended at the Peel Hospital, Galashiels, the Kelso Community Hospital and the Borders General Hospital, Melrose. Notwithstanding that focus, not one of the persons making these notes gave evidence to confirm or explain their findings. Furthermore, although there was much discussion in the evidence about the pursuer having a CTD, no rheumatologist (a specialist in musculo-skeletal disorders) was called to explain the nature of this type of disease, its causes, prevalence or general course and treatment. It is a disease within the expertise of a rheumatologist rather than that of a respiratory physician. Yet the testifying medical experts were all either respiratory physicians or radiologists.

[6] The various medical witnesses were presented with extracts from the GP records. These in turn included records from the hospitals attended. Because much of the evidence of the experts was based upon their interpretation of entries in the records, it is necessary to set out at some length just what entries were referred to, although the weight to be given to the content of these entries may be another issue (infra). The earliest record referred to (7/2 p 215) is dated 1 February 1985, some eleven years after the pursuer's exposure to asbestos had ceased. It does not have any material bearing on the issues in the case. It records the pursuer as having "stiffness & tingling both arms", especially on the right side. He had limitations of his neck movements. A probable diagnosis of cervical spondylosis was made. The first potentially relevant entry is dated 9 August 1985, when the pursuer was recorded as complaining of "arthritic pains in both wrists" and in his left foot "suggestive of polyarthritis". On 1 November 1985, his GP referred to the pursuer having had a red, hot and swollen left ankle, which appeared to have resolved in advance of his visit to the surgery.

[7] On 15 July 1986, the pursuer was complaining to his GP of "swollen joints again" (p 216). He was referred to Peel Hospital, where he was seen at the clinic of Dr AW Logie, consultant physician, in the following October (p 180). This clinic appears to have been a general medical one, not specialising in any particular field. The pursuer's joint pain was noted as was a "minor degree of finger clubbing" (swelling of the soft tissue around the ends of the fingers). A positive diagnosis does not appear to have been forthcoming. However, of some significance, on 9 December 1986 there is a record of a tentative diagnosis in the GP records (p 216) of "SLE". Although there is no note of what led to this, and there was little evidence about the making of it, it seems to have emerged from Dr Logie's clinic (p 178). Indeed the pursuer said that it had been Dr Logie who had first mentioned SLE. "SLE" is Systemic Lupus Erythematosus, a distinct recognised CTD. The diagnosis is repeated in the GP records of 19 January 1987 (p 216), when the pursuer was noted to have "occasional joint pain" in his ankles and elbows. It is mentioned again in an entry for 28 April 1987. Shortly after that, the pursuer was referred to the Royal Infirmary, Edinburgh, for investigation of urological problems. A past diagnosis of "probable SLE" is recorded in his discharge summary (p 176).

[8] In December 1987, the pursuer was back in the Peel Hospital, this time with a history of "Four episodes of gnawing chest pain radiating to the arm and throat associated with nausea and sweating" (p 164). This was thought to have been an episode of pericarditis (inflammation of the membranes around the heart). On examination of his chest, he was found to have "fine bibasal crackles", although the lung fields were reported "clear" on radiology. The diagnosis was SLE. "Crackles", or crepitations or "creps", are sounds heard when examining the chest by stethoscope. They are "bi-basal" when detected in the bottom areas of both lungs.

[9] The pursuer attended his GP on 10 March 1988 complaining of left sided chest pain below the shoulder blade (p 218). He was re-admitted the same day to Peel Hospital (p 162) with a "recurrent history of intermittent night sweats, pyrexia (fevers), general malaise, myalgia (general muscle pain) and joint pains". The chest examination recorded "occasional creps right base, otherwise clear". This time, the diagnosis at Dr Logie's clinic was a more general "Possible connective tissue disorder". The pursuer was discharged after a week but attended his GP again on 21 March with general musculo-skeletal pain recurring along with pyrexia. On 30 March he saw his GP complaining of "severe pleuritic L[eft] sided chest pain". The pleura are the linings of the lungs and chest wall, the inner lining (of the lung itself) being the visceral and the outer lining (of the pleural cavity) being the parietal. The term pleurisy refers to inflammation of these linings and this can cause pleuritic pain. The GP detected effusion (escape of fluid) into the left base of the lung. The pursuer was, once more, returned to the Hospital that day (p 148). He was examined by Dr Logie's senior house officer, Calum Macrae. Dr Macrae recorded (p 159) that there was "no clubbing...". On examining the chest, he observed "some course creps" above the left base. He noted "an ANF (anti-nuclear factor, present in the blood) positive" but "negative double stranded DNA titres (amounts)". An x-ray revealed a left basal effusion. Dr Macrae concluded that the pursuer was "indeed suffering from mixed connective tissue disease". "Mixed" CTD is not the same as SLE. He arranged for the pursuer to have a pleural aspirate (drain) and started him on steroids in the form of 30 mgs daily of Prednisolone (reduced on discharge to 15 mgs).

[10] Back at his GP's surgery on 11 April 1988, the pursuer was noted as "Feeling very well on steroids". A radiology report of the same date recorded "There is a little pleural fluid at the left costophrenic recess". Another, dated a few days later, stated "Pleural shadowing of the left base, lung fields otherwise clear" (7/1 p 104). On 21 April, the GP wrote "? Mixed connective tissue disease", when the pursuer presented with "slight recurrence L[eft] pleuritic pain". Seven days later, after a temporary increase in the Prednisolone, the pursuer's pain was recorded as "all away" and the steroid dose was reduced again. On 16 May, the pursuer was back at Dr Logie's clinic being reviewed by Dr Macrae (7/2 p 158). He was recorded as feeling well with only one recurrence of left axillary (under arm) chest pain. He had had no further fevers, but continued to have mild sweats at night. Chest examination revealed "a few scattered crepitations in the left axilla". Radiology was noted as showing some improvement over the month, with the lung fields appearing clear and there being no evidence of pleural effusion (7/1 p 103).

[11] On 19 September 1988, the pursuer returned to Dr Logie's clinic (7/2 p 155) (by then at the new Borders General Hospital). Under a heading "Presumed SLE", it was recorded that the pursuer was keeping well with no recurrence of his chest pains. The Prednisolone dose was reduced from 10 to 7.5 mgs at that stage. However, when the pursuer reduced it further to 5 mgs in September, he noticed (p 155) a "recurrence of left sided pleuritic chest pain". He thought that he was sweating more than usual. He had Raynaud's phenomenon (colour changes when exposed to the cold) in his hands. The chest was noted by Dr Logie to be "entirely clear".

[12] At the end of the year, the pursuer was suffering pain in his left chest, with some on the right side too. The GP entry was "Pain on deep inspiration" (p 219). Back for a review at the Hospital in January 1989, Dr Logie wrote "Presumed SLE" and once more recorded the pursuer's chest as "clinically clear". The pursuer was still on 5 mgs of Prednisolone at this time. Lung function tests carried out in November 1989 produced:

FEV₁	VC	FEV/VC	FRC	RV	VC	TLC	RV/TLC	TCO	KCO
3.0	3.75	80	2.86	1.66		5.64	29	6.80	1.49

[13] In May 1990, the pursuer was noted as having "some intermittent left lateral chest ache which is neither ischaemic nor pleuritic in character" (p 22). In November 1990, Dr Logie's registrar recorded (p 20) the pursuer's chest as "clear, no rub, no creps". A year later, a further "chest clear" was recorded (p 17). In October 1992, a different registrar wrote (p 13) "Chest is clear, although there were a few scattered coarse crepitations". Lung function tests carried out in November 1993 were:

FEV₁	VC	FEV/VC	FRC	RV	VC	TLC	RV/TLC	TCO	KCO
3.30	4.19	79	3.15	1.34		5.61	24	7.46	1.61

Some time passed before the next series of significant entries.

Medical Notes - 1997-2007

[14] Dr Peter Leslie, consultant general physician at the Borders General Hospital, reviewed the pursuer in May 1997, noting that the prescribed steroids had greatly improved his symptoms of intermittent fever and pleuritic chest pain. In a letter requesting a review by Dr Lambert's rheumatology clinic, which was based at the Western General Infirmary, Edinburgh (p 54), he wrote:

"Recently he describes a feeling as if he is "walking on stones" and there is certainly evidence of peripheral sock type neuropathy (nerve disturbance). His joint pains have mainly involved his ankles but they are of no problem at present. He has an intermittent purpuric type rash involving his legs and possibly a photosensitive rash on his face. When he has symptoms of fever he increases his steroid from the maintenance dose of 2.5 mgs with quick resolution of his symptoms..."

Dr Leslie's diagnoses were: "1 Probable SLE; 2 Raynaud's Phenomenon ? Overlap syndrome; 3 Peripheral neuropathy; 4 Purpuric rash...". Something appears to have gone amiss with the review at the Edinburgh clinic. The pursuer's GP wrote to Dr Lambert about this in November 1997 (p 50). The pursuer seems to have been reluctant to travel to Edinburgh. He was re-referred to Dr Leslie locally (p 49) and was seen by him on 4 March 1998. Dr Leslie wrote back to the GP (pp 45-6) stating:

"I still think the question arises whether [the pursuer] should commence Hydroxychloroquine for management of possible lupus (SLE) and I think this requires a definitive rheumatological opinion".

On 26 March 1998, the pursuer's GP wrote back to Dr Leslie in connection with the SLE diagnosis (p 84). Dr Leslie in turn asked Dr Ruth Richmond, a specialist registrar, to review his notes.

[15] Dr Richmond is subsequently described as a rheumatology registrar and later as a consultant rheumatologist. Her involvement appears to have been the first by a specialist in rheumatology. On 2 April 2008 she wrote (p 82):

"I note original history with polyarthralgia, and later developing pericarditis and pleuritic chest pain. I note he has always had a raised ANA and rheumatoid factor, though double stranded DNA titres have been very low titre (sic) and as far as I can see extractable nuclear antigens have been negative when checked...

It certainly sounds as though he has a connective tissue disease...."

Dr Richmond referred him to the rheumatology clinic, where she would see him again. Her formal diagnoses in the letter to the pursuer's GP (quoted above) did not include CTD.

[16] On 23 June 1998, the pursuer saw Dr Richmond (as rheumatology registrar) at Dr Lambert's local clinic at Kelso Community Hospital. She made certain observations on his history before recording (p 79):

"Currently his Raynaud's is very troublesome...He has an itchy rash over the lower half of his legs which has been present for years, but does not tend to fluctuate, and does seem to be photosensitivity...He has a photosensitive facial rash.

...He has never had joint symptoms since his original onset. He denies pleuritic chest pain, breathlessness or coughs...He does have intermittent fever and sweats which has also been a longstanding feature of his illness, and responds to a slight increase in dose of steroids...

...He has a mild malar rash...He is clubbed and I note this has been documented for a long time. He also has scattered nail fold infarcts and obvious Raynaud's.

...Chest is clear in particular with no evidence fine respiratory creps...

I note features predominantly consistent with SLE. He has been ENA (?ANA) positive over a long period of time, although he doesn't have an elevated double stranded DNA..."

Her diagnoses this time included: "Undifferentiated connective tissue disease; ANA positive; Rheumatoid factor positive; Photosensitivity; Raynaud's phenomenon...". "Undifferentiated" CTD (UCTD) is, by definition, not the same as SLE. Lung function tests carried out in June 1998 produced:

FEV₁	VC	FEV/VC	FRC	RV	VC	TLC	RV/TLC	TCO	KCO
3.05	4.00	76	3.64	1.68	4.38	6.06	28	6.90	1.34

[17] On 28 August 2000, the pursuer was back at his GP complaining of having had right sided chest pain for three weeks (p 228). Radiological examination (p 275) recorded that:

"the lung markings are diffusely increased possibly due to a degree of COPD (chronic obstructive pulmonary disease). No focal lung abnormality. Comparison was made with previous chest radiograph from 1998. There has been no significant change since that time".

On 8 September 2000, Dr Richmond reviewed the pursuer (p 59) and found him to have "a variety of mild symptoms", notably "some arthralga around the right ankle, and right knee, but examination today was unremarkable".

[18] On 19 March 2001 the pursuer's GP recorded him as tender over the right side of the ribs. On 8 January 2002, the pursuer attended his GP complaining yet again of pleuritic pain in the right base and the GP detected crepitations in that area. About a week later (p 230) he was tender over the right lower rib and rhonchi ("wheezes like bagpipes") were detected. A month later, the chest pain was still present but improving. A radiology report of January 2002 (p 274) noted "Lung fields clear".

[19] At the rheumatology clinic in June 2002, the pursuer's CTD was noted as being "in remission". He had no skin rash, had no photosensitivity when on holiday in Ibiza, his Raynaud's was much better and he had no arthritic symptoms, apart from one episode involving a finger joint. Haematology results in 2000, 2002 and 2003 (pp 61, 98, 99) showed his "lymphs" (lymphocytes) count at 1.1 to 1.4 (normal being 1.0 to 4.0), although there was one figure of 0.9 in 2001 (p 93).

[20] On 9 July 2004, Dr Richmond sought (p 133) the views of the general physicians at the Borders General on the correct diagnosis of and treatment for the pursuer. She referred to the pursuer presenting with polyarthralgia in 1986 and continuing joint and steroid responsive chest pain in 1998, amongst other symptoms. She stated:

"I felt that mostly his features were entirely consistent with SLE, he is positive for ANA, though his double stranded DNA has never been elevated".

Dr Richmond referred to bi-basal crepitations being found in June 2004, suggestive of possible early fibrosis. Of substantial significance, she referred to the results of the CT (computerised tomography) scan taken the previous month which showed calcified pleural plaques "which the radiologist felt were more consistent with asbestos exposure". She also mentioned the various lung function tests, which she regarded as stable since 1989. Lung function test results in August 2004 were:

FEV₁	VC	FEV/VC	FRC	RV	VC	TLC	RV/TLC	TCO	KCO
2.70	3.60	75	3.67	1.99	3.69	5.68	35	7.48	1.59

[21] In August 2004, the pursuer was seen by a respiratory physician (Dr JF Faccenda) at the Borders General. He was noted "clubbed" but "Chest auscultation was entirely clear". At this time, the results of the CT scan and the existence of benefits for asbestos related disease were discussed with the pursuer. In October 2004 Dr Faccenda's specialist registrar added "pleural plaques" to the diagnoses (which still included UCTD). The pursuer was noted as having "no respiratory symptoms". It was observed that his claim for asbestos related disease was underway.

[22] In September 2007, the pursuer took an overdose of his co-drydamol pain killers (5/10 pp 2, 39). At that time he was noted as having recently given up smoking 30 cigarettes a day. As late as 20 November 2007, the pursuer's chest was noted as "clear" (6/10 p 42).

Radiology

[23] The radiologist who reached the conclusion concerning asbestos in 2004 did not give evidence. However, the CT scan, which was dated 28 June 2004, an x-ray dated slightly earlier on 15 June and another taken on 18 January 2002 were subjected to anxious scrutiny by the three eminent radiologists who gave evidence. All three were extremely well qualified and experienced in chest x-ray and CT scan interpretation. There was no reason to prefer one over the others by reason of their qualifications or experience. Ultimately, there was consensus on many aspects of the radiology. They all agreed that the pursuer had pleural plaques, with calcification, as a result of exposure to asbestos. They all agreed that the CT scan showed that he had pleural thickening.

[24] The radiologists did lock horns over whether this thickening was "diffuse". In that connection, all agreed that a formal radiological diagnosis of "diffuse" thickening requires a continuous area with dimensions: (i) at least 3 mm in thickness; (ii) at least 5 cms transversely (latitudinally, across the chest); and (iii) at least 8 cms longitudinally (vertically, up and down the chest). This test is stated in a standard text book called "Radiologic Diagnosis of Diseases of the Chest" (2001) by Nestor Muller et al., although it derives from an earlier medical paper in 1989. The more important dimension is the vertical one since the lungs expand more on that axis, as regulated by the diaphragm, than laterally, as determined by rib cage expansion. The figure of 8 cms is a random one, selected simply to distinguish persons likely and not likely to have a disability resulting from such thickening. Eight centimetres is about one quarter of the vertical length of the chest. People can have a disability even if they do not meet the formal criteria for this diagnosis.

[25] All the radiologists agreed that the vertical dimension of the thickening as seen on the CT scan was at least 6 cms. This could be measured physically by ruler on the four lowest slices of the eighteen CT images taken at 1.5 cm intervals during the scan. However, the images did not extend below the area of thickening; i.e. they did not capture the lowest point of the thickening. This presented a difficulty in determining whether the formal criteria for the diagnosis of "diffuse" thickening had been met.

[26] There was some discussion about whether the costophrenic angle had been "obliterated" when seen on a conventional (plain film) x-ray. This is another test for diffuse pleural thickening, deriving from the work of the International Labour Organisation in 2003. The costophrenic angle is at the bottom of the costophrenic sulcus; the lowest area of pleural cavity present on both sides of the body between the diaphragm and the chest wall. It is "obliterated" if the angle cannot be seen on the x-ray image. If it cannot be seen, that is because the thickening of the pleura renders the angle invisible on the image.

[27] At the proof, the pursuer's expert consultant radiologist was Michael Sproule (42), based at the Western Infirmary and Gartnavel General Hospital, Glasgow (CV, 6/14). He produced a somewhat repetitive but clear and succinct report (6/11). He confirmed that he "stuck to" this report, as his examiner put it. It is of some importance to rehearse just what he was "sticking to". In relation to the 2002 x-ray, he writes:

"There is loss of sharp definition of both costophrenic angles and pleural based shadowing extending up the lateral aspect of the right hemithorax. The appearance is...consistent with pleural thickening".

Comparing this with the later 2004 x-ray, he comments:

"...the left costophrenic angle is sharply defined. The appearance on the right side remains the same".

He found, therefore, that the x-rays showed some loss of clarity of the angle on the right side, but not "obliteration", indicating some pleural thickening in that area. Looking at the CT scan, he observes:

"In both hemithoraces there are focal areas of partially calcified pleural thickening which are characteristic of parietal pleural plaques due to previous asbestos exposure.

Posteriorly in the right lower zone there is smooth sheet like thickening which appears to extend into the costophrenic sulcus (the study does not quite cover the entire thorax). The pleural thickening is greater than 5 cm around the hemithorax, 3mm thick and is at least 6 cm in cranio-caudal (head to tail) dimensions. The CT appearance is therefore highly suggestive of diffuse pleural thickening due to a "fibro-thorax". A "fibro-thorax" usually results from a previous exudative effusion which may itself have a number of causes including infection (empyema), trauma (hemothorax), asbestos exposure (benign asbestos induced effusion) or in association with connective tissue disease. Given the presence of parietal pleural plaques due to previous asbestos exposure the appearance is suggestive of diffuse pleural thickening due to previous benign asbestos induced pleural effusions. However, I note that the patient also has a history of connective tissue disease. It is not possible on radiographic criteria to exclude this as a cause of the diffuse pleural thickening. In the absence of a history of infection or trauma, clearly empyema or hemothorax are less likely.

In the lower lung zones bilaterally there are fine dot like and short irregular linear subpleural opacities. These are not confined to the dependent lung or parenchyma adjacent to pleural plaques. The appearance is therefore consistent with mild pleural fibrosis. Given the presence of parietal pleural plaques due to previous asbestos exposure, the findings are suggestive of early asbestosis".

Dr Sproule then summarises (or rather repeats) his position thus:

"1. There are focal areas of partially calcified pleural thickening in both hemithoraces which are characteristic of parietal pleural plaques due to asbestos exposure.

2. Posteriorly, in the right hemothorax there is smooth, sheet like thickening which appears to extend in to the costophrenic sulcus. The CT appearance is suggestive of "fibro-thorax". As discussed above, the presence of parietal pleural plaques due to previous asbestos exposures raises the possibility of diffuse pleural thickening due to previous benign asbestos induced pleural effusions. However, it is not possible on radiographic grounds to exclude diffuse pleural thickening as a consequence of connective tissue disease associated pleural effusion.

3. There are fine sub pleural parenchymal opacities in the lower lung zones which are consistent with mild pulmonary fibrosis. Given the presence of parietal pleural plaques due to previous asbestos exposure, the appearance is suggestive of early asbestosis."

[28] Dr Sproule explained that, as the pursuer had a CTD and had been exposed to asbestos, it was not possible to say which had caused, what he regarded as, the diffuse pleural thickening or the mild pulmonary fibrosis, which he thought was at an early developmental stage. The fibrosis took a reticular or honeycomb like form. Dr Sproule accepted that, on any view, the pursuer was right down "at the margin" of the diagnosis of diffuse pleural thickening. The signs of fibrosis on CT were subtle, not gross or florid. If the thickening and fibrosis had been there since the late 1980s, they were less likely to have been caused by asbestos exposure because greater progression over that period might have been expected.

[29] The first and fifth defenders called Colin Turnbull (61) as their consultant radiologist. He is based at the Western General Infirmary, Edinburgh, and has a special interest in imaging of the lungs (CV 25/9). He "adhered" to his reports (25/2 and 3). In relation to the 2002 x-ray, Dr Turnbull considered it to be "underpenetrated" but thought that it might be showing pleural thickening in the lower third of the right lung. The 2004 x-ray was better and suggested such thickening. However, the costophrenic angles were well defined.

[30] Turning to the CT scan, Dr Turnbull was led through almost all eighteen images, starting with the soft tissue settings and moving onto the lung settings. He described the presence of bilateral pleural plaques with calcification. His main report states:

"...there is more diffuse pleural thickening in the right lower thorax posteriorly which is greater than 3mm thick and greater than 5 cm wide extending for a craniocaudal distance of over 8 cm, meeting radiological CT criteria for diffuse pleural thickening".

He was able to point to the areas of thickening, especially those shown on soft tissue images 12/18 to 16/18. He accepted that it was hard to say where the thickening ended on the images but he had "implied" that it had extended more than the required 8 cms vertically.

[31] On the lung settings, he was able to see reticulation in the lung itself in images 9 to 15/18; that is pulmonary fibrosis. He reports:

"There is bilateral, lower lobe, peripheral, wild ground glass opacification with intralobular interstitial thickening and mild peripheral honeycombing...".

Dr Turnbull concludes:

"The CT scan shows bilateral pleural plaques with associated calcification, parenchymal bands and right lower thoracic posterior diffuse pleural thickening, typical of previous asbestos exposure. There is mild centrilobular emphysema.

There is bilateral, lower lobe, basal, sub-pleural interstitial pulmonary fibrosis with associated minimal fine honeycombing, traction bronchiolectasis and ground glass opacification. These changes, in associated (sic) with the pleural plaques, diffuse pleural thickening, pleural calcification and parenchymal bands could be due to asbestosis.

[The pursuer] also has a diagnosis variously given in the clinical letters of "undifferentiated connective tissue disease" or systemic lupus erythematosus. The changes of insterstitial pulmonary fibrosis on CT scanning in these conditions are indistinguishable in their radiological appearance and extent from those of asbestosis.

It is therefore not possible, on radiological appearances alone, to determine whether the interstitial pulmonary fibrosis in this case is due to asbestosis or connective tissue disease. There are definite radiological signs of previous asbestos exposure and right posterior thoracic diffuse pleural thickening, as detailed above".

He agreed that the pursuer's pleural thickening was "down at the lower reaches", being mild in nature. It was not possible to say "with confidence" that it was interfering with his lung capacity.

[32] Dr Turnbull expressed the view that SLE was a syndrome with specific serological and clinical symptoms and signs. "Undifferentiated" and "mixed" CTD were, in his mind, used interchangeably in the GP records. With all the CTDs there was an association with pleural and pulmonary changes, as there was with asbestos exposure. The changes were indistinguishable radiologically. Dr Turnbull referred to a textbook: "High Resolution CT of the Lung" (third edition) by Webb, Muller and Naidich (7/8 see infra on admissibility), which states (p 219):

"SLE is commonly associated with pleural and pulmonary abnormalities. Pleuritis or pleural fibrosis is present in up to 85% of cases at autopsy, and pleural effusion is often visible on chest radiographs in patients who have SLE".

He also quoted from a paper (6/20): "Idiopathic Nonspecific Interstitial Pneumonia - Lung Manifestation of Undifferentiated Connective Tissue Disease" by Kinder et al published in Volume 176 of the American Journal of Respiratory and Critical Care Medicine (p 691), (2007). This states ("At a Glance Commentary") (p 691):

"Undifferentiated connective tissue disease is a recognised disease entity, but the pulmonary manifestations are not described. Their relationship is unknown".

The paper (Table 4) describes a number of patients with UCTD as having reticulation (fibrosis), as the pursuer has. However, the paper is largely a study of non smoking young women.

[33] In a later report (25/3), Dr Turnbull reviewed x-rays of the pursuer taken in 2006 and 2007 and noted that there was little change since 2002 and 2004. He concludes:

"The lack of any progression of the fibrosis...would tend to favour asbestosis or stable, treated connective tissue disease rather than idiopathic pulmonary fibrosis".

[34] The remaining defenders' consultant radiologist was Arthur Wightman (65), who had been in that post at the Royal Infirmary, Edinburgh, since 1975. He gave evidence at a Commission (7/9) on 18 and 19 February, in advance of the proof, which commenced on 26 February and continued for eight days. It was at this Commission that these defenders attempted to lodge the extract from the Webb, Muller and Naidich book (7/8 supra) and a document called "Diagnosis and Initial Management of Nonmalignant Diseases Related to Asbestos", an official statement of the American Thoracic Society (2003). Although he gave his evidence before the other two consultants, Dr Wightman's testimony was usefully taken as a commentary on the reports of the other two radiologists, as if he had given his evidence last (as would normally have been the case).

[35] Dr Wightman agreed with Dr Turnbull on the presence of pleural thickening, other than the use of the adjective "diffuse". Dr Wightman considered that it was unlikely that the length of the thickening was as much as 8 cms. He too had measured 6 cms, but considered that the next scan (had it existed), being 1.5 cms lower, would have been below the lung, indeed below the diaphragm. He could not say that the thickening did not extend as far as 8 cms, simply that he would not have expected it to do so. He agreed with Dr Turnbull on emphysema as a minor disability. He agreed generally with Dr Turnbull's conclusions but thought that the pleural thickening "might be caused by" rather than being "typical of" previous asbestos exposure. Essentially, like Dr Turnbull, as both asbestosis and CTD were well known causes of interstitial fibrosis, he thought that it was impossible to say which one was the cause. He regarded the "probabilities" as "absolutely equally balanced". Dr Wightman agreed that the more recent x-rays showed no significant change. It followed that he agreed with much of what Dr Sproule had reported, but he considered that CTD was equally likely to have caused the thickening rather than it simply being a cause which could not be excluded. He understood that all the commoner CTDs produced pleural effusions leading to pleural thickening and interstitial fibrosis. Whether the thickening was diffuse or not made no difference. So far as the costophrenic angle was concerned, Dr Wightman did not consider that the x-rays showed any blunting of the angle. Dr Wightman accepted that, were there to be a competition of diagnoses between asbestos exposure and an idiopathic condition, pleural plaques would point towards asbestos. But, he remarked, SLE was a known condition which the pursuer had.

Objection

[36] The only objection insisted upon at the end of the proof was that raised first by the pursuer during the Commission to take the evidence of Dr Wightman concerning the use of passages from the Webb, Muller and Naidich textbook ((supra) lodged provisionally as 7/8) to demonstrate that SLE was commonly associated with pleural and pulmonary abnormalities. The pursuer's complaint was that he had had insufficient time to consider this work and to research its references. The objection was to its late lodging and its incomplete nature. However, the Commission took place a week before the proof. The reference had been intimated on the Friday before the Commission, which had taken place on the following Monday. There had been and was, ultimately, plenty of time to consider and respond to the use of this reference, even if it required to be formally lodged (which is doubtful). The pursuer had subsequently lodged further references in the form of the Kinder paper (supra) and a textbook by Professor Rudd et al (infra). The objection is accordingly repelled.

Physicians

(a) Dr Reid

[37] Peter Reid (44), consultant physician, specialising in respiratory medicine, at the Western General Infirmary, Edinburgh, gave evidence for the pursuer (report 6/6). His testimony lasted almost seven hours, spread over three days of proof. As part of the medical background, he noted that the pursuer was being treated for CTD. His examination revealed finger clubbing, a condition which Dr Reid attributed "most probably" to pulmonary fibrosis, although its precise cause is not known. He also noted the Raynaud's phenomenon, a common manifestation of CTD, although it could occur on its own. Dr Reid appeared to accept the accuracy of the CTD diagnosis because it had been made by a specialist in that field, i.e. a rheumatologist. However, he viewed it as perhaps having shaky foundations. He accepted that Dr Richmond was an expert in the field. However, he pointed out that what she had written (supra) was only that the pursuer had "features predominantly consistent with SLE" and, much later, that "mostly his features were entirely consistent with SLE" before noting that he did not have, as would be expected with SLE, an elevated double stranded DNA. Furthermore, SLE had disappeared as a diagnosis and it had been replaced by UCTD.

[38] Dr Reid detected fine crackles at the bases of both the pursuer's lungs, a sign of possible pulmonary fibrosis. Spirometry produced figures of FEV₁ at 2.8 (predicted (average) 3.71), FVC (forced ventilatory capacity) 3.63 (4.76) and FEV₁/FVC at 77%. These demonstrated a restrictive ventilatory defect; that is a defect affecting the bellows capacity of the lungs caused by pulmonary fibrosis or thickening of the pleura. The defect was not an obstructive one, i.e. one causing a narrowing of the airways such as asthma or CPOD. Looking at the earlier spirometry, FEV₁had fallen from 3.05 (in 1988) and FVC had dropped from 4.19. Although spirometry tests showed an apparent improvement in 1993, Dr Reid thought that this could have been for a number of reasons, including the pursuer simply feeling better on the day of the tests. If there had been an obstructive disease, lung volumes would have increased. That had not occurred. Spirometry also tested the ability of the lung to absorb the gasses in the air (gas transfer). In fibrosis cases, the transfer figures (KCO and TCO) would be expected to drop. That had not happened here, suggesting that something else was occurring such as pleural thickening, which would cause an increase in transfer, effectively cancelling out any predicted drop as a result of fibrosis. Emphysema would also cause a drop in the gas exchange figures, but the CT scans showed the emphysema to be minor. The CT scan showed both pulmonary fibrosis and pleural thickening, thus, Dr Reid reasoned, their interaction was the most probable explanation for the spirometry figures produced over the years. But, he argued, the spirometry ought not be looked at in isolation, as it had its limitations.

[39] At the time of his report (2 April 2005), Dr Reid had noted the CT scan as showing:

"Calcified pleural plaques...anteriorly in both hemithoraces, with some more diffuse pleural thickening in the right posterior hemithorax, with a small fleck of calcification".

He had reported that there was "no evidence of diffuse pleural thickening". He explained that he had underestimated the extent of the thickening because he had not, by then, seen the soft tissue CT images. He had subsequently done so and agreed with his colleague, Dr Turnbull, that they showed:

"...bilateral pleural plaques with associated calcification, parenchymal bands and right lower thoracic posterior diffuse pleural thickening" (report from Dr Turnbull 25/2 (supra)).

Dr Reid described pleural plaques as benign scarring, usually well circumscribed, being a discreet area of thickening up to 2 cm² made up of fibrous tissue. They were strongly associated with asbestos exposure and no other cause was known. The exact pathogenesis of pleural thickening, in this case of the visceral pleura, was not known. It was generally caused by recurrent pleural effusions (exudates containing inflammatory cells) which had healed by scarring the tissue.

[40] Dr Reid agreed with Dr Turnbull that:

"There is bilateral, lower lobe, basal, sub-pleural interstitial pulmonary fibrosis with associated minimal fine honeycombing, traction bronchiolectasis and ground glass opacification. These changes, in associated (sic) with the pleural plaques, diffuse pleural thickening, pleural calcification and parenchymal bands could be due to asbestosis" (25/2 quoted (supra),

except that he would have used the phrase "probably due to" asbestosis rather than the weaker "could be".

[41] Dr Reid said that there were a number of different CTDs. SLE was one in which a particular pattern of symptoms occurred, but there was a whole range of these diseases. The determination of which type a person suffered from was the field of the consultant rheumatologist. The pursuer had originally been seen by a non-specialist and later by a specialist rheumatologist, who had changed the diagnosis from SLE to UCTD. UCTD tended to occur in women and young patients. Furthermore, as the Kinder paper (6/20 (supra)) explained, the pulmonary manifestations of UCTD had not been described in medical literature. But those of asbestos related pleural thickening and pulmonary fibrosis had been so described. These conditions were known to result from asbestos exposure and that, on balance, favoured it as the cause rather than a disease whose effects on the lungs and pleura had not been described in any particular detail.

[42] Passages from a chapter termed Pulmonary Manifestations of Systemic Disease written by Professor Anthony Seaton (chapter 53 of Crofton & Douglas's Respiratory Diseases, 5^th edition (ed Seaton, Seaton & Leitch) (2000)) were put to Dr Reid. These included the following (p 1384):

"Acquired disorders

Connective tissue diseases

Pulmonary manifestations occur frequently in connective tissue diseases. There is considerable overlap between the different diseases, between the associated pulmonary manifestations and between the same pulmonary conditions in the absence of obvious collaged disease. Thus classification of the disorders is rather arbitrary and is likely to remain so until their aetiology is better understood. Those considered in this chapter are summarized in Table 53.1

Table 53.1 Respiratory manifestations of connective tissue diseases

...

Systemic lupus erythematosus

Pleurisy/pleural effusion

...

Interstitial fibrosis

...

Mixed connective tissue disease

Pleurisy/effusion

Interstitial fibrosis

..."

These, it was put to Dr Reid, pointed to fibrosis being a manifestation of CTD. However, although Dr Reid conceded Professor Seaton's academic credentials in relation to respiratory diseases, he would have deferred to the opinion of a rheumatologist in this field rather than to that of Professor Seaton. It was not legitimate to lump all CTDs together and to look at possible manifestations of CTDs in general. Simply saying that a person has a CTD is like saying he has a heart or liver disease. Unless the type can be specified, it is not possible to describe the expected manifestations. If the pursuer had UCTD, then it was the manifestations described as applicable to that CTD that had to be looked at, not those for SLE or "Mixed" CTD. He did accept that pulmonary fibrosis was a common manifestation in SLE patients.

[43] In relation to the paper by Kinder (6/20 (supra)), Dr Reid acknowledged the expertise of Professor Talmage King, the most distinguished of the authors, and described the understanding of interstitial lung disease as evolving. The American use of UCTD was as an umbrella term, different from "Mixed" CTD. All the persons selected in the Kinder study had pulmonary lung disorders. They were selected because of that and not because they had CTDs. The Court could not derive from this paper any information on how many patients with UCTD had pulmonary fibrosis similar to that of the pursuer.

[44] Dr Reid was referred to the report of Dr Graham Crompton (25/1) (infra), his predecessor at the Western General. He agreed with much of its content as regards the pursuer's history, complaints and examination. However, in relation to the interstitial pulmonary fibrosis, Dr Crompton wrote that "This could be asbestosis or a manifestation of connective tissue disease". Dr Reid commented that, although it was possibly a manifestation of CTD, it was more probably a manifestation of asbestos related disease having regard to the high prevalence of that condition in those with a history of asbestos exposure (perhaps 40%), as distinct from patients with CTD (perhaps only 10%). Furthermore, there was diffuse pleural thickening and this was a particular feature of asbestosis which had not been observed with CTDs, especially UCTD. Part of the Webb textbook (7/8 supra) was put to Dr Reid. This tabulated (Table 4-5) "Pleural thickening or effusion" as well as "fibrosis" as CT findings in SLE patients. Dr Reid had not seen this before. He queried the lack of any references for the authors' statement that:

There was no literature suggesting that diffuse pleural thickening occurred as a consequence of SLE. Professor Seaton had written (25/10 p 1389) that:

"SLE is associated with a wide range of pleuropulmonary complications... Pleurisy or pleural effusion is the most common, occurring in about half of all patients".

But, commented Dr Reid, Professor Seaton had not said that it caused diffuse pleural thickening. Professor Seaton had written (p 1390), but had not referenced, that infection and infarction both occurred frequently in SLE. Dr Reid accepted that infection could cause thickening. However, Dr Reid's response was that the pursuer did not have SLE and, even if he had, there was no evidence of infection or infarction. He stressed that, apart from substantive asbestosis, there was nothing in the medical records which might have caused diffuse pleural thickening. He would not concede, other than from a rheumatologist, that the CTD, which the pursuer had, was associated with diffuse pleural thickening. The information about SLE causing such thickening came from autopsy results and not radiology. The Webb textbook entries were not referenced. It was Dr Reid's day to day experience as a clinician that chronic pleural thickening was not seen in SLE patients. If Dr Turnbull were able to advise him that it was of a certain prevalence in CTD patients, then he might change his view, if it were greater than for persons with asbestos exposure. But radiology only provided one part of the puzzle.

[45] A printout of the 1982 Revised Criteria for Classification of SLE from the American College of Rheumatology (25/11) was put to Dr Reid. This said that such a diagnosis was legitimate if a patient manifested four of the eleven conditions listed. Dr Reid explained that the criteria selected were for the purposes of clinical trials. He agreed that the pursuer had been recorded as being photosensitive (criterion 3), but not necessarily arthritic (5) as distinct from arthralgic. He did have serositis (6) and antinuclear antibodies (11) . He also had (9) a haematological disorder in the form of lymphopenia, illustrated by his lymphocyte count being below normal. But Dr Reid was not prepared to accept that the pursuer was "as close as you can get" to SLE, although he would defer to a rheumatologist on that.

[46] Dr Reid did not agree with Dr Crompton that, in the absence of pleural plaques, it would have to be assumed that the pulmonary changes were due to CTD. There had, after all, been a history of asbestos exposure. He did agree with Dr Crompton that, in the absence of CTD, there would be no doubt that the fibrosis was asbestos related. Finger clubbing had also been noted in 1988. He disputed that the presence of long-standing finger clubbing indicated that it was unlikely to be related to asbestosis. Clubbing was not caused by CTD as such, but in connection with pulmonary fibrosis. That fibrosis may have been long-standing.

[47] Dr Reid did not consider that the absence of crackles in 1998 (supra) meant that asbestosis was unlikely. Crackles could be caused by pulmonary fibrosis. The fibrosis might be caused by asbestosis or CTD. Crackles could also be present simply as a result of the presence of fluid or inflammation of the lung. Dr Reid accepted that with asbestosis, once crackles were heard, they would not be expected to go away again. If the crackles were associated with CTD, whether they would go away would depend on the type of CTD and its treatment. Dr Richmond had noted in June 1998 that there was "no evidence fine respiratory creps" (supra 7/2 p 79). It appeared that she had been looking specifically for them. They had been recorded by others in 1987 and 1988 (supra). This was consistent with the presence of fibrosis in the late 1980s, even if the radiology were clear. Their later absence would, conceded Dr Reid, possibly be a pointer away from asbestosis. However, he explained that there were lots of explanations as to why the crackles were not heard. Perhaps the crackles had been missed because of external noises interfering with the auscultation during a busy rheumatology clinic. There was no way of knowing.

[48] It was put firmly to Dr Reid that the appearance and disappearance of crackles was more consistent with the pursuer suffering not from asbestos but an "SLE related condition" and he agreed that he would "go some way with" the cross examiner on that issue. He agreed that disappearing crackles were not consistent with fibrosis caused by asbestos exposure. He did, however, consider it was consistent with benign asbestos pleurisy, resolving itself. At this point he was asked a general question about whether the diagnoses of SLE and asbestosis were equally balanced. His answer to that was that if there was SLE then "it is equally balanced". He was interrupted and prevented from going further by an unfounded objection, indicative of the objector being concerned with that answer, if it had been a general one. Dr Reid appeared somewhat confused about what he had said. He was then asked a very long question with several sub-clauses about whether: "standing back and looking at the history, noting that the physicians from the 1980s onwards, looking at the constellation of facts at that stage, did not consider that the pursuer's condition was asbestosis but SLE or CTD, that on balance it is more likely than not that the pursuer's condition is caused by some form of CTD", or words to that effect. His answer was that "I would contend that they are equally balanced". In re-examination, and in response to somewhat leading questions, Dr Reid explained that he was referring to the findings in the period of the late 1980s, a time when he was unaware of whether asbestosis had been considered. He thought that there was an equal balance then, but not for "the current state of affairs".

[49] Dr Reid accepted that the GP and hospital records revealed the existence of pleural effusion on 30 March 1988 (7/2 p 148, 159 (supra)) and that the pursuer had undergone aspiration of the pleura (p 158). By the following May, the records said there was no evidence of effusion (p 157, 7/1 p 103). Dr Reid accepted that the effusion had gone away after treatment with Prednisolone, but maintained that it was not known whether that had helped. Perhaps the drain had removed the fluid, even if that would have been fortunate where the aspiration was for testing rather than treatment purposes. In relation to the apparent disappearance of pleuritic pain at times, Dr Reid explained that this might simply have been the effect of the pain killers that he was prescribed. Patients on steroids often feel better initially. It was possible that the effusion had been related to CTD and that it had been cured by the drug treatment. It was also possible that it was asbestos related.

[50] Dr Reid also accepted that the medical records showed that the pursuer had chest, possibly pleuritic, pain in 2000 (7/2 p 228 (supra)) and again in 2001 and 2002. He accepted that these could be consistent with infections, but not that they would cause pleural thickening. The pursuer was a smoker and prone to chest infections. But such infections do not cause pleural thickening.

[51] Dr Reid explained that it was difficult to predict how asbestos related pulmonary fibrosis would develop. Asbestosis is slowly progressive. Dr Crompton had concluded (infra) that it was impossible to state "on the balance of probabilities" whether the pulmonary fibrosis was asbestosis or a manifestation of CTD (25/1 p 7). Dr Reid disagreed. In this case there was a very strong history of asbestos exposure, which comfortably exceeded the threshold for causing asbestosis. The prevalence of pulmonary fibrosis in UCTD was not known. Given the prevalence of pulmonary fibrosis in persons with high levels of asbestos exposure, such as the pursuer, the fibrosis in his case was likely to be asbestos related. In addition, Dr Reid repeated, there were the pleural plaques and the diffuse pleural thickening.

[52] Dr Reid accepted the general epidemiology set out thus by Professor Rudd (6/17 supra p 708):

"The interval between the onset of exposure to asbestos and the development of symptoms of asbestosis is commonly 20 years or longer...New lung and pleural lesions continue to appear more than 40 years after first exposure. Asbestos fibres remain in the lungs for long periods, many permanently, and disease may appear and progress long after exposure has ceased.

...

The long latent period contributes to the difficulty in determining the attack rate among exposed persons and its relation to the dose of asbestos inhaled...

The frequency and severity of asbestosis increases with increasing dose of asbestos."

Dr Reid was not able to say when the onset of asbestosis had occurred. His best guess was that it was "some time" before the formal diagnosis in 2004. The disease was progressing, as the lung function tests demonstrated, even if appearances on plain film x-ray were unchanged. There were many factors affecting the progress of the disease and the extent of the dose was only one of them. The time taken between exposure and diagnosis had been longer than average. There had been a long latency period, but not a lot of weight could be put on this. He accepted that if there had been a rapid decline in the pursuer's condition between his own and Dr Crompton's reports, that would have been very rapid for asbestosis and made that diagnosis unlikely.

(b) Dr Crompton

[53] Graeme Crompton (73) gave evidence for the first and fifth defenders. He was a consultant physician until 1999, when Dr Reid succeeded to his post at the Western General. Dr Crompton had an impressive CV (25/8). His overall conclusion (report 25/1) had been that:

"...it is impossible to state whether this man's pulmonary fibrosis is asbestosis or a manifestation of connective tissue disease. I saw (sic) this because the number of patients with pleural plaques who go on to develop asbestosis is similar to the number of patients with a connective tissue disorder who develop pulmonary manifestations. Since there is no way of distinguishing the two disorders on radiological criteria, similarly there is no way of differentiating the two on clinical grounds".

However, having seen all of the medical records, he had changed his view. Having regard to his continuing problems from 1985, Dr Crompton considered that the pursuer had a multisystem disease. He had features of SLE, but no formal diagnosis of this had been possible because of the lack of an elevated double stranded DNA. Back in 1988, Dr Macrae had diagnosed "Mixed" CTD (7/2 p 159 (supra)) because of that, but there was no distinction at that time between "Mixed" and "Undifferentiated" CTD (see eg Crofton & Douglas etc. ((supra) 25/10 p 1384). Indeed, Dr Crompton had, until recently, been unaware of any such distinction. There was a connection between SLE, mixed CTD and pulmonary and pleural disorders. It did not matter which category of CTD the pursuer fitted into. A rheumatologist would say "mixed" even although it was almost SLE. If a person had a CTD, it would not be surprising for him to have a lung problem, although it was more often the pleura and pericardium that were affected.

[54] Dr Crompton was not familiar with the views of Webb et al (7/8 supra) to the effect that SLE could cause pulmonary fibrosis as this was a radiological reference, but he knew that such fibrosis was a manifestation of CTD. Dr Crompton tended to "shy away from" American medical literature, such as the Kinder paper (6/20 (supra)), as he felt that the authors had an inordinate desire to make up new diseases all the time, full of acronyms and synonyms. The paper reads:

"Rheumatologic studies have estimated that up to 25% of patients with features of a systemic autoimmune disease do not fulfil ACR classification criteria for CTD. These patients are considered to have diffuse or undifferentiated CTD. The majority of such cases...after years of follow up do not develop into a "differentiated" CTD (e.g., rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis, mixed CTD). Consequently, it has been proposed that UCTD represents a distinct clinical entity with the following criteria: signs and systems suggestive of a CTD, positive serological results, and disease duration of at least 1 year. The most common clinical manifestations of UCTD include the following: Raynaud's phenomenon. Arthritis/arthralgias, pleuritis/pericarditis, sicca symptoms, cutaneous involvement (photosensitivity, rash), esophageal involvement, fever, and myositis. The specific pulmonary manifestations of UCTD have not been studied".

Dr Crompton was quite happy with the content of this, although the whole paper was based on only 28 patients, all of whom had lung disease. The pursuer did not fulfil the criteria for UCTD used in the Kinder paper and Dr Crompton did not think it relevant to look at its content. The pursuer had four of the eleven criteria for SLE (3, 5, 6 and 11 in 25/11 (supra)). He had started out with SLE. "Mixed" CTD was the same as SLE without the elevated double stranded DNA. If an SLE patient presented with a non SLE manifestation (such as those in Crofton & Douglas etc. (25/10 supra p 1384) then a doctor would be entitled to question whether that manifestation was being caused by the SLE or something else. Crofton and Douglas (6/21 supra, p 1160-1) did not mention chronic pleural thickening as a manifestation of SLE, but any form of pleurisy or pleural effusion could cause thickening. Asbestos related pleural thickening caused the pleural surfaces to be fixed together. Effusion in that place could not recur.

[55] In his report, Dr Crompton sets out two "points in favour of asbestosis", viz. the pursuer's history of asbestos exposure and the radiological evidence of bilateral pleural plaques. He testified that he would have been surprised if Dr Turnbull had considered that the pursuer's diffuse pleural thickening was characteristic of previous asbestos exposure. But he had written earlier in his report that Dr Turnbull had indeed said that the thickening was "typical" of such exposure. Nevertheless, Dr Crompton would not initially, but did eventually, accept that this was a third point in favour of asbestosis. He said that the pursuer did not fulfil the criteria for diffuse pleural thickening, but did accept that the pursuer having pleural plaques was a factor which could be taken into account when deciding whether the thickening was asbestos related. If the pursuer did have a restrictive defect shown in lung function tests then that could be caused by pleural thickening even if that thickening had not shown up on x-ray and would not otherwise be expected to cause symptoms. The persistence of the gas transfer figures despite the presence of pulmonary fibrosis did point to asbestosis as a cause.

[56] Dr Crompton did not consider that the pursuer had finger "clubbing" as distinct from "beaking" (this term not being explained), but, if he did, then it could equally be caused by pulmonary fibrosis caused by CTD as it could by asbestos related fibrosis

[57] Dr Crompton sets out "points in favour of..." CTD (p 7) as including the pleural disease and effusions recorded in 1988 (7/2 pp 158, 159 (supra)) and the pulmonary changes shown on x ray in 1989 and 1992 (pp 104-106). The pursuer had had pleurisy. He had a pleural effusion suggesting an inflammatory process which resolved upon treatment with steroids. This had been preceded by pericarditis. There is no effective treatment for asbestos related pleural effusions. They would not respond to steroids as a CTD related effusion would. The effusion would not have been cured by a diagnostic aspiration. No attempt would be made to drain all the fluid for fear of causing a pneumothorax. Steroids do make people feel better generally but an effusion itself does not cause pain. It is only on successful treatment, when the pleural layers come back together again, that pain would return. Dr Crompton was "nearly 100% confident" that the cause was CTD as no other disease would respond in the way the pursuer had responded to the treatment. The pursuer's history suggested that he had relapsed after dropping the doses of steroids; that the CTD was being barely controlled. The pleuritic pain persisted for two months and that would be sufficient to cause pleural thickening, even it there was no evidence on the x-rays at the time that it did so.

[58] Crackles were, according to Dr Crompton, characteristic findings in asbestosis and all other cases of pulmonary fibrosis. If asbestos related, they did not disappear.

The pursuer had fine bi-basal crackles in December 1987 but these had disappeared by 1998 (7/2 pp 162-4, cf 79-80 (supra)) when Dr Richmond specifically looked for crepitations. This would exclude asbestos related pulmonary fibrosis as a cause. This, at least, was what Dr Crompton said in evidence, even although the significance of the disappearing crackles did not loom large in his report (25/1 p 7). The crackles were noted again in 2002. In August 2004, Dr Faccenda noted that the "chest auscultation was entirely clear" (7/2 pp 130, 126) but Dr Reid had heard crackles in March 2005 and Dr Crompton had no difficulty hearing the crackles in April 2007. The note in September 2007 (6/10 p 42) that the pursuer's chest was clear was in the context of the pursuer being admitted for an overdose and it would not have resulted from a detailed chest examination. The note "chest clear" would be a throwaway line in an out patient clinic.

[59] The first evidence of pulmonary fibrosis was on the CT scan in 2004, so it had appeared some forty to forty five years after the first asbestos exposure and thirty years after the last exposure. The pursuer had a high enough exposure to asbestos to cause problems, so Dr Crompton would have expected the pursuer to have developed fibrosis long before 2004. A longer period of latency after a heavy exposure pointed away from asbestosis, but individuals responded in different ways. Dr Crompton accepted that it was not possible to say how long the fibrosis had existed before the CT scan. It remained invisible on x-ray. Dr Crompton did not consider that it could have existed as far back as 1998, when Dr Richmond had not detected any crackles. But he did accept the idiosyncratic nature of the development of asbestosis described by Professor Rudd (6/17 p 708 (supra)).

[60] If the fibrosis had stemmed from asbestosis then some time would have had to have elapsed for the appearance of the "honey-combing" or "ground glass" opacities, which the pursuer had. If it had stemmed from CTD, a more rapid development could occur than with asbestosis related fibrosis, but the effect of the steroid suppressive therapy was not known. Professor Seaton (supra 1391) did write that "anecdotal reports suggest that [chronic interstitial fibrosis in SLE patients] does not usually respond" to steroids, but Dr Crompton had more experience of CTD patients than Professor Seaton and that experience was that CTD related lung disorders did respond to steroids.

[61] The pursuer had told Dr Crompton in May 2007 that he was short of breath after walking 60-70 yards (25/1 p4). This showed a rapid decline since Dr Reid had seen him in March 2005. This was not typical of asbestosis, which is very slowly progressive. The lung function tests did not support such a change. Although initially stating that there was nothing in the tests to suggest a restriction caused by pleural thickening, Dr Crompton did accept, after some prompting, that the lung function tests did suggest a restrictive ventilatory defect in the late 1980s, 1993 and 1998. Dr Crompton would not initially accept that, in the absence of evidence of pleural thickening, this indicated the existence of pulmonary fibrosis. He did eventually agree that, if there were a genuine restrictive defect, it had to be due to pulmonary fibrosis and/or pleural thickening, if the pursuer only had mild airways obstruction.

[62] Dr Crompton would laugh at the prospect of a mixed diagnosis. It would, in his view, be ridiculous. Doctors were taught not to give two diagnoses when everything could be explained by one. However, Dr Crompton accepted that if the pursuer did not have CTD, he would have no difficulty in saying that his condition was asbestosis. Dr Crompton's mixed diagnosis view seemed to be contradicted by his view that in early 2002, the pursuer was complaining of right basal pleuritic pain and being tender over the right lower rib. Scattered rhonchi, suggesting an obstructive airways disease, were present (7/2 pp 229-230 (supra). Pulmonary problems did not cause rhonchi so, Dr Crompton reasoned, there were two different pathologies.

(c) Dr Winter

[63] John Winter (57), consultant physician with a special interest in respiratory disease at Ninewells Hospital, Dundee, gave evidence for the remaining defenders (report 7/5). He referred to SLE as a multi-system disease, much more common in women than men. UCTD was a diagnostic category for a CTD which did not fit into the accepted CTD boxes, such as Mixed CTD, but he felt out of his depth in this area as he was not a rheumatologist. The pursuer had four of the eleven criteria for SLE: arthritis, photosensitivity, serositis, low lymphocyte count and a positive nuclear factor. There were also entries in the GP notes showing that he had arthritis.

[64] In a long, but clear, answer to a general question on fibrotic changes to the lungs, Dr Winter explained that the CT scan revealed bi-basal fibrosis and pleural thickening, although he had not seen all of the images. The problem with these two changes was that they could be caused by both asbestosis and SLE. There were certain radiological conditions which could lead to a diagnosis of asbestosis, but these were not present. A good history of asbestos exposure was needed, but, if the changes were occurring more than fifteen to twenty years after exposure had ceased, there was some authority for the proposition that they were unlikely to be caused by asbestosis. Here there was an alternative explanation for the pulmonary fibrosis, namely SLE. In his report he had been unable to form a view on which was more likely but, having seen the records, SLE was more likely. In particular, the pursuer had active arthritis in 1985. He had then developed chest pains. An ECG suggested pericarditis. Crackles detected indicated an active inflammatory process in the lung. Thereafter, the pursuer had developed an effusion around the lung, which responded rapidly to steroid treatment. This made SLE more likely than asbestosis. He continued to complain of chest pain. He had skin problems in the 1990s. But his skin and joint problems settled down on treatment. The crackles came and went, also suggesting acute inflammatory problems which had been treated, leaving fibrosis. The cause of that was more likely to be SLE, as it provided a single unifying diagnosis for all the symptoms. If it were possible to explain all the symptoms in this manner, that diagnosis is the most likely. There could be both SLE and asbestosis but, on the "balance of probabilities", SLE was the only cause, although it would not surprise Dr Winter if a lung biopsy showed that it was asbestosis.

[65] Dr Winter considered it significant that the pursuer had a pleural effusion in March 1988 but this had gone by the following May (7/2 p 157), after the prescription of steroids. It was more likely that the steroids had cured the problem, rather than a diagnostic quantity of fluid aspiration. There required to be a lot of fluid, perhaps about half a litre, to show up on x-ray and it was not likely, although it was possible, that this amount had been aspirated.

[66] Dr Winter thought that the latency period between the exposure to asbestos and the discovery of pulmonary fibrosis pointed away from asbestosis. His basis for this was that Parkes (Occupational Lung Disorders, 3^rd ed 1994 p 520, 6/22) states that if fibrosis occurs more than twenty years after exposure, it is less likely to be asbestos related. This was so even if Professor Rudd was of the view that the interval between exposure and symptoms was "commonly 20 years or longer" and "New lung and pleural lesions continue to appear more than 40 years after first exposure". It was not easy to say when the pursuer's fibrosis had started, but it was very minor at the time of the CT scan in 2004. If honeycombing were visible then, the fibrosis could have been there for a few months or even decades.

[67] With asbestosis, crackles in the chest should not go away, as they had done. Crackles indicated something was going on in the lung tissue and not the pleura. Although there could be differences of opinion on whether crackles could be heard at a given time, there were many records stating that the chest was clear, including one from a respiratory physician (Dr Faccenda). Dr Winter had heard crackles, but on 20 November 2007 (6/10 p 42 (supra)) the chest was noted as clear. This suggested that what was happening were inflammatory episodes causing fibrosis in the lung, rather than a problem with the pleura. For there to be fibrosis there had to be some form of injury, whether caused by asbestosis, SLE or radiation. There had to be an inflammatory process. Crackles could be caused by established fibrosis but crackles "on and off" were more consistent with SLE in the lungs rather than asbestosis.

[68] In relation to the pleural thickening, this could be a consequence of both SLE and asbestos exposure. There was no "blunting" of the costophrenic angle as would be expected with asbestosis. It was not possible to say whether the thickening was caused by asbestosis or SLE. Dr Winter had recently considered the Kinder paper (6/20), which had referred to a very rare group of patients with UCTD. The pursuer would not have fitted into this group. Dr Winter agreed with Webb et al (7/8 supra) that SLE could cause pleural fibrosis. He had looked up the references for the propositions in Webb. These were not produced, but Dr Winter was able to describe one of them as demonstrating that a certain proportion of SLE patients had interstitial lung disease (9 out of 34) and another as showing that some had pulmonary fibrosis (3 out of 38). Dr Winter was of the view that there was plenty of literature showing that lung and pleural disease were frequently encountered with SLE patients. He accepted that Crofton and Douglas ((supra) 6/21) did not mention pleural thickening in connection with SLE, but did in relation to asbestosis.

Conclusions of Fact

[69] The pursuer has developed asbestosis, in the form of pulmonary fibrosis, and diffuse pleural thickening as a result of exposure to asbestos during his employment with the defenders.

[70] Although the pursuer initially submitted, somewhat peculiarly, that the radiology should be regarded as "largely neutral", he proceeded, correctly, to found upon it as evidence of the presence of both asbestosis (fibrosis) and diffuse pleural thickening caused by asbestos exposure. That is what the radiology points towards, even although there may be other possible explanations for the fibrosis and the thickening. The starting point when looking at the radiological findings is the undisputed presence of pleural plaques, with calcification, undoubtedly resulting from asbestos exposure. The second area of significance is the pleural thickening. The pursuer submitted that the differences between the radiologists over whether the pleural thickening was "diffuse" were of no significance. However, that is not the case. It is useful to determine whether the thickening is "diffuse" or not in radiological terms in order to assess its cause. It is "diffuse" or as close to that as makes no practical difference. It was not suggested that the plain film x-ray test of obliteration of the costophrenic angle had been entirely met, even if there was some loss of definition. In relation to the CT scan dimensional test, Dr Sproule referred to the thickening as "at least 6 cm" and thus being "highly suggestive" of it being "diffuse". Dr Turnbull reported that it was "over 8 cm", albeit that he said in evidence that he "implied" that, rather than measured it. It was only Dr Wightman who tentatively put forward a case for it not being "diffuse" because, he thought, the next (non existent) CT image would have been below where the pleura of the lungs ought to have been. Although that is no doubt a possibility, the evidence of Drs Sproule and Turnbull that the 8 cm dimension has been reached is preferable even if that achievement is to a degree uncertain. The significance of this dimensional achievement is not just its predictability to produce symptoms (infra) but, as Dr Turnbull concludes in his report, its existence, like the pleural plaques, as "typical of previous asbestos exposure". In this connection, Dr Turnbull was not simply saying, as Dr Wightman did, that the diffuse thickening might be caused by asbestos exposure as one of several options. He was expressing his opinion in writing that it is "typical" as such exposure. From a radiological point of view, the radiologists agreed that thickening might also be caused by a CTD, but none of the radiologists went as far as to express the view that it was typical in patients with a CTD.

[71] The third aspect of the radiology is the fibrosis, which, all agreed, is mild in nature. It is not disputed that fibrosis can be asbestos related or it can be caused by a number of other conditions. As Dr Sproule conceded, if the fibrosis were asbestos related then, if it had existed in the late 1980s, it ought to have progressed beyond its current subtle form. On the other hand, as Dr Turnbull wrote, the fact that it has not progressed at a rapid rate tends to favour asbestosis or a stable or treated CTD. It is impossible to say how long the fibrosis has been present but, as will be seen, it is likely that it was present in the late 1980s.

[72] Before leaving radiology, it should be noted that although it was submitted by the pursuer that Dr Turnbull disagreed with Dr Wightman on whether the vertical or circumferential dimensions were more important as regards causing lung restriction, their evidence seemed to be the same in regarding the vertical as more significant.

[73] Turning to the physicians, a number of difficulties presented themselves in the assessment of their evidence relative to the pursuer's condition. As a preface, the court would not wish to criticise any party for the use of economy in a litigation such as this one where the value of the case, in Court of Session terms, is very small. Keeping the number of medical witnesses to a minimum is sound policy. However, first, where a major issue is a competition of causes between asbestos exposure and a CTD, the absence of expertise in the causes, prevalence, symptoms and treatment of CTDs, especially in males of the pursuer's age, creates a significant evidential gap. It was far from clear that any of the medical witnesses was able to speak with any confidence on this subject, even if Dr Crompton attempted at times to do so. Although the respiratory physicians were able to stress that their departments tended to adjoin those of rheumatology and that they had close contacts with their neighbours, none purported to be especially skilled in CTDs. Secondly, although the parties were keen to focus on particular entries in the medical notes, many of these entries appeared to be being afforded a status well beyond their role as "notes" or as summaries and, in some cases, speculations and conjectures on possible diagnoses. Thirdly, this was compounded by the absence of any of the pursuer's treating physicians over the years, especially someone, such as Dr Richmond, from the rheumatology clinic or a general physician from the Borders General who might have spoken to a final diagnostic conclusion once pleural plaques had been discovered.

[74] It is not without importance to note that, throughout the examination and treatment of the pursuer over at least two decades, asbestos related disease does not appear to have been considered as a possible diagnosis. Once more, the absence of such treating physicians as witnesses should not be taken as a criticism of the parties, since they no doubt had their own good reasons for selecting the witnesses they called. But that absence still presents a gap which the Court has to take note of in reaching its conclusions on the evidence actually presented.

[75] Fourthly, in relation to the use of medical literature, such literature is an entirely legitimate tool, which can be used to bolster or undermine the opinions of the experts. In that connection, the pursuer referred to Davie v Magistrates of Edinburgh 1953 SC 34 (Lord President (Cooper) at 40-41) and to Main v McAndrew Wormald 1988 SLT 141 (Lord Justice Clerk (Ross) at 142). But care must be taken not to imbue a medical textbook (especially one of some vintage) with the same strength as the musings of the Institutional Writers. The helpful dicta of Lord Osborne in Gerrard v Royal Infirmary of Edinburgh NHS Trust 2005 SC 192 (at 221) serves to emphasise that, even in the modern era where hearsay is admissible as proof of fact, the content of a textbook may have very limited evidential value unless expressly adopted by a witness. It is with these general considerations in mind that the evidence of the physicians falls to be examined. Those and, of course, the central concern of whether the pursuer has proved his case on a balance of probabilities, as that phrase is understood in a legal rather than a scientific or medical sense. As Lord Hope observed in Dingley v The Chief Constable, Strathclyde Police 2000 SC (HL) 77 (the Inner House proceedings (1998 SC 548; Lord President (Rodger) at 555, Lord Prosser at 608 and Lord Caplan at 625) of which were referred to by the pursuer) (at 89):

"The function of the judge in a civil case is to decide where the truth lies or whether the case has been made out, on a balance of probabilities. One cannot entirely discount the risk that, by immersing himself in every detail and by looking deeply into the minds of the experts, a judge may be seduced into a position where he applies to the expert evidence the standards which the expert himself will apply to the question whether a particular thesis has been proved or disproved - instead of assessing, as a judge must do, where the balance of probabilities lies on a review of the whole evidence".

[76] The defenders founded strongly upon the approach of Lord Bridge in Wilsher v Essex Area Health Authority [1988] 1 AC 1074, where, in playing down the effect of the dicta in McGhee v National Coal Board 1973 SC (HL) 37, he stressed the need for a pursuer to prove the relevant cause of his condition as a matter of probability where multiple causes were postulated. It is, of course, accepted that such proof is required as a generality, although, in this case, on one view, the onus of proving that the pursuer had a CTD fell on the defenders as the parties averring that fact. Nevertheless, as has often been said, once the evidence in a case has all been heard, issues of onus seldom arise and the question for the Court is simply where the balance of probability has come to rest. It must be in the rarest of civil cases that it remains so finely and evenly balanced after a proper analysis of the evidence, that the Court is forced to hold a case not proved by reason of a failure by a party to discharge a burden of proof.

[77] There was nothing in the qualifications or experience of the respiratory physicians which suggested that the evidence of one of them should be preferred over that of another. They were all very well qualified and experienced and each of their opinions deserves respect. Each may be correct. Each of the physicians had difficulty in answering particular lines of questioning. For example, Dr Reid was undoubtedly floundering when attempting to deal with the "crackles" and Dr Crompton attempted for some time to avoid a direct answer to questions concerning the ventilatory defect shown up in the lung function tests from an early stage. The reason for their difficulties is, no doubt, because there are points clearly for and points plainly against the presence of asbestosis on the one hand and CTD on the other, especially when considered within a short diagnostic time frame.

[78] Overall the wider approach of Dr Reid to the history of the pursuer's condition and treatment and his open minded analysis of that has provided the more acceptable and likely diagnoses, notably his fundamental conclusion that the pursuer does have asbestos related disease in the form of pulmonary fibrosis (asbestosis) and diffuse pleural thickening, as well as a CTD. This is, of course, on the balance of probabilities on a review of the whole evidence. Dr Reid himself appeared to adopt this approach whereas the lasting impression from hearing Dr Crompton and Dr Winter is that they had both determined that it was not possible to say whether asbestos exposure or CTD had "probably" caused the pursuer's fibrosis and pleural thickening simply because both were theoretically capable of doing so as a matter of medical fact. The conclusion that the pursuer has some form of CTD has to be reached primarily because none of the physicians was prepared to dispute its existence, deferring to the rheumatology reports in the records in that regard. However, as Dr Reid did comment, the foundation for that diagnosis is far from being a firm one. But for the lack of challenge on the existence of a CTD, it might have been difficult to accept that existence in the absence of expert rheumatological testimony. The pursuer's CTD is not capable of definitive categorisation. It is not SLE, since the pursuer does not have the necessary elevated double stranded DNA. It is not UCTD, in the American sense, as the pursuer has the necessary elements for American SLE. It may be some form of "Mixed" CTD or UCTD in the British sense.

[79] One of the planks upon which the opinions of Dr Crompton and Dr Winter are based is the notion that if all symptoms can be explained by one diagnosis then that diagnosis ought to be preferred over there being two diseases present. This somewhat fundamental proposition was not put to Dr Reid for his comment. However, it is no doubt a useful aphorism given to medical students and trainee doctors and one to be borne in mind as a generality. But, it cannot be an absolute axiom applicable in all circumstances. This pursuer may well have a CTD, for some reason. But it is accepted that for many years he was also exposed to significant levels of asbestos, sufficient to cause asbestos disease. He has calcified pleural plaques indicating the presence of asbestos particles in his lungs. He also has emphysema caused by smoking. There would appear to be no sound reason not to consider, with an open mind, the possibility of his suffering from two or more conditions at the same time. Dr Reid's approach in this regard is again preferable to those of his colleagues. In that regard, concerning his answer at one point that the diagnoses of SLE and asbestosis were "equally balanced", this was in the context of the evidence available to the physicians in the 1980s and was not a general concession about the position, now that a CT scan has been carried out.

[80] There was no persuasive evidence that diffuse pleural thickening visible on CT images is a common manifestation of CTD. Dr Reid's view on that, subject as it was to persuasion otherwise from a rheumatologist, is again accepted especially his pointing to the absence of medical literature supporting such a proposition and having regard to his reported clinical experience. Dr Reid was the subject of some valid criticism in submissions in relation to his refusal to respond meaningfully to questions about the likely manifestations of the pursuer's CTD without being told what CTD he had. Nevertheless, there is force in his view that, if the defenders are maintaining that the pursuer has pleural thickening and pulmonary fibrosis as a result of a CTD then, in order to demonstrate how that might arise, they ought to be able to state what CTD the pursuer has and then be able to point to the known manifestations of that type as including such thickening and fibrosis. They have not done so. In so far as there is a current categorisation of the pursuer's CTD it is UCTD and, as the Kinder paper points out, the pulmonary manifestations of that disease (at least in its American guise) are not described in medical literature.

[81] All the experts heard crackles from the pursuer's lungs. It was accepted that crackles can be caused by pulmonary fibrosis. Fibrosis caused by asbestos exposure does not necessarily produce crackles. But if there was fibrosis caused by asbestosis then that fibrosis would be permanent. Therefore, once established, any crackles caused by that fibrosis would not disappear and re-appear. It would be a strong point in favour of the defenders' case if it were established that any crackles detected in the pursuer's lungs had disappeared. If they had then they could not have been caused by fibrosis induced by the permanent presence of asbestos particles. Thus, the defenders founded heavily, for example, upon the existence of crackles in December 1987 and both March and April 1988 (supra) and the records in January 1989 that the chest was "clinically clear". In June 1998 Dr Richmond expressly wrote "no evidence fine respiratory creps".

[82] Throughout the records there are references to "chest clear", usually referring to radiological results but sometimes also to what seem to have been stethoscopic examinations. Although Dr Reid's speculation about the surrounding noises of a busy rheumatology clinic is not at all convincing, little weight can be attached to a record stating "no evidence fine respiratory creps" where the author does not give evidence and there is no obvious explanation for that. Even assuming that the record actually means what the defenders maintained it did, namely that there was no evidence of fine respiratory crepitations (which is by no means certain), it has to be borne in mind that this was a chest examination preceding any consideration of asbestos related disease, when such crepitations might have been more carefully looked for. It was an examination by a rheumatologist and not a respiratory physician. The entry is not therefore to be regarded, as the second etc. defenders submitted, as "high quality hearsay" (whatever that may be).

[83] As the defenders conceded in submissions, even although the CT scan showed there to be fibrosis present in the lungs in 2004 and all the experts detected crackles relative to that fibrosis, respiratory physicians (Dr Faccenda and her registrar) had separately failed to detect crackles in 2007, even although the presence of established fibrosis was by then well established. That would seem to suggest, if it were not obvious, that mistakes in the detection of crackles can be made. No doubt they may be more evident at some times than others. At all events, the fact that at some points in the medical records crackles have been noted by some doctors and at others they have not, goes little way towards establishing a pattern of disappearance and re-appearance in clinical terms. In that regard, relative to the medical use of the phrase "chest clear", it is not without significance that the registrar examining the pursuer's chest in October 1992 regarded it as "clear" despite the presence of "a few scattered crepitations". Crackles are detected at various times from 1987 through to 2007. It is likely that they were always detectable upon a careful and detailed examination but that they were not always detected in the context of, in particular, a primary diagnosis of CTD rather than respiratory disease.

[84] The defenders founded upon the apparent resolution of the pursuer's pleuritic pain and the disappearance of the effusion. This, it was argued, was illustrative of a CTD resolved by steroids. Dr Reid struggled under effective cross examination in relation to the disappearance of the effusion and his explanation that the aspiration might have removed it was not convincing. However, so far as pain is concerned, that is, of course, highly subjective. The pursuer was being given doses of steroids which would, no doubt, make him feel better intermittently. He was also taking pain killers. The pursuer was not a particularly good historian, as was illustrated by his surprising inability to recollect past episodes of a variety of pains requiring visits to his local surgery (see (infra) on damages). His reports of pain, the lack of it and its degree may not be very reliable. He was a heavy smoker, prone to chest infections. He may have had an effusion, and indeed pleuritic pain, caused by something other than asbestos exposure, including as a result of whatever CTD he might have. That may well have resolved to some degree upon treatment with steroids. However, that does not lead to a conclusion that the pulmonary fibrosis and pleuritic thickening detected on the CT scan are caused by CTD as distinct from being asbestos related.

[85] Overall, the general picture of the pursuer's history is one of intermittent complaints of pain and of discomfort in his chest. From time to time, he seems to have considered it sufficiently symptom free to avoid calling in at his GP surgery. Given his intake of steroids and painkillers, he may have felt that whatever symptoms he had were resolving to an acceptable level. But the impression from the notes is that the pain and discomfort is seldom reported as disappearing altogether for any prolonged period. It seems to be always there in the background, albeit that, on occasion, the pursuer may have considered it absent on a given date. The lung function tests show that in the late 1980s, he did suffer from a mild restrictive defect. That restriction has continued, and slowly become worse, over the three decades since then. It is not without significance that, over that period too, he was reported as having clubbed fingers; a known consequence of pulmonary fibrosis. Like the crackles, sometimes the clubbing was not detected by some of the doctors over the years, but a sufficient number did find it. It has almost certainly always been present in some degree and is, despite Dr Crompton's view in evidence that it might only be "beaking", present now. This also suggests a continuing pulmonary defect. Dr Crompton, it should be noted, did not state that it was "beaking" in his report. Rather, he said that it was "Clubbing/beaking of fingers (known to be longstanding)". In so far as he maintained that there was no clubbing, his evidence is rejected.

[86] If the pursuer has had fibrosis over this time, then the pursuer's gas transfer figures would have been expected to drop, but they have not done so. There must be a reason for this. Dr Reid's explanation that something else has been happening is a convincing one. It fits in with his persuasive view that the pleural thickening, which has now been confirmed on the CT scan, has been the cause. There has, as Dr Reid stated, been an interaction over the years of the two conditions which, it is now established, the pursuer has, namely pleural thickening and pulmonary fibrosis. In this connection, the lung function tests do not reveal a sharp deterioration in the pursuer's condition between seeing Dr Reid and Dr Crompton. The pursuer has not deteriorated rapidly over this time. He exaggerated his difficulties, as caused by his breathlessness, when seen by Dr Crompton, and to a degree also when giving evidence.

[87] The significance of the latency period depends upon when it is thought that the pursuer developed symptoms of asbestos related disease. If it were thought that these had only occurred when the diagnosis was made in 2004, then clearly the time lapse from the commencement or the cessation of exposure until then might be regarded as a significant pointer away from asbestosis. But, as concluded above, the probability is that the pursuer had some fibrosis, albeit in a mild and very slowly progressing form, from the late 1980s, causing a mild restrictive ventilatory defect. If that is correct, and it is the conclusion reached here, then the pursuer developed symptoms within about fifteen from the cessation of exposure and within thirty years of his initial exposure. These appear to be well within the normal latency periods to be expected for asbestos related disease.

Damages

[88] The pursuer sought a final award of damages and did not insist upon his first conclusion for a provisional sum.

(a) Evidence

[89] The pursuer said that he was currently not well. He suffered from shortness of breath during the day and at night, causing broken sleep. He broke out in sweats during the night. He had pains in his left side. He was unable to walk more than fifty yards or to go up hills, without becoming out of breath. He had been like that for five or six years, but he had got worse in the last four to five years. He had grown "a good bit worse" since seeing Dr Reid. He later said that he had suffered shortness of breath since 1987. He would now use a car if he had to go more than two hundred yards. He had many grandchildren but was unable to engage with the younger ones as he once had with the older children. He needed to take pain killers six or seven times per week. He had suffered from bladder and heart problems but, once treatment of these had been completed, he was told by his GP that something else was wrong. His doctor had told him, he said, that he had to put a label on it and that he would "just put it down as SLE". "They said" there was something wrong with his connective tissue and asked him if he had pains in his joints. He did not have any pain in his joints but did have in his chest. He also had Raynaud's and poor blood circulation in his legs, from the calf down. He was prescribed Prednisolone. He would break out in sweats and began shaking if he withdrew from it. His symptoms recurred if he stopped taking the tablets. He had no recollection of increasing his steroid dose in 1997-98 because of skin or joint pain. He had no recollection of having knee and ankle problems in 2000, or of any joint pain at all. He did have chest problems, although he did not remember pain, in 1997-98 when his lung was drained. He could not remember chest pain in 2000, 2001 or 2002, but he did accept that he had visited his GP regarding chest problems. Finger clubbing had not been mentioned. He used to smoke, latterly 50 grams per week before reducing this to 12.5 grams a week (4 or 5 cigarettes per day) and eventually giving up last year.

[90] The pursuer said that he had first been told that he had an asbestos related condition after Dr Richmond had sent him for the CT scan. Dr Faccenda had told him that he had asbestos in his lungs. After a medical examination, had been told that, for the purposes of industrial injuries disablement benefit, he was 15% disabled. He had received £6,789 in February 2005 (25/7) as benefit for asbestosis.

[91] The pursuer told Dr Reid (30 March 2005) that he was short of breath on exertion such that, although he could walk for about half a mile at his own pace on level ground, he would be short of breath if he had to hurry or climb stairs or inclines. On the Department of Work and Pensions' COPD Disability Rating Scheme scale (25/6) Dr Reid considered that the pursuer was 20% disabled, although he could qualify for 30% if the account to Dr Graham Crompton on 7 May 2007 (infra report 22/1) were true. That was that he had shortness of breath on walking only 60-70 yards, although he could walk long distances on the level if he rested for two or three minutes on feeling breathless. Dr Reid's view was that the pursuer was 15% disabled because of the fibrosis and pleural thickening (mainly the latter) and the additional 5% because of his CTD. Dr Reid regarded the emphysema as "quite minor". In the absence of any evidence of airflow obstruction, he was reluctant to attribute any element of the disability to it.

[92] Dr Reid thought that the comments in his report (6/6 p 7) required alteration in light of the finding of diffuse pleural thickening on CT scanning. He "stuck" with his comment that the asbestosis may be stable but is usually slowly progressive, especially as the pursuer is a smoker. He estimated that "respiratory disability due to asbestosis will progress to a maximum of 30% of his total disability in his life time". He thought that this was unlikely to require any additional care or support. Were he to continue smoking, his emphysema would progress towards causing 15% of his total disability.

[93] In his report, Dr Reid said that the pursuer was at a 5% risk of developing malignant mesothelioma. An assessment of 2% (infra) was too low and applied where a person only had pleural plaques. The pursuer's asbestos exposure had increased the likelihood of him developing lung cancer by fourfold. As he already had an 8% chance of developing lung cancer from his smoking, he had, Dr Reid reasoned, a 32% prospect of lung cancer. This risk would diminish if, as the pursuer said, he had ceased smoking. The pursuer's life expectancy, but for his condition, would be 20.69 years for a man aged 63. His various non asbestos related conditions, including CTD, reduced that by seven years. Dr Reid considered that it was reduced by four years as a result of the asbestos related risks of developing malignant disease. The asbestosis itself would not progress to a fatal degree. The view (infra) that there was no decrease in life expectancy was out of step with the chapter in Professor Rudd's book (6/17).

[94] Dr Crompton was of the view that the pursuer's disability was between 10 and 20% on the scale (25/6 supra). That would be split "50-50" with the pursuer's emphysema and bronchitis. If he had asbestosis then he had a 2% risk of developing mesothelioma. It was not as high as 5%. He was at increased risk of developing lung cancer too, although it was difficult to assess in percentage terms. The ordinary smoker had an 8% risk. Perhaps 20% was appropriate, but it was not as high as four times 8%.

[95] Dr Winter saw the pursuer in April 2007 (report 7/5), when he said he could walk long distances on the flat. If what he had said to Dr Crompton (supra) were correct, then the change was inexplicable. At the time he saw him, Dr Winter thought he was 20% disabled on the scale. On the basis of Dr Wightman's report of the CT scans, Dr Winter thought the emphysema, and COPD, caused half or perhaps three quarters of that with the balance being caused by the pulmonary fibrosis. Any pulmonary fibrosis was minor and it was not possible to say that it contributed to any restriction, although it might do so.

[96] Dr Winter considered that the pursuer was at greater risk of developing lung cancer and mesothelioma as a result of his asbestos exposure and smoking, perhaps at 3% risk for both. Dr Winter would have been prepared to move 2% from this in either direction, and thus 5% was not unreasonable. Professor Rudd's patients (6/17 supra) had different diagnostic criteria, based on chest x rays. Dr Winter dealt many cases of lung cancer in Dundee and made a rough calculation in the witness box of a normal incidence of 11/2 % over a ten year period. Mesothelioma cases were half those of lung cancer. The pursuer's life expectancy as a result of all his various conditions was reduced by 5%; 3% as a result of malignancy.

(b) Submissions

[97] The pursuer sought only solatium and interest. He submitted that a reasonable figure was £30,000, one half of which was attributable to the past. He produced a useful table of various Scottish cases with an up to date revision of the awards made in them. It was accepted that the first five of these cases (Timms v Barclay Curle 2007 CSOH 166, unreported, [2007] CSOH 166; McKenzie v Barclay Curle 2002 SLT 649; Kerr v Newalls Insulation Co 1997 SLT 723; Stanners v Graham Builders Merchants 1995 SLT 728; and Myles v Glasgow District Council 1994 SCLR 1112) involved pursuers with greater disabilities than the present pursuer. However, the pursuer in McKenzie v Cape Building Products 1995 SLT 695, who was aged 52, did have pleural plaques and thickening and sub-pleural fibrotic changes. He had late onset asthma as well, contributing equally to his breathlessness. He was at risk of developing mesothelioma or lung cancer and had been assessed at 15% disabled for Department of Social Security purposes. The award had been £25,000, worth just over £37,500 now, and this had been sustained upon a reclaiming motion (1995 SLT 701). In Lightbody v Upper Clyde Shipbuilders 1998 SLT 884, the award had been £15,000 (over £19,000 now) for a 59 year old with pleural plaques, minor pleural thickening and a small chance of developing mesothelioma. He was described as having a moderate degree of "exertional" breathlessness. The pursuer argued that this award was low and "out of kilter" with other cases. Bateman v Newalls Insulation Co 1987 SCLR 445 was a Sheriff Court award of £14,000 (almost £30,000 now) for what was described as asbestosis (in fact only diffuse pleural thickening) in a 10% disabled 62 years old. Nicol v Scottish Power 1998 SLT 822 was an award of £13,500 (£18,000) for a 52 year old with pleural plaques and an increased risk of developing malignant disease but who had developed anxiety about asbestosis. Finally, there was Campbell v Campbell & Isherwood 1993 SLT 1095, where a 73 year old was awarded £12,000 (£18,250). He suffered from breathlessness, substantially contributed to by bronchitis.

[98] The pursuer also founded upon the English Judicial Studies Board Guidelines which advised £40,750 for "Injuries to Internal Organs" "(C) Asbestos-related Disease" "(c) Asbestosis", involving "Respiratory disability of between 10 to 20 per cent". The "bottom" bracket was £28,830. "(d) Pleural thickening" causing breathlessness carried a range of £23,000 upwards. The pursuer relied upon the table in Kemp & Kemp: Quantum of Damage (K3. Respiratory Organs: Asbestos-Related; p K0004), which incorporated an uplift following on from Heil v Rankin [2001] QB 272, notably upon the English cases of: Seward v Corby Borough Council (2004) Kemp & Kemp K3-017.1 (£40,000 for a 52 year old with similar problems as the pursuer); Snell v Newalls Insulation (1998) Kemp & Kemp K3-018 ((£30,000 for a 72 year old); and especially Ryan v BRB Residuary (2005) Kemp & Kemp K3-019.1 (£20,000 for a 68 year old) and Urwin v Darlington Insulation (1996) Kemp & Kemp K3-021, which was at the bottom end of the scale at £15,000 for a 72 year old with 10% disability.

[99] Interest ought to be at 4% on half of the total from the date of discovery of the disease in June 2004.

[100] The first to fifth defenders submitted that solatium ought to be £20,000 with interest also on half of that figure from the date of diagnosis. They reminded the Court that no damages were available for pleural plaques on their own, or for the prospect of developing a disease in the future or anxiety because of that (Rothwell v Chemical and Insulating Co [2007] 3 WLR 876). On the scale (25/6) the pursuer was 10 to 20% disabled. Half of the disability was smoking related, so the award should reflect a disability level of about 7.5%, or less if Dr Winter was preferred to Dr Crompton. The pursuer had been coy about his breathlessness and the lung function tests did not support any rapid deterioration in his condition. Age was an important factor in the damage assessment. All of the Scottish cases in the table were examined. It was argued that the pursuer in McKenzie v Cape Building Products (supra) was much younger. Lightbody v Upper Clyde Shipbuilders (supra) was a good analogy involving again a younger pursuer but lesser malignancy risks. Nicol v Scottish Power (supra) was an unusual case where a high award was made in respect of the anxiety element. Cook v Wyvern Structures 2001 SLT 1212 was also useful, involving a potential award of £15,000 (£18,000) for 35% disablement. Of the English cases, Ryan v BRB Residuary (supra) was the most helpful. The £6,789 received by the pursuer (25/7) as benefit for asbestosis required to be deducted (Ballantyne v Newalls Insulation [2001] ICR 25).

[101] The remaining defenders adopted these submissions. They submitted that the court should find in fact that: (1) the pursuer suffers from mild breathlessness, causing 20% disablement of which 5% is attributable to pulmonary fibrosis; (2) 15% is attributable to emphysema; (3) the fibrosis is caused by CTD and the emphysema by cigarette smoking; (4) there is no breathlessness caused by pleural thickening; and (5) there is no risk of the pursuer developing malignant disease because of exposure to asbestos.

(c) Award

[102] As noted above, the lung function tests do not warrant the conclusion that the pursuer's pulmonary difficulties have rapidly deteriorated in recent years, although they have grown worse. The pursuer has not had his troubles to seek and has a variety of health problems unrelated to his asbestos exposure, notably significant heart and bladder disease. His asbestos related condition, as manifested in symptoms, consists of a mild restrictive ventilatory defect which causes him breathlessness on exertion. He is only slightly worse than when Dr Reid saw him in March 2005 (see supra on exaggeration). He can walk without much difficulty on level ground but will need to rest if he is required to hurry or climb. He may have occasional disturbed sleep.

[103] The pursuer might just manage to fit into the 20% disability category on the scale produced (25/6 (supra); the categories of which jump from 10% to 20%). Dr Crompton's assessment of between 10% and 20% on the scale seems reasonable. The pursuer's pulmonary disability is therefore assessed at 15%. The condition is very slowly progressive and it may progress to the 20% level, but not to the 30% category. It was accepted that only part of this is caused by asbestos related disease because of the existence of emphysema and, on Dr Reid's analysis, some form of CTD. There were various different proportions attributed by the respiratory surgeons ranging from one quarter of his condition to CTD, but none to his emphysema, from Dr Reid to Dr Winter's half to three quarters being caused by the emphysema and any COPD. On balance, it is reasonable to attribute one half of his 15% disability to asbestos related disease.

[104] The pursuer is at increased risk of developing mesothelioma and lung cancer. Again, various percentage figures were presented. The risk of mesothelioma is very low, and 5% will be taken. Lung cancer risk is higher. Dr Crompton's 20% if the pursuer was still smoking may be too high, and Dr Reid's arithmetical calculation does not seem statistically valid. Perhaps something in the region of 15% may be about right. There must be some reduction in life expectancy, but this will be small. Two to four years seems reasonable having regard to the various figures, ranging from nil to seven (including the CTD element).

[105] Solatium is reasonably assessed at £25,000. In that regard, the submissions on behalf of the first to fifth defenders are accepted as broadly accurate. The Court's task is to award damages for a slowly progressive disabling condition currently assessed as 7.5% attributable to asbestos related disease and carrying with it relatively small risks of malignant disease and consequent possible reduction in life expectancy. Although by no means on all fours with it, the case of Lightbody v Upper Clyde Shipbuilders (supra) is a not unreasonable comparison of all the cases referred to. It did involve a younger pursuer but he had a lower risk of developing a malignant disease. Having regard to the latter and all the other circumstances, a slightly higher award is merited in this pursuer's case.

[106] It was agreed that the £6,789 awarded in February 2005 (25/7) falls to be deducted from the solatium, leaving a principal sum of £18,211. Interest was only sought from the date of diagnosis following upon the CT scan in June 2004. It was not disputed that it should run at 4% on a past element of one half. On that basis, it would run on £12,500 to February 2005, and on the balance of £5,711 thereafter. The interest amounts to about £900. Decree will accordingly be for £19,111.

	[Home] [Databases] [World Law] [Multidatabase Search] [Help] [Feedback]
	Scottish Court of Session Decisions
You are here: BAILII >> Databases >> Scottish Court of Session Decisions >> Hynes v. Lobnitz & Ors [2008] ScotCS CSOH_67 (01 May 2008) URL: http://www.bailii.org/scot/cases/ScotCS/2008/CSOH_67.html Cite as: [2008] ScotCS CSOH_67, [2008] CSOH 67

Scottish Court of Session Decisions