Robert Clayden v State of New Souith Wales

[2001] NSWDDT 6

Dust Diseases Tribunal

of New South Wales

CITATION:	Robert Clayden v State of New Souith Wales [2001] NSWDDT 6
PARTIES:	Robert Clayden State of New South Wales
MATTER NUMBER(S):	194 of 1993
JUDGMENT OF:	Curtis J at 1
CATCHWORDS:	Damages :-
LEGISLATION CITED:
CASES CITED:
DATES OF HEARING:	8th August 2001, 9th August 2001, 13th August 2001, 20th August 2001
DATE OF JUDGMENT:	08/29/2001
LEGAL REPRESENTATIVES:	FOR PLAINTIFF: Mr J Sharpe instructed by Turner Freeman FOR DEFENDANT Mr G Little SC instructed by Hunt and Hunt

JUDGMENT:

1. The plaintiff was employed by the State Dockyard in Newcastle as an apprentice joiner between 1965 and 1970 when he qualified as a tradesman joiner. He then worked at the dockyard as a tradesman joiner between 1971 and July 1977. It is not in contest that during his employment at the dockyard by the defendant the plaintiff was negligently exposed to the inhalation of asbestos dust and fibre, nor is it in dispute that in consequence of the defendant's breach of duty he suffers from asbestos related pleural disease (ARPD). The matter at issue is the extent to which that disease makes any material contribution to the plaintiff’s undoubted breathlessness caused by his tobacco related obstructive airways disease and obesity.

2. Although I feel some sympathy for the plaintiff, the evidence has not led me to the point of actual persuasion that the cause and extent of his breathlessness are as he alleges.

THE PLAINTIFF’S EVIDENCE

3. The plaintiff says that he was in good health until late 1992 when he was 42 years of age. He then began to notice tightness in his throat and chest with a feeling of chest constriction. It should be here noted that until 1989 the plaintiff was a habitual smoker of cigarettes. In response to those symptoms the plaintiff consulted a Dr Moore who arranged a chest x-ray on 4 November 1992. Following upon that x-ray the plaintiff was referred to Dr Deacon who, according to the plaintiff, said that his condition was caused by the asbestos related disease of pleural fibrosis. The plaintiff says that his immediate concern upon being told this, was how long he had left to live, and that shortly thereafter he began to suffer from physical symptoms in addition to shortness of breath, being pains in his chest and under his shoulder blades, a racing heart and a feeling of general malaise. He says that from that time his physical symptoms progressively deteriorated, particularly when he exerted himself. He became progressively more sore in the chest with troubled breathing, particularly on exertion.

4. By July 1996 the plaintiff says his breathlessness was consistent. He had a cough which produced a light brown sputum and chest tightness after carrying anything. During 1999 he asserts that he was taking progressively more and more time off work and that he was suffering regularly from chest infections.

5. In 1998 the plaintiff was absent from work because he had contracted a melanoma on his right ankle which was excised and a skin graft applied. Upon his return to work following the surgery the plaintiff said he became increasingly hard pressed to keep up because of the regular chest infections and increasing breathlessness.

6. In his affidavit the plaintiff asserted that by 1999 he found himself so breathless he was unable to cope with the demands of his work as a supervisor of tradesmen renovating railway carriages in the employ of A Goninan and Co Pty Ltd at Broadmeadow. He said that because he had some seniority and autonomy within that organisation he was able to rearrange his duties and do less physical work and adopt a more managerial and delegatory role. Notwithstanding these changes, increasing breathlessness and inability to cope with the physical demands of the job caused him to accept a redundancy package and retire from work on 30 July 1999 when Goninan laid off most of its staff because of a lack of work. He has not worked since and says he is unable to work.

7. The plaintiff gave the following evidence:

Question Insofar as you were concerned did you take that redundancy or what happened, will you explain to us what happened to you.

Answer I had no intentions of taking any redundancy but the way my health was, and I had discussions when it came up, they were talking about reducing the supervision level. I - in fairness to the company I spoke to my boss and said to him, I said, well, the way my health has been where I've been losing a lot of time through chest infections mainly, that was my problem, I said that when it came to redundancy, I said, 'well, I will think about it if you want to go that way' but he said, 'Well, we don't want to lose you at this stage'.

8. I do not accept this evidence of the plaintiff as to why he took redundancy.

9. The plaintiff in evidence conceded that he had a malignant melanoma removed from his right ankle on 30 July 1998, but asserted in evidence that he was back to normal duties after 2 months (transcript 20) or 9 to 10 months (transcript 17). He said that he was back at normal duties at the time of his redundancy (transcript 20) and that the leg was then causing "hardly any problems at all" (transcript 24) and was "close to fully recovered".

10. The plaintiff in August 1999 accepted a superannuation payout of $146,000 in respect of total and permanent incapacity for work.

11. In a letter of 13 September 1999 from Mr Dennis Gleeson, superannuation manager of A Goninan and Co Pty Ltd, to Howard Smith Group Superannuation Association concerning this claim by the plaintiff for a payment of monies for total and permanent disablement, Mr Gleeson said:

Mr Clayden's health over the past year has diminished to the point that I believe he has been diagnosed as having pleural fibrosis, diabetes, high blood pressure and a serious melanoma.

It has been pointed out to me that Mr Clayden has at times extreme difficulty in breathing and in one incident suffered an air pocket in the lung.

While this is serious in itself, the major problem Mr Clayden has endured during the last 12 months is with the melanoma. Mr Clayden had extensive surgery to his right ankle in July 1998 and at the date of leaving, the wound site had not healed, required daily dressing and the use of a support stocking to control swelling.

Mr Clayden's duties were modified following this operation to alleviate the problems associated with swelling. (PX21).

12. To a form entitled "Employer's statement" submitted to the trustees of the superannuation fund, Mr Gleeson attached a note in these terms:

Mr Clayden's duties were reduced to minimise the amount of walking he needed to do. The duties that Mr Clayden performed before he left Goninan's employment were designed to enable him to perform his duties mainly from his office. This was instigated because Mr Clayden's leg would swell up if he was on his feet or walked for any length of time. A mechanical supervisor that was to be made redundant was continued to be employed while the refurbishment of double decker suburban trains contract continued. This was done so Mr Clayden had very little need to leave his office, allowing him to oversee the contract without aggravating his leg problem. (PX22).

13. It was the evidence of Mr Gleeson that this statement of his was consistent with information received from the plaintiff and from his co-workers and also Mr Gleeson's observation of the plaintiff at the time.

14. It was also the evidence of Mr Gleeson that the trustees required a medical certificate and a statement by the employee before a payment would be made. A letter was sent to the plaintiff at the time requiring completion of an employee's statement (PX29). The plaintiff in evidence first said that he had completed a form for this purpose (transcript 25) and although later he denied this (transcript 37) I do not accept his denial as truthful. In the ordinary course of affairs the payment to him would not have been made without a written statement in his hand or over his signature confirming the employer's representations.

15. In cross-examination the plaintiff conceded that despite his earlier evidence of full recovery that he was on restricted duties because of his leg pain when he left the employment of the respondent (transcript 26) and that the leg was causing him "a lot of trouble at the time" (transcript 30). On 2 August 1999, two days after ceasing work, the plaintiff presented to Dr Foster, the surgeon who had removed his melanoma, complaining of recurrent pain and swelling of his right ankle (DX5). In challenging the plaintiff's evidence of retiring because of incapacitating breathlessness in the light of this material, Mr Little for the defendant put these questions:

Question In fact you were still on restricted duties at the time you retired, were you not.

Answer Yes, to an extent, yes.

(Transcript 26, line 8).
Question In fact prior to you leaving the work you were doing was from your office on the workshop floor, was it not.

Answer Yes.

Question And your breathing did not cause you the slightest problem with doing that work, did it.

Answer Sometimes it did.

(Transcript 26, lines 25 to 29).

16. On 8 July 1999 the plaintiff was examined by Dr M J Deacon. This was shortly before the claim was made for a superannuation payout for total and permanent incapacity. The plaintiff told Dr Deacon that he was considering returning to carpentry.

17. Having seen and heard the plaintiff give evidence I have taken an adverse view, both as to his reliability and as to his credibility. I do not believe that when he left Goninan’s he was incapacitated for his work by reason of his melanoma or his breathlessness. I accept that he is depressed but I do not believe that that illness has blurred in the plaintiff's mind the distinction between truth, exaggeration, hyperbole and misleading statements to either me or the Superannuation Trustees. I cannot accept any contention from the plaintiff which is not supported by persuasive medical opinion.

MEDICAL EVIDENCE IN SUPPORT OF THE PLAINTIFF’S CLAIM

18. No medical practitioner supports the plaintiff's contention that he was incapacitated by reason of breathlessness when he resigned his employment, other than Dr Michael Burns who was qualified by the plaintiff for the purpose of giving evidence in this case.

19. On 10 September 1999 the plaintiff was examined by Dr Burns. This was about 6 weeks after the plaintiff's resignation on 30 July 1999. Dr Burns took this history.

[In the employment of G Goninan from the early 1980s] Mr Clayden was frequently exposed to airborne dust. It was mostly fibreglass sandings of plywood and carriage carpet debris. He was exposed to fumes of paint strippers, contact glues, thinners, et cetera, and a mask was issued to all the workers. He continued there until 30 July 1999 when he took redundancy.

He used to smoke until about 1990. Over the last few years he has been subject to bronchitis and colds and the episodes of bronchitis tend to linger. He is on regular asthma type sprays from his GP who has advised him to apply for a disability pension as Mr Clayden is too breathless to work. He is breathless on hills and stairs and on heavy exertion but can cope with walking along the level.

Dr Burns concluded:
It is not surprising that he found work in the dusty environment at Goninans difficult because he was already short of breath and the temporary irritation usually on a daily basis, from the dust and fibres in the air would have added quite severely to his breathlessness at this time.

20. Dr Burns received no history that the applicant was incapacitated by foot pain or swelling, nor that the work at Goninans in the office was supervisory work conducted from an airconditioned office, requiring no heavy exertion.

21. Significantly, in an earlier report of 6 May 1997 Dr Burns, having examined the plaintiff, expressed his opinion that the plaintiff did not have significant respiratory impairment and that his condition was unlikely to deteriorate.

22. Dr Burns in 1997 believed that upon the basis of high resolution lung scans performed by Dr Michael Jones on 5 May 1997 (PX9) that the plaintiff did have some asbestosis. For the purpose of his report of 13 September 1999 Dr Burns arranged for a further CT scan which was performed by Dr Branson on 10 September 1999 (PX10). Upon this scan and also the scan of 1997 Dr Burns expressed the opinion that "there is good evidence of asbestosis". A further scan was commissioned by Dr Burns from Dr Branson for the purpose of a report of 8 December 2000. In this report Dr Burns observed that the radiological changes in the plaintiff's lungs were "no different than they had been before" but asserted that "with some development of my knowledge" he no longer believed the plaintiff had asbestosis. It is not contended that the plaintiff does in fact have asbestosis. I record the short history of changing opinion to mark the fact that not only may different doctors form different opinions upon the same objective medical testing but that the same doctor may express different opinions upon identical material at different times.

23. In 1997 Dr Burns did not think that the plaintiff had significant impairment. By 13 September 1999 he formed the opinion that the plaintiff was disabled. He changed his assessment of disability, he said in his report of that date, "because of increasing experience in assessing such cases over those 2 and a half years". (He had then been a thoracic specialist for nearly 30 years).

24. For the purposes of his report of 8 December 2000 Dr Burns examined the plaintiff and commissioned respiratory function tests. He said in that report that the respiratory function test showed no deterioration from those tests of September 1999. He expressed the opinion that the plaintiff's respiratory function deficit and disability was then in the order of 10 to 20 per cent in relation to his asbestos related condition and that the plaintiff's condition would slowly deteriorate.

25. The contradiction between the report of 6 May 1997 (no significant impairment, no likelihood of deterioration) and those of 13 September 1999 and 8 September 2000 (significantly disabled and deteriorating) is striking. In a report of 30 May 2001, prepared after a conference with the plaintiff's legal advisers, Dr Burns sought to explain. He said that his 1999 report was based upon new information not available to him in 1997.

26. In 1997 Dr Burns measured the volume of air exhaled by the plaintiff in one second after a deep breath and recorded a volume of 2.5 litres. Such a measurement is known as FEV(1). This was compared to a predicted volume of 4.32 litres exhaled by a healthy man of his age. This reduction in volume is explained by the presence of obstructive airways disease caused by the plaintiff's smoking. This disease causes the fine airways in the lungs to weaken and collapse upon exhalation, trapping much of the inhaled air deeper within the lung. It is characteristic of this disease that the lung expands over time to accommodate, in addition to the trapped air which is called the residual volume (RV), the necessary extra volume for useful respiration. A rise in the total lung capacity (TLC) results from this process which is the sum of the vital capacity (VC) breathed in and out and the residual volume (RV).

27. In opposition to this disease process expanding the TLC, a restrictive disease such as the plaintiff's pleural thickening prevents expansion of the lung by the development of areas of inflexible fibrosis in the pleura surrounding the lung which limits expansion.

28. If the two diseases operate concurrently the TLC may be artificially preserved, resulting in the measurement of TLC consistent with that predicted for a normal healthy lung. It may be then inferred that if a patient has a reduced FEV(1) confirming obstructive disease and yet has a normal TLC, that a restrictive disease is present preventing the necessary expansion of the lung to accommodate the obstructive disease and compounding the plaintiff's symptoms.

29. Dr Burns explains that only when he had access to plethysmographic lung function tests performed in 1999 (PX 12) which showed a normal total lung capacity (TLC) did he appreciate the extent of the restrictive component of the plaintiff's disease.

30. I find myself unpersuaded by this explanation. In 1997 Dr Burns knew that the plaintiff had both obstructive and restrictive lung diseases. The medical text attached to his report of 30 May 2001 advancing the explanation consists of extracts from an article and an editorial in a leading medical journal, "Chest" published in February 1988 and an extract from a text book, the second edition of "Clinical Tests of Respiratory Function" by G J Gibson published in 1996.

31. Dr Burns freely concedes that in the face of a normal TLC in a patient with both obstructive and restrictive lung diseases an estimate of the proportional contribution to the disability made by each disease is speculative (transcript page 62).

32. I do not think for a moment that Dr Burns sought to mislead me with his evidence. His judgment that the plaintiff was disabled in 1999 when he was not disabled in 1997 proceeds, it seems to me, not from the theory he discusses but rather from the totality of his clinical assessment, including in large measure the patient's presentation. The medical theory later advanced by Dr Burns is an attempt to explain the latter presentation but it does not serve to explain the rapid change from the earlier presentation in a disease which progresses very slowly. That change in presentation was also noted by Dr Deacon on 8 July 1999 who was openly sceptical.

33. Because I am unable to accept the plaintiff as an entirely credible and reliable witness I am not persuaded that his presentation to Dr Burns which presentation caused the doctor to change his mind was entirely genuine. Nor am I persuaded that to the extent there was any increase in breathlessness between 1997 and 1999 it was caused by the plaintiff’s restrictive disease rather than his obstructive disease.

34. In any event, Dr Burns, having accepted that the plaintiff is unfit for heavy and strenuous work does not really think that he is that bad. This exchange in evidence is revealing:

MR SHARPE
Question One of the things he complains of, doctor, is an inability to go beach fishing and if he finds he cannot walk on the sand like he used to, that it creates - he is too breathless to do that, is that consistent with that type of problem.

Answer Well, I have to accept what he says. Currently his level of oxygen to the blood is all right so he may cope with that by forcing himself to do it and getting into training and getting into better condition, but I think his breathlessness is consistent with his disability due to the abnormality but it is up to him to overcome it and to do it.

HIS HONOUR

Question What is the relevance of the oxygenation of the blood.

Answer It means that despite the fact that he is breathless he is not in any great danger of - he is still maintaining normal oxygen in the blood. He is not in any desperate straits.

Transcript page 66, lines 19 to 29.

35. I do not think that upon this evidence the plaintiff was then "too breathless to work" as Dr Burns opined on 19 September 1999. The work was mostly sedentary.

36. Because the opinions of Dr Burns are, in my judgment, premised upon a presentation upon which I could not rely, and a rapid increase in symptoms in the absence of objective changes in the pleural thickening shown on CT scan, I look to other evidence to assess the plaintiff's disability as a result of his pleural disease. I do not believe Dr Kinsella, the plaintiff’s general practitioner, can assist as he does not appear to differentiate between the obstructive and the restrictive components of the plaintiff's disease.

37. The evidence of the plaintiff that he resigned after losing a lot of time with chest infections contrasts with the records of Dr Kinsella, who in a report of 22 March 2000 to the plaintiff's solicitors (PX14) said this.

I first saw Robert as a patient at my present practice in July 1998 when he developed a malignant melanoma of the right lower limb (surgically removed and grafted by Dr Hamish Foster) and non-insulin diabetes (well controlled with diet modification only). Over the next 18 months Robert was seen on multiple occasions for the above conditions as well as hypertension and upper GIT symptoms and various other minor complaints regarding his respiratory symptoms . Robert had had recurrent episodes of lung infections requiring oral antibiotics and bouts of shortness of breath on the following dates. 15 September 1998, 13 May 1999, 20 May 1999, 19 January 2000.

These episodes have in all likeness been as a direct result of his pleural fibrosis and I expect this to worsen as the disease progresses.

38. I am not greatly assisted by the transcript of the evidence of Dr Bryant in the matter of Dixon tendered pursuant to s 25. Each plaintiff must be assessed in relation to medical opinion directed to his circumstance, not that of a hypothetical person suffering from a generic disease process.

CONTRARY MEDICAL OPINION

39. Dr Julian Lee first examined the plaintiff on 6 December 1993. He then formed the opinion that the plaintiff had radiological evidence of benign localised bilateral pleural plaques attributable to asbestos exposure. He emphasised, however, that the pleural plaques of this type were unassociated with impairment of function or of the development of such symptoms as shortness of breath and chest discomfort. Dr Julian Lee noted that the plaintiff remained in full time employment and said that "on present evidence there is no reason to anticipate future limitation of his working ability" (DX1).

40. Dr Lee further examined the plaintiff on 18 December 2000. He then formed the opinion that while there was radiological evidence of bilateral pleural plaques and thickening of insufficient dimension to justify the term "diffuse" there was no evidence of asbestosis. He observed a history of chronic bronchitis with mild airways obstruction attributable to cigarette smoking and concluded:

The plaintiff's complaint of dyspnoea is readily attributable to the combined effects of obesity and airflow limitation rather than to the effects of asbestos exposure. There is no radiological evidence of progression and confirmation of debility is provided by the significantly improved vital capacity measurement.

The plaintiff is considered fit for continuing full time employment.(emphasis added)

41. In a later report of 10 July 2001 Dr Julian Lee pointed out that the plaintiff had a long history of chronic productive cough and airflow limitation associated with variability of vital capacity measurement and that these abnormalities of airways function could not be attributed to asbestos exposure. It was also Dr Lee's opinion that the effect of the plaintiff's obesity was to cause a significant reduction in the expiratory reserve volume (ERV) and the fact that this measurement was reduced to 36 per cent of normal was highly significant. Dr Lee said this:

The plaintiff has a long history of chronic productive cough and chronic airflow limitation (associated with variability of vital capacity measurement) for which maintenance inhaled medication was introduced several years ago. Abnormalities of airways function cannot be attributed to asbestos exposure.

The comment by Dr Burns that deterioration in airways function is arrested on cessation on cigarette smoking is incorrect. At best, the effect of smoking cessation on airways function is variable reduction in the rate of deterioration which might otherwise have occurred. There is a progressive annual reduction in forced expiratory volume (FEV1) for a lifelong non-smoker, commencing from early mid-life, of 25 to 30 mls. The equivalent figure associated with prolonged cigarette smoking (20 or more pack years) is 100 mls or greater.

The question to be addressed is the relevant contribution, if any, of the plaintiff’s asbestos exposure to his overall impairment. As indicated in my report of 18 January, the radiological appearances are primarily limited to circumscribed pleural plaques which would have no significant measurable effect on lung function. The trans pulmonary band shadows are not indicative of asbestosis and, in my opinion, the characteristic radiological appearances of this condition are absent.

The plaintiff’s symptomatology and lung function abnormalities are readily explicable on the basis of chronic airflow limitation and obesity.

42. The plaintiff’s solicitors qualified Dr Peter Gianoutsos to give evidence in this case. He examined the plaintiff on 16 December 1993 and reported as follows:

DIAGNOSIS This man has evidence of benign asbestos related pleural disease in terms of pleural thickening and a calcified pleural plaque along with the rounded atelectasis as described in the body of my report. I believe his asbestos related pleural disease is the result of inhalation of asbestos fibres whilst working during all periods of employment at the State Dockyards, Newcastle. In addition, he has evidence of chronic airflow limitation as a bonus issue of his previous smoking. This man is grossly overweight and also suffers from sleep apnoea which I believe may well be corrected by adopting a policy of losing a significant amount of weight. I do not believe there is any significant contribution from the benign asbestos related pleural disease to any of his symptomatology at the present time in terms of breathlessness on effort. I do believe, however, it is important, in somebody like this man with evidence of what appears to be early rounded atelectasis, he should be followed up at yearly intervals with a CT scan of the thorax. (emphasis added)
This report was admitted without objection and the plaintiff’s counsel has not sought to question Dr Gianoutsos upon the alleged deterioration in the plaintiff’s condition.

43. The plaintiff was in 1993 referred by his GP, Dr Moore, to Dr N Saltos with symptoms including breathlessness related to exertion and some headaches. Dr Saltos on 14 May 1993 reported to Dr Moore in these terms:

Mr Clayden seems to suffer with asbestos related pleural thickening, mild chronic obstructive airways disease, hypertension, and possibly early ischaemic heart disease although I am not certain about the last condition. He is also overweight.

As far as the asbestos related problem is concerned, this is quite benign and I do not think it is contributing to his symptoms. There is a risk which cannot be quantified accurately of Mr Clayden developing in the future more serious problems such as mesothelioma. I did not inform him of this.

In terms of medication I suggested that he tries to lose weight, that he continues with his blood pressure therapy, and that he has Bricanyl on a p.r.n. basis and Pulmicort 2 puffs b.d. Although I have not arranged to see him again, I shall be only too happy to do so if it becomes necessary. (emphasis added)

Again this report was tendered by the defendant without objection and without cross-examination

44. Dr M J Deacon has had the advantage of seeing the applicant several times during the period 1993 to 1999 as his treating physician. In a report of 1 March 1993 to the secretary of the Dust Diseases Board Dr Deacon stated that the plaintiff's breathlessness was caused by a combination of obstructive airways disease, obesity and psychological factors with the possibility of some contribution by the pleural fibrosis.

45. In a report of 4 June 1993 to the plaintiff's solicitors Dr Deacon said this.

Mr Clayden's symptoms of tightness in the chest, breathlessness (which is variable) productive cough of some clear mucus, is due primarily to a combination of chronic airflow limitation from cigarette smoking and obesity. He does have quite extensive pleural fibrosis and it is quite likely that this is a contributing factor to his breathlessness. He is not really disabled , able to hold down a normal job and has remarried and runs his home.

The extent to which Mr Clayden's asbestos associated pleural fibrosis is contributing to his symptoms is not clear. I think it is quite likely that there is an association because of the widespread nature of the pleural thickening seen on CT scan. However, in general pleural plaques do not cause disability in themselves. (emphasis added)

46. In 1996 the plaintiff was again examined by Dr Deacon. He complained of breathlessness, some morning cough with some light brown sputum and chest tightness if he tried to carry objects for any distance. He was playing bowls, mowing his grass and working.

47. Upon a further examination by Dr Deacon of 8 September 1999 the plaintiff complained of a recent exacerbation of his airways disease with increased cough, nocturnal wheeze and breathlessness during the day. He had had a course of antibiotics and increased asthma treatment.

48. In a report of 10 March 2000 to the plaintiff's solicitors Dr Deacon said:

Mr Clayton has the following problems: chronic obstructive pulmonary disease. He smoked for 23 years before stopping 11 years ago. The severity of his airflow obstruction from smoking associated small airways disease, has not changed over the last 5 years, according to his pulmonary function tests. His CT scan shows no evidence of any associated emphysema.

Pleural plaques. He has extensive pleural thickening through both hemithoraces consistent with his history of asbestos exposure. I could see no change in these on CT scans between 1997 and 1999.

Intrapulmonary fibrous bands. He has a number of intrapulmonary bands in both lungs which do not appear to have changed between 1997 and 1999. There are no changes of classical asbestosis, i.e. honeycombing, ground glass opacification with loss of the outlines of bronchovascular bundles.

Obesity. His body mass index has not changed over the years and he currently his weight has not been affected by the dietary advice obtained when he developed diabetes 18 months ago.

Diabetes, hypertension, hypertensive heart disease, fatty infiltration of liver. These are not causing any current symptoms but will be major factors in his longevity. He was not aware of his cholesterol levels and is not on any treatment for dyslipidaemia. I do not know the degree of his diabetes and his hypertension is inadequately controlled on the readings I have.

Obstructive sleep apnoea. This is controlled with CPAP and the melanoma of his right ankle is not affecting his health with no sign of any spread from this problem.

Mr Clayden is breathless from a combination of factors. These include airflow obstruction, obesity and pulmonary fibrosis. His airflow obstruction is moderately severe with his FEV(1) being moderately reduced at 51 per cent of predicted with no sign of any asthmatic component and he is non-atopic (negative skin test). CT scan does not show emphysema. He is obese with a body mass index of 32.2 (normal 20-2, overweight 26-30, obese 31-35, severe obesity 36-40, morbid obesity >40). When I saw him he was not getting any regular exercise. He has pleural disease which is not likely in itself to be causing much in the way of symptoms. His total lung capacity is a little reduced which could well be secondary to the pleural disease. He has intrapulmonary fibrous bands. These are secondary to his exposure to asbestos but whether this should be called asbestosis in the absence of classical interstitial disease is a matter of definition. There is mild reduction in diffusing capacity which is still low when corrected for alveolar volume on his lung function tests and this reduction can be attributed to the interpulmonary changes i.e. due to his asbestos exposure.

I can find no evidence of any change in his problems between 1995 and 1999. The apparent increase in historical severity of his breathlessness would require independent confirmation and may be being contributed to by his inactivity following stopping work. (emphasis added)

49. I prefer the opinion of Dr Deacon to Dr Lee as to the extent of the plaintiff's pleural thickening. This is because of evidence by Dr Burns that a normal measure of gas diffusion through the alveoli of the plaintiff's lung termed DLCO/VA is, in the presence of his abnormal DLCO, consistent with pleural thickening. The DLCO/VA measure was 96 per cent on 12 May 1995 (PX8), 91 per cent on 10 August 1999 (PX17) 84 per cent on 10 September 1999 (PX12) and 99 per cent on 4 December 1999. I do not believe this pattern establishes probable deterioration.

50. The asbestos related pleural disease which affects the plaintiff has caused fibrotic changes in the pleura which encases his lung. These changes have inhibited in some measure the ability of his lung to expand and contract. The changes are readily discernible on a CT scan and it is the unanimous medical opinion in this case that the extent of those changes has not been seen to increase on scans taken between 1997 and 1999 despite the applicant's complaints of increased breathlessness.

51. The plaintiff also suffers from obstructive airways disease caused by years of smoking. I believe that this disease has progressed in recent years.

52. On 15 February 1993 Dr G B Field, an eminent respiratory physician, said of lung function testing of the plaintiff that day that:

There is moderate airflow limitation probably associated with premature closing of airways at low lung volumes. Post bronchodilator spirometry might be useful.
On 3 May 1994 and 17 June 1996 lung function tests were repeated and on each occasion the reviewing physician expressed an opinion that there had been no significant changes since the previous study.

53. On 10 August 1999 Professor David McKenzie reviewed the lung function testing of that day and wrote:

There is moderately severe airflow obstruction. Gas exchange is normal. Compared with previous studies there has been a decline in airway functioning. The subject does not appear to be on treatment for airway narrowing. (emphasis added)
On this evidence it does seem probable that the plaintiff's subjective deterioration, such as it is and allowing for exaggeration, has been caused by a worsening of his obstructive airways disease rather than from any deterioration in his restrictive disease.

54. In my opinion the plaintiff’s damages are to be assessed on the acceptance of the opinion of Dr Deacon who treated him over the years from 1993 to 1999. Dr Deacon believes that the plaintiff has pleural disease which is not likely in itself to be causing much in the way of symptoms. Such affliction would not in the ordinary course of events call for any significant award of general damages. The plaintiff's case is, however, exceptional. He has not been favoured with a fortunate life.

55. The plaintiff was born on 11 January 1950 and in 1969 married at the age of 19. He had three children of this marriage. The youngest son, Craig, was born in 1977 with cerebral palsy and died in 1985 at the age of seven. The plaintiff had resigned from the workforce in 1977 to care for his wife, Robin, who was by then very ill with renal failure. She died in 1985. The plaintiff then found work with a company later taken over by Goninan. He remained in that employment until 1999. He married his present wife, Ellen, on 3 March 1990. Happily she is devoted to him.

56. In 1998 the plaintiff was diagnosed with malignant melanoma on his right ankle. In July of that year the melanoma was excised and a skin graft applied. Complications ensued. I have no doubt that the possibility of fatal recurrence plays upon his mind. Before this fear, however, came his fear of dying from an asbestos related disease. Several former workmates of the plaintiff have died from this cause. The plaintiff says, and on this I do accept him, that he is “terrified of being out of breath. I am frightened that I will simply stop breathing when I feel like that" and that "terrible thoughts [race] through my head about whether or not I am dying." He is frightened that he is going to get worse.

57. The plaintiff has been assessed by Dr Leonard Lambeth, a psychiatrist, whose report of 18 July 2001 is before me. Dr Lambeth wrote:

I have no doubt that this man suffers from depression. He is chronically dysphoric and depressed and this would be of moderate intensity. However, for approximately one week in every three he becomes much more severely depressed.

I think the best diagnosis is one of depression - not otherwise specified, according to the diagnostic and statistical manual of mental disorders 4th edition of the American Psychiatric Association.

In my opinion it is more probable than not that his depression is secondary to the asbestos related lung disease...

As far as treatment is concerned I believe that his depression itself requires treatment.

Dr Lambeth went on to say that the plaintiff would need regular psychiatric consultation.

58. The plaintiff's depression was almost certainly present when he decided to stop work. However, it was not advanced to anyone then, nor before me now, as a cause of his decision to stop work. The plaintiff's evidence in relation to the reasons he stopped work is so tainted by contradiction that I doubt I could be persuaded that the depression was a cause in any event.

59. I am, however, persuaded that one effect of the plaintiff's depression is to compound those breathing problems caused by his non compensable obstructive aiways disease.

60. In a diary kept by the plaintiff's wife admitted into evidence (PX24) she has written:

Rob just doesn't seem to be able to cope with stress. He gets really worked up and starts gasping when he starts to get uptight.

61. I do not think that the plaintiff actually gets short of breath when stressed, although both he and his wife believe that he does. The plaintiff in cross-examination at one time stated that he was stressed and asked for a short adjournment. I did not observe him then to be gasping. During two long days in court the plaintiff at no time appeared to be breathless or gasping for air. His problem is one of perception.

62. I also accept the medical opinion that as a result of his asbestos related pleural disease the patient is more prone to suffer chest infections. Dr Kinsella, the treating general practitioner between July 1998 and January 2000 records three episodes of chest infections. Dr Deacon treated him for a chest infection in September 1999 and in March 2001 he was hospitalised for 3 days with pneumonia. I also accept that the asbestos related pleural disease adds in some measure to the breathlessness caused by the plaintiff’s obstructive airways disease and that the compensable disease will slowly worsen. That said, the real blight upon this man's life caused by the defendant's negligence is the pervasive and intractable depression which disturbs the quality of his existence. He is acutely aware of the increased risk of his contracting mesothelioma or lung cancer.

63. I assess general damages in the sum of $80,000. I allow interest on $40,000 at 2 percent for 8 years, a sum of $6,400.

ECONOMIC LOSS

64. I do not accept that the plaintiff has suffered any loss of wages to date as a result of his ARPD. I believe that he is breathless on exertion and unfit for heavy or strenuous work and that that incapacity is in small measure the result of contribution from his ARPD. I am not however persuaded that that breathlessness has to date been productive of economic loss. The plaintiff chose to resign from work that was within his capacity. He was later offered supervisory work within his capacity by Goninans which would have occupied him for 15 weeks during a particular project. He declined.

65. The plaintiff is now 50 years old and it is possible that at some future time he may decide to re-enter the work force. If he should do so the additional component of his breathlessness caused by his ARPD may limit his options. Further occasional chest infections may incapacitate him for several days at a time.

66. Against the possibility of these events (Malec v Hutton) and noting that the plaintiff is in receipt of a Dust Diseases pension, I allow $25,000 as a cushion.

GRIFFITHS v KERKEMEYER

67. Because of the adverse view that I have taken as to the plaintiff’s reliability; the medical opinions of Dr Lee and Dr Deacon which I accept; and the opinion of Dr Burns that the oxygenation of the plaintiff’s blood is not incompatible with his following such leisure pursuits as beach fishing, I reject the plaintiff’s claim for past services. Because his disease may deteriorate I allow the sum of $10,000 for future services.

68. There is to be judgment for the plaintiff in the sum of $121,400.

Mr J Sharpe instructed by Turner Freeman appeared for the plaintiff

Mr G Little, SC instructed by Hunt and Hunt appeared for the defendant