Norrie Williams v Dust Diseases Board

[2006] NSWDC 38

CITATION:	Norrie Williams v Dust Diseases Board [2006] NSWDC 38
HEARING DATE(S):	11/09/2006 - 12/09/2006
EX TEMPORE JUDGMENT DATE:	10/12/2006
JURISDICTION:	Civil (Residual Jurisdiction)
JUDGMENT OF:	Neilson DCJ at 1
DECISION:	Appeal Dismissed; Exhibits to remain in file
CATCHWORDS:	Worker's Compensation (Dust Diseases) Act 1942 - Appeal under s 8I - Whether plaintiff has asbestosis or asbestosis related pleural disease - Indicia of disease diagnosis considered - Whether plaintiff discharges onus of proof
LEGISLATION CITED:	Worker's Compensation (Dust Diseases) Act 1942
PARTIES:	Norrie Williams (Plaintiff / Appellant) Dust Diseases Board (Defendant)
FILE NUMBER(S):	RJ607/04
COUNSEL:	Mr C Heazlewood (Plaintiff / Appellant) Mr J Sheller (Defendant)

JUDGMENT

1 HIS HONOUR: This is an appeal pursuant to s 8I of the Worker’s Compensation (Dust Diseases) Act 1942 from a decision of the Worker’s Compensation (Dust Diseases) Board made on 8 July 2004. On that date the medical authority established under the Act, certified that the plaintiff had not contracted a dust disease within the meaning of the Act. On this appeal the plaintiff seeks to establish that he is suffering from either asbestosis or an asbestosis related pleural disease. Both those conditions are contained in Schedule 1 of the Act.

2 There is no dispute that the plaintiff was exposed to asbestos. It is common ground that the plaintiff has pleural plaques which confirm the plaintiff’s exposure to asbestos. Perhaps the most graphic description of the plaintiff’s exposure to asbestos is contained in the history given by the plaintiff to Dr Anthony Johnson, who examined the plaintiff at his home at Yamba on 4 August 2005. The plaintiff told Dr Johnson that he had been employed over a number of years as a labourer at the Baryulgil Asbestos Mine. Dr Johnson’s history continues thus:

“He did various jobs during his time at the asbestos mine. He initially worked in a quarry, breaking up the rock for two years with a sledgehammer. He helped the crusher and also helped to fill bins with crushed rock. Later he helped store the asbestos fibre in storage bins and then helped bag the fibre. He did recall to me that some of the bags that they used to put the asbestos in had some blue fibre in them. They would shake them out before putting the asbestos from Baryulgil into it.

He also worked in the mill that was beside the quarry. He would feed material with a shovel into the crusher. The end product was then bagged. The product would come down a chute into Hessian bags and it was very dusty. A new mill was built while he was there. The asbestos product would come down in chutes into bags which he would then sew up and place a new bag under the chute. The bags were then put onto a conveyer. He recalls he spent at least three years doing this bagging. He also involved in cleaning up the mill and working on the crusher. He does not recall doing jack hammering or drilling. He cleaned out bins that had contained asbestos material. He stopped working in 1978 and has not worked since. During his time at Baryulgil, he estimates he had daily asbestos exposure.

He lived in Baryulgil Square and built a fibro home himself. The fibro material was supplied by the mine. Originally he lived in a tin hut with bags as doors until he built the fibro home. The table they used was a sheet of fibro. Truckloads of waste from the mill were dumped onto the square to be used as covering for the ground. He also used the bags that the asbestos had come in for blankets.”

3 The plaintiff’s evidence before me largely confirms each part of that history. Mrs Williams also gave evidence which corroborates the plaintiff’s exposure to asbestos and corroborates what the plaintiff had to say about his living conditions. Indeed, it would be fair to say from the evidence of Mr and Mrs Williams, that they were forced to live in what we would nowadays regard as third world conditions.

4 I have no hesitation in accepting the evidence of Mr and Mrs Williams. They did their best to tell me the truth, however, it is clear that with the passage of time, memory fades. There is a dispute about the number of years during which the plaintiff worked at Baryulgil. Mr Williams was cross-examined to suggest that he had informed someone from the Dust Diseases Board, that he had worked at the Baryulgil Asbestos Mine for 10 years only between approximately 1967 and 1977. The plaintiff was adamant in his evidence-in-chief, and in cross-examination, that he had worked at Baryulgil for 23 years.

5 The first specialist to see the plaintiff, who has provided a report, was Dr Peter Gianoutsos, who first examined the plaintiff on 5 February 2002. The plaintiff told Dr Gianoutsos that he worked at Baryulgil between 1956 and 1979, that is a period of 23 years. Dr Gianoutsos goes on to point out that the plaintiff was a little uncertain about the dates but the plaintiff knew that he had worked at the mine for 17 years.

6 Mr and Mrs Williams were blessed with 11 children. Unfortunately four of those children died in infancy. From the timing provided by Mrs Williams, it is clear that the couple were living in Baryulgil at least in 1961, at the time of the birth of their second child. I accept that the plaintiff was employed at the mine for at least 17 years, as he initially told Dr Gianoutsos. However again, whether it was 10 years, 17 years or 23 years, little hangs on that fact, because it is undoubted because of the presence of pleural plaques, that the plaintiff was actively exposed to asbestos dust and fibre.

7 The question for my determination is whether the plaintiff has asbestosis or an asbestos related pleural disease. The existence of that condition is propounded by Dr Gianoutsos. Dr Gianoutsos has seen the plaintiff, not for the purposes of treatment, but for medico legal purposes. He first saw the plaintiff on 5 February 2002 at the Grafton Aboriginal Medical Centre, at the request of the plaintiff’s solicitors Messrs Carroll & O’Dea. The plaintiff had first made an application to the Dust Diseases Board on 7 February 2001. On 13 July 2001, the medical authority constituted under the Act determined that the plaintiff had not contracted a dust disease within the meaning of the Act. The medical authority was comprised at the time by Dr Bryant, Dr Gardiner and by a person whose signature is either that of Dr Julian Lee or of some other thoracic physician. The plaintiff did not appeal from that decision, but clearly consulted solicitors who referred him on to Dr Gianoutsos. At the time of giving its certificate of 13 July 2001, the Board arranged to recall the plaintiff for further examination in May 2004 because of the presence of pleural plaques. That recall led to the certificate of 8 July 2004, which is the subject of this appeal.

8 In his report of 8 December 2005, Dr Gianoutsos conveniently sets out the criteria for the diagnosis of pulmonary asbestosis. He lists the criteria thus:

1.Sub-pleural curvilinear lines.
2.Thickened interlobular septae.
3.Honeycombing effect.
4.Graph ground glass appearance.
5.Long thoraco-mediastinal strands of thickened tissue.

9 It is common ground that neither the fourth or the fifth of those criteria is present. It is common ground that the first and second criteria are present. In contest is whether the third criterion, the honeycombing effect, is present in the current matter. The thrust of the defendant’s case is that the first two criteria are non-specific for asbestosis and do not of themselves permit a diagnosis of asbestosis or of an asbestosis related pleural disease.

10 I shall now consider the question of whether there is a honeycombing effect. According to Dr Gianoutsos a honeycombing effect can be seen in image 17 of a CT scan performed by Dr Fran Newman on 30 January 2002 and reported by Dr Newman on 31 January 2002. Dr Newman’s report is before me. It is exhibit E. The actual CT scan, in particular image 17, has not been put before me and therefore Dr Gianoutsos has not been able to point it out to me in the evidence, where the honeycombing effect is and secondly Dr Anthony Johnson, who gave oral evidence on behalf of the defendant, was not able to have it pointed out to him during the course of cross-examination.

11 Dr Newman herself, for whom Dr Gianoutsos expressed a high professional esteem, does not in her report, state that there is some honeycombing effect present on the radiological appearances. The report is this:

“High resolution scans were performed to assess early changes of asbestosis. 1.5 mm sections were obtained at 10 mm intervals with the patient lying prone. Mediastinal images were also acquired to assess the presence and extent of calcific pleural changes.

Densely calcified pleural plaques on the hemidiaphragms bilaterally have been clearly seen on plain x-rays and are again demonstrated on this examination. There are anterior calcified pleural plaques on the left upper zone and the left posterior sulcus. At both bases the lateral pleura is thickened, but not accompanied by specific nodularity or calcification of plaques. No pleural tumours were identified.

A moderate degree of cardiac enlargement is present and some basal anterior increase in density developed during the examination.

In both lower lobes, extending from the apical segments to the bases there are lines of small peripheral nodules, with vertical extensions to the pleura, the characteristic early findings of pulmonary asbestosis. There were no other intrapulmonary masses seen.”

12 It is noteworthy that Dr Newman refers to the bases of the lateral pleura not being accompanied by any specific nodularity. In Gianoutsos’s report of 5 February 2002, the doctor comments upon this CT scan. He says this of it:

“A CT scan showed evidence of pleural and diaphragmatic calcified plaques, extensive pleural thickening on both sides, most of which was not calcified. In addition there were changes at the lung bases, in particular where there was evidence of thickened inter-lobular septae, curvy linear lines as well as honeycombing of a mild degree at the bases. These changes as described are consistent with a mild degree of pulmonary asbestosis.”

13 The certificate of the Board which is the subject of this appeal was signed by three eminent and well-respected thoracic physicians, Dr Peter Corte, Dr John Mann and Dr Michael Burns. I can describe those gentlemen in that fashion because that is the way that Dr Gianoutsos himself described these gentlemen. The formal certificate of the medical authority commences with a recitation of the authority’s having considered the results of clinical and radiographic examinations of the plaintiff. While that may be formulaic it appears to me to be quite inconceivable that the medical authority and the Board generally would not have arranged for the CT scan of 30 January 2002 to be before it but of course not much weight can be placed upon the decisions of those three eminent practitioners when no attempt has been made to put before me what was actually before them.

14 The next medical practitioner to comment upon the CT scan of 30 January 2002 was Dr Julian Lee, again an eminent thoracic physician who has a lengthy experience in the relevant field. Dr Lee does not specifically comment on the CT scan of 30 January 2001. However, on the first page of the doctor’s report, which lists the material that the doctor relied upon, the tenth item listed is “chest CT scan dated 31 January 2001”. It is clear from the opening sentence that the doctor had available to him both radiographs and CT scans and clearly at times in his list of “documents’ the doctor refers sometimes to radiographs and CT scans and at other times to radiological reports. The inference to be drawn is that Dr Lee did have the CT scan of 30 January 2002. There is no suggestion that the plaintiff had a CT scan on 31 January 2001, so that the doctor’s reference to a report of 31 January 2001 is obviously reference to that of 30 January 2002. In any event, Dr Lee did not find any honeycomb effect.

15 Dr Johnson confirmed in his evidence to me that he did see the CT scan of 30 January 2002 and that he did not see on it any area of honeycomb cysts. Dr Johnson accepted that the most appropriate way to resolve the issues concerning the plaintiff would be to have the CT scans reviewed by an expert radiologist such as Dr Michael Jones. This suggestion was first made by Professor Breslin, whose report was not tendered and who was not called to give evidence. Indeed I had been told that Dr Breslin was to be called in the plaintiff’s case but at the commencement of the hearing learned counsel for the plaintiff advised me that he would not be relying on Dr Breslin’s opinion. The radiological reports were in fact sent to Dr Michael Jones, a specialist radiologist, who was clearly highly regarded, both by Professor Breslin, Dr Johnson and Dr Gianoutsos. Dr Jones reviewed all the radiology and said that there was no honeycomb cyst and therefore the radiological appearances were, “indeterminate”.

16 When Dr Gianoutsos gave evidence he maintained his position that there was a honeycombing effect but did not put it as highly as he had put it in his initial report of 5 February 2002. In that report the doctor said there was “honeycombing of a mild degree” at the bases of the lungs. In evidence Dr Gianoutsos told me that there was a small area of honeycombing which was subtle and not widespread. Here there is a contest about the proper interpretation of a radiological report in particular and radiological reports generally. Dr Lee and Dr Johnson on the one hand, say that they do not show any honeycomb cysts. Dr Gianoutsos on the other, says that there is a small subtle area of honeycomb cysts. Each of those three gentlemen is offering an opinion about what the radiological plates show. The radiological plates have not been put before me, which is a great hindrance to me. However, the appropriate way of resolving this is the way suggested by both Professor Breslin and by Dr Johnson, that is to refer them to a specialist radiologist, who can comment. That was done and the result is that given by Dr Michael Jones that there is no honeycomb cyst. On that basis alone I could not be satisfied on the balance of probabilities that there is any honeycomb cyst.

17 However, there are other matters to be borne in mind. In Dr Gianoutsos’s report of 8 December 2005, Dr Gianoutsos sought to explain away the opinion of Dr Johnson. He said this:

“Dr Johnson referred to the CT scan of the chest of 4 November 2002 but was not privileged to viewing the CT scan of the chest of 30 January 2002, which provided prone views. This is of material importance in assessing these two CT scans of the chest. Dr Johnson also queries a date of the CT scan of 30 January 2002. The scan was performed on 30 January 2002 at the Clarence Valley Imaging Facility and reported on by Dr Fran Newman, radiologist.”

18 Dr Johnson in fact did receive the CT scan of 30 January 2002 and did see it and did not find any honeycomb cyst. Dr Gianoutsos admitted in his evidence that he was in error about his view of Dr Johnson, but it is clear that Dr Gianoutsos attempted to explain away the inconsistent opinion of Dr Johnson by reason of a misapprehension or perhaps by way of a “misrepresentation” as was suggested by learned counsel for the defendant.

19 Clearly, in the same report, Dr Gianoutsos also misrepresented the opinion of Dr Michael Jones. In the report he says this:

“In his overall opinion as outlined on page 2 of that report under item 3, he comments, again: ‘The distribution suggests this might be early unusual interstitial pneumonia (asbestosis).’”

He goes on to say that the absence of honeycomb cysts make the appearance indeterminate.

“I believe it fair to say that there is no evidence of generalised honeycomb cysts, only a relatively small area of honeycomb cysts as I outlined in my review of the prone CT films of the chest of 30 January 2002. The absence of widespread honeycomb cysts does not exclude the diagnosis of early pulmonary asbestosis.”

20 There Dr Gianoutsos refers to “absence of widespread honeycomb cysts” but the issue is not the absence of widespread honeycomb cysts, it is the absence of any honeycomb cyst that is important. Read as a whole I accede to the submission put to me by learned counsel for the defendant, that there was an attempt by Dr Gianoutsos to misrepresent what Dr Jones had been saying.

21 However there are a number of other criticisms that can be levelled at the opinion of Dr Gianoutsos. The first concerns what Dr Gianoutsos has described as “extensive pleural thickening on both sides”. Dr Gianoutsos’s opinion is that there is such thickening and it is a consequence of exposure to asbestos.

22 Dr Julian Lee believes that there was not pleural thickening, but rather extensive bilateral extra-pleural fat deposits. In his report of 7 June 2005, Dr Lee expressed this opinion.

“The radio-density of extra-pleural fat deposits is similar to the sub-cutaneous tissues and permits differentiation from more radio-dense diffuse pleural thickening.”

23 Dr Lee has explained why it is that he can distinguish between pleural thickening and extra-pleural fat deposits. Dr Johnson, in his report of 24 August 2005, said this on this issue:

”There is pleural thickening, which on my view of the films, is of the same density as the sub-cutaneous fat, so it is likely to be extra pleural fat.”

24 This was again a question addressed by Dr Michael Jones. He said this, of the first CT scan:

“A prone high-resolution CT scan on 30 January 2002 re-demonstrates thick, densely calcified typical asbestos pleural plaques over both sides of the diaphragm, and shows that the pleural shadowing in both mid and lower zones laterally is due to extra pleural fat, and not due to pleural plaques or diffuse pleural thickening”.

25 Of the CT scan of 4 November 2002, Dr Jones said this:

“The extra pleural fat is redemonstrated in the lateral lower zones:-"

26 The second point made by Dr Jones in his opinion is this:

“Mr Williams has one area of circumscribed pleural thickening in the posterior left mid-zone, but no evidence of diffuse pleural thickening. Pleural density seen on the chest x-rays are shown by CT to be extra pleural fat and therefore unrelated.”

27 Again, on the question of interpreting the x-rays I believe I am best guided by the expert radiologist. I therefore cannot accede to the position adopted by Dr Gianoutsos that the plaintiff was suffering from pleural thickening. I accept that there is some extra pleural fat deposits which Dr Gianoutsos has misread as being pleural thickening.

28 Another area which I found the evidence of Dr Gianoutsos to be unsatisfactory was that concerning the use of the “race correction factor”, which is applied in pulmonary function tests. Mr Williams is an Aborigine. Dr Johnson made the point in his evidence that there are different race correction factors for a number of races where the clear exception to the general rule is the Caucasian race and most other races having a lesser pulmonary capacity. The race correction factor applied in the case of Mr Williams is 85 per cent of that expected of Caucasians. In order to establish the extent of the incapacity that the plaintiff has, due to his asbestos related condition, Dr Gianoutsos argued that the race correction factor should not be applied. He told me that it was inappropriate to apply it because of the plaintiff’s height and weight, making him very similar to a Caucasian. When measured by Caucasian standards, the plaintiff’s lung function tests show a significant abnormality. However, if the race correction factor is applied, there is little, if any, abnormality.

29 In his evidence Dr Johnson explained how the race correction factor is arrived at. He explained that for every human being there are statistics available to estimate what a normal lung function test should be. For every human being they are based on four factors: height, weight, sex and race. In other words, there are expected outcomes for a man of the plaintiff’s height and weight, as well for a man of the plaintiff’s race. The reason for discounting the fact that Mr Williams is an Aborigine, is without any validity when one looks at the relevant criteria. It appeared to me that Dr Gianoutsos has decided to not apply the race correction factor in order to boost the extent of the plaintiff’s alleged incapacity, due to the alleged asbestos condition. In other words it appeared to me to be explicable by Dr Gianoutsos’s advocacy on behalf of the plaintiff, rather than by his role as an expert witness.

30 There is indeed a further problem with the evidence of Dr Gianoutsos. Dr Gianoutsos had lung function tests performed in his rooms on 3 March 2006 and sent the plaintiff along to have the same tests conducted at Royal Prince Alfred Hospital Clinic on 2 March 2006. The evidence of Dr Gianoutsos was that after he had tested the plaintiff he sent the plaintiff off to the clinic to have the same tests redone. I think that there may be a misstatement of dates in the reports. Nothing turns on that. However there is a discrepancy between the testing carried out by Dr Gianoutsos and that conducted by the Clinic. Of that discrepancy, Dr Gianoutsos says this:

“The discrepancy between the results I obtained on simple pulmonary function testing in my rooms and that obtained in the Department of Respiratory Medicine Laboratory at the Royal Prince Alfred Hospital, relates to the race correction factor of 85 per cent being applied, giving what I believe to be a falsely high value for the FEV 1 and the FVC. This man is not of small stature and he is about average height, and his weight of 90 kilograms gives him a BMI putting him in the obese category. I therefore do not believe the race correction factor should be applied to this man.”

31 I set out that not because of its reference to the race correction factor, but because of this. When one looks at the discrepancies between the testing of Dr Gianoutsos and the testing at Royal Prince Alfred Hospital Clinic, the discrepancy is not explicable solely by the race correction factor. The mathematics do not work out. Dr Gianoutsos accepted that in cross-examination and said that there may have been some lessened effort on the part of the plaintiff when he was tested in the doctor’s rooms. However, it could also be explicable by some other factor. In any event, the important thing to note is that the alleged reason for the discrepancy, according to Dr Gianoutsos is not the real reason for the discrepancy. There is some other reason as well.

32 Another matter relied upon by Dr Gianoutsos is his finding at each of his examinations, of a crackle within the lung. However, in cross-examination Dr Gianoutsos conceded that that was a symptom of dyspnoea. There is no dispute that the plaintiff has dyspnoea. The question is to what is it due? And, in particular, is it due to asbestosis or an asbestosis related pleural disease? In evidence Dr Gianoutsos maintained that one should look at the plaintiff’s case in globo, to look at the whole picture and to take into account the plaintiff’s undoubted exposure to asbestos. I do that, but I also must take into account other evidence, which appears to have been largely ignored or downplayed to some extent, by Dr Gianoutsos. One of the practitioners who was supposed to examine the plaintiff was Dr Michael O’Rourke, Professor of Medicine at the University of New South Wales, a specialist cardiologist at St Vincent’s Clinic here in Sydney. The plaintiff was supposed to see Dr O’Rourke on 19 April 2005 but did not attend. However, Dr O’Rourke did prepare a report based on the medical material that was put before him. In that report the doctor says this:

“I note that there is some lack of agreement amongst respiratory consultants as to the contribution of intrinsic pulmonary pleural disease to Mr Williams’ symptoms and clinical state. There is no disagreement that there is accompanying cardiac disease of sufficient severity as to be causing a major contribution to Mr Williams’ symptoms. These views are set out in some detail in the letters by Dr Breslin and Dr Lee. Mr Williams has suffered from myocardial infarction and has marked cardiomegaly on chest x-ray with symptoms consistent with congestive cardiac failure. He has been treated for congestive cardiac failure, complicated by atrial fibrillation. He is not receiving any Warfarin in the presence of atrial fibrillation to limit likelihood of peripheral (including cerebral) embolism. He is being treated for hypertension and has longstanding diabetes melitis treated with diet and Diaformin. He has symptoms suggestive of obstructive sleep apnoea. He is markedly limited by exertional dyspnoea. There is some suspicion of hepatic impairment. Lung scans show evidence of pulmonary congestion attributable to cardiac disease.”

33 Further in his report, Dr O’Rourke expressed the view that it was his belief that dyspnoea was principally due to cardiac disease on the material provided to him.

34 On the question of prognosis, the doctor offered a very poor prognosis because of the plaintiff’s cardiac condition. A similar prognosis is offered by Dr Gianoutsos in that he accepted the plaintiff’s longevity would be determined by his cardiac condition rather than his pulmonary condition.

35 Further in his report, Dr O’Rourke said that he considered that it was accepted that the plaintiff was disabled as a consequence of dyspnoea, but that the dyspnoea was attributable to the plaintiff’s cardiac disease. It would appear to me that Dr Julian Lee was expressing much the same condition. For example he said this and this also makes the point that the first two criteria of the five accepted by Dr Gianoutsos as relevant to the diagnosis of asbestosis are not specific for the condition:

“Pulmonary venous congestion, rather than asbestosis, is the likely explanation for the minor areas of sub-pleural septal thickening in an individual with radiological evidence of gross cardiomegaly and receiving treatment for heart failure.”

36 Dr Johnson, who saw the plaintiff on 4 August 2005, obtained from the plaintiff a history that he was diagnosed with heart disease in approximately 1985 and that put the plaintiff onto sickness benefits and ultimately the disability pension. In other words the plaintiff’s incapacity as far as the Department of Social Security was concerned, arose because of his cardiac condition.

37 A fair reading of Dr Johnson’s report indicates that as far as he was concerned, the plaintiff is not disabled or incapacitated by reason of an asbestos related pulmonary condition but he does accept the plaintiff has a disablement due to the cardiac condition.

38 My reading of the medical evidence establishes that the first two criteria of the five criteria specified by Dr Gianoutsos could be explicable solely by the plaintiff’s cardiac condition. His symptoms could be mediated solely by the cardiac condition. In those circumstances one must have some direct evidence of asbestosis in order to accept that that is the cause or even a cause of the plaintiff’s pulmonary condition. At the current time it is possible that the plaintiff does have asbestosis or an asbestos related pleural disease. However, that cannot be determined at this stage. If further radiological investigations do reveal honeycombing, then it must be accepted that the plaintiff does have an asbestos related pleural disease or asbestosis. Equally, from my understanding of the evidence, if it is established in the future that the plaintiff has either the honeycombing effect or the ground glass appearance or the long thoraco-medisternal strands of thickened tissue, then he does have an asbestos related pulmonary condition. However none of those things are in evidence at the current time on the balance of the evidence before me.

39 I am not satisfied on the balance of probabilities that the plaintiff is suffering from either asbestosis or asbestos related pleural disease. As I understand it, those conditions cause subtle changes which may and usually do progress with the passage of time. It is four and a half years since the plaintiff had the CT scan of 30 January 2002 and it would be quite prudent that the plaintiff be again examined by that procedure before he is recalled before the Board in July 2007, in ten months time. That may show some honeycombing effect. If so there would be grounds for holding that the plaintiff had asbestosis or an asbestos related pleural disease. However, at the current time I cannot be persuaded that the plaintiff has discharged the onus of proof which is upon him, of establishing on the balance of probabilities that he does suffer from a specified dust disease.

40 For those reasons the appeal is dismissed.

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