Seltsam Pty Ltd v Mcguiness; James Hardie & Coy Pty Ltd v Mcguiness

[2000] NSWCA 29

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(Decision by: Stein JA)

Seltsam Pty Ltd
vMcguiness; James Hardie v Coy Pty Ltd v Mcguiness

Court:

Judges: Spigelman CJ

Stein JADavies AJA

Subject References:
NEGLIGENCE
proof of negligence
causation
whether exposure to asbestos caused renal cell carcinoma
use of epidemiological studies EVIDENCE
opinion evidence
expert opinion
Evi-dence Act 1995 (NSW) s79 DUST DISEASES
Appellate Jurisdiction of Supreme Court
Dust Diseases Tribunal Act 1989 s32

Legislative References:
Compensation Court Act 1984 - The Act
Courts Legislation Amendment Act 1998 - The Act
Dust Diseases Tribunal Act 1989 - The Act
Evidence Act 1995 - The Act
Interpretation Act 1987 - The Act

Case References:
-

Hearing date: 2 and 3 August 1999
Judgment date: 7 March 2000

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Decision by:
Stein JA

Introduction

[187] These are two appeals from a decision given by Judge Maguire in the Dust Diseases Tribunal on 13 July 1997. His Honour adjudged the plaintiff, Robert George McGuiness, entitled to a verdict against the appellants (Seltsam and James Hardie) in the sum of $159,959.

[188] Subsequent to delivery of the judgment the plaintiff died and the proceedings have continued in the name of his widow, Yvonne McGuiness, as the legal personal representative of his estate.

[189] The principal issue in contention before the Tribunal was causation. Likewise on the appeal although liability was argued, albeit faintly. In its notice of appeal, James Hardie had challenged the jurisdiction of the Tribunal but this was abandoned at the hearing of the appeal. Seltsam had included in its Notice of Appeal grounds relating to admissibility of material under s25(3) of the Dust Diseases Tribunal Act 1989, damages and procedural fairness. These grounds were not pursued.

[190] The appeal was argued on the basis that it was a rehearing. After judgment was reserved a question arose as to whether, in light of the decision in Fishburn v Elcom [1999] NSWCA 401, the appeal was confined to questions of law and the admissibility of evidence. This was because the Court of Appeal held that the amendments to s32(1) of the Dust Diseases Tribunal Act 1989 by the Courts Legislation Amendment Act 1998 had retrospective effect. The Court accordingly gave leave to the parties to file further written submissions which they did. I agree with Spigelman CJ that Fishburn was correctly decided but that it does not apply to the instant appeals because they were instituted prior to the 1998 amendments coming into force.

The Judgment of the Trial Judge

[191] His Honour delivered an extempore judgment at 6pm on Sunday, 13 July 1997 after sitting for the best part of 10 days commencing on 2 July 1997 with a bedside hearing of the plaintiff's evidence. When examining the reasons expressed by the trial judge in the judgment, the circumstances in which the hearing took place must be kept in mind.

[192] After finding jurisdiction and negligence, His Honour turned to the issue of causation, which involved conflicting expert opinion.

[193] Before embarking on an analysis of causation, the trial judge found that the plaintiff was suffering from primary renal cell carcinoma (RCC). There was ample evidence to support this finding. Although Seltsam had challenged this conclusion on diagnosis in its notice of appeal, the ground was not pursued at the hearing of the appeal.

[194] His Honour noted that there were two questions which arose for consideration on causation. First, was it more probable than not that the inhalation of asbestos dust and fibre was capable of contributing to the contraction of renal cell carcinoma? Second, was the plaintiff's RCC, more probably than not, caused or contributed to by the inhalation of asbestos dust and fibre at the factory premises of the appellants?

[195] It is apparent from the hearing in the Tribunal that there was substantial conflict between the evidence of two epidemiologists, Dr Margaret McCredie and Professor Joseph McLaughlin, although there was considerable additional opinion evidence proffered by a large number of other witnesses, mostly in the cases presented by the appellants.

[196] The trial judge summarised Dr McCredie's evidence, which culminated in her opinion that on the balance of probabilities obesity and exposure to asbestos material contributed to causation of the plaintiff's RCC. Dr McCredie had relied, in part, on the Mandel report, an international study of renal cell cancer and occupation published in 1995. Both she and Professor McLaughlin had been signatories to that report. The report was obviously significant and His Honour isolated six passages from it as relevant to his determination of the issue.

[197] His Honour then proceeded to briefly summarise the evidence of Dr Burns, a thoracic surgeon and Dr Nankivell, a consultant physician and nephrologist, both called in the plaintiff's case. Turning to the expert witnesses called by the appellants, His Honour referred to Professor McLaughlin's conclusion that the epidemiologic evidence for an association between asbestos and RCC was scanty and problematic. Further, that while cigarette smoking and obesity significantly contributed to the plaintiff's cancer, his exposure to asbestos 'played no role'. According to Professor McLaughlin, any argument to the contrary was purely speculative.

[198] The trial judge briefly summarised the evidence of the expert witnesses called by Seltsam and James Hardie.

[199] Judge Maguire then returned to the task of considering the epidemiological dispute. He commented that the conclusions of epidemiologists were the product of scientific judgment. He saw the Mandel report as important in determining the conflict in the evidence between Dr McCredie and Professor McLaughlin. His Honour returned to the passages from Mandell which he had earlier cited. In particular, the judge said that he was concerned to understand what the authors meant when they used the words 'confidently concluded' in relation to the link between asbestos exposure and kidney cancer. His Honour then referred to the evidence of witnesses on the issue and to counsels' submissions. He concluded that in the Mandel study both Dr McCredie and Professor McLaughlin 'were advancing as their scientific judgment the probability of the link contended for by the plaintiff'. Having so found, His Honour turned to the second question and concluded that there was evidence (which he accepted) that the plaintiff's RCC was caused or contributed to by his inhalation of asbestos dust and fibre at the premises of the appellants.

Causation

[200] The issue of causation in this appeal may be approached by the court in two ways. First, by confining itself to the judgment and seeking to discern whether it contained error. Second, by examining the whole of the relevant evidence and determining whether His Honour's conclusions on the two stage process for determining causation were reasonably open on the evidence, or indeed whether the Court of Appeal would so conclude after an examination of the evidence, s32 of the Dust Diseases Tribunal Act giving a full appeal.

[201] Was His Honour, or for that matter the Court of Appeal, entitled to draw the inference that the causal relationship was established on the balance of probabilities? As the Chief Justice observes in his judgment, the common law test of the balance of probabilities is not satisfied if only a possibility is established. The plaintiff has to establish that the condition from which he suffers is caused or materially contributed to by the defendant's wrongful conduct not that it might have been so caused, Tubemakers v Fernandez (1976) 50 ALJR 720 and in the Court of Appeal, (1975) 2 NSWLR 190 especially at 197 and 199. This does not mean that a plaintiff cannot adduce expert evidence of the possibility and that this may be considered by the Court in determining whether causation has been established on the balance of probabilities. Evidence of possibility is, of course, often the stuff of epidemiological evidence.

[202] In Chappel v Hart (1998) 156 ALR 517 McHugh J (at 523) reiterated that the existence of the relevant causal connection is determined according to common sense ideas and not by philosophical or scientific theories of causation. He cited Mason CJ in March v E & MH Stramare Pty Ltd (1991) 171 CLR 506 at 509 as explaining the reason for such a distinction. Mason CJ had said:

In philosophy and science, the concept of causation has been developed in the context of explaining phenomena by reference to the relationship between conditions and occurrences. In law, on the other hand, problems of causation arise in the context of ascertaining or apportioning legal responsibility for a given occurrence. [p523 para23]

[203] In March the Court, having rejected the 'but for' test as the exclusive test of causation, preferred the common sense view of causation. McHugh J continued in Chappel v Hart:

Before the defendant will be held responsible for the plaintiff's injury, the plaintiff must prove that the defendant's conduct materially contributed to the plaintiff suffering that injury. In the absence of a statute or undertaking to the contrary, therefore, it would seem logical to hold a person causally liable for a wrongful act or omission only when it increases the risk of injury to another person. If a wrongful act or omission results in an increased risk of injury to the plaintiff and that risk eventuates, the defendant's conduct has materially contributed to that injury occurring. [p524 - p525 para27]

See also Gaudron J in Naxakis v Western General Hospital (1999) 73 ALJR 782 at 31 and Callinan J at 127.

[204] Also in Chappel v Hart Hayne J said:

I have said that the resolution of the question of causation will often be asserted without lengthy articulation of reasons. Since it is a question of fact resolved as a matter of common sense and experience, the conclusion is often reached intuitively. The description of the steps involved in that kind of process is difficult and is apt to mislead. Articulating the reasoning will sometimes appear to give undue emphasis to particular considerations. No doubt if policy and value judgments are made, they should be identified. But the lengthy analysis which I have made should not be taken as intending to state any qualification upon the generality of the propositions recognised in cases like March v E & M H Stramare Pty Ltd. Causation is a question of fact to be resolved as a matter of common sense. I have made the extended analysis which I have in order to draw out the various considerations which I consider bear upon the resolution of a difficult and unusual case, not because I consider that a trial judge should be expected (except, perhaps, in the most unusual case) to do more than record the conclusion that he or she reaches about whether the plaintiff's damage was caused by the defendant's negligence. [p562 para148]

[205] In Bennett v Minister of Community Welfare (1992) 176 CLR 408 at 412 - 413 Mason CJ, Deane and Toohey JJ stated:

In the realm of negligence, causation is essentially a question of fact, to be resolved as a matter of common sense (Fitzgerald v Penn (1954) 91 CLR 268 at p277 - p278, per Dixon CJ, Fullagar and Kitto JJ; March v Stramare (E & M H) Pty Ltd (1991), 171 CLR 506 at p515, per Mason CJ; p522 - p523, per Deane J. In resolving that question, the "but for" test, applied as a negative criterion of causation, has an important role to play but it is not a comprehensive and exclusive test of causation; value judgments and policy considerations necessarily intrude (March v Stramare (E & M H) Pty Ltd). [p412 - p413]

[206] Further, the High Court has predicated that a robust approach is required to the issue of causation, see Kirby J in Chappel v Hart at 93. Again, as Handley and Beazley JJA remarked in Commonwealth v McLean (1996) 41 NSWLR 389 at 410, a tribunal of fact (causation being a question of fact) is entitled to find causation as a matter of common sense 'from the sequence of events, although medical science does not suggest an affirmative answer, provided it does not exclude such a finding'. To the extent to which counsel for the appellant James Hardie, Mr Gee QC, appears to submit that common sense and intuition have no part to play in considering epidemiological evidence, I reject the proposition.

[207] The appellants contend that His Honour's finding on causation was in error because a number of the criteria said to be necessary to demonstrate the link between asbestos exposure and RCC were not present. In particular, they rely on the need for consistency in epidemiological studies, the lack of any strength of association in the studies and the absence of any dose response relationship.

[208] Some of the difficulties of epidemiological evidence, in the context of the legal standard of proof, was commented on by Fitzgerald JA in E.M. Baldwin & Son Pty Ltd v Plane & Anor; Jsekarb Pty Ltd v Plane & Anor (1999) Aust Torts Reports 81 - 499 at 65, 640:

The pragmatic assessment of probable cause as a basis for tortious liability cannot be wholly constrained by the scientific and philosophical purity of epidemiology, which essentially depends upon a comparison of data obtained in controlled circumstances.

and

The problems associated with the use of comparative epidemiological studies in connection with causation are magnified when there are multiple possible causes which are capable of operation individually or in a variety of combinations. The law does not require the dismissal of a claim because there are no epidemiological studies available which permit the direct comparison considered necessary by an epidemiologist.

[209] Turning to an examination of the principal epidemiologic evidence before the Tribunal. First to Dr McCredie. She has a distinguished curriculum vitae having obtained a doctor of philosophy in 1982 on cancer epidemiology, her thesis being 'Analgesics and Cancer of the Kidney, Ureter and Bladder'. Since 1990 she has been the Chief Epidemiologist of the Cancer Epidemiology Research Unit at the NSW Cancer Council. She has written extensively on kidney cancer.

[210] In 1993 she and J H Stewart carried out a population based case-control study on 'Risk Factors for Kidney Cancer in NSW: IV Occupational Factors' published in the British Journal of Industrial Medicine. The study found that exposure to asbestos significantly increased the risk for RCC by a factor of 1.58, a link seen more clearly among men - relative risk 1.73 with a 95% confidence interval (C1) of 1.04 to 2.89. It may be noted that if the confidence interval exceeds 1.00 there is a significantly increased risk. Certainly a risk which is seen as statistically significant.

[211] The study involved 489 cases of RCC, 147 of renal pelvic cancer and 523 controls. It was this study which was subsequently used, with necessary modifications, as part of the Mandel study.

[212] The Mandel report was published in 1995 in the International Journal of Cancer. It is entitled 'International Renal-Cell Cancer Study. IV Occupation'. It had eight authors, including Dr McCredie and Professor McLaughlin. Other authors include Professor Mandel from the University of Minnesota, two professors from Germany, one from Denmark and two from Sweden. The study is described as a multicenter collaborative case-control study 'to evaluate factors possibly related etiologically to RCC'. The study included six case studies in five countries with a common study protocol and similar data collection. Professor McLaughlin coordinated the study. He said that he was in charge, that he was running it and was the principal investigator.

[213] For the purposes of the Mandel study, and no doubt to conform with the common study protocol, the NSW study was trimmed to 250 cases with 248 controls. This eliminated telephone responses and was limited to face to face interviews. The Mandel study had a total of 1,732 cases and 2,309 controls over the six study centres. This included 200 cases in the asbestos industry compared with 187 controls. The relative risk result was 1.4, meaning that a worker exposed to asbestos was 40% more likely to contract RCC than a person who was not exposed. The CI (95% confidence interval) was 1.1 to 1.8. This meant that it was statistically significant. However, the study revealed no clear pattern of increasing risk with increasing duration of exposure.

[214] The Mandel report said that 'generally' population based case-control studies were not the most accurate method for ascertaining occupational risks. Cohort studies of workers in a specific occupation or exposure were a better approach. I note that there seems to be universal agreement on this statement. However, the report continues that, despite the limitations, the study confirmed an association with exposure to asbestos.

[215] Important to the evidence adduced in the Tribunal, the report stated:

Several investigators have found increased risks of kidney cancer associated with exposure to asbestos (Selikoff et al 1979; Enterline et al 1987: Maclure, 1987; Smith et al 1989). Experimental evidence lends support to a causal link. Asbestos fibres have been found in the kidneys of individuals with high exposures (Huang et al 1988) and in the kidneys of exposed animals (Kanazawa et al 1970). Finn and Hallenbeck (1985) found more asbestos fibres in the urine of asbestos workers than in non-exposed controls. Case-control studies not showing an association with asbestos exposure had small numbers of exposed workers. (McLaughlin et al 1984: Yu et al 1986; Asal et al 1988; Brownson, 1988; Partanen et al 1991; McLaughlin et al 1992). Our study, with 200 exposed cases provides additional evidence that asbestos increases the risk of kidney cancer. Nevertheless, further research of asbestos-exposed workers is needed to demonstrate a relationship with either duration of employment or amount of exposure before a causal association can be confidently concluded. [Emphasis added]

[216] The conclusion was that:

.... although renal-cell cancer is not usually linked with occupation, we observed a number of associations, most of them consistent with previous reports. Our finding for asbestos supports a number of earlier studies and suggests a relation with renal-cell cancer. The other occupational associations we observed lack the consistency in the literature of the asbestos finding . But the risk for exposure to other petroleum products such as jet fuel, heating oil, kerosene and diesel fuel, warrants further investigation. [Emphasis added]

[217] Before considering the evidence given by Dr McCredie and Professor McLaughlin to the Tribunal, it is convenient to refer to one other publication. Professor McLaughlin and others wrote a chapter on Renal Cancer in a book entitled Cancer Epidemiology and Prevention 2nd Edition, Oxford University Press 1996. It said:

.... renal cell cancer is not generally considered an occupationally associated tumor. However, asbestos has been linked to kidney cancer in several studies. Two cohort studies, one of insulators (Selikoff et al, 1979) and one of asbestos products workers (Enterline et al, 1987), reported significantly elevated mortality rates for kidney cancer. An association between asbestos exposure, mostly from work in shipyards, and renal cell cancer was suggested in a Boston-area case-control study (Maclure, 1987). There is some evidence from autopsy surveys and animal studies that asbestos fibers can be deposited in the kidney (Smith et al, 1989). Most case-control studies of renal cell cancer have found no association with asbestos exposure (McLaughlin et al, 1984; Yu et al, 1986; Goodman et al, 1986; Asal et al, 1988b; Brownson, 1988; Partanen et al, 1991), although their power to detect risks for asbestos exposure is generally low because of the small number of exposed workers. However, case-control studies from Australia (McCredie and Stewart, 1993) and Denmark (Mellemgaard et al, 1994d) observed elevated risks for self-reported exposure to asbestos.

[218] It may be assumed that this was written by Professor McLaughlin before the completion of the Mandel study since it does not refer to it.

[219] In her report tendered to the Tribunal Dr McCredie stated:

Cancer results from multiple serial damage to DNA at sites which control cell growth and development. Although each episode of DNA damage may have a single cause, any one cancer will inevitably have a number of different causes. In the case of renal cell carcinoma, most of the causes are unknown or imperfectly understood. However, it is known that (1) smoking increases the risk for this cancer by a factor of approximately 1.5 to 2.0, the risk being higher in those who have smoked more (McCredie and Stewart, 1992a; McLaughlin et al, 1995); (2) obesity as measured by body mass index (weight [kg]/height [m]) increases the risk for renal cell carcinoma by about the same amount (McCredie and Stewart, 1992b; Mellemgaard et al, 1995); and (3) the majority of population-based epidemiological studies which have the power (sufficient number of subjects studied) to detect such an association (see following paragraph) have found an increased risk of about 1.5-to 2.0-fold linked with exposure to asbestos - in most studies exposure has been assessed according to the respondent's report without verification. [Emphasis added]

[220] In support of her opinion Dr McCredie cited cohort studies, in particular Selikoff and Enterline, as well as case-control studies, including the Mandel report. She concluded that on the balance of probabilities the plaintiff's obesity and exposure to asbestos materially contributed to the causation of his RCC.

[221] In her oral evidence Dr McCredie said that her study with Stewart found a moderately increased risk for workers exposed to asbestos over the non-exposed. She acknowledged that dose response was desirable, but said that it was not essential. Dr McCredie also acknowledged that 'recall bias' was a problem with case-control studies and that cohort studies carried more weight. However, case-control studies were still useful and reliable and there was consistency between the six controls (in five different countries) the subject of the Mandel report. There was also consistency with cohort studies, particularly the larger studies of Selikoff and Enterline. Biological plausibility also existed and assisted in her conclusion.

[222] She was cross-examined about the reanalysis by Maclure of his work and agreed that it was no longer statistically significant. However, she maintained that it still showed a modestly raised increased risk. Dr McCredie said that smoking and obesity are more widely accepted risk factors than asbestos, an opinion shared by all witnesses. Nonetheless, she noted that her studies (and Mandel) had revealed a similar order of risk magnitude for asbestos. Nevertheless, she accepted that the evidence for asbestos exposure as a link to RCC was not as strong as smoking and obesity.

[223] In terms of criteria to test whether a link had been established, Dr McCredie maintained:

a)

That there was a relationship between the exposure to asbestos and the disease in the sense that the exposure proceeded the disease.

b)

That the strength of the relationship had been shown, for example a relative risk of 1.4 in Mandel.

c)

That there was a general (or sufficient) consistency of results in epidemiological studies.

d)

While dose response effect was absent in Mandel, this was not essential.

f)

There was biological plausibility and this was confirmed by other evidence eg. Dr Nankivell, Dr Burns and Professor Breslin.

[224] In his report prepared for the Tribunal Professor McLaughlin, whom His Honour acknowledged as a eminent epidemiologist, said that the majority of RCC are of unknown aetiology with two recognised causes, cigarette smoking and obesity. There were other possibilities but these did not include asbestos exposure. The epidemiological evidence for an association between asbestos and an increased risk of RCC was 'scanty and problematic'. Of 50 cohort studies of asbestos-exposed workers, only two had reported an increased risk of kidney cancer. A 'few' case-control studies had done so, but these were problematic because of recall bias, eg. McCredie and Stewart. Professor McLaughlin said that this study contained methodological flaws. The Maclure study had serious methodologic problems and, when finally completed, was no longer statistically significant.

[225] Professor McLaughlin concluded his report with the unequivocal statement that asbestos exposure 'did not contribute to Mr McGuiness' renal cell cancer'. Further, he stated that the plaintiff's exposure to asbestos 'played no role in the development of his cancer', adding that 'to argue otherwise is purely speculative'.

[226] In his oral evidence before the Tribunal Professor McLaughlin was even more emphatic and dogmatic. He divided the various possible causes of RCC into three categories. The first 'level of confidence' accepted obesity and smoking as a cause. The second level related to 'implicated factors' where, to use his expression, the jury is still out, eg hypertension and/or diuretics, phenacetin and hip replacement surgery. The third and lowest level was speculative only. This level included asbestos exposure.

[227] In coming to a scientific judgment on the issue, a number of principles were relevant which had evolved from the Bradford Hill criteria. These were much the same as enumerated by Dr McCredie. Important among them was consistency in the epidemiological studies - between different controls and different people - and between cohort and case studies.

[228] Professor McLaughlin was particularly critical of the Maclure case study - Maclure had, he said, rushed into print with premature publication of incomplete data. He was asked why Maclure was uncritically relied on in the Mandel report. He gave two answers. At first, he said it was an 'oversight'. Later he said that Maclure was a friend and he didn't want to rub his nose in the dirt. Coming from such an eminent scientist, I find both these answers extraordinary.

[229] The Professor was highly critical of case-control studies. Given this position, one might ask why he associated himself, as one of the authors, with a multi-national case-control study in six centres spread among five countries. Indeed, as I have mentioned, he agreed that he was the coordinator of the Mandel study and set the parameters and methodology for it. It is apparent that he was among the principal authors, if not the principal author.

[230] Professor McLaughlin was asked what was meant by the reference in the Mandel study to it providing 'additional' evidence that asbestos increases the risk of kidney cancer. With respect to the Professor, I do not think that he answered the question.

[231] The Professor was also cross-examined about his claim of 50 cohort studies and he agreed that only nine were relevant as kidney cancer studies. He said that the weight of the evidence amongst the studies was either 'no effect' or a 'slight effect'. As to the cohort studies, he said that there was 'no over-whelming consistency pointing in the direction of an increased risk'. A dose response consistency was not present. Professor McLaughlin was questioned about the meaning of the words 'confidently concluded' in the Mandel report. He agreed that they went well beyond a mere preponderance of evidence or balance of probabilities.

[232] Since the way the case was run before the Tribunal was an epidemiological contest, essentially between Dr McCredie and Professor McLaughlin, I think that the trial judge was entitled to spend only a relatively short time on discussing the evidence of the other expert witnesses, see Hayne J in Chappel v Hart at 562. Some of the evidence of the other witnesses supported Dr McCredie and some Professor McLaughlin. Turning to them briefly, it first may be seen that Drs Burns and Nankivell gave evidence of biological plausibility. Asbestos is a known carcinogen. Asbestos can travel outside the lung to the parietal pleura, the peritoneum, and the testes. Asbestos fibre has been found in the urine of experimental animals fed asbestos and in autopsy specimens in humans. Also, it has been found in the kidneys of experimental rats. The connection was therefore biologically plausible. Professor Breslin confirmed this, as did Dr Jurgen Stahl. Professor Berry said, putting it around the other way, that one could not say that it was not biologically plausible. On the other hand, Dr Katelaris thought this was extremely doubtful. Professor McLaughlin, however, appeared to accept that the connection was biologically plausible. So did Dr McCredie. The preponderance of the evidence was therefore in favour of biological plausibility.

[233] Professor Ferguson (an occupational physician), Dr Katelaris (a urologist), Dr Lee (a thoracic physician), Professor Henderson (a pathologist), Professor Berry (an epidemiologist) and Professor Breslin (a thoracic physician) all opined that the link between exposure to asbestos and RCC had not been established.

[234] Dr Stahl had prepared a report which noted the 'trend' towards acceptance of asbestos as a possible contribution. Professor Henderson wrote an 'Addendum' to Dr Stahl's report acknowledging the trend in recent literature but concluding that the evidence was unconvincing at this time.

[235] Professor Ferguson said that he remained to be convinced. No link had been established with any certainty. The Professor was critical of some of the epidemiological studies, including Selikoff. He accepted that it was unnecessary to meet all of the Bradford Hill criteria but the more important ones should be satisfied.

[236] Professor Berry said that there was no association established which he would accept as causal. McCredie and Stewart, and for that matter Mandel, provided no extra evidence. Furthermore, a 40% relative risk (RR) was only a weak to moderate relationship. While smoking has the same RR, a lot more work had been done on that link than with asbestos. He agreed that one needed to look at the extent of the consistency between studies and the trend. Professor Berry also said that when the Mandel authors mentioned 'confidently concluded', they would not have had the balance of probabilities in mind.

[237] Dr Lee thought that the strength of association was insufficient. The epidemiological evidence was insufficient. He accepted that it was relatively common to find conflicting results in the field of epidemiology and that it was necessary to balance the evidence. Dr Katelaris considered that the asbestos link was speculative and not proven and that there were methodological flaws in the epidemiological studies. Professor Breslin agreed that the relationship was unproved but the detection of asbestos in many organs suggested that it was not implausible.

[238] This brief summary of some of the evidence of the witnesses reveals that they do little more than express reasons for agreeing with either Professor McLaughlin or Dr McCredie. The interesting aspect of their evidence is that, for the very most part, their opinions are based on the same material. It is their interpretation of the material that may differ. In addition, with few exceptions, the opinions are expressed by witnesses who are not epidemiologists. For these reasons I do not think that a great deal of assistance is gained from their evidence of reviews of the epidemiological literature. The issue comes down more to whether Professor McLaughlin is preferred over Dr McCredie or vice versa.

[239] In my opinion, there are a host of reasons why the trial judge was entitled to prefer Dr McCredie and find that, on the balance of probabilities, the link between asbestos exposure and RCC was established. Further, the plaintiff's RCC was, more probably than not, caused or contributed to by his inhalation of asbestos at the workplaces of the appellants. In Kavanagh v Akhtar (1998) 45 NSWLR 588 at 597 Mason P (adopting Gaudron J in Chappel v Hart at 519-520) pointed out that the common sense approach applied to this question also. On an assessment of the whole of the evidence, the conclusion of the trial judge on causation was well open to him. Indeed, although without the benefit of seeing and hearing the expert witnesses, I would come to the same conclusion. In this respect, I respectfully disagree with the Chief Justice. I will attempt to explain in the succeeding paragraphs why I have so concluded.

[240] One cannot gainsay that the Mandel report is an important document in the study of occupational exposure to asbestos and RCC. It purports on its face to study the relationship in a very significant collaborative case study covering six centres in five different countries. It claimed to be the largest RCC study ever. This was never challenged. The study was carried out by eminent epidemiologists using a shared study protocol and common data collection processes. The Mandel study involved a significant number of cases and brought together the results of case-control studies in Denmark, Uppsala in Sweden, Minnesota in the USA, New South Wales, Australia as well as Berlin and Heidelberg in Germany. At least one year's exposure was a prerequisite. At the time of trial, Mandel was the most up-to-date study available on the subject. The report accepted that case-control studies were not as accurate as cohort studies but concluded that, despite the limitations, an association with asbestos was confirmed.

[241] Mandel then reviewed previous studies, including the cohort studies of Selikoff and Enterline and the case-control studies of Maclure and Smith. The authors also referred to case studies which had not shown an association, including McLaughlin et al (1984) and McLaughlin (1992). It noted, however, that these studies had small numbers of exposed workers.

[242] What can be said about this discussion in Mandel and the apparent reliance on prior reports and studies? The cohort studies of Selikoff and Enterline are relied on without any criticism. This is difficult to reconcile with Professor McLaughlin's strident criticism in his evidence, unless he later changed his mind. Maclure is relied on in Mandel, well after his retraction, if that is what it was. Professor McLaughlin says that Maclure's inclusion was an oversight. This is hardly likely. Then he says, as a I have already observed, that it wasn't mentioned because Maclure was a friend and he (Professor McLaughlin) didn't want to rub his nose in the dirt. As I have said, I find this answer quite extraordinary. If it is to be believed, it means that a study pointing in a certain direction, but known to be fatally flawed, was allowed to remain as evidence in an important international report on RCC and its causes, because of a friendship. One should bear in mind the role of peer review in assessing papers for publication in medical scientific journals.

[243] There is also a more fundamental criticism of Professor McLaughlin's evidence before the Tribunal. If case-control studies were so unreliable because of recall bias and other expressed confounding problems, why did he allow himself to be associated, and in such a prominent fashion, with the Mandel study. After all, he was its leading light, its coordinator, and he decided the rules. It beggars belief. Why since he apparently had such a poor view of the NSW study of McCredie and Stewart, considering it to be badly flawed, did he allow it to be used in the Mandel study? Again, it is easy to infer that his evidence before the Tribunal is just not believable.

[244] It must be remembered that Professor McLaughlin signed the Mandel report and, one is entitled to assume, must be prepared to take responsibility for its content and expressions of opinion. I am unable to accept that he would have signed off on it if he did not subscribe to its content.

[245] It appears that Professor McLaughlin now seeks to resile from the statement in the Mandel report that the study - indeed 'our study' - provides additional evidence that asbestos increases the risk of kidney cancer. Why this is so is difficult to discern. So far as the evidence goes, there has been no new information since Mandel which would cause Professor McLaughlin to change his mind. Indeed, one is entitled to assume that the additional evidence of the Mandel study built on the evidence which already existed.

[246] This is confirmed by the further conclusions of the Mandel study that although kidney cancer is not usually linked to occupation 'we observed a number of associations, most of them consistent with previous reports'. There is more. 'Our finding for asbestos supports a number of earlier studies and suggests a relation with renal-cell cancer'. With respect to Professor McLaughlin, his evidence before the Tribunal cannot stand with these statements. The Mandel report concludes by stating that other occupational associations observed lacked the consistency of the asbestos finding. For exposure to petroleum products further investigation was warranted. Contrast this with Professor McLaughlin's evidence before the Tribunal of three levels of association. Level one, smoking and obesity are proven. Level two - the jury is still out on hypertension and diuretics, and level three, which is merely speculative, includes asbestos. Indeed, asbestos is downgraded within the speculative category because Professor McLaughlin stated quite categorically, that there is no connection. With respect to the evidence given by Professor McLaughlin in the Tribunal, it cannot stand alongside that which he has put his pen to in the Mandel report. It is as different as chalk and cheese.

[247] Nor does Professor McLaughlin's evidence stand credibly against what he wrote in the chapter on Renal Cancer in the text book on cancer epidemiology and prevention. This has been set out earlier. Again, the same sources are referred to uncritically, including Maclure. Indeed, McLaughlin quotes case-control studies, including his own, which have found no association, but says that their power to detect risks for asbestos exposure was generally low because of the small number of exposed workers.

[248] The appellants place particular reliance on the part of the Mandel study which expresses the need for further research of asbestos exposed workers. No one can deny the need for more research. However, reliance is placed on the need for this further research in order 'to demonstrate a relationship with either duration of employment or amount of exposure before a causal association can be confidently concluded' (emphasis added). Confident conclusions are the language of science. Professors McLaughlin and Berry agreed, the former assuming that the words connoted a higher standard than the balance of probabilities.

[249] Reading the Mandel report as a whole, it is apparent that it is saying that there is a link shown by previous studies and by the combined international case study which arrived at an increased relative risk of 40%. Further, Mandel is saying that this is statistically significant. However, to be satisfied to a degree in excess of the balance of probabilities - for scientists to be able to 'confidently conclude' that there is a causal connection, will require further research.

[250] In my opinion, there was more than sufficient evidence before the Tribunal for it to conclude that, on the balance of probabilities, exposure to asbestos can cause or materially contribute to the contraction of RCC. The inferences drawn by His Honour were permissible, open and rose well above conjecture. Acceptance of the evidence of Dr McCredie before the Tribunal, the contents of the Mandel study and the preference for Dr McCredie's evidence over Professor McLaughlin, which is more than available when his evidence is scrutinised, all lead to this conclusion. In my view, there was sufficient evidence to satisfy His Honour to a level of actual persuasion to meet the probability test. His Honour may not have expressed his reasons for preferring Dr McCredie over Professor McLaughlin with great detail or precision but the circumstances of the trial (which I have explained) make this understandable. The judge was clearly entitled to accept Dr McCredie over Professor McLaughlin for reasons I have discussed. Moreover, I think that he was correct to do so and my own assessment of the evidence would lead me to the same conclusion. I am also of the view that His Honour plainly turned his mind to the strength and quality of the epidemiological evidence in determining the question of causation. I do not see any failure on His Honour's part to take account of a relevant consideration. Merely because he did not consider every aspect of the extensive epidemiological evidence does not make him guilty of failure to take account of a relevant consideration. I say this particularly taking into consideration the circumstances of the trial mentioned earlier.

[251] It also seems to me that the appellants seek to place too much reliance on epidemiology. The evidence makes it plain that there is no such thing as a perfect epidemiological study. As Professor McLaughlin said, there is no epidemiology study which cannot be criticised. Professor Berry agreed.

[252] There was no requirement for the trial judge to accept the evidence of Professor McLaughlin. Indeed, as I have shown, there were good reasons to prefer Dr McCredie. At least Dr McCredie's evidence before the Tribunal was consistent - and consistent with what she wrote in the Mandel study (along with Professor McLaughlin). Professor McLaughlin was asked whether the Mandel report still represented his current views. He responded in the affirmative with the proviso that it be read as a whole and things were not taken out of context. I think that the Mandel report is clear on its face and, as I have already indicated, when read as a whole. After all, it is not a very long document and is written in plain terms. As I have said, Mandel is clearly inconsistent with the evidence of Professor McLaughlin before the Tribunal. A fair reading of Mandel cannot lead to a conclusion that, as Professor McLaughlin urges, the evidence for an association between asbestos and RCC is 'scanty and problematic'.

[253] Because the science of epidemiology involves questions of judgment, experience and interpretation to be applied to gathered statistics, it is not surprising that criticism may be made about individual studies, whether they be case studies or cohorts. It is equally unsurprising that two highly qualified epidemiologists may express different opinions on the same material. An examination of the epidemiologic evidence of other witnesses also discloses divergences of opinion based on the same material. See, for example, Professor Berry and Dr Stahl as against Professor Henderson and Dr Katelaris.

[254] Quite apart from the epidemiologic evidence, there was evidence of a non-statistical nature supporting the plaintiff's case on causation. This was the evidence of biological plausibility, which supports a common sense approach to causation. It includes the plaintiff's lengthy and heavy exposure to asbestos dust and fibre, asbestos being a known carcinogen. Latency between exposure and onset of disease is consistent with other asbestos-related diseases (Drs Nankivell and Burns). Asbestos fibres may be carried to the kidney and found in urine. Experiments show that asbestos can cause cancer in the kidney of animals. RCC results from multiple serial damage to DNA at sites of cell growth (Dr McCredie). The evidence of Dr Nankivell, Dr Burns, as well as some of the evidence called by the appellants, supports the non-statistical direct evidence on biological plausibility.

S79 Evidence Act 1995

[255] The appellant Seltsam submits that certain evidence was wrongly admitted by the trial judge since it was in breach of s79 of the Evidence Act 1995. In particular, the submission concerns the opinion of Dr Burns on epidemiology and the opinion of Dr McCredie on medical issues. It is submitted that each witness lacked the specialised knowledge to proffer such an opinion.

[256] S79 provides:

If a person has specialised knowledge based on the person's training, study or experience, the opinion rule does not apply to evidence of an opinion of that person that is wholly or substantially based on that knowledge.

[257] In making the submission on behalf of Seltsam, Mr Burbidge QC relies on statements made in H G v R (1999) 160 ALR 554 at 563 (Gleeson CJ) at 566 (Gaudron J) and at 584 (Hayne J).

[258] The submission may be disposed of shortly. No objection, based on s79, was taken to any part of the evidence of Dr Burns or Dr McCredie. If there was a vice in this evidence, it is one which is equally applicable to many of the expert witnesses called by the appellants. Not only was no objection taken, no submission was made to His Honour to disregard any part of their evidence as contrary to the Evidence Act. Further, no identifiable ground of appeal refers to the issue. I do not think that intermediate Courts of Appeal should encourage these kinds of submissions in the circumstance just disclosed. In any event, the relevant witnesses clearly had sufficient specialised knowledge based on their training, study and experience to qualify them in order to give an opinion. It may be accepted that the weight of such opinion may be diminished by the degree of specialised knowledge. Their evidence, on the matters challenged, was however admissible and not in breach of the section. H G v The Queen is quite a different case and its facts are far divorced from this appeal.

Liability

[259] The issue of negligence and foreseeability occupied very little time on the hearing of the appeal although liability was addressed in the written submissions of the parties. Seltsam did not expand on its written submissions. James Hardie did, but only to the extent of a brief submission being made by Mr McIntyre of Counsel.

[260] The thrust of his submission, and this was in common with Seltsam's submission, was that, at the relevant time, exposure to asbestos was within the threshold limit values (or standards) of the National Health and Medical Research Council (NH & MRC). Accordingly, there was not then thought to be a foreseeable risk of injury.

[261] There was an abundance of evidence before the Tribunal of the actual knowledge of each appellant of the dangers to workers of being exposed to asbestos dust and fibre, and that it could lead to asbestosis. His Honour found that the plaintiff's exposure to asbestos dust and fibre while working for James Hardie was very considerable, although not as significant as Seltsam. The plaintiff gave evidence of his exposure and His Honour summarised this. James Hardie called no evidence contradicting the plaintiff. The documents before the Tribunal make it plain that both appellants appreciated that there was no safe level of exposure to asbestos dust and fibre. That James Hardie may have been one-step ahead of the NH & MRC does not affect foreseeability in the light of the evidence of knowledge referred to above. See Beazley JA in Bendix Mintex v Barnes (1997) 42 NSWLR 307 at 334 - 335 and CSR v Wren (1997) 44 NSWLR 463 at 477. I agree with the judgment of the Appeal Division of the Supreme Court of Victoria in Thompson v Johnson & Johnson Pty Ltd [1991] 2 VR 449 at 494 where it said:

Whether or not the NH & MRC recommended that a warning be given was not determinative of the question of reasonable care, for to accept that proposition would permit the respondents to abrogate the duty of reasonable care owed by them. It is not the response of such a body which determines whether a person in the position of the respondents is or is not negligent. That is for the courts to decide.

[262] As stated by Windeyer J in Mount Isa Mines Ltd v Pusey (1970) 125 CLR 383 at 402 foreseeability does not require foresight of the particular event causing the harm. It does not suppose foresight of the particular harm that occurred. The plaintiff need not prove a distinct or particular injury but only that the injury suffered falls into a class of injury which ought reasonably have been foreseen as a consequence of conduct. The plaintiff had a significant and prolonged exposure to asbestos dust and fibre from the age of 15 years, until his retrenchment in 1991. He was exposed to asbestos dust and fibre for much of his 41 years of employment with the appellants. That his exposure caused a cancer in the kidney as opposed to the lung, the pleura or peritoneum, does not mean that it falls into a different class and was not foreseeable (Chapman v Hearse (1961) 106 CLR 112.

[263] The submission on negligence and foreseeability by each appellant is rejected.

Orders

[264] I would propose the following orders. Both appeals be dismissed with costs. Cross-appeal dismissed with no order as to costs.