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

[2000] NSWCA 29

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(Judgment by: Spigelman CJ)

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

Court:

Judges:
Spigelman CJStein JA
Davies 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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Judgment by:
Spigelman CJ

[1] I have read the judgments of Stein JA and Davies AJA in draft. It is unnecessary to repeat their Honours' outline of the relevant evidence. I will, however, supplement that outline to some extent.

[2] This case gives rise to some of the issues considered in Commonwealth v Bell, (Court of Appeal, 11 August 1998, unreported). That case turned on the way the trial was conducted. It did not resolve the issue of causation between asbestos exposure and renal carcinoma.

Nature of the Appellate Jurisdiction

[3] S32 of the Dust Diseases Tribunal Act 1989 ("the Act"), was replaced by Schedule 11 of the Courts Legislation Amendment Act 1998 ("the 1998 Amendment Act"). The new s32 limits appeals to this Court to a party "dissatisfied ... in point of law or a question as to the admission or rejection of evidence". It was modelled on s32 of the Compensation Court Act 1984.

[4] The 1998 Amendment Act amended Schedule 3 of the Act by the inclusion of:

"4 S32 as in force before the commencement of Schedule 11 to the Courts Legislation Amendment Act 1998 does not apply to decisions of the Tribunal made before that commencement."

[5] Judgment in the present case was delivered on 13 July 1997. The Appellant, James Hardie & Co Pty Ltd, filed its appeal on 24 July 1997. The Appellant, Seltsam Pty Ltd filed its appeal on 1 August 1997. The relevant provisions of the Courts Legislation Amendment Act 1998 were proclaimed to come into force on 4 December 1998.

[6] Accordingly, at the time the appeals in the present case were instituted, the relevant provision was s32(1) in its original form namely:

"32(1) If a party to any proceedings before the Tribunal is dissatisfied with a decision of the Tribunal, the party may appeal against the decision to the Court of Appeal."

[7] It is this section which, by force of cl4 of Schedule 3 of the Act, "does not apply to decisions of the Tribunal made before that commencement".

[8] In Fishburn v Electricity Commission of New South Wales (1999) NSWCA 401, this Court determined that s32 of the Act in its amended form applied to the case before the Court. This judgment was handed down after this Court reserved judgment in the present case. The Court then sought and received further submissions on the nature of the appellate jurisdiction applicable in this case.

[9] The proper construction of cl4 of Schedule 3 was not in issue in Fishburn because the appellant accepted the retrospective effect of the new s32 (at [3]). This concession was properly made. The decision of the Tribunal in that case was handed down on 13 November 1998 and the notice of appeal was filed on 9 December 1998 ie after the new s32 came into force. In the present case, as I have noted, the appeals had already been instituted before the 1998 amendments came into force.

[10] The reasoning in Fishburn was, in my respectful opinion, plainly correct with respect to appeals instituted after the date on which Schedule 11 of the 1998 Amendment Act came into effect. The position is, in my opinion, otherwise with respect to appeals that had been instituted prior to that date.

[11] The words which must be construed state that s32, as in force at a particular date, "does not apply" to decisions of the Tribunal made before that date. S32 as so "in force" stated, relevantly; "a party ... dissatisfied with a decision ... may appeal".

[12] The words of the new cl4 of Schedule 3 of the Act - "decisions of the Tribunal made before that commencement" - encompass two kinds of decisions: those from which an appeal has been instituted and those from which no appeal has been instituted. The position of the latter is clear: the new s32 applies, the old s32 "does not apply". With respect to the former, the terminology of the old s32 was permissive: "may appeal". An appellant which had instituted an appeal before the relevant date has exercised its statutory right to do so. In such a case, there was no further work for s32 to do.

[13] The usual presumption is that legislation operates prospectively. That presumption applies to cl2 of Schedule 11 of the Courts Legislation Amendment Act 1998 which inserted cl4 into "Schedule 3 - Savings Transitional and other Provisions" of the Act. The presumption is not, in my opinion, displaced. Cl1 of Schedule 11 of the 1998 Amendment Act omitted s32. It did not omit the section with retrospective affect.

[14] Cl4 of Schedule 3 does work which is not done by the repeal of s32. It constitutes a "contrary intention" within s5(2) of the Interpretation Act 1987, so that an unexercised right of appeal is not a "right accrued" within s30(1)(c) of the Interpretation Act 1987. It is not, however, sufficiently explicit to constitute a "contrary intention" with respect to an appeal that has in fact been exercised.

[15] The Parliament must express an intention to remove the jurisdiction of a court which has already been invoked, in clear and unambiguous terms. (See Bropho v Western Australia (1990) 171 CLR 1 at 17-18; Magrath v Goldsbrough Mort & Co Ltd (1932) 47 CLR 121 at 128, 134; R v Cain (1985) 1 AC 46 at 55-56). The formulation under consideration - "decisions of the Tribunal made before that commencement" - is not clear and unambiguous in this regard. It should be read down to apply only to decisions of the Tribunal in which no appeal has been instituted.

[16] This is a case in which s30(1)(b) of the Interpretation Act 1987 applies:

"The amendment ... of an Act ... does not:

(b)

affect the previous operation of the Act ... or anything duly ... commenced under the Act ..."

[17] The "previous operation" of the old s32 had resulted in the exercise of the right to appeal. Alternatively, that appeal had been "duly commenced". Neither the omission of the old s32, nor the inclusion of cl4 in Schedule 3, "affects" the appeals so instituted.

[18] The Appellants invoked s30(1)(c) of the Interpretation Act. There is no need to consider the applicability of that provision in the alternative.

Causation: The Trial Judge's Reasons

[19] The causation issue posed for the Tribunal was whether the Respondent's renal cell carcinoma was sufficiently related to his exposure to asbestos so as to enable the Tribunal to attribute responsibility for the injury to the Appellants.

[20] His Honour approached the issue of causation, in accordance with the Respondent's submissions, by asking two questions:

(i)

Is inhalation of asbestos, more probably than not, capable of causing or contributing to the contraction of renal cell carcinoma?

(ii)

Was Mr McGuiness' renal cell carcinoma, more probably than not, caused or contributed to by the inhalation of asbestos at the defendants' premises?

[21] His Honour answered the first question he posed on the basis of his assessment of the epidemiological evidence. The conflict of expert epidemiological evidence had emerged as a central focus in the course of the trial.

[22] The first question - Is the agent capable of causing the disease? - is sometimes referred to by epidemiologists as "general causation". The second question - Did the agent cause the disease in this case? - is sometimes referred to as "specific causation". Epidemiological evidence - both the statistics and the interpretation - may play a role with respect to both questions. For legal purposes, the relevant question is the second.

[23] When answering the second question His Honour did not refer expressly to the epidemiological evidence. He did, however, refer to the opinions expressed by the Respondent's experts. Their opinions were based, almost exclusively, on the epidemiological studies.

[24] It is instructive to set out His Honour's reasoning with respect to the second question - the determinative legal issue - which he posed for his consideration. This was as follows:

"That brings me to the second proposition that the plaintiff must establish, that is, that not just persons in general can be affected in the way contended for, but that his own renal cell carcinoma was, more probably than not, caused by or contributed to by the inhalation of asbestos dust and fibre. That is a different question. There is opinion evidence to support the plaintiff's case. Some of it comes from Dr Burns; some of it comes from Professor McCredie. There are other factors that Mr Letcher of Queens Counsel advances in support of a favourable finding. He says, firstly, that there was heavy exposure of this known carcinogen, and I found that there was, particularly in relation to the dust extractor. He says that there was exposure over a long period, and I find that there was. Dr McCredie is not of course a medical practitioner, but in a passage that I have quoted, she refers to successive insults to the material.

Notwithstanding her lack of medical training, I think that that was a view that she was entitled to express. Certainly there was no objection to her expressing that view, and it having been expressed by her, it became an issue in the case which was not dealt with either by way of cross-examination or by the calling of any other evidence.

Mr Letcher also advances, in support of this contention, that the plaintiff's light smoking experience and heavy asbestos infection, support the view advanced by Dr Burns, that the asbestos more probably than not, contributed to the condition. He says, and I think this is valid, that if smoking can be minimised as a possibility, then any other candidate for causality must have its prospects enhanced. He also points to the fact that another candidate, namely diuretics, is negated here by the uncontradicted evidence of the plaintiff.

Mr Letcher also points out and I think there is some force in this, that on the evidence, some at least of the dust and fibre inhaled by this man, went beyond the inside of the lung, and to the pleura, that is it had started to advance through the anatomical system. That I think, validly supports the proposition advanced by Dr Burns that more probably than not, it had got into the right kidney and more probably than not, it contributed to the contraction by the plaintiff, of the renal cell carcinoma."

[25] It is not entirely clear to what His Honour was referring when he said that Dr McCredie had made mention of "successive insults to the material". It is likely to have been the following passage in her report of 2 July 1997, which His Honour had earlier quoted:

"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."

[26] It appears from his reasons that His Honour identified four factors which, cumulatively, led him to draw the inference that the inhalation of asbestos at the Appellants' premises caused, or materially contributed to, the Respondent's renal cell carcinoma:

(i)

Asbestos is a "known carcinogen" which "had started to advance through the anatomical system" of the Respondent.

(ii)

The Respondent's exposure to asbestos was significant ("heavy").

(iii)

The significant exposure contrasts with lesser or no exposure to other "candidates for causality" ("light smoking experience" and no "diuretics").

(iv)

The opinion evidence of Dr Burns and Professor McCredie.

[27] Of some significance in the present case is that there was no direct evidence that any asbestos had reached Mr McGuiness' kidney. The needle biopsy was negative. No other relevant tests were tendered.

[28] His Honour made no reference to the epidemiological studies in the context of answering the second question he posed for himself. His discussion of epidemiology occurred in the context of the first question, namely whether or not asbestos was "capable" of causing renal cell carcinoma.

[29] I am of the view that His Honour did not take into account the strength or quality of the epidemiological evidence in answering the second question: causation in the specific case of the Respondent.

[30] Because of the urgency with which it had to be delivered, His Honour's judgment is not subject to criticism for omission. In any event, it is not necessary to state conclusions on causation in lengthy reasons. As Justice Hayne has said, such a conclusion is "often reached intuitively" (Chappel v Hart (1998) 195 CLR 232 at [148]). However His Honour expressly refused to consider certain matters. He said:

"I propose not to examine or deal with all or indeed any of the particular criticisms advanced by Mr McIntyre of counsel and Mr Burbidge of Queen's Counsel for their respective clients. These matters are matters which if I were an epidemiologist I might look at to appraise the work of another epidemiologist. That is not my task."

[31] The submissions which His Honour set aside as irrelevant, were directed to the assessment of the strength and quality of the epidemiological studies.

[32] In this respect I believe His Honour fell into error. The strength of the association between asbestos exposure and renal cell carcinoma, and other aspects of the quality of the epidemiological research, particularly inconsistencies amongst the various studies, were relevant considerations which His Honour was obliged to take into account. They were relevant, as a fact on which, in part, to base an inference as to the causal relationship in the particular case and also, indirectly, in order to assess the two expert opinions which His Honour did take into account and which were substantially, if not exclusively, based on those studies.

[33] This error justifies the intervention of the Court. On the basis that the old s32 applies, this Court must assess the evidence for itself.

Expert Evidence

[34] The trial judge placed particular reliance on the opinions of two experts called by the Respondent: Dr McCredie, an epidemiologist and Dr Burns, a medical practitioner.

[35] Dr McCredie concluded her report of 2 July with the statement:

"On the balance of probabilities, obesity and exposure to asbestos materially contributed to the causation of renal cell carcinoma in this case ." (emphasis added)

[36] This conclusion was based on her analysis of the epidemiological studies which she summarised as follows:

"The majority of population based epidemiological studies which have the power (sufficient number of subjects studied) to detect such an association ... 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."

[37] In cross-examination, Dr McCredie's assertion of an opinion as to causation in the individual case was qualified, but not withdrawn:

"Q I think you said earlier, doctor, that your speciality in epidemiology is one looking at statistics and populations and diseases and that your discipline does not permit you to make a particular diagnosis for a particular patient.

A That's exactly right."

and

"Q ... but you are not in a position, I would suggest, to say that this man's cancer on the balance of probabilities was materially contributed to by his asbestos exposure, are you.

A I have said so.

Q I realise you said so, doctor, but I had the impression from your evidence earlier that all you were saying you were able to do, was to look at statistics and give an opinion as to whether or not exposure to a particular substance may or may not have an association with the development of cancer.

A That's true." (Black AB 176).

[38] Dr McCredie was an epidemiologist and, as His Honour indicated, her opinion was based on that expertise. There was nothing in the nature of clinical experience on which she could draw. Dr Burns, who had such experience relied, almost exclusively, on epidemiological studies.

[39] In his report of 26 June 1997, Dr Burns concluded that:

"In my opinion on the balance of probabilities, his asbestos exposure while working with Wunderlich & Hardies in the period 1950 to 1984 contributed to the development of his renal carcinoma."

[40] The question he was addressing was "Can such a tumour be attributable to asbestos exposure?". In this context he referred to the "close association between cigarette smoking and the development of renal carcinoma". He then said:

"The association between asbestos exposure and renal carcinoma has not yet been so clearly accepted."

[41] Dr Burns went on to refer to four matters as the foundation of his opinion, to which he also referred in his oral evidence:

(i)

The fact that asbestos fibre has been found in urine and in the kidneys.

(ii)

"Asbestos is generally accepted to be a carcinogen in general [mesothelioma, lung cancer]."

(iii)

"[Asbestos] ... has been shown to be a carcinogen in the rat kidney."

(iv)

The epidemiological studies, specifically those of Selikoff, Enterline and the withdrawn Maclure study, together with the review of the literature by Smith, McCredie and Stewart, and the Mandel study.

[42] The first matter establishes a possibility of a connection: "biological plausibility", as it was referred to in the evidence.

[43] The second matter involves the identification of asbestos as a suspect substance.

[44] The third matter, animal laboratory experiments, is a permissible, albeit limited, basis for the opinion.

[45] The fourth matter is the epidemiological studies, to which I will refer further below.

[46] Nothing in Dr Burns' opinion turned in any way on the circumstances of the particular case. He referred to the fine needle biopsy of Mr McGuiness which disclosed nothing of relevance. There was no reference to any testing which could have established the presence of asbestos in the kidney or urine of the Respondent.

[47] The Respondent also relied on a report from Dr Nankivell of 25 June 1997. In his report, Dr Nankivell relied on the epidemiological studies to which I will refer.

[48] Dr Nankivell concluded:

"On the balance of probabilities this past exposure to asbestos could have made a material contribution to the development of his renal cell carcinoma."

[49] The language of possibility ("could") contrasts with the positive conclusion of Dr Burns and Dr McCredie. It appears that Dr Nankivell was interpreting the epidemiological studies. He did not bring to bear clinical or other relevant experience.

[50] On behalf of the Respondent Seltsam, Professor McLaughlin gave evidence about the epidemiological studies. He focused on the recognition amongst epidemiologists of the link between renal cell cancer and cigarette smoking and obesity. He asserted that evidence for all other putative risk factors was weak, inconclusive or contradictory, when compared with that observed for cigarette smoking and obesity. He said:

"The epidemiological evidence for an association between asbestos and an increased risk of renal cell cancer is scanty and problematic."

[51] He noted that of almost 50 cohort studies, which he regarded as the most informative type of study for an occupational exposure, only two had reported an increase of kidney cancer. He noted that although a few case control studies had reported an association with asbestos, this type of study design is problematic for purposes of evaluating occupational exposures, because of recall bias.

[52] In the course of his oral evidence he said that he did not believe that the literature demonstrated a causal relationship between asbestos exposure and renal cancer.

[53] Dr Katelaris in a report dated 5 July 1997 asserted that the link between asbestos exposure and renal cell carcinoma had not been proved.

[54] Dr Lee in a report dated 7 July 1987 concluded that the epidemiological evidence was limited and of insufficient strength to permit a conclusion that a causal relationship existed.

[55] Professor Berry in a report of 6 July 1997 reviewed the literature and a number of the studies. He concluded that there was "suggestive evidence" that exposure may lead to an increased risk of kidney cancer, however the evidence was not conclusive.

[56] Professor Breslin also referred to the various studies and said that they did not establish "a firm association" and that it could not yet be accepted that exposure to asbestos increases the risk of development of renal cancer.

[57] Dr Stahl identified "a trend in the more recent literature which favours a possible contributory relationship given the finding of asbestos bodies in renal cell carcinoma tissue and in the urine, and apparently the increased relative risk of developing this tumour after appropriate asbestos exposure".

[58] Professor Henderson provided an addendum to Dr Stahl's comments. He noted that the recent literature demonstrated no more than a statistical association. He said that the presence of asbestos fibre in renal tissue or urine was "a simple topographical or anatomical association with no obvious link between the fibres and cancer". He concluded that evidence of a causative or contributory effect was "unconvincing or inconclusive" and:

"It is certainly my view that this does not equate to a probability of causation or material contribution by asbestos at the level of 50% or greater (in other words the relationship at this time is no more than speculative or possible and it does not achieve probability status)."

Use of Epidemiology: General

[59] Epidemiology is the study of the distribution and determinants of disease in human populations. It is based on the assumption that a disease is not distributed randomly in a group of individuals. Accordingly, subgroups may be identified which are at increased risk of contracting particular diseases.

[60] Epidemiological evidence identifies associations between specific forms of exposure and the risk of disease in groups of individuals. Epidemiologists do make judgments about whether a statistical association represents a cause-effect relationship. However, those judgments focus on what is sometimes called in the epidemiological literature "general causation": Whether or not the particular factor is capable of causing the disease. Epidemiologists are not concerned with "specific causation": Did the particular factor cause the disease in an individual case?

[61] Epidemiology, according to one exhibit, "provides a systematic method for identifying and quantifying health risks" (J K McLaughlin and R Brookmeyer "Epidemiology and Biostatistics" in McCunney (ed) A Practical Approach to Occupational and Environmental Medicine (1994)).

[62] Epidemiology provides two types of material: first, the statistical measurement of an association between exposure and disease and, secondly, interpretation of the data to determine general causation. The second function may be performed by an epidemiologist who had no association with the study or studies which provide the raw data.

[63] Dr McCredie and Professor McLaughlin, whose qualifications are set out by Stein JA and Davies AJA, gave evidence concerning the science of the epidemiology, both about its general nature and about the procedure by which epidemiological evidence is used as a basis for an inference of a causal relationship between exposure and a particular disease. References to these matters are also contained in various specific studies relating to the alleged relationship between asbestos and various forms of disease which were tendered in evidence. Furthermore, the article by McLaughlin and Brookmeyer, referred to above, is an overview of the discipline.

[64] There is now a substantial legal literature on the use of epidemiology which is consistent with the evidence tendered in this case. In Australia, see Christie "Toxic Tort Disputes: Proof of Causation and the Courts" (1992) 8 Environmental Planning and Law Journal 302; Marley & McMichael "Disease Causation: The Role of Epidemiological Evidence" (1991) 155 Medical Journal of Australia 9.

[65] In the United Kingdom, there is a summary of the literature in the judgment of French J in Reay v British Nuclear Fuels (1994) 5 Med LR 2.

[66] As would be expected, however, the largest legal literature is from the USA, based on a substantial case law to which I will presently refer. Of particular significance is a compilation prepared by the Federal Judicial Centre entitled Reference Manual on Scientific Evidence (1994), especially the chapter "Reference Guide on Epidemiology" at 122-192. The journal literature is extensive: B Black & D E Lilienfeld "Epidemiological Proof in Toxic Tort Litigation" (1984) 52 Fordham L Review 732; R E Hoffman "The Use of Epidemiological Data in the Courts" (1984) 120 American Journal of Epidemiology 190; M Dore "A Proposed Standard for Evaluating the Use of Epidemiological Evidence in Toxic Tort and Other Personal Injury Cases" (1985) 25 Howard Law Journal 677; H M Ginzburg "Use and Misuse of Epidemiological Data in the Courtroom" (1986) 12 American Journal of Law & Medicine 423; G E Marchant & M S Baram "The Use of Risk Assessment Evidence to Prove Increased Risk and Alternative Causation in Toxic Tort Litigation" (1990) FICC Quarterly 95; R P Charrow & D E Bernstein Scientific Evidence in the Courtroom: Admissibility and Statistical Significance After Daubert Washington Legal Foundation (1994); Goldberg "Scientific Evidence, Causation and the Law - Lessons of Bendectin (Debendox) Litigation" (1996) 4 MedLR 32; Berger "Eliminating General Causation: Notes Towards a New Theory of Justice and Toxic Torts" (1997) 94 Columbia Law Review 2117; R Parker "Understanding Epidemiology and Its Use in Drug and Medical Device Litigation" (1998) 65 Defence Counsel Law Journal 35.

[67] Most epidemiological studies identify the strength of an association by a measure called relative risk (RR). RR is defined as the ratio of the incidence of disease in exposed individuals compared to the incidence in unexposed individuals. If the relative risk equals 1.0, the risk in exposed individuals is the same as the risk in unexposed individuals. If the relative risk is greater than 1.0 the risk in exposed individuals is greater than the risk in unexposed individuals.

Epidemiological Studies

[68] The epidemiological study to which his Honour made primary reference was the Mandel Study ("The International Renal Cell Cancer Study" (1995) 61 International Journal of Cancer 601). Professor McLaughlin and Dr McCredie were co-authors of the study. It was the most recent study in evidence before his Honour, both directly and indirectly, as a basis for the expressions of opinion by the Respondent's experts.

[69] The Mandel Study identified the Relative Risk as 1.4 and the 95% confidence interval as ranging from 1.1 - 1.8. The identification of a 1.4 RR and a "confidence interval" of 1.1-1.8 in the Mandel study meant that the RR of 1.4 is the best estimate of the increased risk, but the authors have a 95% confidence that that increase falls somewhere between 1.1 and 1.8. An RR of 1.4 is a moderate statistical increase well below the level of 2.0 RR, which the United States authorities, to which I will refer, use as a point of reference.

[70] The Mandel study indicated that there was no dose response relationship between exposure to asbestos and renal cancer. Workers who had had an occupational exposure of between one to eight years showed an RR of 1.5; those exposed between nine and twenty-four years showed an RR of 1.5; and those exposed between twenty-five and fifty-seven years showed a reduced RR of 1.2. The absence of a dose response relationship is of significance in assessing the evidence.

[71] The conclusion of the Mandel Study was:

"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."

[72] An earlier report by McCredie and Stewart was a case report forming part of the Mandel Study ("Risk Factors for Kidney Cancer in NSW" (1993) 50 British Journal of Industrial Medicine 349-354). This study identified a 1.58 RR with a 95% confidence interval of 1.02 - 2.44. Dr McCredie described the 1.58 RR as "a moderately increased risk" and as "moderate". However, with respect to the confidence interval, the fact that the lowest level of the 95% confidence level was 1.02 meant that, in her opinion, there was "a significantly increased risk". The fact that the 95% confidence interval was above 1.0 meant that she was "statistically sure that there is an increased risk". I note that the Mandel Study also began the 95% confidence interval at above the 1.0 level, ie at 1.1.

[73] The third study to which both Dr Burns and Dr McCredie referred was that of Selikoff "Mortality Experience of Insulation Workers in the United States and Canada 1943-1976" (1979) Annals New York Academy of Sciences 91. This was a study of 17,800 asbestos insulation workers. The figures indicated that expected deaths from cancer of the kidney in this sample size was about 8, whereas the actual observed number of deaths from cancer of the kidney was more than double that at 19. This suggested an RR of 2.2, however reassessment in a follow up paper had brought this down to 1.7.

[74] Dr Burns and Dr McCredie also referred to the Enterline study "Asbestos and Cancer a Cohort Follow-Up to Death" (1987) 44 British Journal of Industrial Medicine 396-401. This was a study of 1,074 retired asbestos workers. The report indicated that 2.54 cases of kidney cancer would have been expected but 7 cases were observed, giving an RR of 2.758. This study reported a higher RR for renal cancer than for lung cancer which, Professor Henderson said, was a surprising finding for a study of asbestos exposure.

[75] There was also a study conducted by Maclure upon which Dr Burns said that he had relied. However, after certain statistical errors had been pointed out to the author of the report, it had in fact been withdrawn as, inter alia, Professor McCredie indicated. This was the only study to which, on the evidence, it was not appropriate to give weight.

[76] According to Professor McLaughlin, there had been forty-seven occupational cohort studies of asbestos exposed workers. The overwhelming majority made no reference to renal carcinoma, a fact to which the Professor attached significance. Of the nine studies which did refer to renal cancer two of them reported an increased level of risk:

A study by Acheson "Cancer in a Factory Using Amosite Asbestos" (1984) International Journal of Epidemiology of 5,969 employees in an insulation board factory concluded that 2 cases of such cancer had been observed in the sample whereas 1.4 would have been expected, a ratio of 1.4.

A study by Hughes et al "Mortality of Workers Employed in Two Asbestos Cement Manufacturing Plants" (1987) of 6,931 employees reported 7 cases observed against 5.3 expected, a ratio of 1.32.

These increases in risk would also be described as moderate.

[77] Seven other studies had not reported any increased risk. These included:

Clemmesen and Hjalgrim-Jensen "Cancer Incidence Among 5,686 Asbestos-Cement Workers followed from 1943 through 1976" (1981) 5 Ecotoxicology and Environmental Safety 15 reported 3 cases observed against 5.38 expected, a ratio of 0.55. (Obtained by deducting results for bladder cancer from those for the urinary system).

A study by Peto et al "Relationship of Mortality to Measures of Environmental Asbestos Pollution in an Asbestos Textile Factory" (1985) 29 Annals of Occupational Hygiene 305 of 3,211 men reported 1 death observed from cancer of the kidney against 4.07 expected, a ratio of 0.24.

A study by Raffn et al "Incidence of cancer and mortality among employees in the asbestos cement industry in Denmark" (1989) 46 British Journal of Industrial Medicine 90, of 7,996 men indicated that 12 cases were observed as against 15.39 expected, a ratio of 0.78.

A 1984 study by Liddell "Cancer Mortality in Chrysolite Mining and Milling: Exposure in Response" (1984) of 1,925 men employed in a chrysotile mining and milling in Quebec reported 13 observed cases against 13 expected, a ratio of 1.00.

A 1994 study by De Klerk et al "Diseases in Miners and Millers of Crocidolite from Wittenoom, Western Australia" (Blue AB 1304) of 6,499 men. Dr De Klerk gave oral evidence that in this cohort study, there was 1 observed case of renal cancer against 3 or 4 expected.

Use of Epidemiological Evidence

[78] Epidemiology is, as I have noted above, concerned with the study of disease in human populations. It is not, of itself, directed to the circumstances of an individual case. For the purpose of determining whether exposure to a particular substance is the legal cause of a particular disease, epidemiology only provides evidence of possibility.

[79] Evidence of possibility, including expert evidence of possibility expressed in opinion form and evidence of possibility from epidemiological research or other statistical indicators, is admissible and must be weighed in the balance with other factors, when determining whether or not, on the balance of probabilities, an inference of causation in a specific case could or should be drawn. Where, however, the whole of the evidence does not rise above the level of possibility, either alone or cumulatively, such an inference is not open to be drawn.

[80] The common law test of balance of probabilities is not satisfied by evidence which fails to do more than establish a possibility. See especially the unanimous joint judgment of the High Court in St George Club Ltd v Hines (1961-62) 35 ALJR 106 at 107 where the court referred to Bonnington Castings Ltd v Wardlaw (1956) AC 613 as authority for the following proposition :

"In an action at law a plaintiff does not prove his case merely be showing that it was possible that his injury was caused by the defendant's default."

[81] In Tubemakers of Australia Ltd v Fernandez (1976) 50 ALJR 720 at 724, Mason J referred to:

"...the ordinary onus of proof which rests upon a plaintiff to establish on the probabilities that a medical condition or disability from which he suffers is 'caused or materially contributed to' by the defendant's wrongful conduct (Bonnington Castings Ltd v Wardlaw [1956] AC 613, at 620 per Lord Reid). Consequently as the decision in that case demonstrates, the plaintiff will fail if all that he can show is that his disability might have been so caused...".

[82] See also Cole v Commonwealth of Australia (1961) 62 SR(NSW) 700 at 708. In Roulstone v Tetley (1966) 2 NSWR 389 at 394, Walsh J made a clear distinction between a "theoretical possibility" and "future probabilities", as approved on appeal in Tetley v Roulstone (1960-61) 34 ALJR 495 at 497 and see 496. Further see Sydney County Council v Furner (1991) 7 NSWCCR 210 at 213-217.

[83] The law in Australia is, in my opinion, as stated by Glass JA in this Court in Fernandez v Tubemakers of Australia Ltd (1975) 2 NSWLR 190 at 197:

"The issue of causation involves a question of fact upon which opinion evidence, provided it is expert, is receivable. But a finding of causal connection may be open without any medical evidence at all to support it: Nicolia v Commissioner for Railways (NSW) (1970) 45 ALJR 465, or when the expert evidence does not rise above the opinion that a causal connection is possible: EMI (Australia) Ltd v Bes [1970] 2 NSWR 238; appeal dismissed (1970) 44 ALJR 360N. The evidence will be sufficient if, but only if, the materials offered justify an inference of probable connection. This is the only principle of law. Whether its requirements are met depends upon the evaluation of the evidence."

[84] It is often difficult to distinguish between permissible inference and conjecture. Characterisation of a reasoning process as one or the other occurs on a continuum in which there is no bright line division. Nevertheless, the distinction exists.

[85] Lord Macmillan in Jones v Great Western Railway Co (1930) 47 TLR 39, in the context of stating that a possibility that a negligent act caused injury was not enough, said (at 45):

"The dividing line between conjecture and inference is often a very difficult one to draw. A conjecture may be plausible but is of no legal value, for its essence is that it is a mere guess. An inference in the legal sense, on the other hand, is a deduction from the evidence, and if it is a reasonable deduction it may have validity as legal proof. The attribution of an occurrence to a cause is, I take it, always a matter of inference."

[86] After referring to this passage, Sir Frederick Jordan in Carr v Baker (1936) 36 SR(NSW) 301 said (at 306):

"The existence of a fact may be inferred from other facts when those facts make it reasonably probable that it exists; if they go no further than to show that it is possible that it may exist, then its existence does not go beyond mere conjecture. Conjecture may range from the barely possible to the quite possible."

[87] As Lord Wright put it in a frequently cited passage in Caswell v Powell Duffryn Associated Collieries Ltd [1940] AC 152 at 169-170:

"Inference must be carefully distinguished from conjecture or speculation. There can be no inference unless there are objective facts from which to infer the other facts which it is sought to establish. In some case the other facts can be inferred with as much practical certainty, as if they had been actually observed. In other cases the inference does not go beyond reasonable probability. But if there are no positive proved facts from which the inference can be made, the method of inference fails and what is left is mere speculation or conjecture."

[88] The test is whether, on the basis of the primary facts, it is reasonable to draw the inference. (See eg Layton v Vines (1952) 85 CLR 352 at 358).

[89] In my opinion, evidence of possibility, including epidemiological studies, should be regarded as circumstantial evidence which may, alone or in combination with other evidence, establish causation in a specific case.

[90] Proof on the balance of probabilities, indeed on the beyond reasonable doubt standard, may be established on the basis of circumstantial evidence. As Lord Cairns said in Belhaven and Stenton Peerage [1875] 1 AC 278 at 279:

"My Lords in dealing with circumstantial evidence, we have to consider the weight which is to be given to the united force of all the circumstances put together. You may have a ray of light so feeble that by itself it will do little to elucidate a dark corner. But on the other hand, you may have a number of rays, each of them insufficient, but all converging and brought to bear upon the same point, and, when united, producing a body of illumination which will clear away the darkness which you are endeavouring to dispel."

[91] Causation, like any other fact can be established by a process of inference which combines primary facts like "strands in a cable" rather than "links in a chain", to use Wigmore's simile. (Wigmore on Evidence (3rd ed) para2497, referred to in Shepherd v R (1990) 170 CLR 573 at 579).

[92] In the present case, the primary facts consist, in large measure, of epidemiological studies.

[93] With respect to many diseases, medical science is able to give clear and direct evidence of a causal relationship between a particular act or omission and a specific injury or disease. There are, however, fields of inquiry where medical science is not able to give evidence of that character. There are cases in which medical science cannot identify the biological or pathological mechanisms by which disease develops. In some cases medical science cannot determine the existence of a causal relationship. Such a state of affairs is not necessarily determinative of the existence or non-existence of a causal relationship for purposes of attributing legal responsibility. Epidemiological evidence may be able to fill the gap. It is of particular potential utility in the field of what is often referred to as "toxic torts", especially in case of diseases with long latency periods.

[94] In circumstances where the aetiology of a disease is uncertain, or subject to significant scientific dispute, the Courts are not thereby disenabled from making decisions as to causation on the balance of probabilities. As Herron CJ said in EMI (Australia) Ltd v Bes [1970] 2 NSWR 238 at 242:

"Medical science may say in individual cases that there is no possible connection between the events and the death, in which case, of course, if the facts stand outside an area in which common experience can be a touchstone, then the judge cannot act as if there were a connection. But if medical science is prepared to say that it is a possible view, then, in my opinion, the judge after examining the lay evidence may decide that it is probable. It is only when medical science denies that there is any such connection that the judge is not entitled in such a case to act on his own intuitive reasoning. It may be, and probably is, the case that medical science will find a possibility not good enough on which to base a scientific deduction, but courts are always concerned to reach a decision on probability and it is no answer, it seems to me that no medical witness states with certainty the very issue which the judge himself has to try."

[95] In Fernandez v Tubemakers [1975] 2 NSWLR 190, the plaintiff's medical witness gave evidence to the effect that the relevant trauma was a "possible cause". Mahoney JA distinguished two issues - first whether the trauma was a possible cause and secondly whether it was the actual cause in the case (see also Barnes v Hay (1988) 12 NSWLR 337 at 353) - and said (at 199):

"The question remains whether, accepting that the trauma was a possible cause of the condition, it was open to the jury to infer that, in this case, it was the actual cause of it. The evidence, or the process of reasoning, sufficient to warrant this conclusion may, again, vary with the circumstances of the case. However, before the possible cause, the trauma, can in this particular case be inferred to be the cause of the condition, the cause must be related to the condition, not merely temporally, but 'sufficiently closely'."

[96] His Honour referred to the judgments in EMI (Australia) Ltd v Bes, set out the extract from Herron CJ which I have quoted above, and concluded (at 200):

"In such a case as the present, the question would be whether the evidence showed the connection between the possible cause and the condition which occurred was sufficiently close to warrant a reasonable mind, faced with the problem of determining the question upon the evidence before it, concluding that the possible was the actual cause."

(This passage was quoted with approval by the Full Court of the Supreme Court of Victoria in Dahl v Grier (1981) VR 513 at 523).

[97] In Jones v Dunkel (1958-59) 101 CLR 298 at 305 Kitto J said:

"...I agree that no ground for an inference is to be found in general considerations as to the likelihood of negligent conduct occurring in the condition which existed at the time and place of the collision. One does not pass from the realm of conjecture into the realm of inference until some fact is found which positively suggests, that is to say provides a reason, special to the case under consideration, for thinking it likely that in that actual case a specific event happened or a specific state of affairs existed."

[98] The Courts must determine the existence of a causal relationship on the balance of probabilities. However, as is the case with all circumstantial evidence, an inference as to the probabilities may be drawn from a number of pieces of particular evidence, each piece of which does not itself rise above the level of possibility. Epidemiological studies and expert opinions based on such studies are able to form "strands in a cable" of a circumstantial case.

[99] Do the epidemiological studies show the connection between inhalation of asbestos and renal cell carcinoma to be "sufficiently close" (to use Mahoney JA's formulation) "to warrant a reasonable mind concluding that the possible was the actual cause"?

[100] Do the epidemiological studies "positively suggest" (to use Kitto J's formulation) that inhalation of asbestos materially contributed to renal cell carcinoma?

[101] Do those studies, in combination as "strands in a cable" with other relevant facts, including biological plausibility and the laboratory experiments, establish a basis for an inference that inhalation of asbestos caused the Respondent's cancer?

Increased Risk and Mere Possibility

[102] Some of the epidemiological evidence suggests some increase in risk. On the approach I believe to be appropriate, that evidence and that conclusion are circumstantial facts which may be taken into account as "strands in the cable" for the purpose of drawing the inference that the particular exposure caused or materially contributed to the injury in the specific case.

[103] Mason P has concluded that the law does not regard an increase in risk as satisfying the legal requirements of causing, or materially contributing to, injury. (See Bendix Mintex Pty Ltd v Barnes (1997) 42 NSWLR 307 esp at 315-316).

[104] In that case, Beazley JA said at 339A that the onus of proof of causation "is not discharged by establishing that a particular matter cannot be excluded as a cause of the injury". The authority to which Her Honour referred, Sydney County Council v Furner (1991) 7 NSWCCR 210, stated that proposition as a conclusion from the principle that a mere possibility is not enough. As noted above, authority binding on this Court establishes that principle. Beazley JA does not draw the conclusion that an increase in risk is not capable of establishing causation.

[105] The Respondent relied on an observation by McHugh J in Chappel v Hart supra [272] where His Honour, noting that "increases" in this context includes "creates", said:

"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 the injury that the plaintiff suffers whether or not other factors also contribute to that injury occurring. If, however, the defendant's conduct does not increase the risk of injury to the plaintiff, the defendant cannot be said to have materially contributed to the injury suffered by the plaintiff."

[106] Although His Honour's was a dissenting judgment, this passage has subsequently been referred to with approval. (See Naxakis v Western General Hospital (1999) 73 ALJR 782 at [31] per Gaudron J, and [127] per Callinan J).

[107] The starting point of McHugh J's analysis was that it had been established on the balance of probabilities that the conduct did create or increase the risk of injury, "and that risk had eventuated".

[108] This starting point is the very matter in issue in the present case. Was there evidence on the basis of which the trial judge could conclude, on the balance of probabilities, that there was an increased risk of injury and that that risk had "eventuated" in the specific disease of the Respondent?

[109] If there was such evidence then, to use the words of both Gaudron J (at [31]) and Callinan J (at [128]), the tribunal of fact was "entitled" to find that the conduct which increased risk, materially contributed to the injury - entitled, but not, of course, required to so find.

[110] There is, a similar line of authority based on McGhee v National Coal Board [1973] 1 WLR 1. In that case, Lord Reid said (at 5):

"From a broad and practical viewpoint I can see no substantial difference between saying that what the defendant did materially increased the risk of injury to the pursuer and saying that what the defendant did made a material contribution to his injuries."

[111] In Page v Smith (No 2) [1996] 1 WLR 855, where the issue was whether a motor vehicle accident had materially contributed to the conversion of a pre-existing condition of chronic fatigue syndrome from a mild and intermittent state to a chronic condition, Sir Thomas Bingham MR (as his Lordship then was) said (at 858):

"First it was said that the judge was wrong to refer to a material increase of the risk, which was clearly an echo of the difficult decision of the House of Lords in McGhee v National Coal Board [1973] 1 WLR 1. In my judgment there is force in that criticism. In the McGhee case the question was whether the plaintiff could recover when, although the defendant's negligence had exposed him to an increased risk of contracting dermatitis, he could not show that he had probably suffered damage as a result of exposure to that risk. In the present case, the question is not whether the plaintiff was exposed to an increased risk of exacerbation of his existing symptoms, but whether the accident did in fact have that result. It was not, in my view, a case concerned with risk at all."

[112] As I understand this reasoning, it is equivalent to the phrase "and that risk eventuates" of McHugh J in Chapell v Hart.

[113] The learned author of McGregor on Damages (16th ed, 1997) also uses the word "difficult" to describe McGhee (at p145n):

"This difficult decision is to be regarded as one of policy rather than logic".

(See also Tilbury Civil Remedies, vol 1, (1990) para3066-para3068).

[114] In Wilshir v Essex Area Health Authority [1987] QB 730, Sir Nicholas Browne-Wilkinson (as his Lordship then was) delivered a dissenting judgment, which was referred to with approval in the successful appeal to the House of Lords ([1988] AC 1074 at 1090-1091). His Lordship (at 780A) refused to extend, what he described as "an illogical decision taken on grounds of policy", and concluded at 780B "... it was fundamental to the decision in the McGhee case that the dermatitis was undoubtedly physically caused by brick dust". In that case, the brick dust was established to be a source of the disease and the negligent exposure increased the risk of suffering that disease.

[115] The role of increased risk in the McGhee line of authority was explained by the House of Lords in Kay v Ayrshire and Arran Health Board (1982) 2 All ER 417. In that case the issue was whether or not an overdose of penicillin had been established to have caused deafness. As Lord Griffiths put it (at 422):

"The principle in McGhee v National Coal Board will only fall for consideration if it was first proved that it was an accepted medical fact that penicillin in some cases caused or aggravated deafness."

There was no such evidence in that case.

[116] Furthermore in Kay, Lord Ackner explained McGhee's case in the following terms (at 427):

"In McGhee's case the absence of washing facilities was known to be a factor which increased the risk of dermatitis arising from the circumstances in which the pursuer worked. In this case, as previously stated, there is no evidence to incriminate the overdose of intrathecal penicillin."

[117] In Cubillo v The Commonwealth (Federal Court of Australia, 14 December 1995, unreported) at 76-77 Foster J explained the McGhee line of authority as depending on the proposition that the plaintiff's condition could only have been caused by one factor.

[118] The issue in the present case is whether an increased risk did cause or materially contribute to the injury actually suffered.

[119] There is a tension between the suggestion that any increased risk is sufficient to constitute a "material contribution", and the clear line of authority that a mere possibility is not sufficient to establish causation for legal purposes. The latter is too well established to be qualified by the former. The reconciliation between the two kinds of references is to be found in the fact that, as in Chappel v Hart and in the cases that suggest the former, the actual risk had materialised. The "possibility" or "risk" that X might cause Y had in fact eventuated, not in the sense that X happened and Y had also happened, but that it was undisputed that Y had happened because of X.

[120] The epidemiological evidence in the present case can be expressed in terms of "increased risk". However, in its application to determining causation in the specific case of the Respondent that evidence never rises above the level of a possibility. Whether or not the increased risk "eventuated", is the issue which must be determined. The Respondent's reliance on the passage from McHugh J was, in my opinion, misplaced.

U S Case Law

[121] The use by American courts of Relative Risk established by epidemiological studies for purposes of inferring causation in an individual case, is set out in the following extract from the Federal Judicial Centre's, Reference Manual supra (p178-p179):

"The civil burden of proof is described most often as requiring the fact finder to 'believe what is sought to be proved ... is more likely true than not true'. The relative risk from an epidemiological study can be adapted to this fifty percent plus standard to yield a probability or likelihood that an agent caused an individual's disease. The threshold for concluding that an agent was more likely the cause of a disease than not is a relative risk greater than 2.0. Recall that a relative risk of 1.0 means that the agent has no effect on the incidence of disease. When the relative risk reaches 2.0, the agent is responsible for an equal number of cases of disease as all other background causes. Thus, a relative risk of 2.0 implies a fifty percent likelihood that an exposed individual's disease was caused by the agent. A relative risk greater than 2.0 would permit an inference that an individual plaintiff's disease was more likely than not caused by the implicated agent. A substantial number of courts in a variety of toxic substance cases have accepted this reasoning."

[122] The authors of the study went on to say (at p179-p180):

"The discussion above assumes that the only evidence bearing on cause in fact is epidemiological. Such an assumption is unlikely, and a variety of additional pieces of evidence, although less quantifiable, affect a fact finder's assessment. Biases in the epidemiological studies might justify a conclusion that the real magnitude of increase risk is greater or lower than that revealed in the study. The dose to which the plaintiff was exposed might be greater or lesser than those in the epidemiological study, thereby requiring some extrapolation. In addition, there might be factors peculiar to the plaintiff - excess exposure to another known cause, pathological mechanism, family history of disease, or conflict in diagnoses - that modify any probability based solely on the available epidemiological evidence.

This additional evidence bearing on causation has led a few courts to conclude that a plaintiff may satisfy his or her burden of production even if a relative risk less than 2.0 emerges from the epidemiological evidence. For example genetics might be known to be responsible for fifty percent of the incidence of the disease. If genetics can be ruled out in an individual's case, then a relative risk greater than 1.5 might be sufficient to support an inference that the agent was more likely than not responsible for the plaintiff's disease."

[123] The authors referred to a number of authorities in support of these propositions.

[124] In Manko v The United States 636 F Supp 1419 (1986), affirmed in relevant Pt830 F 2d 831 (8th Cir. 1987) and subsequently quoted with approval in DeLuca v Merrell Dow Pharmaceuticals Inc 911 F 2d 941 (3rd Cir. 1990) at 958-959, the Court stated (at 1433-1434):

"Epidemiology is the study of the available data to determine whether a causal relationship exists between an event and the outbreak of a disease. The first step in analysing whether there is a causal relationship between an event and the outbreak of a disease is to determine whether the causal relationship is biologically possible. Both plaintiff's experts and defendant's experts agree that it is biologically possible for the swine flu vaccination to cause GBS (Guillain-Barr Syndrome).

Because a causal relationship between the swine flu vaccinations and GBS is biologically possible, the next inquiry is whether there is a statistically significant association between the vaccination and the outbreak of the disease. This association is determined by mathematical computation that produces a ratio for the relative risk of contracting the disease. The relative risk ratio is computed by dividing the observed number of cases of a particular disease for a particular time period (numerated data) by the expected number of cases of that disease for the same time period based on historical information not influenced by the event in question (denominated data).

A relative risk of 'one' is the expected rate of contracting a disease in a population not influenced by the event under investigation. A relative risk of 'two' means that the disease occurs among the population subject to the event under investigation twice as frequently as the disease occurs among the population not subject to the event under investigation. Phrased another way, a relative risk of 'two' means that, on the average, there is a fifty percent likelihood that a particular case of the disease was caused by the event under investigation and a fifty percent likelihood that the disease was caused by chance alone. A relative risk greater than 'two' means that the disease more likely than not was caused by the event." (p1433-p1434).

(See also Hall v Baxter Healthcare Corp 947 F Supp 1387 (1996) at 1403).

[125] In Daubert v Merrell Dow Pharmaceuticals Inc. 43 F 3d 1311 (9th Cir. 1991) the United States Court of Appeals for the ninth circuit had before it an issue as to whether or not the drug Bendectin caused birth defects. The Court said (at 1314):

"Not knowing the mechanism whereby a particular agent causes a particular effect is not always fatal to a plaintiff's claim. Causation can be proved even when we don't know precisely how the damage occurred, if there is sufficiently compelling proof that the agent must have caused the damage somehow . One method of proving causation in these circumstances is to use statistical evidence. If fifty people who eat at a restaurant one evening come down with food poisoning during the night, we can infer that the restaurant's food probably contained something unwholesome, even if none of the dishes is available for analysis. This inference is based on the fact that, in our health conscious society, it is highly unlikely that fifty people who have nothing in common except that they ate at the same restaurant would get food poisoning from independent sources."

[126] The relevant issues were identified by the Court as follows (at 1320):

"California tort law requires plaintiffs to show not merely that Bendectin increased the likelihood of injury, but that it more likely than not caused their injuries. See Jones v Ortho Pharmaceutical Corp 163 Cal App 3d 396, 403, 209 Cal Rptr 456 (1985). In terms of statistical proof, this means that plaintiffs must establish not just their mother's ingestion of Bendectin increased somewhat the likelihood of birth defects, but that it more than doubled it - only then can it be said that Bendectin is more likely than not the source of their injuries. Because the background rate of limb reduction defects is one per thousand births, plaintiffs must show that among children of mothers who took Bendectin the incidence of such defects was more than two per thousand."

[127] In a footnote to this passage, the Court said (at 1320, fn13):

"No doubt there will be unjust results under the substantive standard. If a drug increases the likelihood of birth defects, but doesn't more than double it, some plaintiffs whose injuries are attributable to the drug will be unable to recover. There is a converse unfairness under a regime that allows recovery to everyone that may have been affected by the drug. Under this regime, all potential plaintiffs are entitled to recover, even though most will not have suffered an injury that can be attributed to the drug. One can conclude from this that unfairness is inevitable when our tools for detecting causation are imperfect and we must rely on probabilities rather than more direct proof."

[128] The Court went on to refer to Deluca, supra, and the requirement that the relative risk ratio exceed two, and said (at 1321):

"A relative risk of less than two may suggest teratogenicity, but it actually tends to disprove legal causation, as it shows that Bendectin does not double the likelihood of birth defects."

[129] The evidence before the Court in that case included epidemiological evidence, the evidence of the effect on laboratory animals and comparison between the chemical structure of the pharmaceutical in question and other pharmaceuticals with a known effect. The Court concluded that this combination of evidence never rose above the level of establishing that the drug Bendectin could "possibly" have caused the injury.

[130] A similar issue to that arising in the present proceedings was considered by the United States District Court for New York in Re Joint Eastern and Southern District Asbestos Litigation 758 F Supp 199 (1991). The issue was whether or not exposure to asbestos was a cause of colon cancer. The Court held that the balance of probabilities test required a relative risk of 2.0. It emphasised that this was applicable in a case where a plaintiff had to rely on epidemiological evidence alone (202-203). This case was overruled on appeal on the basis that in that particular case the plaintiff did in fact have evidence additional to the epidemiological evidence, namely clinical evidence based on the plaintiff's own medical records and personal history. Accordingly, the United States Court of Appeal for the Second Circuit did not need to rule on the test which the trial judge applied (see in Re Joint Eastern and Southern District Asbestos Litigation 964 F 2d 92 (2nd Cir. 1992) at 97.

[131] Litigation about the possible link between asbestos and colon cancer returned to the United States Court of Appeals of the Second Circuit in 1995, in a case in which the District Court for the Southern District of New York had entered judgment as a matter of law in favour of the defendant. Allowing the appeal, the appellate court found that the evidence before the Court was sufficient to leave the matter to the jury. (See in Re Joint Eastern and Southern District Asbestos Litigation 827 F Supp. 1014 (1993) and on appeal 52 F 3d 1124 (2nd Cir. 1995)). The appellate court summarised the decision below in the following terms (at 1127-1128):

"The District Court based its decision on its findings that:

(1)

the plaintiff's epidemiological evidence was insufficient to support a causal connection between asbestos exposure and colon cancer, and

(2)

the plaintiff had failed to present affirmative clinical evidence to overcome the paucity of statistically significant epidemiological proof."

[132] The Court referred to the risk ratio of 2.0 in terms of a "standardised mortality ratio" ("SMR"). The Court summarised the test adopted by the District Court in the following way (at 1128):

"In order for plaintiff to present a jury question on the issue of causation, the District Court noted that she bore the burden of demonstrating that asbestos exposure was "more likely than not" the cause of Maiorana's colon cancer ... This burden could be met either through studies conclusively establishing an SMR of more than 2.0, or through epidemiological evidence falling short of 2.0 in combination with "clinical or experimental evidence which eliminates confounding factors and strengthens the condition between the causal factor and the disease specifically in the circumstances surrounding the plaintiff's case of (the disease)."

[133] This statement of the relevant test does not appear to have been doubted in the appeal. The case on appeal turned on whether or not the District Court had impermissibly undertaken the jury's role in the way it assessed the scientific evidence and also whether or not it had ignored the references to the quality of the evidence in the judgment of the Court on the previous appeal. In the event, the appellate court held that there was evidence fit to go to a jury.

[134] The Court concluded (at 1133):

"We acknowledge that sufficiency poses unique difficulties with trial courts in toxic or carcinogenic tort cases, such as the one before us, which hinge on competing interpretations of epidemiological evidence. By its nature, epidemiology is ill suited to lead a fact finder towards definitive answers, dealing as it does in statistical probabilities and the continual possibility of confounding causal factors ...In light of the inherent uncertainties shrouding issues of probabilistic causation, the decision of a District Court on whether a plaintiff's epidemiological evidence is sufficient to get to the jury should be guarded by the well established standards governing judgment as a matter of law - whether, viewed in a light most favourable to the non-moving party, "the evidence is such that, without weighing the credibility of the witnesses or otherwise considering the weight of the evidence there can be but one conclusion as the verdict that reasonable (jurors) could have reached." ...Applied to epidemiological studies, the question is not whether there is some dispute about the validity or force of the given study, but rather, whether it would be unreasonable for a rational jury to rely on that study to find causation by preponderance of the evidence."

[135] Some of the American cases indicate that the RR of 2.0 should not be applied as a rigid mathematical formula. Others appear to apply it in that way.

[136] The predominant position in Australian case law is that a balance of probabilities test requires a court to reach a level of actual persuasion. This process does not involve a mechanical application of probabilities. (See Briginshaw v Briginshaw (1938) 60 CLR 336 at 361-362; Jones v Dunkel (1959) 101 CLR 298 at 304-305; West v Government Insurance Office of NSW (1981) 148 CLR 62 at 66; State Government Insurance Commission v Laube (1984) 37 SASR 31 at 33; Sir Richard Eggleston Evidence, Proof and Probability (2nd ed, 1983) esp Ch 10; The Hon Mr Justice K J Carruthers "Some Observations on the Standard of Proof in Marine Insurance Cases" (1988) 62 ALJ 199 esp at 208-209; The Hon Mr Justice D H Hodgson "The Scales of Justice: Probability and Proof in Legal Fact Finding" (1995) 69 ALJ 731 esp at 732-733; Hamer "The Civil Standard of Proof Uncertainty: Probability, Belief and Justice" (1984) 16 Syd LR 506 esp at 509-512; Robertson and Vignaux "Probability: the Logic of the Law" (1993) 13 Oxford J of Legal Studies 457; Hodgson "Probability: the Logic of the Law Response" (1995) 15 Oxford J of Legal Studies 51 esp at 58-59; Note (1997) 71 ALJ 33; Ligertwood "Australian Evidence" (3rd ed, 1998) pp14ff; Redmayne "Standards of Proof in Civil Litigation" (1999) 62 Mod LR 167).

[137] In Australian law, the test of actual persuasion does not require epidemiological studies to reach the level of a Relative Risk of 2.0, even where that is the only evidence available to a court. Nevertheless, the closer the ratio approaches 2.0, the greater the significance that can be attached to the studies for the purposes of drawing an inference of causation in an individual case. The "strands in the cable" must be capable of bearing the weight of the ultimate inference.

Assessment of Epidemiological Evidence

[138] The American authorities make reference to a list of factors, referred to in the submissions in this Court as "postulates", which are taken into account by epidemiologists in the course of considering whether or not a causal relationship should be inferred from a statistical association. In United States case law and literature, these "postulates" are referred to as the "Bradford-Hill criteria" or, less often, as the "Koch postulates". The former is the usage in Australia , as in England. This is a reference to criteria formulated by Sir Austin Bradford Hill, then Professor Emeritus of Medical Statistics at the University of London, in his Presidential address to the Section of Occupational Medicine: "The Environment and Disease: Association or Causation" (1965) 58 Proc R Soc Medicine 295.

[139] There is widespread acceptance amongst epidemiologists of the principles or postulates which are applied to assess the evidence of a statistical correlation or association. In evidence in the present case, is the article by McLaughlin and Brookmeyer, which contains the following summary:

" Key Principles in Interpreting Epidemiological Studies

1

Strength of the Association In general the higher the risk estimate, the less likely the finding is a result of confounding or bias ...

2

Dose Response Effect If the risk of the disease rises with increasing exposure, a causal interpretation of the association is more plausible ...

3

Time Sequence The exposure or risk factor must precede the disease ...

4

Consistency Results from other epidemiological studies of the exposure-disease association should be similar. If similar results are found in different populations using various study designs, the plausibility of a causal interpretation is increased. An alternative explanation of bias or confounding would have to apply to each of the different studies, a highly implausible explanation.

5

Biological Coherence Does the exposure-disease association make biological sense given what is known of the natural history of the disease? Do animal experiments support the association? Do other types of collateral evidence support the association, such as secular trends of the exposure factor in the disease? Unfortunately, for many diseases little is known about their aetiologies, so the informational background by which to judge biological coherence is often limited. Thus, failure of this broad principle does not necessarily weaken the plausibility of a causal interpretation.

The first three principles can be applied to an individual study and used to assist the findings. The last two principles referred to results outside their particular study and relate more to external issues of coherence or consistency. All of the criteria or principles should be viewed as guidelines. Except, perhaps, for time sequence, none is required for a causal interpretation."

[140] These postulates or criteria are uncomplicated statements of commonsense propositions. (See French J in Reay v British Nuclear Fuels supra (at 13)).

[141] The postulates or criteria are all matters which a court can take into account in determining whether or not it should infer, on the balance of probabilities, that a particular exposure caused injury in the specific case before the court. The approach of epidemiologists with respect to the identification and application of the postulates may be of assistance to the court by force of their reasoning. They do not constitute a scientific opinion which a court is constrained to accept.

[142] When assessing expert evidence on causation, the legal concept of causation requires the court to approach the matter in a distinctively different manner from that which may be appropriate in either philosophy or science, including the science of epidemiology.

[143] The commonsense approach to causation at common law is quite different from a scientist's approach to causation. (See National Insurance Co of New Zealand Ltd v Espagne (1961) 105 CLR 569 at 591; March v E & M H Stramare Pty Ltd (1990-91) 171 CLR 506 at 509, 522, 530-531; Chappel v Hart (1998) 195 CLR 232 esp at [6]-[7], [23], [62]-[64], [93], [111], [122]. An inference of causation for purposes of the tort of negligence may well be drawn when a scientist, including an epidemiologist, would not draw such an inference.

[144] The Appellant James Hardie submitted that with respect to issues of medical causation, a court should not infer causation where scientists, including epidemiologists, would not do so. This submission is inconsistent with a long line of authority and should be rejected.

[145] As is often the case with evidence of experts, evidence on causation may in fact be more in the nature of submissions than opinion evidence properly so called. In a technical area it is sometimes helpful to have submissions articulated by a person with technical expertise, without the intermediation of counsel. That is not to say that there are not many occasions when lay explanation, indeed translation, of such technical evidence is required.

[146] In the present case, no issue was raised with respect to "time sequence" or "biological coherence". There was, however, disagreement amongst the experts on the "strength of association" and "consistency" criteria. The absence of a dose response relationship was also referred to. These disputes affect both the direct use of those studies as "strands in the cable" and the extent to which reliance can be place on expert opinions, based on those studies, with respect to causation in the specific case.

[147] Like all the postulates, the proposition that the stronger the association the lower the probability that it would occur without a causal relationship, is a commonsense proposition which a court will readily accept. The same is true of the proposition that inconsistency of results undermines an inference of causation.

Admissibility of Opinions

[148] Senior Counsel for Seltsam submitted that the opinion expressed by Dr McCredie as to causation in the individual case and the opinions expressed by Dr Burns about the epidemiological studies were not admissible. He submitted that neither had "specialised knowledge" within s79 of the Evidence Act 1995 (NSW). Dr McCredie was an epidemiologist without the medical knowledge required to express a conclusion on causation in the specific case. Dr Burns was a medical practitioner, not an epidemiologist. Reliance was placed on the observations of Gleeson CJ in H G v R (1999) 160 ALR 554 at [39]-[40] and [43]-[44].

[149] No objection to admissibility was taken at the trial. In the ordinary course, the words "not admissible" in the Evidence Act, including in the opinion rule found in s70 to which s79 is an exception, means "not admissible over objection", in accordance with the practice of the courts of which the Parliament was aware when it passed the Evidence Act. (See R v Reid (1999) NSWCCA 258 at [5]). If this appeal were being conducted under the new s32 of the Dust Diseases Tribunal Act and the court were concerned to identify "a question as to the admission of evidence", it may have been necessary to consider whether the special circumstances of this trial were such as indicate that the delays involved in objecting to evidence were so inappropriate as to require a qualification of the general proposition I have advanced. It is not, however, necessary to do so.

[150] I have no difficulty with a medical practitioner drawing on and assessing epidemiological studies. I have greater difficulty with an epidemiologist expressing an opinion about causation in the individual case. Dr McCredie did so. Professor McLaughlin expressed the opposite opinion. As I understand the position, epidemiology is concerned with populations, not individual cases. As no objection was taken, this issue was not fully explored below. I am not prepared to hold, for the first time on appeal, that the opinions were not admissible under s79.

Conclusion

[151] It is necessary to bring together the strands in the cable and determine whether an inference that asbestos exposure caused or materially contributed to the Respondent's renal cell carcinoma should be drawn. In my opinion the answer is in the negative.

[152] As I have indicated above, in my opinion, Judge Maguire expressly refrained from considering the strength and quality of the results of the epidemiological studies which were in evidence before him.

[153] As I have also noted above, a circumstantial case can involve drawing a conclusion on the balance of probabilities, or indeed beyond reasonable doubt, on the basis of facts which are expressed only in terms of possibility. Whether or not the inference is open or should be drawn, depends on the quality of the underlying facts, particularly in terms of the degree of 'possibility' which is involved.

[154] His Honour's judgment does not contain any findings which identify, or in any way consider, the degree of possibility. That is not, in the circumstances of this case, a criticism of His Honour's reasons. The judgment had to be, and was, delivered under conditions of great urgency, so that the Respondent could know the outcome before he died. In another case, this may have given rise to an error of law in terms of inadequacy of the reasons. That was not the case here.

[155] However, the trial judge did not simply fail to give reasons. He said he would not consider the detailed submissions made to him about the epidemiological studies. In this, as I have said above, in my opinion he erred. This justifies the intervention of the court and, indeed, may well have done so even if the new s32 of the Act were applicable to the case.

[156] One of the factors which His Honour took into account - as did Dr Burns - was that asbestos is a "known carcinogen". This is not a fact entitled to much, if any, weight.

[157] In Kay v Ayrshire and Arran Health Board supra 417, the issue was whether an overdose of penicillin had caused deafness. Lord Mackay of Clashfern said (at 425):

"The next step is to consider whether there is evidence that the overdose materially increased the risk of deafness. In my opinion, it is not right to ask whether it materially increased the risk of neurological damage when the evidence available distinguishes between different kinds of neurological damage ...I cannot accept that it is correct to say that because evidence shows that an overdose of penicillin increases the risk of particular types of neurological damage found in these cases that an overdose of penicillin materially increases the risk of a different type of neurological damage, namely that which causes deafness when no such deafness has been shown to have resulted from such overdose."

[158] In the present case there was evidence before His Honour that other "known carcinogens" are not causally related to forms of cancer, other than certain specific types.

[159] The Mandel study, to which His Honour made extensive reference, found that exposure to radiation or radioactive materials did not suggest any relationship with renal cell carcinoma. (Reporting a RR of 0.7). Other material in the evidence is equivocal. One survey co-authored by Professor McLaughlin describes any such relationship as "weak".

[160] Furthermore, the evidence before the Court indicated that asbestos has been found in various parts of the human body, without any suggestion of adverse consequences. Exposure of the skin to asbestos does not appear to result in skin cancer.

[161] His Honour's references to "heavy exposure" and "heavy asbestos infection" in His Honour's reasoning suggests that His Honour applied an intuitive judgment that the greater the exposure to asbestos, the more likely it would have the particular consequence.

[162] This was one of the very matters on which His Honour had a body of expert evidence. Epidemiologists do take into account whether or not studies indicate that a dose response relationship exists. When relying on the "heavy" extent of asbestos exposure, His Honour did not expressly consider the epidemiological evidence on this issue.

[163] The Mandel study, on which His Honour placed particular reliance, does not suggest that the degree of exposure is material. It is a feature of that study that no dose response relationship between asbestos and renal cancer was suggested. Indeed, the relative risk went down with greater exposure: a "reverse response". The relative risk was identified as 1.5 for occupational exposure between one to eight years; 1.5 for occupational exposure between nine and twenty-four years; and 1.2 for occupational exposure between twenty-five and fifty-seven years. This reduction is the opposite to that which His Honour inferred and on which he appeared to rely. The evidence does not support "heavy exposure" as a "strand in the cable" in the process of inferring causation in the individual case.

[164] His Honour also referred with approval to the submission that there had been "heavy exposure" to asbestos and that this contrasted with what was described as a "light smoking experience". His Honour accepted the proposition that if "smoking can be minimised as a possibility, then any other candidate for causality must have its prospects enhanced." His Honour made no reference to obesity, which the epidemiological evidence clearly indicated was a known risk factor and which Dr McCredie had identified as a relevant causal factor in the case of the Respondent.

[165] His Honour's reasoning appears to turn on the proposition that the scope of relevant causal factors was limited to a choice between smoking and asbestos exposure. Nothing in the medical literature or the epidemiological literature or the expert evidence suggests that the issue came down to a choice between these two factors: smoking or asbestos.

[166] Indeed in her report of 2 July 1997, (Blue AB Vol 4 p24) Dr McCredie said:

"In the case of renal cell carcinoma, most of the causes are unknown or imperfectly understood".

This appeared to be accepted by all the experts.

[167] In such a case, the fact that one known risk factor is of diminished significance, says little, if anything, about another alleged risk factor. This case was not fought on the basis that the cause was either smoking or asbestos.

[168] As Dixon CJ said in Jones v Dunkel supra at 305, the balance of probabilities test:

"...does not authorise a court to chose between guesses, on the ground that one guess seems more likely than another or the others. The facts proved must form a reasonable basis for a positive conclusion affirmatively drawn of the truth of which the tribunal of fact may reasonably be satisfied."

[169] The assessment of conflicting expert witnesses is subject to well known restrictions on an appellate court reviewing findings of fact. His Honour placed reliance on the opinions expressed by Dr Burns and Dr McCredie. He did not reject the other experts based on any assessment of their credibility. The various experts gave detailed reasons for their analyses of the epidemiological studies which are able to be assessed by this Court.

[170] This is not a case in which the experts drew on anything in the nature of clinical experience or "feel". (See X & Y v Pal (1991) 23 NSWLR 26 per Mahoney JA at 34). The experts articulated their positions in writing and in oral evidence, in a manner capable of assessment by an appellate court.

[171] If there had been any evidence relevant to the Respondent personally, for example if asbestos had been detected in his kidney, the basis for an inference of causation in the individual case would have been quite different. However, what His Honour had before him was evidence of possibilities: the fact that asbestos can reach the kidney, the laboratory experiments on rats, the positive epidemiological studies.

[172] I have set out above in summary form the general conclusions of the epidemiological studies. They show two things:

(i)

The increased risk, where detected at all is generally low to moderate.

(ii)

Many studies do not show any increased risk.

[173] It must be borne in mind that references to increased risk in the studies and the epidemiological literature are references to increases in human populations. The application of that information to the case of a specific individual requires a separate and distinct step by way of inference.

[174] In my opinion, the extent of increased risk indicated by all but one, or perhaps two, of the epidemiological studies is too small to justify an inference of causation, either alone or in combination with other factors including biological plausibility, the laboratory experiments and the expressions of professional opinion which were, in large measure, based on the epidemiological evidence.

[175] The relative risk factors in the range of 1.32 to 1.58 for four of the six positive studies are well below the level of 2.0 which could satisfy a balance of probability test according to the U S case law. Whilst I do not hold that such a level is required, the fact that the increased risk of most positive studies is only of a low to moderate degree, significantly undermines their importance as a basis for inferring causation in an individual case.

[176] One study shows a significant ratio of 1.7 and another a particular significant ratio of 2.758. These studies cannot, on their own sustain an inference of causation, unless the other studies, both positive and negative, are given minimal weight. There is no basis in the evidence for doing so.

[177] The seven cohort studies which indicated no increased risk reported an RR range of 0.24 to 1.0. Other studies of asbestos exposure did not show any results with respect to renal cell carcinoma.

[178] Dr McCredie and other witnesses gave evidence that greater weight should be given to some studies rather than others, on the basis of a range of specific matters eg sample size, length of exposure, anomalous results. Nevertheless all the studies were accepted to be entitled to weight in the epidemiological assessment.

[179] Dr McCredie asserted that there was sufficient consistency. This was an observation based on giving particular weight to the studies which she believed had a sufficient sample size of long periods of exposure. For example, the Wittenoom Study had a large sample size, but she discounted its results because of the substantial proportion of the sample which had been employed for short periods.

[180] Dr McCredie's evidence would have greater force if the studies on which she did rely suggested the existence of a dose response relationship. They do not. It is not, in my opinion, appropriate to give studies like the Wittenoon Study minimal weight as Dr McCredie suggested.

[181] On the other hand some of the studies on which Dr McCredie placed reliance were case control studies affected by recall bias. Furthermore, the study which suggested an RR of 2.758, produced anomalous results in finding low rates for lung cancer from exposure to asbestos. While these studies are entitled to weight they are not entitled to determinative weight.

[182] When the negative results of the seven studies entitled to be given weight is combined with the small to moderate increased risk of all but two of the positive epidemiological studies, the effect of the evidence when combined as strands in a cable, does not, in my opinion, support an inference of causation in the specific case of the Respondent.

[183] Epidemiological studies and expert epidemiological opinion evidence on general causation go no further than establishing a possibility. Applying a common sense test of causation to the evidence of possibility in the present case does not, in my opinion, justify an inference of causation on the balance of probabilities in the individual case.

[184] In my opinion, the appeals should be allowed.

[185] This was a case of significance for the Appellants beyond the individual case. It was fought below and in this Court as if it were a test case. For that reason I would not disturb His Honour's order as to costs. Each party should bear its own costs of the appeals.