Seltsam Pty Ltd v McGuiness - [2000] NSWCA 29

NEW SOUTH WALES COURT OF APPEAL

CITATION: Seltsam Pty Limited v McGuiness; James Hardie & Coy Pty Limited v McGuiness [2000] NSWCA 29

FILE NUMBER(S):
40456/97
40463/97

HEARING DATE(S): 2 - 3 August 1999

JUDGMENT DATE: 07/03/2000

PARTIES:
Seltsam Pty Limited (Appellant) (40456/97)
Robert George McGuiness (First Respondent)
James Hardie & Coy Pty Limited (Appellant) (40463/97)
Robert Geroge McGuiness (First Respondent)

JUDGMENT OF: Spigelman CJ Stein JA Davies AJA

LOWER COURT JURISDICTION: Dust Diseases Tribunal

LOWER COURT FILE NUMBER(S): DDT 51/93

LOWER COURT JUDICIAL OFFICER: Judge Maguire, QC

COUNSEL:
R Burbidge QC/S Rushton (Appellant - Seltsam)
C Gee QC/J McIntyre (Appellant - James Hardie)
J T Rush QC/G Farmer (First Respondent)

SOLICITORS:
Toomey Pegg & Drevikovsky (Appellant - Seltsam)
A O Ellison & Co (Appellant - James Hardie)
Turner Freeman (First Respondent)

CATCHWORDS:
NEGLIGENCE - proof of negligence - causation - whether exposure to asbestos caused renal cell carcinoma - use of epidemiological studies
EVIDENCE - opinion evidence - expert opinion - Evidence Act 1995 (NSW) s 79
DUST DISEASES - Appellate Jurisdiction of Supreme Court - Dust Diseases Tribunal Act 1989 s 32 - D

LEGISLATION CITED:
Compensation Court Act 1984
Courts Legislation Amendment Act 1998
Dust Diseases Tribunal Act 1989
Evidence Act 1995
Interpretation Act 1987

DECISION:
Appeals allowed
Set aside order 2 of the Dust Diseases Tribunal
Each party to bear his and its own costs of the appeals

JUDGMENT:

THE SUPREME COURT

OF NEW SOUTH WALES
COURT OF APPEAL
CA 40456/97
CA 40463/97
DDT 51/93
SPIGELMAN CJ
STEIN JA
DAVIES AJA
Tuesday, 7 March 2000

SELTSAM PTY LTD v McGUINESS & ANOR
JAMES HARDIE & COY PTY LIMITED v McGUINESS & ANOR

Negligence - proof of negligence - causation - whether exposure to asbestos caused renal cell carcinoma - use of epidemiological studies

Evidence - opinion evidence - expert opinion - Evidence Act 1995 (NSW) s79

Dust Diseases - Appellate Jurisdiction of Supreme Court - Dust Diseases Tribunal Act 1989 s32

A plaintiff was awarded damages in the Dust Diseases Tribunal for renal cell carcinoma which was found to be caused by the defendants’ negligence in exposing him to asbestos.

The principle issue raised in the appeal was the use of epidemiological evidence to prove causation. A preliminary issue was whether the appellate jurisdiction of the Supreme Court was determined by s32 of the Dust Diseases Tribunal Act 1989 as in force before amendment by the Courts Legislation Amendment Act 1998.

Held: (Allowing the appeal)

Nature of Appeal

(Per Spigelman CJ, Stein JA and Davies AJA agreeing)

Section 32 of the Dust Diseases Tribunal Act as in force before it was amended by the Courts Legislation Amendment Act applies to an appeal instituted before the commencement of the amended provision. Fishburn v Electricity Commission of New South Wales (1999) NSWCA 401 distinguished.

Parliament must express an intention to remove the jurisdiction of a court which has already been invoked in clear and unambiguous words. Bropho v Western Australia (1990) 171 CLR 1; Magrath v Goldsbrough Mort & Co Ltd (1932) 47 CLR 121. The transitional provisions inserted in the Dust Diseases Tribunal Act by the Courts Legislation Amendment Act do not evince such an intention with respect to appeals instituted before the commencement of the amended s32. Section 30(1)(b) of the Interpretation Act 1987 applied.

Causation: General

(Per Spigelman CJ, Davies AJA agreeing)

Epidemiological evidence that exposure to a substance is a possible cause of an injury may be used to establish that the exposure is the legal cause of the injury.

The balance of probabilities test is not satisfied by evidence which fails to do more than establish a possibility: St George Club Ltd v Hines (1961-62) 35 ALJR 106; Tubemakers v Fernandez (1976) 50 ALJR 720; Fernandez v Tubemakers of Australia Ltd (1975) 2 NSWLR 190.

Causation is not established by showing that a defendant’s act or omission increased the risk of injury to a plaintiff when the risk had not eventuated: Chappel v Hart (1998) 195 CLR 232; Naxakis v Western General Hospital (1999) 73 ALJR 782; McGhee v National Coal Board [1973] 1 WLR 1 considered.

Causation in an individual case can be established by a process of inference from circumstantial evidence which combines primary facts like “strands in a cable”. Epidemiological evidence of the effects on populations of exposure to a substance is circumstantial evidence which may form part of this process of inference.

Evaluation of epidemiological studies considered.

Causation: Facts of the Instant Case

(Per Spigelman CJ and Davies AJA, Stein JA dissenting)

The trial judge did not take into account the strength or quality of the epidemiological evidence including the strength of association identified in, and inconsistencies between, the various studies.

The evidence does not support a finding that asbestos exposure caused or materially contributed to the respondent’s renal cell carcinoma.

(Per Stein JA)

A finding that exposure to asbestos caused the respondent’s renal cell carcinoma was open to the trial judge.

Liability

(Per Stein JA)

There was evidence of actual knowledge of the appellants of the dangers to workers of being exposed to asbestos. That the exposure was within the threshold limit value of the National Health and Medical Research Council at the time does not affect the foreseeability of injury resulting from it.

Orders

Appeals allowed.
Set aside order 2 of the Dust Diseases Tribunal.
Each party to bear his and its own costs of the appeals.
***********
THE SUPREME COURT
OF NEW SOUTH WALES
COURT OF APPEAL
CA 40456/97
CA 40463/97
DDT 51/93
SPIGELMAN CJ
STEIN JA
DAVIES AJA
Tuesday, 7 March 2000
SELTSAM PTY LTD v McGUINESS & ANOR
JAMES HARDIE & COY PTY LIMITED v McGUINESS & ANOR
JUDGMENT
SPIGELMAN CJ: 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.
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
Section 32 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.

The 1998 Amendment Act amended Schedule 3 of the Act by the inclusion of:
“4 Section 32 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.”
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.
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.”
It is this section which, by force of clause 4 of Schedule 3 of the Act, “does not apply to decisions of the Tribunal made before that commencement”.
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.
The proper construction of clause 4 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 i.e. 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.
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.
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. Section 32 as so “in force” stated, relevantly; “a party … dissatisfied with a decision … may appeal”.
The words of the new clause 4 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.
The usual presumption is that legislation operates prospectively. That presumption applies to clause 2 of Schedule 11 of the Courts Legislation Amendment Act 1998 which inserted clause 4 into “Schedule 3 - Savings Transitional and other Provisions” of the Act. The presumption is not, in my opinion, displaced. Clause 1 of Schedule 11 of the 1998 Amendment Act omitted s32. It did not omit the section with retrospective affect.
Clause 4 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.
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.
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 …”
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 clause 4 in Schedule 3, “affects” the appeals so instituted.
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
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.
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?
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.
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.
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.
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.”
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.”
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.
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.
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.
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.
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.”
The submissions which his Honour set aside as irrelevant, were directed to the assessment of the strength and quality of the epidemiological studies.
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.
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
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.
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)

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.”
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).
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.
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.”
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.”
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.
The first matter establishes a possibility of a connection: “biological plausibility”, as it was referred to in the evidence.
The second matter involves the identification of asbestos as a suspect substance.
The third matter, animal laboratory experiments, is a permissible, albeit limited, basis for the opinion.

The fourth matter is the epidemiological studies, to which I will refer further below.
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.
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.
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.”
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.
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.”
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.
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.
Dr Katelaris in a report dated 5 July 1997 asserted that the link between asbestos exposure and renal cell carcinoma had not been proved.
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.
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.
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.
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”.
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
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.
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?
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)).
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.
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.
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.
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.
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.
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

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.
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.
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.
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.”
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, i.e. at 1.1.
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.
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.
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.
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.

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

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.
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.
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 CastingsLtd 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.”
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…”.

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.
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.”
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.
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.”
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.”
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.”
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).
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.
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.”
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) para 2497, referred to in Shepherd v R (1990) 170 CLR 573 at 579).
In the present case, the primary facts consist, in large measure, of epidemiological studies.
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.
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.”
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’.”
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).
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.”
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.
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) paras 3066-3068).

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 (pp178-179):

“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 pp179-180):

“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 part 830 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.” (pp1433-1434).

(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 Benectin the incidence of such defects was more than two per thousand.”

127 In a footnote to this passage, the Court said (at 1320, fn 13):

“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 The Queen (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.

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.

265 DAVIES AJA: As the Chief Justice and Stein JA have dealt with all the issues in the appeal, I limit my comments to the issue of causation, on which I agree with the reasons and conclusions of the Chief Justice. I agree with the Chief Justice and Stein JA on the nature of the appellate jurisdiction.

266 This appeal is one in which it is important for an appellate judge to consider carefully the issues and the material that were before the trial Judge. Although the trial Judge, his Honour Judge Maguire, at the end of a week’s hearing of a case which had been brought on as a matter of urgency, gave an impressive judgment, an appellate judge necessarily has more time available in which to consider the matter.

267 As Stein JA has pointed out, the reasons for judgment show that the trial Judge treated the case essentially as if it turned on a contest between the two epidemiologists, Dr Margaret McCredie on the one hand and Professor Joseph McLaughlin on the other. The trial Judge preferred Dr McCredie’s view, in particular because he considered that a statement expressed in a study, in which both Dr McCredie and Professor McLaughlin had participated, was inconsistent with the view which Professor McLaughlin was expressing to the Court. In my view, for reasons I shall later state, that approach was wrong. In my opinion, as a result of his Honour’s approach, matters put on behalf of the present appellants, the employers, were not considered.

268 In the circumstances of this case and having regard to the issues, which are ones that can be resolved from a reading of the medical reports and of the transcript of the evidence, and in which the benefit that a trial Judge may have from hearing the witnesses give their oral evidence has little application, I consider that I should examine the matter for myself. Such an approach was adopted by each member of the Court in Bendix Mintex Pty Ltd v Barnes (1997) 42 NSWLR 307. See, particularly, Mason P at p 319 and also State Rail Authority of New South Wales v Earthline Constructions Pty Ltd (In Liq) (1999) 73 ALJR 306.
269 I need not discuss at length the principles of causation which were fully examined in Bendix Mintex Pty Ltd v Barnes. The present case does not raise the issue which led to the dissent of Stein JA in that case. The following are principles enunciated in Bendix Mintex Pty Ltd v Barnes:- Causation is a question of fact to be determined by the application of commonsense to the facts of each case: see March v E & M H Stramare Pty Ltd (1991) 171 CLR 506; Bennett v Minister of Community Welfare (1992) 176 CLR 408; Bendix Mintex Pty Ltd v Barnes at pp 315-316, 335, 345. In a negligence claim, it is sufficient for a plaintiff to establish that his or her injuries were caused or materially contributed to by the defendant’s wrongful conduct: see Kilgannon v Sharpe Bros Pty Ltd (1986) 4 NSWLR 600; Bendix Mintex Pty Ltd v Barnes at pp 311, 335, 345. The onus is on the plaintiff to prove causation on the balance of probabilities: see Bonnington Castings Ltd v Wardlaw [1956] AC 613; McGhee v National Coal Board [1973] 1 WLR 1; Wilsher v Essex Area Heath Authority [1988] AC 1074; March v E & M H Stramare Pty Ltd; Bendix Mintex Pty Ltd v Barnes at pp 315, 339, 349. The onus is not discharged by establishing that a particular matter cannot be excluded as a cause of the injury: see Bendix Mintex Pty Ltd v Barnes at pp 318, 339.

General Facts

270 Mr McGuiness was born on 25 November 1934 and was 62 years of age at the time of the trial. From 1950 until 1984, he worked at a factory at Rosehill in which asbestos was used, inter alia, in the manufacture of fibro-cement sheeting and mouldings. That factory had been conducted originally by Wunderlich Limited and was taken over by James Hardie & Coy Pty Limited in 1977. In 1984, Mr McGuiness was transferred to the Dispatch Section of the James Hardie Camellia Fibro Plant and he worked there until he ceased work in April 1991. In that Plant, large quantities of flat sheet and corrugated fibro were stored and moved. It appears that, in the early years, Mr McGuiness may have come into contact with both crocidolite (blue asbestos) and chrysotile (white asbestos), but for the most part he encountered chrysotile.

271 The proceedings in the District Court commenced in 1993 after Mr McGuiness had been diagnosed as having pleural plaques, which were presumed to have been asbestos related. However, the plaques did not develop but remained benign and were not incapacitating. In 1997, Mr McGuiness was diagnosed as suffering from renal cell cancer of the left kidney. This was a fast growing malignancy which spread to the spine and was invading the lung. At the time of the trial, Mr McGuiness had only a short time to live.

The Nature and Sequence of Events

272 It is not in dispute that renal cell cancer has a cause or causes. It is not in dispute that Mr McGuiness, in the course of his working life, would have inhaled and may have ingested asbestos fibres and dust and that, if the intake of asbestos was a cause of renal cell cancer, then the period over which the inhalation and ingestion of asbestos occurred was consistent with the development of the cancer.

273 However, consistency is not enough. Although renal cell cancer is one of the less frequent cancers, it is common throughout the population. Moreover, Mr McGuiness was at an age at which renal cell cancer is commonly found and, although the cause of most renal cell cancers is unknown, there were at least two factors which were generally accepted as having a causal relationship with renal cell cancer. One was obesity, from which Mr McGuiness suffered throughout most of his life, and another was smoking. Mr McGuiness was a moderate smoker.

274 These basic facts do not support an inference of a causative link between asbestos and Mr McGuiness’ renal cell cancer, merely an inference that a connection was possible because of Mr McGuiness’ long encounter with asbestos.

Medical Facts

275 The following are the principal facts concerning renal cell cancer which were referred to in the evidence and which appear to be uncontroversial, notwithstanding that they were not stated by the trial Judge:

(1)      Most cancers, particularly environmental cancers, are thought to result from successive insults to the DNA structure of cells until eventually a catalyst or event occurs which causes a change in a cell, this cell becoming a rogue cell which multiplies rapidly.
(2)      In renal cell cancer, where there is no predominant risk factor, the preconditioning is “most likely to be a whole swathe of causes”.
(3)      Renal cell cancer appears to have a relationship with aging. Most renal cell cancers are found in men aged in their 60’s and 70’s.
(4)      Asbestos is a known causal agent of mesothelioma, asbestosis and lung cancer. As Mr McGuiness’ cancer was located in the substance of his kidney, not in the outer lining, it is appropriate to look at asbestosis and lung cancer rather than at mesothelioma. Asbestosis and lung cancer, but not mesothelioma, are dose response conditions.
(5)      Lung cancer appears to have a relationship with asbestosis. Asbestosis may be a necessary or usual precondition to lung cancer. Mr McGuiness suffered from neither asbestosis nor lung cancer, or at least showed no signs thereof.
(6)      Obesity and smoking are accepted causes of renal cell cancer; but the risk ratios of about 1.5 to 2 are relatively low. The reasons for the relationships are not known; but it is thought that there may be something in tobacco, such as an oxidant, or in the diet, which may be the contributing factor. Diet is suspected but not proven to contribute to renal cell cancer. The ingestion of a number of chemicals and minerals which are known carcinogens is a suspected cause. Hypertension is also suspected of having a causal relationship. However, although many factors are suspected to contribute to renal cell cancer, it is a cancer found in the community generally, and no predominant cause has been identified. In most cases of renal cell cancer, no cause is identified.
(7)      Although asbestos is a known carcinogen or causal agent of mesothelioma, asbestosis and lung cancer, it has not been shown to have that effect in relation to other parts of the body. For example, contact between asbestos and the skin does not appear to cause cancer. In laboratory tests, the injection of asbestos into the kidneys of rats has been shown to cause cancer. However, such experiments are not a reliable indicator of the human experience.
(8)      Asbestos has been found throughout the body including the brain, the heart, the lymph nodes, the adrenal glands, the kidneys and elsewhere. Asbestos may enter the body either through inhalation or by way of ingestion through the gut.
(9)      Long thin asbestos fibres greater than 8 micrometres in length and certainly more than 5 micrometres in length appear to be necessary to induce carcinomas or mesothelioma. The fibres recovered from renal tissue have been extremely short. A paper by Patel-Mandlik recorded the range of fibre in renal tissue as between .1 micrometre through to a maximum of 2.5 micrometres with the great majority of fibres falling within the range of .4 to .6 micrometres.
(10)     Although the contact which Mr McGuiness had with asbestos was undesirably high and was described by the trial Judge as “heavy” and may well have been a, or the, cause of his pleural plaques, it did not lead, in his case, to mesothelioma, asbestosis or lung cancer.
(11)     A fine needle aspiration taken from Mr McGuiness’ left kidney did not disclose the existence of asbestos fibre. The biopsy was, however, a very small section.

276 The above points were the main facts which, together with the epidemiological evidence, were relied upon by the medical practitioners who gave evidence in Mr McGuiness’ case. They do not seem to me to justify an inference that asbestos had a probable, as distinct from a possible, causal connection with Mr McGuiness’ renal cell cancer.

The Medical Practitioners

277 The medical experts called on behalf of Mr McGuiness drew an inference of probability from the fact that there are likely to be many causes which contribute to bring about renal cell cancer, from the fact that, as asbestos can reach the kidneys, it is possible that asbestos exposure was a contributing cause of Mr McGuiness’ cancer and from the fact that asbestos is a known carcinogen. On the other hand, the employers’ experts pointed out that, although asbestos has been found in many parts of the body, including the brain, the heart, the lymph nodes and so on, it has not been identified by practitioners or by pathologists working in those fields as a cause of cancer in those areas or, more importantly, as a cause of renal cell cancer.

278 The employers’ experts pointed to the fact that asbestos has not been shown to cause cancer other than mesothelioma, asbestosis and lung cancer. They further suggested that, even if asbestos could cause renal cell cancer, it was improbable that it did so in Mr McGuiness’ case. They pointed out that, if asbestos caused renal cell cancer, the cancer would be dose related and therefore, if the asbestos were inhaled, they would expect there to be at least a sufficient inhalation to cause asbestosis. Mr McGuiness did not show signs of asbestosis. The degree of pleural plaque formation is a reasonably good guide to the degree of asbestos exposure. Mr McGuiness’ plaques were minor. They suggested that, if the asbestos had been ingested, by being swallowed with other dust, it would have been filtered passing through the gut into the bloodstream and then to the kidneys. Asbestos is not an established cause of stomach cancer and the asbestos fibres found in the gut have been small, not of the length of the fibres known to cause cancer in the chest.

279 I do not propose to set out in detail the evidence of each particular medical practitioner. On behalf of Mr McGuiness, evidence was called from, inter alia, Dr M W Burns, a Thoracic Physician, and Dr B J Nankivell, a Consultant Renal Physician. Both expressed the view that the contact which Mr McGuiness had with asbestos in the course of his work was a probable cause of his renal cell cancer. Both expressed their opinions by reference to the epidemiological evidence and to the fact that asbestos was a carcinogen. Dr Burns seems to have relied principally upon the epidemiological evidence, including a study by Maclure, in respect of which the author later recanted. Dr Nankivell relied, not only upon the epidemiological material, but also upon the nature of cancer, the consistency of the time delay in the case of Mr McGuiness and the known effects of asbestos. Neither doctor gave evidence that he had personally encountered a case where asbestos fibres had been found to be associated with renal cell cancer. Indeed, Dr Nankivell confused chrysotile, the white asbestos, with crocidolite, the blue asbestos.

280 Called on behalf of the employers were, inter alia, Professor D W Henderson, a Specialist Pathologist with an interest in epidemiology and who for many years has been concerned with the problems of asbestos related diseases and neoplasia in particular, Professor D A Ferguson, a Consultant Occupational Physician and an Emeritus Professor at the University of Sydney who has specialised in the field of occupational medicine, Associate Professor A B X Breslin, a Consultant Thoracic Physician, and Dr J Lee, a Thoracic Physician. These medical practitioners relied upon the epidemiological evidence but their evidence was not limited to that. The effect of their evidence was that the medical profession has not accepted that asbestos is a cause of renal cell cancer. Dr Breslin said, “[T]he majority of authorities at this stage won’t accept that it is established that renal cancer is caused by asbestos exposure” and “[I]t is a possibility and … that is why all these studies have been done trying to establish whether it actually happens rather than just a possibility”. Dr Breslin said that he had never seen a renal cancer that he thought was due to asbestos exposure. The employers’ experts considered that the connection between asbestos and renal cell cancer was unlikely to be found because the conditions that had been observed in relation to asbestosis and lung cancer, including the length of the fibres and the body’s response to those fibres, had not been observed in kidneys, where such asbestos fibres, as have been found, have been of a very small size. Moreover, the employers’ experts thought that, even if asbestos could cause renal cell cancer in some cases, it was unlikely that asbestos inhalation or ingestion was a contributing factor to Mr McGuiness’ cancer, as he had not inhaled sufficient asbestos to cause lung cancer or asbestosis.

281 To my mind, the evidence given by the employers’ medical experts is the more persuasive. Dr Burns and Dr Nankivell considered that, as it is likely that the development of renal cell cancer has many causes, then asbestos, which is known to cause cancer elsewhere in the body, was probably a cause of Mr McGuiness’ cancer. That is clearly a tenable view. However, I am persuaded that the weight of the medical evidence is against it. I am also influenced by the fact that there is no evidence from any medical expert that he or she has encountered in the course of his or her practice, a case or cases of renal cell cancer which he or she has attributed to asbestos. Anecdotal evidence to that effect, such as one encounters in other areas of medico-legal disputes, is absent, notwithstanding the long history of the mining and use of asbestos in Australia. I am also influenced by the point that, if Mr McGuiness had encountered sufficient asbestos to cause cancer, one would have expected him to show signs of asbestosis or lung cancer, for their connection with asbestos is a strong one. Renal cell cancer is considered to be, in relation to environmental carcinogens, a dose related cancer.

The Epidemiological Evidence

282 Although his Honour did not expressly say so, he appears to have taken the view that, absent support from the epidemiological studies, the medical evidence would not justify a finding of causation. The trial Judge, however, then treated the matter as if it were a contest between the evidence of Dr Margaret McCredie on the one hand, who said that, in her view, on the epidemiological evidence available, Mr McGuiness’ exposure to asbestos was a cause of his renal cell cancer, and that of Professor Joseph McLaughlin, on the other hand, who expressed the view, inter alia, that the epidemiological evidence justified the conclusion that a causal relationship between asbestos and renal cell cancer did not exist. His Honour’s approach excluded consideration of the view that the epidemiological material was inconclusive.

283 There is, indeed, much to be said for the view that the epidemiological evidence is inconclusive, that it does not show positively either that there is a causal connection between asbestos and renal cell cancer or that there is no such connection.

284 Most studies, and there have been many of them, have found no association between asbestos and renal cell cancer. However, the Selikoff study in 1979, the Enterline study in 1987 and the Maclure study in 1987 reported a link between asbestos and renal cell cancer. The lastmentioned report was later thought to have had a flaw in its methodology and Maclure recanted. Dr McCredie, who has been connected, inter alia, with the Cancer Epidemiology Research Unit at the New South Wales Cancer Council, later participated with J H Stewart in a study of asbestos and kidney cancer in New South Wales in respect of the years 1989-1990. That study, which was a population-based study, reported that exposure to asbestos significantly increased the risk of renal cell cancer by a factor of 1.6, that is to say that there was a 60 per cent increase in risk.

285 That particular study was undertaken as part of an international study into renal cell cancer, a study which was headed by J S Mandel and in which Dr McCredie, Professor McLaughlin and others participated. In that study, called “the Mandel study”, there were six study centres in five countries: Australia, Denmark, Germany, Sweden and the USA. There was a common study protocol and the instruments for data collection were similar. That overall study found an increase risk of renal cell cancer associated with exposure to asbestos and placed the risk at 1.4. The vital conclusion of the Mandel study read as follows:

“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.”

Note the last sentence which indicated that, while the study itself showed an increased risk, further research was required to ascertain whether the causal relationship existed.

286 There were good reasons for the qualification which the authors of the report put upon their finding. The first was that the risk ratio was a modest one. The risk ratios in relation to mesothelioma and lung cancer are of a different order entirely. Secondly, the study was a population-based case-study, a form of study which the report itself acknowledged was not the most accurate or efficient study method for ascertaining a specific occupational risk. Thirdly, the study did not show a dose related effect. Indeed, the McCredie-Stewart study reported that the risk for renal cell cancer was fivefold higher in those whose exposure began after rather than before 1956. The finding was the reverse of that which would have been expected. Finally, the Mandel study was only one of a number of studies which had been undertaken. It was one of the studies which reported a positive relationship between asbestos and renal cell cancer, but the majority of studies were to the contrary.

287 In epidemiology, consistency is important. Epidemiology seeks to arrive at a conclusion with respect to a medical issue through the use of mathematical techniques. Neither the McCredie-Stewart study nor the Mandel study established, as a fact, that exposure to asbestos was causally related to renal cell cancer. Neither the McCredie-Stewart study nor the Mandel study expressed itself in that way. Both studies reported an increased risk. There is no question about that. But they were studies which needed to be taken into account with other studies before a general conclusion could be reached. They increased the possibility that a causal relationship existed. But they did not establish that it did so.

288 In two other studies reported at about the same time, one being a follow-up study of the Wittenoom cohort by N H de Klerk and others, which was published in 1994, and the other a Canadian study on Cancer Mortality in Chrysotile Mining and Milling by Douglas Liddell also published in 1994, no increased risk was found relating asbestos to renal cell cancer.

289 The view that the epidemiological studies show no more than a possibility that asbestos may be related to renal cell cancer has been expressed in the textbooks. A work by Richard Doll and Julian Peto in 1986 on Asbestos-Related Malignancy concluded in relation to renal cell cancer, “In the absence of any positive experimental evidence these data [earlier studies including the Selikoff study] do not, in our opinion, justify the belief that asbestos can cause this type of disease”. In 1992, Professor D Greenberg and Professor V L Roggli, writing on the pathology of asbestos-associated diseases said, in relation to renal cell cancer, “Overall, in the authors’ opinion, the balance of the evidence available at present does not support an association between asbestos exposure and renal cell carcinoma.” More recently, in Cancer Epidemiology and Prevention, of which the editors were Schoddenfeld and Fraumeni, published in 1996, in a chapter on renal cancer by McLaughlin, Blot, Devesa and Fraumeni Jr, the following was stated:

“Unlike bladder cancer, the most common tumor of the urinary tract, 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 fibres 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.”

That chapter was written before the Mandel report was issued, but subsequent to the McCredie-Stewart study.
Material Considerations

290 The evidence of Dr McCredie which the trial Judge accepted was that, “On the balance of probabilities, … exposure to asbestos materially contributed to the causation of renal cell carcinoma in this [Mr McGuiness’] case”. The evidence of Professor McLaughlin which the trial Judge rejected, was that, “On the balance of probabilities … His [Mr McGuiness’] exposure to asbestos played no role in the development of his cancer”. However, it was not necessary for his Honour to choose between these two views. Dr McCredie and Professor McLaughlin were epidemiologists. Another view was that the epidemiological evidence was inconclusive. Studies other than the Mandel study were relevant and so was the detailed medical evidence.

291 The trial Judge unfortunately took a narrow view of his function. His Honour said, inter alia:

“No Common Law judge is an expert in epidemiology. Even if one were, he would be required to leave his epidemiological hat on the peg when coming to judge any case, even one where epidemiology lay at its very heart. … 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 Queens Counsel for their respective clients [the employers]. These matters are matters which if I were an epidemiologist I might look to, in appraising the work of another epidemiologist. That is not my task.” (emphasis added)

292 As a result of this narrow approach to his task, the trial Judge turned his attention to the Mandel study, which he said was “at the heart of the issues that I must determine”. His Honour then rejected Professor McLaughlin’s evidence, set out above, on the ground that it was inconsistent with the Mandel study, as that study has reported a positive relationship. To approach the matter in that way was to fail to consider the Mandel study in its context, to fail to take account of the criticisms which Professor McLaughlin and others had made of its results and to fail to consider whether the epidemiological evidence as a whole supported the claimed connection between asbestos and renal cell cancer. The trial Judge deliberately shut his mind to these matters considering it not to be part of his function to do so.

293 By concentrating his attention on the words of the Mandel study, the trial Judge also excluded from his consideration the evidence given by the employers’ medical experts that the medical profession generally has not accepted that asbestos is a cause of renal cancer and, further, that the conditions which had been observed in relation to asbestosis and lung cancer had not been observed in relation to the kidneys. Nor did the trial Judge appear to take into account many of the medical facts I have set out above or of the view that it was unlikely that Mr McGuiness’ renal cancer would have been caused by asbestos as his exposure to asbestos had not led to asbestosis or lung cancer. Epidemiological results must be examined with care if they appear to be inconsistent with known medical or biological facts.

294 The “Bradford-Hill Criteria” which set out relevant factors against which epidemiological results should be examined are cited in Reay v British Nuclear Fuels (1994) 5 Med LR 1 at 13-14. Amongst those factors, the strength of the association reported and the need for consistency, for biological plausibility and for dose response are emphasised.

295 His Honour, however, did not consider the Mandel study in the context of the evidence as a whole, or even in the context of the epidemiological evidence as a whole. By excluding from his consideration such of the epidemiological evidence and of the medical evidence as threw doubt upon the result of the Mandel study, his Honour excluded important material from his consideration.

296 The trial Judge also failed to point out that the finding of the Mandel study, an increased risk of 1.4, which was a modest increase in risk, was not a strong basis for a finding that asbestos was a cause of cancer in the particular case, Mr McGuiness’ case, particularly in light of the fact, to which I have already referred, that in most cases of renal cancer no cause is identified. It is a cancer found in the community generally, particularly amongst men in their 60’s and 70’s.

297 Contrary to the approach taken by the trial Judge, the duty of a trial judge is to consider the substance of the matters before him and to make all relevant findings of fact, whether or not they be of a technical nature. As Sir Owen Dixon said in his address on “Science and Judicial Proceedings”, Jesting Pilate at pp 16, 22:

“When a judge is confronted with some question which depends upon a scientific inquiry however ill equipped he may be for the task, he is expected to acquire from the evidence of experts a sufficient knowledge of the subject to make him appreciate and even form a judgment upon the scientific facts, inferences and deductions which contribute to a correct solution to the question.
.....
There is no escape from the general necessity of investigating difficult and complicated sets of facts, and these can never be separated from considerations including any special branch of knowledge which may affect them.”

In Mifsud v Campbell (1991) 21 NSWLR 725, at 728, Samuels JA put the matter succinctly when he said:
“[I]t is an incident of judicial duty for the judge to consider all the evidence in the case.”

Conclusion

298 In my opinion, the current state of the epidemiological evidence, as disclosed by the evidence of this case, is that a causal relationship between asbestos and renal cell cancer has not been established. Some studies have shown a positive relationship. The McCredie-Stewart and the Mandel studies showed a modest increase in risk. However, taking the epidemiological evidence as a whole, the position is that the link between asbestos and renal cell cancer remains a possibility, which has not been established as a matter of probability. In this circumstance, I would not accept the evidence of Dr McCredie that, “On the balance of probabilities, … exposure to asbestos materially contributed to the causation of renal cell carcinoma in this [Mr McGuiness’] case”.

299 In my opinion, the trial Judge placed undue weight on the Mandel study. I do not read that study as expressing a view other than that the study itself showed a positive causal relationship between asbestos and renal cell cancer, the risk factor being 1.4. I do not read the study as reporting that the causal relationship had been established on the balance of probabilities. Not only did the study itself not say that, but it was only one of a large number of studies. Its results had to be assessed in the light of its findings, the nature of the study, the inconsistency in the dose relationship and, finally, the inconsistency of the study with most other epidemiological studies. In my opinion, the study was written in the context that all these matters would have to be taken into account. Its conclusions should be read accordingly.

300 I am, moreover, of the view that, having regard to both the epidemiological evidence and the medical evidence to which I have referred and which I need not repeat, it would be wrong to draw an inference of causation in this particular case.

301 It follows, in my opinion, that the evidence before the Court does not justify a finding, on the balance of probabilities, that asbestos exposure was a cause of Mr McGuiness’ renal cell cancer. Although I have discussed the issue under several headings, I have, nevertheless, considered the totality of the evidence in coming to this view.

Orders

302 I would allow the appeal. I agree with the orders proposed by the Chief Justice.

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LAST UPDATED: 07/03/2000