Evans v Queanbeyan City Council

J D Heydon Cross on Evidence (8th Ed 2010) at 304 [7160] fn 123

J F Stephen, A Digest of the Law of Evidence (5th Ed 1887) at 11 Category: Principal judgment Parties: Appeal:

Lola Merle Evans as Executrix of the Estate of Keith Henry Evans - Appellant

Queanbeyan City Council - First Respondent Amaca Pty Ltd (Under NSW Administered Winding Up) (Formerly James Hardie & Coy Pty Ltd) - Second Respondent

Lola Merle Evans as Executrix of the Estate of Keith Henry Evans - Applicant

Dust Diseases Tribunal of New South Wales - First Respondent Queanbeyan City Council - Second Respondent Amaca Pty Ltd (Under NSW Administered Winding Up) (Formerly James Hardie & Coy Pty Ltd) - Third Respondent Representation: Counsel:

J L Sharpe - Queanbeyan City Council G M Watson SC/J C Sheller - Amaca Pty Ltd Submitting appearance - Dust Diseases Tribunal Solicitors:

Thompson Cooper Lawyers - Queanbeyan City Council DLA Piper Australia - Amaca Pty Ltd IV Knight, Crown Solicitor - Dust Diseases Tribunal File Number(s): CA 2010/112912 Decision under appeal Citation: Evans v Queanbeyan City Council [2010] NSWDDT 7 Date of Decision: 2010-04-20 00:00:00 Before: Curtis J File Number(s): 2009/199

HEADNOTE [This headnote is not to be read as part of the judgment] In November 2006 Mr Keith Evans was diagnosed with lung cancer. Mr Evans smoked between 20 and 35 cigarettes a day for approximately 40 years up to 1991. He also experienced occupational exposure to asbestos dust of variable intensity. Mr Evans worked for Queanbeyan City Council from 1975 until 1990. Amaca Pty Ltd was an important manufacturer of asbestos building products throughout Mr Evans' working life. In the Dust Diseases Tribunal, Mr Evans' widow, Mrs Lola Evans, claimed that Mr Evans' lung cancer was caused by exposure to asbestos dust in circumstances imposing responsibility on the respondents. Judge Curtis was not satisfied on the balance of probabilities that Mr Evans' lung cancer was caused by exposure to asbestos: Evans v Queanbeyan City Council [2010] NSWDDT 7. Mrs Evans appeals against that decision. The Court held, dismissing the appeal:

1. The law as to negligence requires that a plaintiff prove on the balance of probabilities that the defendant's wrong caused or materially contributed to his or her loss; it is not sufficient for the plaintiff to show that the wrong materially increased the risk of harm, where medical science does not permit any further proof: [20]-[22]; [56], [93], [103] St George Club v Hines Ltd (1961) 35 ALJR 106; Amaca Pty Ltd v Ellis [2010] HCA 5; 240 CLR 111; Tabet v Gett [2010] HCA 12; 240 CLR 537; Gett v Tabet [2009] NSWCA 76; 254 ALR 504; Seltsam Pty Ltd v McGuiness [2000] NSWCA 29; 49 NSWLR 262 applied. Sydney South West Area Health Service v Stamoulis [2009] NSWCA 153 distinguished and doubted.
2. Although there was evidence of a biological synergistic effect of asbestos dust and tobacco smoke in causing lung cancer, the primary judge was entitled to reject, as inconsistent with the epidemiological evidence, the hypothesis that both agents probably worked together in a majority of cases and thus in respect of Mr Evans' carcinoma: [7]-[19], [80]-[83].
3. The appeal being limited, relevantly, to a decision of the Tribunal in point of law, the fact that there was evidence both supportive of and adverse to the plaintiff's claim precluded a successful appeal based on an assessment of that evidence: [70], [99]. Dust Diseases Tribunal Act 1989 (NSW), s 32(1).
4. The primary judge did not err in undertaking his own calculations as to the level of exposure to asbestos dust and the resultant relative risk. His Honour was entitled to reach his own conclusion as to the level of exposure, based on the evidence before him and to apply the procedure for determining relative risk revealed in the epidemiology: [6], [104]-[110]. Dasreef Pty Ltd v Hawchar [2011] 21; 277 ALR 611 distinguished.
5. The primary judge did not adopt a 'but for' test of causation, to the exclusion of proper consideration of material causation in circumstances where two agents operated causally: at [3]-[5] and [85]-[99]. Amaca Pty Ltd v Ellis [2010] HCA 5; 240 CLR 111 distinguished. (per Allsop P)
6. To the extent that English case-law supports liability based on a material increase in risk, adoption of such a principle in this jurisdiction must lie with the High Court: [52]. McGhee v National Coal Board [1973] 1 WLR 1; Fairchild v Glenhaven Funeral Services Ltd [2002] UKHL 22; [2003] 1 AC 32; Barker v Corus UK Ltd [2006] UKHL 20; [2006] 2 AC 572; Sienkiewicz (Administratrix of the Estate of Enid Costello Deceased) v Greif (UK) Ltd [2011] UKSC 10 discussed.

Judgment 1ALLSOP P: I have read the reasons of Hodgson JA and Basten JA. Subject to what (largely by way of elaboration) appears below, I agree with them. I agree with the orders proposed by Basten JA. 2The appellant, Mrs Lola Evans (the widow and executrix of the estate of Mr Keith Evans), appeals in point of law against the orders made by the Dust Diseases Tribunal (Curtis J) that there be judgment for the defendant. Various complaints were made as to legal error in his Honour's approach. 3The appellant's first complaint is that the primary judge imposed a but-for test of causation in circumstances where such a case was not put forward by the appellant. That argument should be rejected. At [144] of his reasons, the primary judge set out the arguments put forward by Mr Little SC (who, with Mr Foord, appeared for Mrs Evans below and on appeal): "Mr Little SC argues that: (a) In all cases where lung cancer is contracted following exposure to the carcinogens cigarette smoke and asbestos, each agent materially contributes to the development of the disease. (b) In the alternative, the fibre burden of Mr Evans was probably sufficient to materially contribute to his lung cancer in any event." These were arguments based on causation by material contribution. 4The primary judge's conclusion at [201] of his reasons was expressed in terms of these arguments: "I am not persuaded that it is more probable than not that any contribution of asbestos to the cause or progression of Mr Evans' lung cancer was, in the light of his smoking history, material." 5His Honour's reasoning between those points ([145]-[162] as to (a) set out at [3] above, and [163]-[194] as to (b) set out at [3] above) dealt with the matter in this way. The primary judge did not limit himself to a but-for test in the way complained of. 6The appellant's second complaint is that the judge impermissibly used his position as an expert tribunal going outside the evidence in calculating fibre load: cf Dasreef Pty Ltd v Hawchar [2011] HCA 21; 277 ALR 611. This argument should be rejected. The task undertaken by the primary judge at [31]-[62] was not shown to adopt a process or conclusion to have been derived outside the evidence. 7The appellant's third complaint (which is related to the first complaint) was that the primary judge impermissibly used the epidemiological evidence beyond the reason for which it was led by the appellant. The appellant submitted that epidemiological evidence was only led to prove that asbestos was a carcinogenic agent. The primary judge, wrongly, it was submitted, used it to reject a proposition that the relative risk from asbestos (whether alone or in conjunction with smoking) was less than 2 (and so not proved to be more probable than not). 8This third complaint should be rejected. As I said above, the structure of the primary judge's reasons after [149] revealed that he dealt with a case based on material contribution. The first argument put forward ((a) at [3] above) was that for which Dr Leigh contended - that in a manner not fully understood, tobacco and asbestos always worked together synergistically in causing lung cancer. According to this hypothesis, the asbestos can be taken to materially contribute to the cancer as part of one intermingled causative agent. The essence of the proposition was described at [145]-[148] of his Honour's reasons. His Honour said that the proposition that this occurred, in all cases, was "theoretically sound": [145]. His Honour found, however, as follows (at [149]-[150]): "[149] I am persuaded that asbestos and cigarette smoking may act in combination in contributing to the development of lung cancer. [150] I am not persuaded that in all cases, and in particular in this case of Mr Evans, that the contribution of asbestos must have occurred, or if it did, that the contribution was material. " (Emphasis in original.) 9These were plainly factual findings. Reasons for these findings were given in the paragraphs that followed. If those reasons contained legal error the factual findings might be vulnerable. Before turning to the reasons and the complaints made of them, something should be said about the question posed in [150] whether the contribution of asbestos "must" have occurred. The question can be seen to reflect some of the language used in Amaca Pty Ltd v Ellis [2010] HCA 5; 240 CLR 111 at 133 [52] and [53], and 134 [60]. It might be, perhaps, that, rather than a question framed in terms of certainty ("must"), it would have been sufficient for it to be concluded that it was probable in any given case that smoking and asbestos worked synergistically together to cause cancer. In any event, that is not how the case was run and his Honour cannot be criticised for positing and answering the proposition put forward by Mrs Evans as the foundation for her relief. 10The first reason for the factual conclusion in [150] is set out in [151]: "First, because both Professor Breslin and Professor Tattersall, while accepting the theory, dismissed the contribution of asbestos in Mr Evans' case because of its relative insignificance. I accept that a contribution may be material although it is minor but I believe that, in context, the opinions of both medical experts are to the effect that the contribution was not minor but insignificant, that is to say, immaterial." 11This reason was said to be illogical; and illogicality was said to reveal legal error. Assuming without deciding the second of those propositions (cf Amaba Pty Ltd v Booth [2010] NSWCA 344), the illogicality was said to flow from the judge's own findings at [168] and [177] in which he found "significant asbestos exposure": "[168] My finding of 21.9 fibre/ml/years is approximately six times greater than Mr Roger's estimate of 3.24 fibre/ml/years and Mr Pickford's 'probable' scenario of 3.4 fibre/ml/years. It is nearly double Mr Pickford's 'worst case' scenario. This finding is compatible with the description 'significant asbestos exposure'. It is also consistent with the circumstance that the cumulative dose of asbestos fibre required to double the risk of contracting lung cancer requires a significant exposure for a prolonged period of time. ... [177] The presence of diffuse pleural thickening does indicate significant asbestos exposure, but I have no evidence that correlates the presence of diffuse pleural thickening with an increased risk of contracting lung cancer. Professor Breslin says he took into account the presence of the pleural thickening." 12The error in this argument is revealed by an examination of the evidence of both Profs Breslin and Tattersall. The "relative insignificance" of the asbestos exposure for the theory of multiplicative or synergistic operation of smoking and asbestos was, for Prof Tattersall, lower than 25 fibre/ml/years (the "absolute bottom end of any risk calculation for lung cancer": Black 138 (T p 133)). Professor Breslin gave similar evidence based on Professor Pooley's measurement: see [110] and [111] of the primary judge's reasons. These views from the two experts, who accepted the theory of the multiplicative or synergistic operation of tobacco and asbestos, provided the factual foundation for the primary judge's conclusion. There was a difference between significant exposure and significant or material contribution. 13Further, the presence of pleural thickening was recognised by the primary judge to indicate significant asbestos exposure ([177]), but there was not evidence acceptable to him that this amounted to an increased risk of cancer: [170]-[177] and [111]. This, likewise, was a factual conclusion. 14The second reason for the factual conclusion in [150] is set out in [152]: "Secondly, because Dr Leigh concedes that in a particular case the contribution of asbestos may play a very small part, and that he could not say that, more probably than not, Mr Evans would not have contracted his cancer in the absence of the asbestos exposure." (Emphasis in original.) 15As to [152], whilst the primary judge referred to Dr Leigh's evidence (at Black 89 (T p 86)) that he could not say that more probably than not Mr Evans would not have contracted his cancer in the absence of the asbestos exposure, I do not conclude from that that his Honour was not continuing to deal with the question of material contribution. 16The third reason for the factual conclusion in [150] is set out in [153]: "Thirdly, because epidemiological studies predict that among the class of persons who share Mr Evans' smoking history, the greatest number of those who contract lung cancer after exposure to an equivalent asbestos fibre burden are persons who would have contracted the disease in any event." 17As to [153], again this might be seen as relevant to a "but-for" test and causation otherwise based on material contribution of asbestos through synergistic operation. It deals with the proposition at [150] at a level of analysis beyond that put by the appellant. To that extent, it may not be a relevant reason for the conclusion in [150]. It does not, however, undermine the primary foundation for [150] - the evidence of Profs Breslin and Tattersall that the multiplicative or synergistic theory does not apply to the case of Mr Evans, even though they accepted the theory. 18The fourth reason for the factual conclusion in [150] is set out in [154]-[155]: "[154] Fourthly, because, even if asbestos and smoking combined causally in the development of lung cancers in all cases, the contribution of asbestos to the development of lung cancer in smokers may take the form of hastening the development of the cancer. That would reconcile the certainty of epidemiological prediction that a certain number of lung cancers will develop in smokers in any event, with the plausible biological theory that the additional risk factor of asbestos exposure will contribute to that inevitable development by way of acceleration. [155] That acceleration may be minimal or substantial and yet not change the inevitability of the tumour's appearance. If a motor car without brakes travels at a certain speed toward a collision there comes a time when any additional impetus by way of acceleration will not affect the inevitability of disaster." 19As to [154]-[155], this reason was not the subject of debate at trial. With respect to the learned trial judge, I do not understand the relevance of [154]-[155] to the factual conclusion in [150]. Nevertheless, it does not undermine [150] insofar as that paragraph is supported by Professors Breslin and Tattersall. 20The appellant's fourth complaint is based on a fundamental legal question. The appellant submitted that the primary judge failed to apply what should be taken to be the law of causation concerning tortious wrongs in Australia. It was submitted that in circumstances were the defendant created a risk of injury and that injury eventuated and, in circumstances where medical science did not permit a causal conclusion to be drawn on the balance of probabilities, it was sufficient to attribute causal responsibility to a defendant that it materially increased the risk to the plaintiff of suffering that injury. As I understand the submission, the causal connection of material contribution may (not necessarily must) be drawn from that increase in risk alone. Reliance was placed on Fairchild v Glenhaven Funeral Services Ltd [2002] UKHL 22; [2003] 1 AC 32; Barker v Corus UK Ltd [2006] UKHL 20; [2006] 2 AC 572; Sienkiewicz (Administratrix of the Estate of Enid Costello Deceased) v Greif (UK) Ltd [2011] UKSC 10; McGhee v National Coal Board [1973] 1 WLR 1; Resurfice Corp v Hanke 2007 SCC 7 ; [2007] 1 SCR 333; Sydney South West Area Health Service v Stamoulis [2009] NSWCA 153; Adeels Palace Pty Ltd v Moubarak [2009] HCA 48; 239 CLR 420; and Bonnington Castings Ltd v Wardlaw [1956] AC 613. 21The primary judge, concluded at [201] (see [4] above) that any contribution of asbestos to Mr Evans' cancer was not material. His Honour, however, did not approach the matter by reference to the above proposition. If he had done so, the evidence may have permitted a relevant causal conclusion, on that hypothesis. 22The submission should, however, be rejected. Subject to the views of the High Court in respect of any development of the common law or to the operation of any legislation, it can be concluded that at common law, as a general proposition, the increasing of risk of harm by a tortious act is, alone, insufficient for a conclusion of causation by material contribution to that harm or for a conclusion of responsibility in law for that harm. 23It can be accepted that in Resurfice Corp v Hanke at 342-343 [24]-[25], the Supreme Court of Canada expressed the framework for "material contribution" in the absence of a positive conclusion from the "but-for" test as follows: "However, in special circumstances, the law has recognized exceptions, to the basic 'but for' test, and applied a 'material contribution' test. Broadly speaking, the cases in which the 'material contribution' test is properly applied involve two requirements. First, it must be impossible for the plaintiff to prove that the defendant's negligence caused the plaintiff's injury using the 'but for' test. The impossibility must be due to factors that are outside of the plaintiff's control; for example, current limits of scientific knowledge. Second, it must be clear that the defendant breached a duty of care owed to the plaintiff, thereby exposing the plaintiff to an unreasonable risk of injury, and the plaintiff must have suffered that form of injury. In other words, the plaintiff's injury must fall within the ambit of the risk created by the defendant's breach. In those exceptional cases where these two requirements are satisfied, liability may be imposed, even though the 'but for' test is not satisfied, because it would offend basic notions of fairness and justice to deny liability by applying a 'but for' approach." 24Further, it can be accepted that the House of Lords and now the United Kingdom Supreme Court has modified the common law in the United Kingdom by accepting that, at least as a special rule in mesothelioma claims, fairness and justice demand that the factual link between the wrongful act and the harm to the plaintiff need only be a wrongful exposure of the plaintiff by the defendant to an amount of asbestos that would materially increase the risk of mesothelioma: Fairchild; Barker v Corus; and Sienkiewicz. In Sienkiewicz, the statements of principle may also be seen not to be limited to mesothelioma. 25Further, it can be accepted that at the foundation of the House of Lords' views in Fairchild and Barker v Corus and of the Supreme Court's views in Sienkiewicz was a re-interpretation of McGhee (contrary to the interpretation given to it by the House of Lords in the 1980s) that supported the appellant's fundamental proposition underlying her fourth complaint. McGhee was not, of course, a mesothelioma case. 26The unanimous decision of the House of Lords in Fairchild can be expressed by reference to the headnote: "... where an employee had been exposed by different defendants, during different periods of employment, to inhalation of asbestos dust in breach of each defendant's duty to protect him from the risk of contracting mesothelioma and where that risk had eventuated but, in current medical knowledge, the onset of the disease could not be attributed to any particular or cumulative wrongful exposure, a modified approach to proof of causation was justified; that in such a case proof that each defendant's wrongdoing had materially increased the risk of contracting the disease was sufficient to satisfy the causal requirements for his liability; and that, accordingly, applying that approach and in the circumstances of each case, the claimants could prove, on a balance of probabilities, the necessary causal connection to establish the defendants' liability." 27The skill of the author of the headnote was able to avoid reference to the different ways this was expressed by their Lordships. Aspects of these differences emerged in Barker v Corus . Nevertheless, what was common to the several views of their Lordships in Fairchild was the necessity to depart from the common law's usual rule of the need for proof on the balance of probabilities in circumstances where it could be unjust for there to be no recovery. See in particular Fairchild at 66 [32] per Lord Bingham of Cornhill, 69 [40] per Lord Nicholls of Birkenhead, 73 [56] per Lord Hoffmann and 112 [155] per Lord Rodger of Earlsferry. These views reflected the expression of the matter by Justice (now Chief Justice) McLachlin at the commencement of an article written by her Ladyship in 1998, "Negligence Law - Proving the Connection" in N J Mullany and A M Linden (Eds) Torts Tomorrow: A Tribute to John Fleming (LBC Information Services, Sydney 1998). The foundational legal and moral premise that can be seen in Fairchild and in the introductory comments in the above article is that tort law, as an aspect of the rule of law, is concerned with righting wrongful conduct. If self-evident wrongs (so characterised by legitimate human perceptions) are not recognised by the law's rules, and thus go unremedied, people who legitimately feel themselves victims will be left with a sense of injustice. A legitimate sense of injustice should not be the product of the rule of law. 28The avowed change to causal principle by the House of Lords that materially increasing the risk of injury was sufficient factual tortious involvement for causation (or attribution of responsibility) to be established was narrowly confined by all their Lordships in Fairchild : at 40 [2] and 55 [21] per Lord Bingham, 70 [43] per Lord Nicholls, 74 [ 61] per Lord Hoffmann, 91 [108] per Lord Hutton and 118 [170] per Lord Rodger. Crucial to that confinement were factors such as the causal element being singular (only exposure to asbestos) and the inability of medical science to explain cause in terms of a balance of probabilities. 29Further illumination of the policy-based change to the common law in Fairchild can be seen from the lively debate in the judgments in Barker v Corus as to what was, in fact, decided in Fairchild . At issue in Barker v Corus was the extent of several liability of the wrongdoers who had exposed the plaintiff to the asbestos, causing a material increase in risk of contracting mesothelioma. Though all their Lordships (with a caveat by Lord Rodger: Barker v Corus at 610 [100]-[102]) came to the view that the exceptional approach in Fairchild should extend to circumstances where not all the exposure was tortiously caused by the defendants, a restriction was placed on the principle being that there must be one causative agent: Barker v Corus at 587 [24] per Lord Hoffmann (his Lordship recanting his view in Fairchild that this limitation was unprincipled), 599 [64] per Lord Scott of Foscote, 611 [104] per Lord Walker of Gestingthorpe and 615 [121] per Baroness Hale of Richmond. Save for Lord Rodger, all were agreed that the extent of responsibility of individual defendants should be measured by reference to the extent to which they had increased the risk, based on the respective length and intensity of exposure: Barker v Corus at 589-590 [35]-[36] per Lord Hoffmann, 599 [62] per Lord Scott, 612 [109] per Lord Walker and 616 [126] per Baroness Hale. The majority, recognising that it was justice and fairness that had given rise to the exceptional rule, thought that justice and fairness should limit the defendants' respective liabilities by reference to the wrongful exposure. Lord Rodger dissented on this point - all defendants were liable in full, the change in rule in Fairchild being a relaxation of the rules of causation - thus each caused the damage. 30At this point, the Parliament intervened with the Compensation Act 2006 (UK), which reflected Lord Rodger's view in Barker v Corus as to the responsibility of defendants in mesothelioma cases, and not the majority's view of fairness. 31The above discussion of Fairchild and Barker v Corus reveals, at once, the policy questions involved in any conclusion that increasing risk is sufficient for a conclusion of causation or causal responsibility or legal responsibility. Such policy questions are a matter for the High Court, not this Court. 32Fairchild , Barker v Corus and Sienkiewicz all discuss Bonnington Castings and McGhee . Before saying something about these cases, it is to be noted that the common law of Australia has long recognised a legitimate causal connection, in circumstances where a but-for analysis does not give a clear answer, which can be described as "material contribution". The defendant's tortious acts amount to a cause of the plaintiff's injury if the plaintiff establishes that his or her injuries are "caused or materially contributed to" by the defendant's wrongful conduct: March v Stramare (E & MH) Pty Ltd [1991] HCA 12; 171 CLR 506 at 514 per Mason CJ with whom Toohey J and Gaudron J agreed. For this proposition the Chief Justice in March v Stramare cited Duyvelshaff v Cathcart & Ritchie Ltd (1973) 47 ALJR 410 at 417 per Gibbs J; Tubemakers of Australia Ltd v Fernandez (1976) 50 ALJR 720 at 724; Bonnington Castings at 620; and McGhee at 4, 6, 8 and 12. See also the use of the phrase "caused or causally contributed to" in Norton Australia Pty Ltd v Streets Ice Cream Pty Ltd [1968] HCA 61; 120 CLR 635 at 643 per Barwick CJ. Mason CJ's comments in March v Stramare were made in the context of his Honour's discussion of concurrent or successive tortious acts each amounting to a cause and not in the context of materially increasing the risk of the harm that eventuates. 33The passage from the judgment of Gibbs J in Duyvelshaff at 417, cited by Mason CJ was as follows: "The general principle is clear, that the plaintiff must prove, on the balance of probabilities, that the breach of duty caused or materially contributed to his injury: Bonnington Castings Ltd v Wardlaw [1956] AC 613, at 620; McWilliams v Sir William Arrol & Co Ltd [1962] 1 WLR 295; Wigley v British Vinegars Ltd , supra. This means that 'it is for the plaintiff to prove on a balance of probabilities both that the safety measures would have been effective and that the injured person would have made use of them had they been available': Wigley v British Vinegars Ltd ([1964] AC, at 325) In some cases the fact that the employer is in breach of his statutory duty may itself provide some prima facie evidence of a causal connexion between the breach and the subsequent damage: McWilliams v Sir William Arrol & Co Ltd ([1962] 1 WLR, at 302) or, in other words, 'the breach of duty coupled with an accident of the kind that might thereby be caused is enough to justify an inference, in the absence of any sufficient reason to the contrary, that in fact the accident did occur owing to the act or omission amounting to the breach of statutory duty': Betts v Whittingslowe (1945) 71 CLR 637, at 649. Nevertheless, the burden of proving the causal connexion between the breach and the damage remains on the plaintiff." 34I will return to Betts v Whittingslowe [1945] HCA 31; 71 CLR 637 shortly . The above passage, however, is not authority for the proposition that tortiously increasing the risk of harm suffices for causation of harm. Nor is the reference by Mason CJ to his Honour's own reasons in Tubemakers . In that case, there was a contest about the condition of the plaintiff's hand being attributable to the injury suffered by the plaintiff caused by the defendant's negligence. Mason J (as his Honour then was) said at 724: "In my opinion, this evidence left it open to the jury to infer that on the probabilities the injury caused or materially contributed to the occurrence of the condition. In drawing such an inference the jury was entitled to have regard, in addition to the matters referred to by Dr Sweeney in his evidence, to other significant circumstances: (a) that before the accident the respondent had suffered no disability in his right hand; (b) that the condition made its appearance shortly after the accident; and (c) that no alternative cause was established or indeed suggested in evidence. The combination of these circumstances, taken together with Dr Sweeney's evidence, provided in my opinion a sufficient basis from which the jury could draw an inference favourable to the respondent. Reaching this conclusion involves no departure from 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; at 618, 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 St George Club Ltd v Hines ( 1961) 35 ALJR 106 at 107; [1962] ALR 39 at 41, where it was pointed out that mere proof of default followed by injury does not show that the default caused the injury)." Mason J (in Tubemakers ) then referred to passages in the reasons of Taylor J in Australian Iron and Steel Ltd v Connell [1959] HCA 54; 102 CLR 522 at 531-532 and 532-533 and Dixon J in Adelaide Stevedoring Co Ltd v Forst [1940] HCA 45; 64 CLR 538 at 569 as elaborating "with varying degrees of emphasis the general onus which lies upon the plaintiff on an issue of causation where the issue lies outside the realm of common knowledge and experience and falls to be determined by reference to expert medical evidence". 35Australian Iron and Steel was a case in which the respondent's husband collapsed and died whilst walking from home to the train station on his way to work. A claim was made under the workers' compensation legislation. Taylor J considered the relationship between exertion and the injury and said the following at the above-cited pages: "... the question is not whether exertion may have been a factor in causing death but whether it is probable that it was, and this must fail ( sic ) to be determined by the evidence in the case. No doubt cases have arisen and will continue to arise where the character and sequence of events may strongly suggest that exertion played a material part in bringing about death (cf Adelaide Stevedoring Co Ltd v Forst (1940) 64 CLR 538). But this is not such a case and it is necessary to remember that it is for the applicant to make out a case and that liability is not established merely by proving that exertion may have been a material factor. ... No doubt we are permitted to know that coronary disease is the cause of many deaths and that sometimes death occurs when the victim is at rest. At other times it occurs whilst he is engaged in some activity which calls for a degree of exertion. In the latter category there will, doubtless, be found cases where exertion was a factor contributing to death whilst in other cases the connexion between the exertion and the death will be no more than temporal. Whether there is a causal, as opposed to a merely temporal, connexion may possibly appear, sometimes, from a significant sequence of events. At other times it may be established by more precise evidence but such a connexion must be shown by a balance of evidence in order to establish liability." 36In Forst , Dixon J had said at the above-cited page: "... I think that upon a question of fact of a medical or scientific description, a court can only say that the burden of proof has not been discharged where, upon the evidence, it appears that the present state of knowledge does not admit of an affirmative answer and that competent and trustworthy expert opinion regards an affirmative answer as lacking justification, either as a probable inference or as an accepted hypothesis." 37None of these passages supports a proposition of causation by increased risk. Indeed, they are to the contrary, unless the increased risk is part of a body of evidence from which it can be legitimately inferred on the balance of probabilities that the tortious act caused or materially contributed to the injury. 38In Bonnington Castings silica dust that caused the pursuer's pneumoconiosis came from two sources in his employer's factory: "innocent" dust from the pneumatic hammer at which he worked in respect of which no known practical method of extracting or preventing dust was available; and "guilty" dust from swing grinders that were fitted with an extraction device which was negligently not kept free from obstruction. The medical evidence permitted the conclusion that pneumoconiosis was caused by the gradual accumulation of silica dust inhaled (guilty and innocent dust together). The guilty dust being material in its contribution to the disease, causation was proved at 618 per Viscount Simonds, agreeing with Lord Reid, 620-623 per Lord Reid, 623-624 per Lord Tucker and 625-626 per Lord Keith of Avonholm. The "guilty" dust as part of an accumulation was a materially contributing factor or cause. See in particular Lord Reid at 620-621. Mason J in Tubemakers and Mason CJ in March v Stramare specifically referred to Lord Reid's speech in Bonnington Castings at 620, where his Lordship said the following: "It would seem obvious in principle that a pursuer or plaintiff must prove not only negligence or breach of duty but also that such fault caused or materially contributed to his injury, and there is ample authority for that proposition both in Scotland and in England. ... ... the employee must in all cases prove his case by the ordinary standard of proof in civil actions: he must make it appear at least that on a balance of probabilities the breach of duty caused or materially contributed to his injury." 39None of these passages supports a proposition of proof of causation by increased risk.

The question of onus of proof 40Before dealing with McGhee , it is necessary to say something about Betts v Whittingslowe and the question of onus of proof. All evidence is of course weighed according to the proof which it is in the power of one side to have produced and in the power of the other to have contradicted: Blatch v Archer (1774) 1 Cowp 63 at 65; 98 ER 969 at 970. The practical approach to the drawing of inferences and conclusions from available evidence that is taken by the courts can be illustrated by many cases: Hollis v Young [1909] 1 KB 629; Dunlop Holdings Ltd's Application [1979] RPC 523 at 544; Hampton Court Ltd v Crooks [1957] HCA 28; 97 CLR 367 at 371-372; Parker v Paton (1941) 41 SR (NSW) 237 at 243; and J D Heydon Cross on Evidence (8 th Ed 2010) at 304 [7160] fn 123 and cases and references there cited. Thus, "in considering the amount of evidence necessary to shift the burden of proof, the Court has regard to the opportunities of knowledge with respect to the fact to be proved which may be possessed by the parties respectively": J F Stephen, A Digest of the Law of Evidence (5 th Ed 1887) at 11 cited in Cullen v Welsbach Light Company of Australasia Ltd [1907] HCA 3; 4 CLR 990 at 1013-1014. 41The circumstances in which the law will provide for rules of shifting onuses or rules of evidence or rules of substantive law that affect proof is, in part, a matter of legal policy. There is a variety of circumstances in which the law provides either forensically or substantively for a shift in onus. The fact that the wrongful conduct has itself made proof difficult may found a rule about who bears the relevant onus. In transport cases, shifting evidential onuses are sometimes employed to disentangle causation issues by reference to capacity for proof: for example in deviation cases and cases of cargo damage under bills of lading where a largely internationally accepted regime of onus shifting exists. Bailment is a relationship under which the onus lies upon the defendant upon proof of the damage to, or non-return of, goods bailed. The present circumstances, however, do not amount to a recognised category of shifted onus. Personal injury is asserted to be caused, or materially contributed to, by the defendant's wrong. The task of the plaintiff is to prove such on the balance of probabilities. This involves direct evidence or inference that must amount to more than conflicting inferences of equal degree or probability such that any choice is conjecture. The conclusion must be affirmatively drawn: Holloway v McFeeters [1956] HCA 25; 94 CLR 470 at 480-481; Jones v Dunkel [1959] HCA 8; 101 CLR 298 at 305; and Luxton v Vines [1952] HCA 19; 85 CLR 352 at 358-359. Common experience and expert evidence will be relevant, and the former may provide the foundation for the inference when the latter cannot: Forst at 563-564; and EMI (Australia) Ltd v Bes [1970] 2 NSWR 238 at 242, unless the expert evidence regards an affirmative inference as lacking justification: Forst at 569; and Tubemakers at 724; cf Australian Iron and Steel v Connell at 535-536 per Menzies J. 42The notion of "balance of probabilities" does not import a conclusion of mathematical or mechanical precision: Jones v Sutherland Shire Council [1979] 2 NSWLR 206 at 227-228 per Mahoney JA; and Seltsam Pty Ltd v McGuiness [2000] NSWCA 29; 49 NSWLR 262 at 275-278 [80]-[98]. 43It is in this context of proof of facts that the question of the defendant's wrongful conduct materially increasing the risk of the relevant harm must be assessed. In Betts v Whittingslowe at 649, Dixon J said the following: "It is not necessary to inquire whether their Lordships meant more than that the breach of duty coupled with an accident of the kind that might thereby be caused is enough to justify an inference, in the absence of any sufficient reason to the contrary, that in fact the accident did occur owing to the act or omission amounting to the breach of statutory duty. In the circumstances of this case that proposition is enough. For, in my opinion, the facts warrant no other inference inconsistent with liability on the part of the defendant." (Emphasis added.) 44Dixon J was discussing the decision of the English Court of Appeal in Vyner v Waldenberg Brothers Ltd [1946] 1 KB 50, in which, in the context of factories and shops legislation, the Court (Scott LJ, Mackinnon LJ and Morton LJ) had said at 55: "If there is a definite breach of a safety provision imposed on the occupier of a factory, and a workman is injured in a way which could result from the breach, the onus of proof shifts on to the employer to show that the breach was not the cause. We think that that principle lies at the very basis of statutory rules of absolute duty." (Emphasis added.) 45Dixon J was using the conjunction of breach and the occurrence of the harm as part of the fact finding process of drawing the relevant inference, not as a basis for a shift of onus that can be seen in Vyner. ( Vyner , it should be noted, was expressly over-ruled in Bonnington Castings .) That is how Betts v Whittingslowe has been interpreted by the High Court in Roads and Traffic Authority (NSW) v Royal [2008] HCA 19; 82 ALJR 870 at 878 [31] per Gummow J, Hayne J and Heydon J and 897 [143] per Kiefel J and by this Court and other intermediate courts of appeal in Australia: Gett v Tabet [2009] NSWCA 76; 254 ALR 504 at 556 [254] and 557 [256] (and the cases there cited); and Flounders v Millar [2007] NSWCA 238 at [4]-[38]; cf John Pfeiffer Pty Ltd v Canny [1981] HCA 52; 148 CLR 218 at 242 in a context of statutory duty. It should be noted, however, that there are dicta inconsistent with this approach in the High Court: Bennett v Minister of Community Welfare [1992] HCA 27; 176 CLR 408 at 420-421 per Gaudron J; Chappel v Hart [1998] HCA 55; 195 CLR 232 at 238-239 per Gaudron J, 257-259 per Gummow J and 273 per Kirby J; and Naxakis v Western General Hospital [1999] HCA 22; 197 CLR 269 at 279. It must be recognised, however, when one is assessing Gummow J's view in Chappel v Hart (in contrast to that in Royal ) that the Court in Chappel v Hart (and Bennett ) was dealing with a duty to warn: see the discussion in Elbourne v Gibbs [2006] NSWCA 127 at [59]-[75] per Ipp JA and North Sydney Council v Binks [2007] NSWCA 245 at [93] per Basten JA. In this respect, the character of the duty and its relationship with the required causal connection may be seen to highlight the relevance of the governing rule of responsibility in the inquiry: Environment Agency v Empress Car Co (Abertillery) Ltd [1998] UKHL 5; [1999] 2 AC 22 at 29. Further, one view of Gummow J's position in Chappel v Hart may be that his Honour was doing no more than drawing an inference in an orthodox manner (if I may respectfully put it that way) in the absence of other evidence. 46The need for an affirmative inference of the above character is inconsistent with the fundamental legal proposition founding the appellant's fourth complaint. Also inconsistent with it are the decisions in this Court in Bendix Mintex Pty Ltd v Barnes (1997) 42 NSWLR 307 at 315-316 per Mason P and 339 per Beazley JA; TC by his Tutor Sabatino v State of New South Wales [2001] NSWCA 380 at [59]; Seltsam at 278-280 [102]-[120] per Spigelman CJ and at 306 [268] per Davies AJA; and Gett v Tabet [2009] NSWCA 76 at [254]. Further, the necessary relationship between liability for increase in risk and loss of a chance places the appellant's fundamental proposition in conflict with the High Court's decision in Tabet v Gett [2010] HCA 12; 240 CLR 537.

McGhee 47It is necessary to deal with McGhee , not least because of the changed interpretation of the case by the House of Lords and United Kingdom Supreme Court. In McGhee , the pursuer who worked in a brickworks contracted dermatitis. He was usually employed in emptying pipe kilns, but shortly before he felt excessive irritation of the skin he had been sent to empty brick kilns where work was hotter and dustier. Shortly thereafter, he went off work suffering dermatitis. The breach of duty relied upon (and admitted) was not providing washing facilities after finishing work in the brick kilns. The medical evidence was to the effect that the dermatitis was caused by repeated minute abrasions of the outer skin followed by some damage to underlying cells, of a kind not scientifically understood. Profuse sweating over time softened the skin and made it easily injured. Dust would adhere to the skin in the kiln and exertion would cause abrasion. Washing was the only practical way of removing the danger. His bicycling home caked with sweat and dust would only exacerbate the position. Enough, however, was known about the disease to enable a conclusion that it was not like pneumoconiosis in that it was not caused by all the dust and sweat and exertion. However, it was clear that not providing showers materially increased the risk of contracting dermatitis. The House of Lords found for the pursuer. 48Two interpretations have been placed on the case. The first is reflected in Lord Bridge's analysis (adopted by all members of the House) in Wilsher v Essex Area Health Authority [1988] AC 1074 that McGhee did not stand for any principle that the onus of proof was reversed or that material increase in risk alone was sufficient. McGhee was said to be (with the exception of Lord Wilberforce's opinion) an example of a robust and pragmatic approach to inferential fact finding of material contribution. This had been also how the House of Lords had interpreted it in Kay v Ayrshire and Arran Health Board [1987] 2 All ER 417. This was also the view of Lord Hutton in Fairchild. This interpretation was also the foundation of Bendix and Seltsam . The second interpretation is reflected in the analysis of Lord Bingham, Lord Nicholls, Lord Hoffmann and Lord Rodger in Fairchild that in circumstances such as McGhee either a material increase in risk is an adequate "causal" link or no relevant distinction was to be drawn between materially increasing the risk and materially contributing to (that is causing) the injury. This interpretation of McGhee also founds the United Kingdom Supreme Court's decision in Sienkiewicz , to the extent that that decision stands as support for the appellant's fundamental proposition. 49There are a number of references in the High Court to McGhee : Bennett at 420-421 per Gaudron J; March v Stramare at 514 and 516 per Mason CJ; Chappel v Hart at 273-274 [93] per Kirby J; RTA v Royal at (2008) 82 ALJR 870, 888-889 [94] per Kirby J and 897-898 [143] per Kiefel J; Amaca Pty Ltd v Ellis [2010] HCA 5; 240 CLR 111 at 123 [12]; and Tabet v Gett at 558 [40] per Gummow ACJ and 588 [149] per Kiefel J. 50The issues of the relationship between breach and causation and between causing an increase in risk, material contribution and onus of proof were expressly left open in Bennett at 416, and were expressly disavowed by the plaintiff/respondent in Amaca Pty Ltd v Ellis see 123 [12]; nor were the points taken in the High Court in Tabet v Gett . 51The importance of the question left open by Mason CJ, Deane J and Toohey J in Bennett at 416 ("the question whether a failure to take steps which would bring about a material reduction of the risk amounts to a material contribution to the injury") can be seen from the references by Mason CJ in March v Stramare at 514 to McGhee at 4, 6, 8 and 12 as support for the law's recognition of "material contribution" as an element of causation. It can be accepted that the re-interpretation of McGhee by reference to what is at these pages has some force. Lord Reid at 4-5, Lord Wilberforce at 6, Lord Simon of Glaisdale at 8 and Lord Salmon at 12 appear to found their reasoning on material increase in risk founding the causal link in cases where proof of more is otherwise not possible. (I express no concluded view on the question of the proper interpretation or understanding of McGhee .) The leaving open of the consideration of the question in Bennett can be taken as a recognition that the references in March v Stramare at 514 to the pages of McGhee to which I have referred did not already establish a proposition which is consistent with the re-interpretation of McGhee in Fairchild and later cases. This is particularly the case given the limited purpose of the citation of McGhee in March v Stramare at 514. 52Given the state of the law otherwise to which I have referred, a re-analysis of the cases on causation by reference to the interpretation of the speeches in McGhee in accordance with the views of the House of Lords and Supreme Court in Fairchild, Barker v Corus and Sienkiewicz awaits the attention of the High Court. In my view, it is not open to this Court to accept the appellant's fundamental proposition underpinning her fourth complaint. This is so certainly in the absence of a direct attack in this Court on cases such as Bendix and Seltsam as plainly wrong.

Conclusion 53The law is to be understood as requiring that, in a tortious claim such as this, a plaintiff must prove on the balance of probabilities that the defendant's wrong caused or materially contributed to his or her loss, not just that the defendant's wrong materially increased the risk of such harm and that medical science does not permit any further proof. As the High Court said in St George Club v Hines Ltd (1961) 35 ALJR 106 at 107: "In an action at law a plaintiff does not prove his case merely by stating that it was possible that his injury was caused by the defendant's default."

Stamoulis 54It is necessary to deal with Stamoulis , which was relied on by the appellant to found the proposition. Both Hodgson JA and Basten JA have discussed it. The reasons of Ipp JA (with whom Beazley JA, a member of the bench in Gett v Tabet , agreed), the additional comments of Beazley JA and the reasons of Giles JA are all founded on an expression of legal principle which is consistent with authorities that I have discussed and which is inconsistent with the appellant's fundamental proposition underpinning her fourth complaint: [2009] NSWCA 153 at [29]-[30], [37] and most importantly [122]-[127] and [134]-[141]. Whether or not the evidence in Stamoulis was sufficient to enable the inference of cause or material contribution to be drawn need not be analysed. It was a factual conclusion reached by their Honours. The comments of Spigelman CJ in Seltsam at 275 [84] and Lord Macmillan in Jones v Great Western Railway Co (1930) 144 LT 194 at 202 as to the difficulty in identifying the dividing line between inference and conjecture are relevant in this respect. More importantly for present purposes, the legal principle expressed by all three judges was in accordance with the views that I have expressed above that are inconsistent with the appellant's fundamental proposition underpinning her fourth complaint. 55The above does not deal with the Civil Liability Act 2002 (NSW), s 5D, which provision is irrelevant to proceedings (such as this) brought under the Dust Diseases Tribunal Act 1989 (NSW), s 11: see the Civil Liability Act , s 3B(1)(b). 56HODGSON JA : I agree with the orders proposed by Basten JA, and I agree substantially with his reasons. I would add the following reasons of my own. 57The table prepared by the primary judge and set out in Basten JA's judgment suggests that if, in a case where a person has both smoked and been exposed to asbestos, it is possible that cancer has been caused either by the smoking alone or by the asbestos alone or by the synergistic effects of the two, the statistics could not support a finding on the balance of probabilities that the asbestos was a substantial contributing cause, operating either alone or in combination with the smoking. 58However, if it had been established that, where a person has both smoked and been exposed to asbestos, the two operated synergistically (either in all cases, or in the particular case of Mr Evans) and that the contribution of the asbestos was significant (at least in the case of Mr Evans), then this could have supported a finding that the asbestos was a substantial contributing cause of the cancer suffered by Mr Evans. It might however have then been necessary to deduct from any damages a sum reflecting the chance that cancer would have developed without the exposure to asbestos; although it appears that in this case such a deduction may have been quite small, having regard to the figure of ten percent mentioned in par [88] in Basten JA's judgment. 59This approach seems consistent both with Sydney South West Area Health Service v Stamoulis [2009] NSWCA 153 and Amaca Pty Limited v Ellis [2010] HCA 5; (2010) 240 CLR 111. 60In Stamoulis , a carcinoma of the plaintiff's left breast metastasised into her lungs and brain. The plaintiff brought a claim against two radiologists who examined a mammogram taken in March 2006, but did not recommend further investigation. The plaintiff was diagnosed as having cancer as a result of a further mammogram in January 2007. The evidence was that, had the tumour been detected and treated in March 2006, the plaintiff would have had a 62 percent chance of not experiencing metastasis; but in the event, she had a lesser 58 percent chance of not experiencing metastasis. The Court of Appeal held that that would have been sufficient to establish causation. 61As pointed out by Basten JA, it may be questioned whether Stamoulis is consistent with Tabet v Gett [2010] HCA 12; (2010) 240 CLR 537. At best for the appellant, it would have to be understood on the basis that what came home was a materially increased risk (increased by ten percent from 38 percent to 42 percent), which was an indivisible whole, incapable of being divided into separate components of a "base" risk of 38 percent and an increase to this risk of four percent. However, had the plaintiff been otherwise successful, this analysis would suggest that it would then have been necessary to make a deduction from any verdict referable to the 38 percent chance that metastasis would have occurred in any event: cf Malec v JC Hutton Pty Ltd [1990] HCA 20; (1990) 169 CLR 638. 62In Ellis , the analysis was not applicable, because it was not established that smoking and cancer must work together, or that they must have worked together in that particular case: see Ellis at [53]-[54]. In my opinion, it is clear that the High Court was not satisfied that smoking and asbestos had in fact worked together in that case. 63The primary contention of the appellant was that the evidence in this case was different from that in Ellis ; and that the evidence did establish that smoking and asbestos had worked together synergistically in this case. It was submitted for the appellant that the primary judge erred in law in rejecting that contention, in the following paragraphs of his judgment: 149. I am persuaded that asbestos and cigarette smoking may act in combination in contributing to the development of lung cancer. 150. I am not persuaded that in all cases, and in particular in this case of Mr Evans, that the contribution of asbestos must have occurred, or if it did, that the contribution was material. 151. First, because both Professor Breslin and Professor Tattersall, while accepting the theory, dismissed the contribution of asbestos in Mr Evans' case because of its relative insignificance. I accept that a contribution may be material although it is minor but I believe that, in context, the opinions of both medical experts are to the effect that the contribution was not minor but insignificant, that is to say, immaterial. 152. Secondly, because Dr Leigh concedes that in a particular case the contribution of asbestos may play a very small part , and that he could not say that, more probably than not, Mr Evans would not have contracted his cancer in the absence of the asbestos exposure. 153. Thirdly, because epidemiological studies predict that among the class of persons who share Mr Evans' smoking history, the greatest number of those who contract lung cancer after exposure to an equivalent asbestos fibre burden are persons who would have contracted the disease in any event. 154. Fourthly, because, even if asbestos and smoking combined causally in the development of lung cancers in all cases, the contribution of asbestos to the development of lung cancer in smokers may take the form of hastening the development of the cancer. That would reconcile the certainty of epidemiological prediction that a certain number of lung cancers will develop in smokers in any event, with the plausible biological theory that the additional risk factor of asbestos exposure will contribute to that inevitable development by way of acceleration. 64It was also submitted that what was said in par [151] was inconsistent with a statement in par [177] of the judgment that the presence of diffuse pleural thickening in Mr Evans' lungs indicated "significant asbestos exposure". 65I think there is force in some of the criticisms of those paragraphs. If it had been proved that smoking and asbestos worked synergistically in the case of Mr Evans, and if it had also been proved that the contribution of the smoking to this synergistic working was significant, then it would not matter that it had not been proved that "Mr Evans would not have contracted his cancer in the absence of the asbestos exposure" (par [152]). Further, contrary to what is suggested in par [154], acceleration of development of something that would have happened later could support a claim for damages; although that kind of claim was never made in this case. 66However, crucially in par [150], the primary judge was not persuaded that in all cases or in this case the contribution of asbestos must have occurred in combination with that of smoking (and I take it that this means he was not persuaded on the balance of probabilities that it did so in this case). Further, in par [151], the primary judge indicated lack of satisfaction that any contribution of the asbestos was significant. I do not see any inconsistency of this with par [177]: exposure to asbestos could be significant, yet a judgment could be made that its contribution to the causation of cancer in a heavy smoker was not significant. 67I do not think those views of the primary judge were vitiated by any of the errors in pars [152] or [154]. This means that neither of the thresholds suggested by my earlier analysis was passed: it was not shown that the contribution of asbestos was indivisible from that of the smoking, and it was also not shown that this contribution was significant. 68BASTEN JA : Most disputes which reach tribunals and courts turn not on some uncertainty as to the correct legal principle to be applied, but on the facts. Courts do not act upon facts in some absolute sense, but only decide what, on the evidence before them, is (in a civil case) probably true. In other areas of social activity, including scientific investigation, it is unusual to treat as objectively true something of which all that can be said is that it is more probably true than untrue. That is a circumstance with which courts must grapple in cases where critical evidence comes from experts involved in scientific investigation. This case involved evidence from specialists in epidemiology, pathology, thoracic medicine, other medical specialties and from industrial hygienists, many of whom were eminent in their fields. 69The issue in dispute was whether the lung cancer contracted by the late Mr Evans was caused by his exposure to asbestos dust in circumstances imposing responsibility on either or both of the respondents. The first respondent (Queanbeyan City Council) was Mr Evans' employer from 1975-1990; the second respondent (Amaca Pty Ltd) was an important manufacturer of asbestos building products through much of Mr Evans' working life. If it had been shown that Mr Evans' lung cancer was caused by exposure to asbestos, further questions would have arisen as to the responsibility of each of the respondents for such exposure. Thus, liability in negligence would require those respondents to have failed to exercise reasonable care to protect Mr Evans from exposure to asbestos dust as a worker, or as a user of asbestos products. These latter questions did not arise in the present case because the appellant failed at the first hurdle: Judge Curtis, sitting in the Dust Diseases Tribunal, was not satisfied on the balance of probabilities that Mr Evans' lung cancer was caused by exposure to asbestos: Evans v Queanbeyan City Council [2010] NSWDDT 7. Mr Evans' widow appeals against that decision. 70Tribunals are usually established to improve access to justice, especially for the less well-off members of the community, who may have small claims which do not justify the expenditure of large sums of money. In other cases, such as the Dust Diseases Tribunal, an alternative to the ordinary civil courts may be established with flexible procedures to permit speedy determination of claims of persons possibly suffering from a terminal illness. Despite the procedures of civil courts having the overriding purpose of facilitating the just, quick and cheap resolution of the real issues in dispute, their ability to do so is relative. Further, injustice may be reduced, but expense and delay increased, by the provision of general rights of appeal from tribunals. To that end, the Dust Diseases Tribunal (in common with many other statutory tribunals) is not subject to appeals by way of rehearing. Its decisions are subject to judicial review, but a dissatisfied party's right of appeal is limited to "a decision of the Tribunal in point of law or on a question as to the admission or rejection of evidence": Dust Diseases Tribunal Act 1989 (NSW) ("the Tribunal Act "), s 32(1). To the extent that either party is dissatisfied with a decision of the Tribunal which cannot be described as being "in point of law" (leaving to one side questions of evidence) the result may be to prefer finality and expedition over the "just" outcome, always assuming that a full right of appeal is apt to promote the just resolution of disputes. 71It is natural for judges to seek to promote just outcomes. Where an appellate court perceives that an injustice has been suffered, due to erroneous fact-finding, there is a tendency to press the limits of the statutory right of appeal to allow the injustice to be remedied. Fidelity to the statutory language may, however, preclude intervention. 72One form of injustice is to fail to achieve similar results in like cases. That can occur when there is evidence to support a decision either way in two cases, the judge in the first case preferring the evidence tending in one direction, whereas the judge in the second case prefers the other evidence. One claimant may succeed and the other fail in circumstances where their circumstances and the expert evidence is not materially different. The statutory right of appeal would not permit interference in either case. As will be explained below, this case illustrates an aspect of that paradox.

Nature of case in Tribunal 73Mr Evans was a tolerably heavy smoker for a considerable period of time. He commenced smoking in about 1941, at 14 or 15 years of age, and continued smoking until 1990. The primary judge held that Mr Evans smoked between 20 and 35 cigarettes a day for approximately 40 years: at [16]. Over roughly the same period, he suffered occupational exposure to asbestos dust of variable intensity, depending upon the work he was undertaking at the relevant time. A quantitative assessment of such exposure is extraordinarily difficult, with any degree of accuracy. It depends on anecdotal evidence as to the occasions of exposure, the periods of exposure on each occasion and the levels of dust from time to time. Precision is impossible. Nevertheless, techniques have been devised to permit the calculation of total exposure measured as fibres/ml/years. 74Exposure to asbestos dust can give rise to a number of conditions, including asbestosis, asbestos related pleural diseases, lung cancer and mesothelioma. This case is concerned with lung cancer. Although it is not presently possible for medical science to say whether a particular instance of lung cancer is caused by exposure to asbestos or not, knowledge supports a correlation between the level of exposure and the occurrence of that disease. Accordingly, establishing Mr Evans' level of exposure, to the extent that that could be done, was a relevant factual inquiry. His Honour found that Mr Evans had a total exposure over the whole of his working life of 21.9 fibre/ml/years: at [62]. The apparent level of precision is misleading - his Honour did not suggest otherwise: rather, he "recognised the difficulty of reconstruction and attempted to make generous assumptions as to his exposure": at [167]. He accepted that this was a finding of "significant asbestos exposure": at [168]. 75Because Mr Evans was not able to demonstrate, by medical evidence, the cause of his particular disease, it was, arguably, necessary for him to rely upon epidemiology. Epidemiology involves a statistical analysis of various populations. Although it too may produce calculations resulting in precise figures, the position is often misleading and the figures are no more accurate than the underlying source material. The evidence was not expressed in terms of degree of certainty or range of possible error, referrable to the basic data. 76Broadly speaking, epidemiology can be used in two quite different ways. One is to calculate the risk of disease in a population, for example of persons who are exposed to asbestos dust or smoke cigarettes. This exercise is of relatively limited significance for present purposes, except to show that even amongst heavy smokers, or those who have significant asbestos exposure, the incidence of lung cancer is relatively low. The second kind of exercise, relied upon in the present case, may take a population with a particular disease and estimate the likelihood that in any particular case the disease resulted from one of a number of causes. Thus, with a particular cohort or population of lung cancer sufferers, tables can be produced indicating the "relative risk" that a particular cancer arose from a particular cause where the causes which are not sought to be investigated are broadly lumped together as "background risk" and accorded the numerical value of 1. When the relative risk in respect of a particular cause reaches 2, it can be said that any particular cancer suffered by a person subjected to that cause is as likely to have resulted from that cause as from the background risk. Alternatively, the cohort can be divided in percentage terms into the various causes. Adopting the latter approach, the primary judge prepared a table in which the background incidence of lung cancers was 100 in a given population and then showing the percentages attributable to smoking, asbestos and the combined effect of smoking and asbestos exposure, reflecting Mr Evans' circumstances: at [140]. Cause of Cancer No. of Cancers % Background (RR 1) 100 7% Additional cancers attributable to smoking alone (RR 10.7) 970 63% Additional cancers attributable to asbestos alone (RR 1.43) 43 3% Additional cancers attributable to the synergistic effect of smoking and asbestos exposure 417 27% Total 1530 100%

77These figures reflected exposures in the range of those experienced by Mr Evans. The table, taken at face value, demonstrated two critical matters. The first was that the total of all of the cancers attributable in some measure to asbestos exposure amounted to 30% of the cohort, whereas those attributable solely to smoking constituted 63% of the cohort. That is, in respect of any individual cancer afflicting a person who both smoked and was subjected to asbestos dust, there was a one-in-three chance that asbestos was in some part responsible and a two-in-three chance that it was attributable to smoking alone. On those figures, it could not be said of any individual cancer that it was more probably than not attributable, even in part, to asbestos exposure. If that were the only relevant material, or if it were material, taken alone, upon which the primary judge was entitled to rely, and did rely, the appeal must fail. 78The second matter illustrated by the table is that there is a "synergistic effect" in respect of smoking and exposure to asbestos dust. The precise mechanism by which this effect works is not scientifically established. It may be hypothesised that there is a biological reaction taking place in the lung, although the reaction is not presently understood.

A universal "synergistic effect"? 79Of critical importance for the appellant's case was the evidence of Dr James Leigh, who has a distinguished record in research and clinical work, broadly in the area of thoracic medicine, but with a particular emphasis on asbestos-related disease and epidemiology. A critical passage at page 6 in the report of 22 July 2009 prepared by Dr Leigh, set out by the primary judge at [66], was in the following terms: "While the precise mechanism of interaction between asbestos and tobacco smoke in causing lung cancer is not known, it is not possible in my view to separate their effects on the individual case when both have acted, as they must do to some extent from a purely physico-chemical point of view, and it is thus more probable than not, that in this situation, the lung cancer was the singular result of the two factors acting together." 80In a passage from his oral evidence, also set out by the primary judge, Dr Leigh, after being referred to two published papers, stated (Tcpt, 25/03/10, p 91(30)): "They certainly strengthen my opinion that if both agents are present then both are acting biologically in producing either tumours or the early stages of carcinogenesis in the form of mutations. They actually demonstrate a more than additive interaction between the tobacco agent and the asbestos, in fact, in a biological sense as opposed to [an] epidemiologic sense." 81The appellant argued that this evidence of a biological effect allowed the trial judge to be satisfied that asbestos, on the probabilities, contributed to Mr Evans' lung cancer. That is, where both agents were present, a reaction will usually occur, meaning that both would contribute to any instance of lung cancer. In legal terms, causation was thus established. On this approach, it was not necessary to go to the epidemiology, which provided no conclusion as to the role of asbestos in a particular case. Curtis J, did not, however, accept this submission. Rather, he accepted the evidence of Dr Berry, the primary epidemiologist, that such a conclusion was inconsistent with the epidemiology, which, although it showed the synergistic effect of the two agents in combination, did not suggest that the synergistic effect operated in all cases, indeed the contrary. In evidence accepted by the primary judge, Dr Berry said of the biological modelling, "that if it did not agree with the epidemiological data it must be incorrect": at [194]. 82The synergistic effect is not merely a theory of physical or chemical inter-reaction of the two agents in a person's lung. Nor is it, subject to an argument addressed below, an effect which can be identified in a particular individual. It is, his Honour found, capable of assessment in epidemiological terms. Thus, he stated at [131]: "There is a synergistic effect between asbestos and smoking in the causation of lung cancer so that the combined effect of asbestos exposure and smoking on the risk is approximately multiplicative. The effect of the synergy can be given mathematical form by multiplying together the relative risks of smoking and asbestos and deducting the sum of those risks."

Double agent effects in a particular case 83The primary judge was entitled to accept Dr Berry's evidence and hence reject, as inconsistent with the epidemiology, the hypothesis that smoking and asbestos work together in all (or more than 50% of) cases. That is not to say that the hypothesis is erroneous: rather, it is to say that the trial judge was not satisfied that it was probably correct. If, as Dr Leigh explained, and his Honour accepted, there is a synergistic effect, it is obviously important to understand how the mechanism works, so that it will be possible to say whether it must operate in all cases, or only in some, and if some, in more or less than half. The evidence was contentious in this respect. The epidemiology demonstrated that, after taking into account the numbers of persons who would suffer from lung cancer if exposed to asbestos or to cigarette smoke at certain levels , there will be more who suffer as a result of exposure to both agents. For the purposes of the appellant's case, the trial judge had to be satisfied that, in more than half the cases of double exposure, including people who would have suffered from lung cancer as a result of smoking alone, the exposure to asbestos nevertheless contributed. 84One question may be whether it would sufficient to show a universal contribution in circumstances where it could not be shown that the tortious agent (asbestos exposure) resulted in an earlier contraction of the disease, or a more serious disease. If, for example, both were found to be contributing causes, but that the injured worker would have suffered from lung cancer as a result of his or her smoking in any event, the analysis of the hypothetical circumstances required in Malec v JC Hutton Pty Ltd [1990] HCA 20; 169 CLR 638 would operate. Thus, if the tortious event could be shown to have led to an injury two years earlier than it would have been suffered absent the tortious event, the damages would be limited to the suffering inflicted over that period. But if the damage would not have occurred earlier, nor been more intense, causation may have been proved, but no loss attributable to the tortious exposure. These issues do not arise in the present case.

Application of 'but for' test 85The next point concerns remarks by his Honour which appear to apply the so-called "but for" test. Thus, at [81], his Honour stated: "Notwithstanding his opinion that both smoking and asbestos contributed to the development of Mr Evans' lung cancer, Dr Leigh was unable to say that, more probably than not, Mr Evans would not have contracted the cancer in the absence of the asbestos exposure." 86Taken in isolation, that passage might indicate the application of a wrong test. As explained by Deane, Gaudron and McHugh JJ in Malec , the issue in that appeal concerned "the valuation of a plaintiff's damage, caused by the tortious conduct of the defendant, after it is found that it is more likely than not that the damage would have occurred in any event as the result of conditions or events for which the defendant is not legally responsible": at 640. Causation of injury and assessment of loss are separate exercises. 87The questioning upon which the primary judge relied in making the statement set out above (at Tcpt, 84(29) and 86(41)) involved the same latent ambiguity as his statement. Thus, in the latter passage, his Honour asked: "Q. Paragraph 65 of Ellis the High Court, Doctor, said it was not shown to be more probable than not that asbestos was the cause of [or?] a necessary condition for his cancer. Are you able to express an opinion whether or not Mr Evans would have contracted cancer without the asbestos. A - Yes, he could've. Q. Are you able to say whether it's more probable than not, that is can you know more probably than not that he would or would not have contracted the cancer without the asbestos. A - Well, it would depend on what the court accepts as to the relative exposures. So I can't really answer that in this particular case." 88The first problem with this exchange was the ambiguity as to whether the witness was being asked to assume that Mr Evans contracted cancer. If the hypothetical were addressed before he contracted cancer, relying upon an unspecified level of cigarette smoking but no exposure to asbestos, the chance of him contracting cancer would have been well below 50%, particularly as one of the circumstances was that he had ceased smoking some years before he contracted cancer. However, it cannot have been assumed that he did contract cancer, or the question would have been meaningless. (The parties accepted that less than 10% of people who smoked as heavily as Mr Evans contract lung cancer.) 89Secondly, the context of the question requires reference to the judgment of the High Court in Amaca Pty Ltd v Ellis [2010] HCA 5; 240 CLR 111 at [65]. The context in which this passage arose needs to be identified. Like the present case, Amaca v Ellis involved a smoker exposed to asbestos dust. Importantly, the case came before the High Court following an appeal from a trial court to the Court of Appeal of Western Australia. The appeal was by way of rehearing and involved a review of the evidence: it was not limited to identification of legal error on the part of the primary judge. In that context, the High Court reviewed evidence given by Dr Leigh in that case. Their Honours stated: "[33] Dr Leigh gave evidence about research into the possible biological mechanisms for the synergistic effect, and noted that some research suggested that tobacco smoke and asbestos act at different stages of the development of cancer. He expressed the opinion that: 'While the precise mechanism of interaction between asbestos and tobacco smoke in causing lung cancer is not known, it is not possible in my view to separate their effects in the individual case when both have acted and it is thus more probable than not, that in this situation, the lung cancer was the singular result of the two factors acting together . It is however true that exposure to either factor alone is capable of causing lung cancer.' (emphasis added) [34] The meaning and effect of this passage of Dr Leigh's report was much debated in the course of the argument of the present appeals. In terms, the proposition advanced by Dr Leigh in this passage of his opinion was that when both smoking and asbestos cause cancer, the cancer is 'the singular result of the two factors acting together'. That proposition, if taken literally, would not address the question in issue in these cases. The question for decision in these cases is whether asbestos was a cause of the cancer. [35] Reading his opinion as a whole, it is evident that Dr Leigh did not express the view that, if a smoker has been exposed to asbestos and develops lung cancer, the asbestos exposure is, or is probably, a cause of that cancer. Dr Leigh expressly acknowledged not only that the precise mechanism of interaction between asbestos and tobacco smoke is not known, but also that it remains possible (for what he described as "legal or administrative" reasons) 'to partition attributability to smoking and asbestos under a variety of mathematical risk models'. To read the passage from his evidence about 'singular result of the two factors acting together' as saying that, if a smoker has been exposed to asbestos and develops lung cancer, the asbestos exposure is necessarily (even probably) a cause of the cancer, would not be consistent with his acknowledgement that the probability of causal connection can be divided ('partition[ed]') between the two carcinogens." 90The trial judge was found to have erred in two respects. First, his Honour had looked at cumulative exposure without considering the respective responsibilities of each defendant (a question not reached in the present case) and had treated a material contribution to risk as sufficient to demonstrate causation. Their Honours identified the relevant question as whether it was "more probable than not that the negligence of the defendant was a cause of [the plaintiff's] cancer": at [51]. They then addressed the first step in the plaintiff's argument which was that "smoking and asbestos must work together". In response to that their Honours stated at [54]: "It may be accepted (at least for the purposes of debate) that the synergistic or multiplicative effect suggests that in some cases the two carcinogens will have contributed to the development of an individual patient's cancer. But the proposition which the plaintiff advanced was an absolute proposition of universal application: smoking and asbestos must work together and they must have worked together in this case. That proposition was not established." 91Their Honours identified the issue in this way because that was the way in which the plaintiff had put his case. Assuming that it would be sufficient if it were established that smoking and asbestos worked together more often than not, the evidence in Amaca v Ellis did not establish any such proposition. Their Honours concluded at [65]: "It was not shown to be more probable than not that asbestos was a cause of (a necessary condition for) his cancer. It was not shown that exposure to asbestos made a material contribution to his cancer. Material contribution was not shown because a connection between [the plaintiff's] inhaling asbestos and his developing cancer was not demonstrated." 92In the present case, Dr Leigh explained his opinion in a manner which meant that the evidence before the Tribunal differed from that before the Courts in Amaca v Ellis . However, in order to succeed by demonstrating error in point of law, the appellant needed to demonstrate that Dr Leigh's evidence stood alone, in the sense that it was not contradicted, or that if contradicted, there was some erroneous application of legal principle in failing to accept his evidence in preference to other material. Not only did Dr Leigh not stand alone, but he did not have unequivocal support from any other witness. In a sense, it does not matter whether Dr Leigh obtained support; the real question is whether there was probative evidence to the contrary. If there were, his Honour was entitled to accept it. In any event, the supportive evidence relied on by the appellant was inadequate for the purpose. For example, the appellant relied on two passages in the evidence of Dr Nicholls, a consultant thoracic physician. In his report of 29 April 2009, Dr Nicholls stated: "There is considerable debate as to whether asbestos exposure in the absence of asbestosis increases the risk of bronchogenic carcinoma. However, I believe there is good evidence of a synergistic effect of smoking and asbestos exposure on the risk of developing lung cancer. Thus, I believe that his exposure to asbestos is definitely a contributing factor to his subsequent development of lung cancer." 93A number of comments may be made in respect of this evidence. First, if there is "considerable debate" on a point, it is difficult to see how one conclusion rather than the other could be said to be based on "no evidence". Secondly, his Honour accepted that there was a "synergistic effect". Thirdly, increase in risk of developing lung cancer does not equate with a material contribution to the development of a particular cancer. This was a fallacy exposed in Amaca v Ellis . What the evidence needed to show was that where the two agents coexisted, exposure to asbestos was a contributing factor in at least half of all cases. 94A second passage, from a report of Dr Nicholls dated 18 December 2009 read as follows: "There is evidence that asbestos exposure is associated with an increased risk of lung cancer even in the absence of asbestosis. There is also evidence of a multiplicative risk of smoking and asbestos exposure in causation of lung cancer. ... Mr Evans has pleural plaques confirming his occupational history of exposure to asbestos. In view of the above comments, I believe it is impossible to ignore the effects of asbestos as a cause of the development of lung cancer in this gentleman." 95This passage is somewhat vague in its import and could only provide limited support to Dr Leigh. It was not the subject of elaboration or cross-examination when Dr Nicholls gave evidence. 96The appellant also sought to call in aid the evidence of Professor Tattersall. Professor Tattersall did not provide unequivocal support for the plaintiff's case at trial. In his report of 20 August 2009 he expressed the belief that "on the balance of probabilities occupational exposure to asbestos dust and fibre ... did NOT cause or make a material contribution to the development of Keith Evans' lung cancer". The appellant, however, relied upon Professor Tattersall's evidence before the Tribunal. The following exchange took place (Tcpt, pp 137-138): "Q. Now, are you prepared to accept that there is some interaction between the carcinogens produced by tobacco smoke and asbestos fibre, particularly amphibole asbestos fibre. A - I think there is an interaction in lung tissue between the effects of cigarette exposure and asbestos fibre exposure, but I'm not sure there's any effect on asbestos fibres per se. Q. Right, so it is fair to say that a biological level the two act together in lung tissue. A - I think there is evidence that they can coexist and there is evidence that they can cause lung damage, the extent to which they interact has been a subject of considerable controversy over recent years. Q. Are you aware of the recent animal studies that have been conducted into the relationship between the carcinogens from tobacco smoke and amphibole asbestos. A - I have seen some of those papers, yes. Q. And you would accept from those would you not, that there is both a biological and genotoxicity effect for those two acting together to cause tissue damage, is that not so. A - I don't recall how the asbestos in those experiments was actually administered to the animals, but I am aware of experiments which have shown an interaction between biological tissues containing asbestos and products of cigarette smoke." 97The further passage appeared in the evidence of Professor Tattersall (Tcpt, p 141) in response to a question from the primary judge: "Q. ... We have heard from Dr James Leigh, who says that theoretically, because epidemiological studies that showed incidents of lung cancer with asbestos, secondly because asbestos has been shown to be a primary carcinogen in laboratory tests and thirdly because the combination of asbestos and tobacco products can together act, in animal studies and laboratory tests, in combination to produce cancers, that as a matter of theory all exposure to both tobacco and asbestos would have a concurrent that the asbestos contribution did something although it may be very minor. As a matter of theory, do you reject that reasoning. A - I accept it's a plausible hypothesis. I think the evidence you're referring to is incomplete and relates to animals given exposure in particular ways and cell culture experiments are, I think highly artefactual. The epidemiological evidence, as I understand it, is more discriminatory and as far as I am aware, in non-smokers the evidence that asbestos exposure causes a peranc or lung cancer is not supported by the evidence." 98There are aspects of this statement which are not entirely clear, but it did not provide unequivocal support for the hypothesis that in all or at least a majority of cases, the agents interact.

Reliance upon Smith's case 99There was discussion in the course of argument, both before the Tribunal and in this Court, as to the assistance which might be obtained by the appellant from Workers Compensation (Dust Diseases) Board of NSW v Smith, Munro and Seymour [2010] NSWCA 19. In fact, that case provides little assistance. The legal principle was, of course, the same, namely that the plaintiffs had to establish that their exposure to asbestos was, on the balance of probabilities, a contributing factor to their individual carcinomas: at [67]. There was evidence before the primary judge in that case as to the circumstances in which the synergistic effect operated. In particular, it was "not entirely clear from the evidence ... whether the synergistic effect operated universally": at [67]. This Court held that there was evidence on which her Honour could so find. Because the appeal was limited to a question of law, the challenge to the finding as to causation therefore failed. Subject to what follows, the same result must obtain in the present case. Indeed, the reasoning is stronger in the present case because it is an appeal by the plaintiff, who bore the onus of proof and, at least in theory, might not have succeeded even if all the evidence was in favour of the view that exposure to asbestos contributed to the lung cancer because it would do so in a majority of cases: see Azzopardi v Tasman UEB Industries Ltd (1985) 4 NSWLR 139 at 156 (Glass JA, Samuels JA agreeing). To interested parties reading these cases, it might be thought that similarly placed plaintiffs should, if the law is properly administered, either always succeed or always fail. The reason why that is not so is that the medical evidence is not a fixed quantity, but a variable. Further, because the medical evidence is contestable and contested, the outcomes may legitimately differ. This is a function of the shortcomings of medical science, not of the administration of justice.

Reliance on Stamoulis 100The appellant also sought to obtain support from the judgments of this Court in Sydney South West Area Health Service v Stamoulis [2009] NSWCA 153. In that case, the plaintiff had undergone a mammogram in February 2006. The radiologists, exercising reasonable skill and care, should have detected a cancerous growth: they did not. A second investigation in January 2007 discovered the breast cancer. There was a risk that the tumour would metastasize. Epidemiological evidence indicated that, if diagnosed in February 2006, the chance of metastasis was about 38%; if not diagnosed until January 2007, the chance rose to 42%. The plaintiff's tumour metastasized, leading to her subsequent death. The Court held that the 10% increase in risk, resulting from the delayed treatment, followed by the materialisation of the risk, was sufficient to demonstrate that the tortious conduct materially contributed to the metastasis. 101This authority does not assist the appellant, for two primary reasons. First, the nature of the epidemiology is quite different: it was concerned with direct risk of metastasis, depending upon the stage at which the first carcinoma was detected and treated. It did not take a cohort of women whose tumours had metastasized and determine the effect of the delay. There was no similar case run for the appellant. Had there been, he would have needed to identify the risk of a man with his smoking history contracting lung cancer (said by counsel in the course of argument to be either 6% (for the appellant) or less than 10% (for the respondent)) and add to that the increased risk due to exposure to asbestos dust at the level experienced by the appellant (there was no indication of any figure in this respect). 102Secondly, the reasoning in Stamoulis is not self-evidently correct, to the extent that it relied upon the epidemiology. By the time the metastases occurred, it was clear that the plaintiff was one of the 42 women in every 100 who would suffer that development. The critical question was whether she was one of the 38 whose tumour would have metastasized in any event, or one of the additional four in respect of whom the consequence flowed from the delay in obtaining treatment. Unless there were other material factors, specific to the plaintiff's case, the chance that she was in the critical group, rather than the base group, was 10.5%. On that evidence alone, it could not be said that the delay in treatment, on the probabilities, contributed to her metastasis. 103Had there been evidence similar to that in Stamoulis in the present case, it would still not have been open to this Court to follow the reasoning in Stamoulis , to the extent that it equated a material increase in risk with a material contribution (in a causative sense) to the condition which eventuated. That reasoning was rejected by this Court in Gett v Tabet [2009] NSWCA 76; 254 ALR 504, decided before Stamoulis , but subsequently confirmed by the High Court in Tabet v Gett [2010] HCA 12; 240 CLR 537.

Other challenges 104The appellant raised a number of subsidiary complaints. First, the primary judge had undertaken his own calculations as to the level of exposure to asbestos dust and the resultant relative risk. There seemed to have been a number of elements to this challenge. The first was that such a calculation was not called for in any event because it was not necessary to establish a material contribution to the carcinoma. The effect of the other evidence in that respect has been discussed above. 105A second element was that in calculating the level of exposure to asbestos, the primary judge rejected the calculations of two industrial hygienists called by the respondent, but failed to simply adopt the evidence of Professor Pooley, tendered by the appellant, based upon examination of the fibre burden in a sample of tissue obtained from Mr Evans' lung. As the appellant noted, Professor Pooley was not cross-examined. However, his conclusion was expressed in very general terms, to the effect that "[t]he levels of amphibole asbestos fibres detected are well in excess of those considered to be related to an environmental asbestos exposure but are equivalent to a low level occupational exposure": report, 6 November 2009. There was debate as to the significance to be attached to the number of fibres detected and their length. There was also debate as to the rate at which fibres would have cleared from the lungs, given that Mr Evans had not been exposed to asbestos for some 18 years at the date the sample was taken: at [183]. 106The trial judge discussed this evidence at [178]-[186], but concluded, in effect, that it did not assist him in determining the level of exposure because the original fibre burden in Mr Evans' lungs was unknown: at [186]. 107This material was considered as part of a submission that a numerical estimate of asbestos exposure was not possible and that the objectively assessable evidence was that of the presence of pleural plaques and diffuse pleural thickening. 108The structure of the reasons of the primary judge may have been unfortunate in relation to this discussion. His Honour determined his preferred figure for the number of fibre years of exposure before addressing these arguments. Nevertheless, the fact that he accepted a figure more than six times that proposed by the defendants' industrial hygienists, makes it difficult for the appellant to establish legal error. His Honour's acceptance that there was "significant asbestos exposure" was consistent with at least some of the evidence as to the inference to be derived from the pleural plaques. He further noted that there was "no evidence that correlates the presence of diffuse pleural thickening with an increased risk of contracting lung cancer": at [177]. In that respect, there was an implicit contrast with the correlation which might be based on asbestosis, a condition from which Mr Evans did not suffer. 109It should be noted that a ground of appeal which complained that the calculations were undertaken "in the absence of available satisfactory evidence" does not in terms identify any error of law. There was evidence available from which his Honour could draw inferences and make calculations and indeed could have made calculations less favourable to the appellant. Whether the evidence was "satisfactory" was a matter for him to determine, so long as it could be described as rationally probative as to the existence of a fact in issue. As noted in Amaba Pty Ltd v Booth [2010] NSWCA 344 at [23]: "Implicit in the statement that there is no evidence to 'support' a particular finding, is the characterisation of a relationship between the evidence and the finding. It is the same relationship inherent in the concept of "relevance", on which the laws of evidence depend. That relationship depends on a process of reasoning which must be logical or rational. Thus, evidence is relevant which, if accepted, 'could rationally affect (directly or indirectly) the assessment of the probability of the existence of a fact in issue in the proceeding': Evidence Act 1995 (NSW), s 55(1). As explained by Gleeson CJ, Heydon and Crennan JJ in Washer v Western Australia [2007] HCA 48; 234 CLR 492 at [5]: 'The word 'rationally' is significant in this context. In order to establish relevance, it is necessary to point to a process of reasoning by which the information in question could affect the jury's assessment of the probability of the existence of a fact in issue at the trial.'" 110To complain that the trial judge made his own calculations is not, in the context of this trial, to complain that he acted without any evidence, or that he usurped the functions of the experts. He relied on the available material and drew inferences. Whether the inferences were reasonably open, in the sense of being logically available, involves an evaluative judgment, which is to be assessed by the court exercising appellate or supervisory jurisdiction. If this were the basis of complaint, it must be rejected. 111Secondly, the appellant asserted error in point of law in "failing to give reasons for rejecting the proposition that the increase in risk demonstrated by his Honour's own calculations was capable on its own of proving material contribution": ground 1(g). With respect, that ground also contains the seeds of its own destruction. An increase in "risk" does not demonstrate a material contribution unless the "risk" shows that the tortious agent more probably than not contributed to the injury. In this context, talk of "risk" is somewhat misleading. Risk usually identifies the chance of a future occurrence; what is relevant in the present case, is a causal link between two events in the past. As has already been explained, the cause of the carcinoma need not have been only one agent, or another. Agents may have worked in combination. The fact that they undoubtedly do work in combination in some circumstances will be sufficient to demonstrate a contribution by the tortious agent if it is more likely than not that the tortious agent contributed in more than half the cases. Because that fact was not unequivocally demonstrated on the evidence, it is not possible to complain of error in point of law because his Honour failed to accept evidence which did support such a conclusion. It is only when such evidence has been accepted that it is necessary to consider whether the contribution was in fact material, as opposed to insignificant or insubstantial. That question was not reached in the present case. 112Finally, it should be noted that Queanbeyan City Council filed a notice of contention noting that a decision as to the aggregate exposure of Mr Evans to asbestos dust did not answer the question about the particular responsibility of each defendant. That statement was neither true nor relevant. The negative conclusion reached by the primary judge did answer the question, in favour of each defendant. The further question identified accordingly did not arise. It is not necessary to say more about the contention. 113The appellant has failed to identify a decision of the Tribunal in point of law which was shown to be erroneous. Accordingly, the appeal must be dismissed. The appellant must pay the costs of the respondents in this Court.

Judicial review application 114To avoid the possibility that there may have been jurisdictional error or error of law on the face of the record which did not fall within the appellate jurisdiction of this Court under s 32 of the Dust Diseases Tribunal Act , the appellant also commenced proceedings by way of summons under s 69 of the Supreme Court Act 1970 (NSW), seeking relief in the nature of certiorari, quashing the orders of Judge Curtis. The grounds in the summons were the same as those in the notice of appeal. Reliance on the summons proved unnecessary, and its presence cannot have significantly affected the costs incurred. It is appropriate to dismiss the summons with no order as to costs.

DISCLAIMER - Every effort has been made to comply with suppression orders or statutory provisions prohibiting publication that may apply to this judgment or decision. The onus remains on any person using material in the judgment or decision to ensure that the intended use of that material does not breach any such order or provision. Further enquiries may be directed to the Registry of the Court or Tribunal in which it was generated. Decision last updated: 05 August 2011