NSWQA – asbestos exposure + smoking = lung cancer / material contribution & causation



The decision is an appeal from Quirk DCJ. Whilst many of the issues of the appeal concern matters unique to the Dust Disease Tribunal & Board, there is a helpful for discussion about the principles of causation and when inferences can be drawn per Basten JA, Allsop P and Handley AJA agreeing:

124 There remains for analysis the challenge to inferences drawn from primary facts. In Azzopardi v Tasman UEB Industries Ltd [1985] 4 NSWLR 139 at 156, Glass JA identified as the first stage of the judicial process, “determining the facts by way of primary findings and inferences”. Primary facts may, of course, be inferred from particular evidence. However, the process of drawing inferences from such facts is a discrete exercise. Thus, if the driver of a car gives evidence that he put his foot on the brake pedal to no effect, it may be inferred that the brakes failed. The cause of the failure may involve a further inference of a different kind. The further inference may be that there was a mechanical defect in the car. In some circumstances that inference can be drawn on the basis of general experience and commonsense; in other cases it may depend upon inquiry into the operation of the mechanism (if available) or it may depend upon expert assessment.

125 The inference that one event caused another because of a temporal relationship will rarely be available, absent some element of connection between the two events. (A mere temporal connection between an increase in the export of apples from Canada and an increase in the rates of lung cancer in the UK is unlikely to demonstrate a causal connection.) In many cases there will be a question whether commonsense can provide an answer or whether an inference can only be drawn on the basis of specific expertise. The application of the well-known statement of McHugh J in Chappel v Hart [1998] HCA 5; 195 CLR 232 at [27] that “[i]f a wrongful act or omission results in an increased risk of injury to the plaintiff and that risk eventuates, the defendant’s conduct has materially contributed to the injury that the plaintiff suffers whether or not other factors also contributed to that injury occurring”, may well depend upon which of the categories is invoked. Indeed, the appellant’s argument in the present case depends upon the falsity of that approach in relation to smokers who are exposed to asbestos (both agents which increase the risk of lung cancer) where lung cancer has materialised. It is doubtful whether, in such a case, “commonsense” can permit the inference that exposure to asbestos dust probably contributed to the disease. Similarly, the reference to “commonsense” approved in March v Stramare (E & MH Pty Ltd) [1991] HCA 12; 171 CLR 506 at 515, taken from the judgment of Lord Reid in Stapley v Gypsum Mines Ltd [1953] AC 663 at 681 may not operate uniformly in different kinds of case. In some cases such an approach may be inappropriate. There will then be a question as to whether inappropriate reliance upon commonsense to draw a causal link can constitute an error of law in circumstances where illogicality in the drawing of inferences is said not to give rise to an error of that kind.

128 These particular questions are sometimes referred to as “general causation”, causal mechanism and “specific causation”. In Seltsam Pty Ltd v McGuiness [2000] NSWCA 29; 49 NSWLR 262 the worker suffered (and died from) a renal cell carcinoma following exposure to asbestos dust, whilst working for the appellant. “Commonsense” may suggest that exposure to a known carcinogen, followed by a carcinoma would give rise to the inference, on the probabilities, that the exposure caused the condition. However, commonsense may be an inadequate guide. A commonsense, but uninformed, view could gain legitimate support from scientific evidence that the carcinogen was known to enter or pass through the kidneys. Further support may be given to the potential inference by expert evidence of a plausible explanation of a mechanism, although the operation of the mechanism has not been observed. That may provide an element of “biological plausibility”: see Spigelman CJ at [41]-[42]. Biological plausibility may be strengthened by observation of a known mechanism in laboratory experiments or by epidemiological studies. These are matters for expert analysis and explanation, not commonsense.

129 In Seltsam, the Chief Justice noted the manner in which epidemiological evidence could be used. (Indeed, many of the comments would extend to other forms of medical science.) However, his Honour commenced with the proposition that the establishment of a possibility would not satisfy the common law test requiring proof on the balance of probabilities in civil litigation: at [80]. That comment is equally applicable in the case of a statutory claim which depends upon the civil standard of proof. Although not designed to determine the cause of a particular condition in an individual, epidemiological evidence allows for a probabilistic or stochastic approach (to use the language of Professor Henderson), as a form of circumstantial evidence, capable of combination with other evidence, in order to establish causation in a specific case: see Seltsam at [89]. As noted by Spigelman CJ in Seltsam at [67]:

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

individuals is greater than the risk in unexposed individuals.”

130 Statistically, it is only when the relative risk reaches 2 that the chance that the condition was caused by the identified agent is equal to the chance that it was caused by some other mechanism. Accordingly, where the relative risk is greater than 2, it may be said that the epidemiology will support an inference that the condition was more probably than not caused by the agent under consideration: Seltsam at [121]. Spigelman CJ, continued, at [137]:

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

131 The analogy of “strands in a cable” may not operate where the epidemiological evidence is the only strand capable of supporting a claimant’s case. However, his Honour’s reasoning requires consideration of what is involved in the establishment of a relative risk. In particular, there are two elements which may reduce the significance for legal purposes of the attribution of 50% probability which flows only from a relative risk of 2.0. The first is that statistical analysis will involve a degree of potential error, so that, instead of a single figure, it might be more accurate to identify a range, together with the confidence level which is achieved at a particular point in the range. The studies routinely identify what is described as a “95% confidence interval”. That is not necessarily a test which the law would apply in respect of causation. Secondly, it is not merely the uncertainty of the studies which must be taken into account, but also the uncertainties surrounding the individual to whom the risk analysis is applied in the course of the litigation. The difficulty, even the impossibility, of knowing with any degree of precision the intensity or duration of exposure to asbestos dust in respect of a deceased worker, prevents meaningful calculations being undertaken at any level of precision and allows for an element of evaluative judgment on the part of the trial judge.

156 The whole of the appellant’s case was ultimately founded on the proposition that each of the workers died from a lung cancer, the cause of which could not be directly established, but which was likely to be, predominantly, cigarette smoking.

157 There were statements in the evidence which suggested that some of the experts misapprehended the questions asked of them or the issues before the Court. For example, Dr Leigh gave evidence which suggested ambivalence as to the distinction between a factor materially contributing to a condition and one materially contributing to the risk of the condition. However, there is no suggestion that her Honour fell into error in failing to draw that distinction. Secondly, there was evidence from Professor Berry which suggested that he thought that even where asbestos contributed to a condition, the condition could not be attributed to asbestos inhalation unless the contribution reached 50%. While her Honour did not make a numerical assessment of the contribution of asbestos to the lung cancers of any of the three workers, it is clear that she did not accept that the contribution exceeded 50%, nor did it need to do so to be “material”.

Brisbane Barrister – David Cormack

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