In a unanimous decision by their Honours FRENCH CJ, GUMMOW, HAYNE, HEYDON, CRENNAN, KIEFEL AND BELL JJ the High Court has considered a sensitive and scientifically challenging causation issue, namely; the interaction of smoking and asbestos exposure in the cause of lung cancer.
I refer to my earlier posting concerning the Court of Appeal of NSW in WORKERS COMPENSATION (DUST DISEASES) BOARD OF NSW v SMITH, MUNRO AND SEYMOUR  NSWCA 19 as an example of the customary approach to this difficult causation issue, which has now drastically changed.
The High Court judgment at face value sweeps aside such arguments and as foreshadowed by the High Court:
A paradoxical result?
It was submitted that the conclusion that causation was not established in this case entailed a paradox. If consideration of the results of the population studies described in evidence in this matter does not permit the inference that Mr Cotton’s cancer was caused or contributed to by exposure to asbestos, no claim by an individual in Mr Cotton’s position could succeed. And yet, the argument continued, the population studies showed that exposure to asbestos was a cause of cancer in some cases. How then could it be right to reach a result that entailed the corollary that all individual claims would fail?
The answer to the question can be expressed in several different ways. All depend upon the basic and unpalatable fact that no scientific or medical examination can now say, with certainty, what caused Mr Cotton’s cancer or lung cancer in any other particular case. As explained at the outset of these reasons, despite this uncertainty, the courts must, and do, “reduce to legal certainty [a question] to which no other conclusive answer can be given”. The courts do that by asking whether it is more probable than not that X was a cause of Y. Saying only that exposure to asbestos may have been a cause of Mr Cotton’s cancer is not a sufficient basis for attributing legal responsibility. Observing that a small percentage of cases of cancer were probably caused by exposure to asbestos does not identify whether an individual is one of that group. And given the small size of the percentage, the observation does not, without more, support the drawing of an inference in a particular case. The paradox, if there be one, arises from the limits of knowledge about what causes cancer.
The crux of the evidence before the High Court was that whatever evidence was accepted the material contribution of asbestos exposure alone was at its highest 23%:
The basis on which the description “more dangerous” was attached to exposure to both smoking and asbestos was not identified in argument. At least in part it seems to have been used as a qualitative description of the synergistic effect examined earlier in these reasons. But the critical question is whether the exposure to asbestos was a cause of Mr Cotton’s cancer.
To the extent to which the plaintiff’s description “more dangerous” was intended to reflect some quantitative measure of the probability that one carcinogen rather than another was a cause of cancer, it was a proposition not supported by the evidence. None of the witnesses whose evidence is examined earlier in these reasons assigned a probability greater than 23% to the chance that Mr Cotton’s cancer was caused by exposure to asbestos (whether alone or in combination with smoking). Professor Berry put that probability as low as 1%; Dr Leigh put it at between 2 and 12% (or 5 and 20% if higher exposure figures were used). Professor de Klerk considered the probability that Mr Cotton’s cancer was due to asbestos exposure alone was only 3% and due to exposure to both was 20%. The witnesses who expressed an opinion on the matter agreed that the probability that Mr Cotton’s cancer was caused by smoking alone was high (Professor de Klerk said 67%; Professor Berry said 92%).
If the description of exposure to smoking and asbestos as “more dangerous” than exposure to one or the other was intended to reflect a quantitative comparison of risk, it is a description that did not accurately reflect the evidence given by the witnesses about the relative risks of smoking compared with the relative risks of exposure to asbestos. And if the description “more dangerous” was intended to convey no more than that those who were exposed to both smoking and asbestos were at greater risk of developing cancer than those who were exposed to only one of those carcinogens, it is necessary to bear steadily in mind that the evidence did not establish that smoking and asbestos must work together.
This third step in the plaintiff’s argument was not made good.
The plaintiff relied on:
The relevance of material contribution –
“What is a material contribution must be a question of degree. A contribution which comes within the exception de minimis non curat lex is not material, but I think that any contribution which does not fall within that exception must be material.”
Particular attention was given to what was meant by saying that any contribution that was not de minimis must be material.
It is important to recognise the context in which this statement was made. The issue in Bonnington Castings was whether exposure to silica dust from poorly maintained equipment caused or contributed to the pursuer’s pneumoconiosis, when other (and much larger) quantities of silica dust were produced by other activities at the pursuer’s workplace. Those other activities were conducted without breach of duty. As Lord Reid rightly pointed out, the question in the case was not what was the most probable source of the pursuer’s disease: dust from one source or the other. The question was whether dust from the poorly maintained equipment was a cause of his disease when the medical evidence was that pneumoconiosis is caused by a gradual accumulation of silica particles inhaled over a period of years.
This description of the issue of causation in Bonnington Castings shows how different it is from the issue of causation in this case. The issue in Bonnington Castings was whether one source of an injurious substance contributed to a gradual accumulation of dust that resulted in disease. The issue here is whether one substance that can cause injury did cause injury. Or, to adopt and adapt what Starke J said in Adelaide Stevedoring Co Ltd v Forst, was Mr Cotton’s cancer “intimately connected with and contributed to” by his exposure to asbestos? Questions of material contribution arise only if a connection between Mr Cotton’s inhaling asbestos and his developing cancer was established. Knowing that inhaling asbestos can cause cancer does not entail that in this case it probably did. For the reasons given earlier, that inference was not to be drawn in this case. Questions of what is a material contribution do not arise.
I recommend the judgment be read in its entirety.
Brisbane Barrister – David Cormack