Further to earlier postings regarding Booth, I refer you to the High Court summary and note the majority dismissed the appeal, with the exception of Heydon J. The issue for determination was whether the trial judge’s rationale, which was not displaced on appeal that “there was an overwhelming inference of causation”, could be established on the evidence. The trial judge found that exposure to asbestos dust liberated from brake linings manufactured by Amaca and Amaba “materially contributed to Mr Booth’s contraction of mesothelioma.”. The appellants contended the evidence did not support such a finding. The evidence which was relied upon in particular was that of Professor Douglas Henderson, a professor of pathology and in particular his finding that: “almost universally accepted that all asbestos exposure, both recalled and unrecalled, will contribute causally towards the ultimate development of a mesothelioma”. The trial judge concluded in this respect :
“At issue between the parties in this case is the proposition that all exposure to chrysotile asbestos, other than trivial or de minimis exposure, that occurred in a latency period of between 26 and 56 years, materially contributed to the cause of Mr Booth’s mesothelioma. I resolve that issue in favour of the plaintiff.”
The appellants contended there was no basis for this finding and in particular relied upon epidemiological evidence that the nature of the fibres and exposure was not sufficient to establish causation.
It should be said immediately that the present case is not of the kind considered in Amaca Pty Ltd v Ellis. In that case the evidence of a very limited exposure to asbestos coupled with epidemiological evidence simply did not support an inference that asbestos exposure was a factual cause of the deceased person’s fatal lung cancer. In particular, and by way of contrast with the present case, it was not argued in Amaca Pty Ltd v Ellis that it could be concluded, independently of epidemiological analysis, that exposure to asbestos was a cause of the cancer. It is necessary now to consider the relationship between risk and causation in the circumstances of this case.
In summary, a finding that a defendant’s conduct has increased the risk of injury to the plaintiff must rest upon more than a mere statistical correlation between that kind of conduct and that kind of injury. It requires the existence of a causal connection between the conduct and the injury, albeit other causative factors may be in play. As demonstrated by medical evidence in this case and in particular by Professor Henderson’s evidence, a causal connection may be inferred by somebody expert in the relevant field considering the nature and incidents of the correlation. The Bradford Hill criteria provide a guide to the kind of considerations that lead to an inference of causal connection. As noted above, they may include reference to relative risk ratio as an indicator of the strength of the association. Where the existence of a causal connection is accepted it can support an inference, in the particular case, when injury has eventuated, that the defendant’s conduct was a cause of the injury. Professor Henderson offered that inference of specific causation by reference to Mr Booth’s exposure to the products of both Amaca and Amaba. Where such an inference is drawn, the probability that it is correct is not to be determined only by reference to epidemiologically based ex ante probabilities. In Betts v Whittingslowe, Dixon J employed apposite logic when he said:
“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.” (emphasis added)
That logic encompasses the case of an ex ante probability, of accident given breach, supported by a causal explanation linking breach and accident. In this case an explanatory causal mechanism was proposed in the medical evidence.
Lord Reid applied similar logic in Gardiner v Motherwell Machinery and Scrap Co Ltd when he said:
“when a man who has not previously suffered from a disease contracts that disease after being subjected to conditions likely to cause it, and when he shows that it starts in a way typical of disease caused by such conditions, he establishes a prima facie presumption that his disease was caused by those conditions.”
It is enough for present purposes to say that an inference of factual causation, as against both Amaca and Amaba, was open on the evidence before the primary judge. The cumulative effect mechanism involving all asbestos exposure in causal contribution to the ultimate development of a mesothelioma had been propounded and was accepted by his Honour. It depended upon an understanding of physiological mechanisms. It did not depend upon the epidemiology. Whether or not medical science in the future vindicates or undermines that theory, is not to the point. That is not a question which can be agitated on these appeals. The cumulative effect mechanism, accepted by his Honour, implicated the products of both Amaca and Amaba in the development of Mr Booth’s disease. The primary judge’s interpretation of the expert evidence and his conclusions from it, were open as a matter of law.
It is not necessary in this case to consider the application of any modified concept of causation of the kind developed in Fairchild v Glenhaven Funeral Services Ltd. That concept was, as Lord Phillips of Worth Matravers PSC pointed out in Sienkiewicz v Greif (UK) Ltd, a response to “ignorance about the biological cause of the disease” which rendered it “impossible for a claimant to prove causation according to the conventional ‘but for’ test”, a result which would have caused injustice to claimants. In those cases, legal causation was extended beyond the limits of factual causation. In the result, a new head of tortious liability appears to have been created. The understanding of the aetiology of mesothelioma in Fairchild did not encompass the cumulative effect mechanism accepted by the primary judge in this case. In Sienkiewicz, Lord Phillips observed that:
“The possibility that mesothelioma may be caused as the result of the cumulative effect of exposure to asbestos dust provides a justification, even if it was not the reason, for restricting the Fairchild/Barker rule to cases where the same agent, or an agent acting in the same causative way, has caused the disease, for this possibility will not exist in respect of rival causes that do not act in the same causative way.”
The present case proceeds upon the foundation of findings, based on evidence before the primary judge, that Mr Booth’s exposure to the chrysotile asbestos in brake linings manufactured by Amaca and Amaba not only prospectively increased the risk of his contracting the disease but, in the event, causally contributed to its development and continuation.
Gummow, Hayne and Crennan JJ
Even if the issue is one to which other disciplines may not be able to give any conclusive answer, questions of causation, as a step in the ascertainment of rights and the attribution of liability in law, call for sufficient reduction to certainty to satisfy the relevant burden of proof for the attribution of liability. In Tubemakers of Australia Ltd v Fernandez, Mason J, with the concurrence of Barwick CJ and Gibbs J, referred to a statement by Dixon J as elaborating the general onus which lies upon the plaintiff where the issue of causation lies outside the realm of common knowledge and experience. In Adelaide Stevedoring Co Ltd v Forst, Dixon J said:
“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.” (emphasis added)
The “but for” criterion of causation proved to be troublesome in various situations in which multiple acts or events led to the plaintiff’s injury, for example, where the development of a particular medical condition was the result of multiple conjunctive causal factors. In such cases what may be unclear is the extent to which one of these conjunctive causal factors contributed to that state of affairs. These situations have been addressed by the proposition stated by Lord Watson in Wakelin v London and South Western Railway Co that it is sufficient that the plaintiff prove that the negligence of the defendant “caused or materially contributed to the injury”. In that regard, reference may be made to the well-known passage in the speech of Lord Reid in Bonnington Castings Ltd v Wardlaw. Of that case it was said in the joint reasons in Amaca Pty Ltd v Ellis:
“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.” (emphasis in original)
It should be emphasised that the resolution of the issue before this Court in Ellis does not govern the issues in the present appeals. Ellis involved alternative causes of the plaintiff’s lung cancer, asbestos inhalation and inhalation of tobacco smoke; the plaintiff had not shown that it was more probable than not that exposure to asbestos had made a material contribution to his cancer; but the evidence in the present case, to which further reference will be made, was that, unlike the situation regarding lung cancer, exposure to asbestos is effectively the only known cause of mesothelioma.
77. Several points respecting this evidence should be noted. The first is that the appellants called no expert clinicians, rather relying upon cross-examination of the four experts called by Mr Booth and upon Professor Geoffrey Berry, a biostatistician and epidemiologist. The second is that Professor Henderson, Dr Heiner and Professor Musk had each encountered cases of mesothelioma where the only identified exposure to asbestos was from working with brake linings. Professor Musk said in evidence that he had “seen brake lining exposed mechanics with mesothelioma who [did not] appear to have had significant other exposure”. Professor Henderson concluded his written report of 2 March 2009:
“I would also emphasise that my consultation and referral files now include many cases of pleural malignant mesothelioma for whom chrysotile-tremolite only exposure derived from new brake linings was the only identified pattern of exposure.”
The third point concerns what, in Fairchild v Glenhaven Funeral Services Ltd, Lord Bingham of Cornhill said was the state of medical knowledge in about 2000 respecting the cause of mesothelioma:
“the condition may be caused by a single fibre, or a few fibres, or many fibres: medical opinion holds none of these possibilities to be more probable than any other, and the condition once caused is not aggravated by further exposure”.
The reasons of the Court of Appeal in that litigation had included the passage:
“It was therefore common ground on these appeals that it could not be said whether a single fibre of asbestos was more or less likely to have caused the disease, alternatively whether more than one fibre was more or less likely to have caused the disease. In the latter event, it could not be shown that it was more likely than not that those fibres came from more than one source. In other words, none of these scenarios could be proved on the balance of probabilities. Similarly, it could not be proved on the balance of probabilities that any one man’s mesothelioma was caused cumulatively by exposure to asbestos dust in more than one employment.”
The “single fibre” theory was not accepted in the evidence in the present case as representing current expert opinion. In the course of his cross-examination, Dr Leigh said of the proposition that mesothelioma could be generated from a single fibre that this was not physically possible. In his evidence-in-chief Professor Henderson gave a long answer to a question that he explain his statement that each of multiple asbestos exposures contributes to the causation of mesothelioma. His answer included the following:
“[W]hen there are multiple episodes of asbestos exposures and the individual concerned inhales increasing numbers of fibres on different occasions, that contributes to the total burden of asbestos fibres deposited in the lung and translocated to the pleura and it is thought that mesothelioma develops because of an interaction between the asbestos fibres and the mesothelial cells by way of secondary chemical messengers[. A]nd to simplify the answer, the point is that the more fibres there are the greater number of fibres there will be interacting with mesothelial cells which themselves undergo proliferation and so the progress goes on with increasing numbers of mesothelial cells interacting with increasing numbers of fibres, so that the ultimate development of mesothelioma and its probability of development will be influenced by the numbers of fibres interacting with mesothelial cells over multiple periods of time and probably over multiple different generations of mesothelial cells[. A]nd I think this is a fairly well accepted model now and it flies in the face of what used to be called the one fibre hypothesis that mesothelioma came about from a single fibre interacting with a single mesothelial cell which in biological terms is a ridiculous proposition.”
Finally, it should be noted that the witnesses were appreciative of the need to indicate the relative degrees of strength of the conclusions they reached. For example, Professor Henderson expressed “at a high order of confidence” his opinion that chrysotile has the capacity to cause malignant mesothelioma; and, “cautiously … ‘on the balance of probabilities'”, his opinion that exposure to dust derived from brake linings which contain chrysotile asbestos has the capacity to cause mesothelioma.
The United Kingdom authorities
The expert evidence in the present case shows that the limits in medical knowledge disclosed by the (now discredited) “one fibre” theory accepted in the evidence in Fairchild have been removed by further advances in medical science. However, in the United Kingdom the decision in Fairchild has left in place a common law principle, now supplemented by a statutory regime, designed to bridge what Professor Jane Stapleton has called an “evidentiary gap”. The problem of legal coherence which thus is presented was recognised in Fairchild by Lord Rodger of Earlsferry when he observed:
“In future more may be known. As Mr Stewart rightly observed, in the course of submissions that were both helpful and sensitive, this may change the way in which the law treats such cases. But the House must deal with these appeals on the basis of the evidence as to medical knowledge today and leave the problems of the future to be resolved in the future.”
“The special rule of causation applied to mesothelioma was devised because of ignorance about the biological cause of the disease. It was accepted in Fairchild and Barker[] that this rendered it impossible for a claimant to prove causation according to the conventional ‘but for’ test and this caused injustice to claimants. It is not possible properly to consider the issues raised by this appeal without reference to what is known about mesothelioma. This has been summarised in many cases, and much of my own summary in Bryce v Swan Hunter Group plc of what was known 25 years ago remains true today. The cases under appeal did not involve the introduction of detailed evidence of what is known today about mesothelioma, proceeding on the basis that findings in previous cases could be taken as read.” (emphasis added)
The case which Amaca and Amaba were required to meet thus differed significantly in its evidentiary foundation from that in Fairchild and in Sienkiewicz.
83. Mr Booth developed his case in the following steps: (1) he had contracted mesothelioma; (2) the only known cause of that disease is exposure to asbestos; (3) the expert evidence at trial, accepted by the primary judge, was that: (a) exposure to asbestos contributes to the disease; and (b) the prospective risk of contracting the disease increases with the period of significant exposure; (4) Mr Booth had two periods of significant exposure; (5) it is more probable than not that each period of exposure made a material contribution to bodily processes which progressed to the development of the disease.
84. The response of the appellants was to emphasise that step (3) did not make proper allowance for the epidemiological evidence which they had presented. The appellants relied upon 19 studies upon the incidence of mesothelioma in automotive mechanics. These had been published in peer reviewed literature. In particular, the appellants relied upon three analyses of the literature, by Wong, Goodman and others, and Laden and others.
85. For example, Wong concluded that “there is no evidence to support or even to suggest an association between an increased risk of mesothelioma and exposure to brake linings or clutch facings among garage mechanics”. However, in the course of his cross-examination, Professor Berry said that although Wong had found “no significant evidence of effect”, for himself he accepted that there might be some risk due to chrysotile exposure as a result of working with brakes, “for example drilling holes in them to make them fit the car”.
86. The discipline of epidemiology, and its application in answering issues of causation in litigation, was described by Lord Phillips in Sienkiewicz as follows:
“Epidemiology is the study of the occurrence and distribution of events (such as disease) over human populations. It seeks to determine whether statistical associations between these events and supposed determinants can be demonstrated. Whether those associations if proved demonstrate an underlying biological causal relationship is a further and different question from the question of statistical association on which the epidemiology is initially engaged.
Epidemiology may be used in an attempt to establish different matters in relation to a disease. It may help to establish what agents are capable of causing a disease, for instance that both cigarette smoke and asbestos dust are capable of causing lung cancer, it may help to establish which agent, or which source of an agent, was the cause, or it may help to establish whether or not one agent combined with another in causing the disease.”
Lord Mance JSC left for consideration on another occasion the question whether “epidemiological evidence can by itself prove a case”, that is to say, a plaintiff’s case. Sienkiewicz was decided on other grounds, namely, that as a matter of law Fairchild applied.
In the present case, the plaintiff, Mr Booth, did not challenge the reception of epidemiological evidence, represented principally by studies in published papers, which was tendered by the defendants. Rather, his attitude in this Court was close to that of Lord Mance in Sienkiewicz, namely that such evidence can be admissible and relevant but its weight will depend upon the nature of the evidence and the particular factual issues before the court.
The epidemiological evidence, considered by itself, did leave open the inference that cumulative exposure to asbestos increased the risk of contracting mesothelioma by developing bodily processes to an irreversible point. Further, as Dr Leigh emphasised in his report, inability to demonstrate epidemiologically a statistically significant increase in risk in motor mechanics, relative to other occupational categories, does not, in any way, negate a causal inference in an individual case where, beyond the general background environment, the only asbestos exposure was incurred in that occupation.
Professor Henderson accepted that epidemiological data respecting work with brake linings was inconclusive. But he wrote in his report that “[o]ne of the problems with epidemiological studies on this issue is that they do not clearly distinguish between dedicated brake mechanics versus general automotive mechanics or garage mechanics”. That report further stated that a dedicated brake mechanic includes one “who frequently machined/ground new and not heat-altered brake linings”. Mr Booth had done grinding work throughout the periods in question. Professor Henderson also discounted the epidemiological data for other deficiencies in the methodology employed. Dr Leigh, who is trained in epidemiology, gave what the primary judge described as cogent evidence, criticising the methodology and case design upon which many of the studies were based.
It was open to the primary judge to decide that he was “not persuaded that the epidemiological evidence specific to automotive mechanics is adverse to the submission that causation has been proved in this particular case”.
The Court of Appeal, with respect, correctly concluded:
“Findings as to the cumulative effect of exposure to asbestos were undoubtedly open. [Mr Booth’s] witnesses, including Professor Henderson and Dr Leigh, sought to reconcile that approach with the epidemiology which suggested there was no increased risk in the case of brake mechanics. It was open to his Honour to accept their evidence, as he did. The underlying proposition put forward by the appellants, that the epidemiology was conclusive, in accordance with the principles applicable to such evidence, did not give rise to a question of law, but to a question of fact, which his Honour resolved against the appellants.”
Causation inferred from risk
The plaintiff did submit that even if Professor Henderson’s evidence did not support the view that every exposure to asbestos was causative of mesothelioma, but only added to the cumulative risk of mesothelioma, it was open to the trial judge to infer causation from the increased risk of injury. The submission cited authority which did not support it, for it held that an increase in risk does not by itself support a conclusion of causation. Indeed, Amaba submitted, the trial judge’s reasoning proceeded on the opposite view. A key element of the trial judge’s reasoning on causation, under the heading “Specifically”, was that 70% of the asbestos fibres to which the plaintiff was exposed in 1953-1962 were from Amaca products, and 70% of the asbestos fibres to which the plaintiff was exposed in later years were from Amaba products. This amounted respectively to 10% and 20% of “the additional fibre burden beyond background which caused [the plaintiff’s] mesothelioma.” The trial judge arrived at these figures thus:
“Professor Berry says that it may be appropriate to assume that the background exposure of [the plaintiff] to asbestos fibre as a consequence of general low-level concentrations of asbestos in urban air corresponds to a lifetime risk of 70 per million.
The brake repair work increased the background causal component of 70 per million lifetime risks by a further 30.6 per million lifetime risks. Expressed in terms of cause, the brake work increased by approximately 44 per cent that fibre burden which comprised the background risk.” (emphasis added)
The reasoning treats “risk” and “cause” as being identical. Amaba’s submission is to be accepted.
The trial judge’s alternative route to causation
The trial judge considered that an:
“overwhelming inference of causation may be drawn from the following facts:
(1) [The plaintiff’s] mesothelioma was caused by the inhalation of asbestos fibre;
(2) Mesothelioma very rarely occurs in persons who have not been exposed to asbestos fibres beyond the background level that pervades urban environments;
(3) For a total of 27 years, week in and week out, [the plaintiff] was additionally exposed to asbestos fibres liberated from asbestos brake shoes by his own work, and by the work of others in his vicinity,
(4) The previous exposure, in the course of home renovations and truck loading was, in comparison, trivial.”
Amaca accepted propositions (1) and (2). Amaca attacked proposition (3) on three grounds. It did not discriminate between Amaca-Amaba brake exposure and other brake exposure. It insinuated that the additional exposure referred to was very substantial, when in fact it was only 10% for Amaca and 20% for Amaba, even on the trial judge’s controversial calculations. Thirdly, the reasoning did not explain why it should be concluded, more probably than not, than between 1953 and 1962 changes occurred in the plaintiff’s body leading to him later developing the symptoms of mesothelioma which were attributable to Amaca’s fibres, or that between 1962 and 1969, and between 1971 and 1983, changes occurred in the plaintiff’s body leading to him developing the symptoms of mesothelioma which were attributable to Amaca’s fibres in combination with other fibres.
Amaca also attacked proposition (4). The home renovation could create an additional four cases per million per lifetime: that was not trivial relative to the additional seven cases per million per lifetime for Amaca.
Amaca was correct to submit that this alternative route to causation suggested by the trial judge was neither an “overwhelming inference” nor available at all.
The “but for” test
The trial judge did not inquire whether the plaintiff had established that but for the Amaca and Amaba exposures he would not have contracted mesothelioma. The “but for” test is a necessary but not sufficient test for causation. There was specific evidence that it was not satisfied, and for the reasons given above, there was no evidence that it was satisfied.
Brisbane Barrister – David Cormack