The Limitations of Medical Science
40. I reject the submission that medical science cannot support the proposition that all asbestos inhaled materially contributes to the causes of mesothelioma.
41. Professor Henderson is an eminent pathologist. Pathology, he said, is "the study of disease processes in the broadest sense, including their causes, mechanisms of development, characteristics once they have developed, and their natural history."
42. Professor Henderson's professional and academic interests over the last 35 years have concentrated upon asbestos related disorders. He is the senior editor and a major contributor to the textbook "Malignant Mesothelioma" published in New York in 1992.
43. Dr James Leigh is an occupational physician who holds a PhD in that discipline. He has been a researcher in the field of asbestos related diseases for almost 30 years.
44. Both Dr Heiner and Professor Musk are Respiratory Physicians with extensive clinical experience with mesothelioma.
45. In support of his first submission Mr Watson relies upon the following passage from the judgment of Dixon CJ in Jones v Dunkel (1958-1959) 101 CLR 298 at 305:
But in any case we are not concerned with a choice among rival conjectures. In an action of negligence for death or personal injuries the plaintiff must fail unless he offers evidence supporting some positive inference implying negligence and it must be an inference which arises as an affirmative conclusion from the circumstances proved in evidence and one which they establish to the reasonable satisfaction of a judicial mind. It is true that "you need only circumstances raising a more probable inference in favour of what is alleged". But "they must do more than give rise to conflicting inferences of equal degree of probability so that the choice between them is mere matter of conjecture". These phrases are taken from an unreported judgment of this Court in Bradshaw v. McEwans Pty. Ltd. (Unreported, delivered 27th April 1951). which is referred to in Holloway v. McFeeters [1956] HCA 25; (1956) 94 CLR 470 , by Williams, Webb and Taylor JJ. The passage continues: "All that is necessary is that according to the course of common experience the more probable inference from the circumstances that sufficiently appear by evidence or admission, left unexplained, should be that the injury arose from the defendant's negligence. By more probable is meant no more than that upon a balance of probabilities such an inference might reasonably be considered to have some greater degree of likelihood." (at pp 480, 481) But the law which this passage attempts to explain does not authorise a court to choose between guesses, where the possibilities are not unlimited, on the ground that one guess seems more likely than another or the others. The facts proved must form a reasonable basis for a definite conclusion affirmatively drawn of the truth of which the tribunal of fact may reasonably be satisfied. (at p305)
46. In his paper Science and Judicial Proceedings: Seventy-Six Years on Published in 2010 84 ALJ 244, Chief Justice Robert French, discussing an address by Sir Owen Dixon on Science and Judicial Proceedings delivered to the Medico-Legal Society of Victoria on 13 September 1933, observed that:
Today medical science is informed in both theory and its practical application by many other disciplines and sub-disciplines including physics, chemistry and molecular biology. Its diagnostic tools use concepts and techniques undreamed of in 1933. There are, however, many elements of medical judgments which are still probabalistic in their character. Biological systems are so complex and affected by so many factors that predictions about their behaviour or inferences about their status often have to be expressed in terms of probabilities.
47. Mr Watson contends that, because Professor Henderson, Dr Leigh, Dr Heiner and Professor Musk each concede that the biological process of causation is incompletely understood, and because several alternative and competing theories of causation have been canvassed in the evidence, the proposition that all fibres contribute to the development of the mesothelioma is merely a guess, and not a legitimate inference.
48. He suggests that several competing theories of causation emerge from the evidence. These are said to be the single fibre theory; the mechanical theory based on the physical properties of asbestos; the chemical theory; and the complete carcinogen theory.
49. The evidence does not support this submission.
50. No witness accepted the single fibre theory. Professor Henderson rejected it as ridiculous, and Dr Leigh as silly. Professor Musk conceded that, depending upon fibre type, a single incident of inhaling asbestos of more than a minimal dose may explain the development of a mesothelioma 30 to 40 years later. He did add that: "it may not require any further exposure, but the risk increases as the dose of asbestos that is inhaled increases". (Emphasis added).
51. Because the defendants call no medical evidence, it is unnecessary to review in further detail the evidence from the plaintiff's medical witnesses. I think it sufficient to observe that the mechanical theory and the chemical theory of causation are not competing but complementary, and that the complete carcinogen theory is not incompatible with the proposition that all exposure materially contributes to the development of the mesothelioma.
52. The plaintiff's experts, conceding that some of the steps necessary to form the opinion on purely deductive and scientific grounds are yet to be discovered, are each of the opinion that all asbestos fibres contribute to the development of a mesothelioma. They adopt that theory as most probably according with the actual aetiology of the disease. Their conclusions are not guesses, but reasonable inferences drawn from the current state of medical knowledge.
53. Ultimately it is for the Tribunal to draw the necessary inference from the established facts with the assistance of medical evidence.
54. In EMI (Australia) Ltd v Bes [1970] 2 NSWLR 238 at 242, Heron CJ said:
Medical science may say in an individual case that there is no possible connection between the events and the death, in which case, of course, if the facts stand outside an area in which common experience can be the touchstone, then the judge cannot act as if there were a connection. But if medical science is prepared to say that it is a possible view, then, in my opinion, the judge, after examining the lay evidence, may decide that it is probable. It is only when medical science denies that there is any such connection that the judge is not entitled in such a case to act on his own intuitive reasoning. It may be, and probably is, the case that medical science will find a possibility not good enough on which to base a scientific deduction, but courts are always concerned to reach a decision on probability and it is no answer, it seems to me, that no medical witness states with certainty the very issue which the judge himself has to try.
55. Uninstructed by medical evidence, I would not regard Mr Watson's suggestion that mesothelioma may be contracted by exposure to a threshold dose, with further exposure irrelevant, as consistent with the epidemiological evidence that the incidence of mesothelioma increases in proportion to increased dose.
56. Because most people exposed to asbestos fibres do not contract mesothelioma, it is thought that persons contracting the disease suffer from some underlying genetic susceptibility.
57. If the threshold dose were sufficient to explain the contraction of the disease in those persons, then increasing doses should yield few further cases of mesothelioma. The fact that the incidence rises with increasing dose suggests that the further exposure plays a causative part in the aetiology of the disease.
58. In E.M. Baldwin & Son Pty Ltd v Plane (1998) 17 NSWCCR 434 the Court of Appeal considered the evidence of Professor Henderson concerning the cumulative process by which asbestos fibres liberated from locomotive brake blocks caused mesothelioma. At [89], Fitzgerald AJA, (with whom Meagher JA and Beazley JA agreed) said this:
…Jsekarb's submission that the Tribunal had no basis for acceptance of Professor Henderson's "cumulative effect" was wrong. There was no contrary view proffered by an appropriate expert with Professor Henderson's qualifications and expertise, and his opinion was based on his experience, related to published statistics, information (e.g. the Australian Mesothelioma Register) and opinions, logically defensible, and at least to some extent, supported by other experts. [94]
…
Professor Henderson was undoubtedly the pre-eminent expert witness on the aetiology or pathogenesis of mesothelioma
… the Tribunal was entitled, and, in my opinion, correct, to accept Professor Henderson's "cumulative effect" theory, and to reject Jsekarb's fundamental proposition that inhalation of more than one amphibole form of asbestos fibre raises a number of separate, independent, possible causes of mesothelioma.[95]
59. 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.
60. Over 10 years have elapsed since the decision in E.M. Baldwin & Son Pty Ltd v Plane, yet the defendants in this case call no medical evidence to suggest that the "cumulative effect" theory may not be accepted because of further advances in medical knowledge.
61. His Honour the President in (Re Jones-Mashman) Amaca Pty Ltd v CSR Ltd No 2 [2009] NSWDDT 24 (unreported) determined, for the purpose of s25B of the Dust Diseases Tribunal Act 1989, that all asbestos exposure within an acceptable latency period makes a material contribution to the cause of mesothelioma.
62. Upon the facts in this case I specifically determine for the purpose of s25B that all exposures to chrysotile asbestos, other than trivial or de minimis exposure, occurring in a latency period of between 25 and 56 years, materially contributes to the cause of mesothelioma.
Improbability of the Causal Mechanism
63. I reject each of these submissions. It has been demonstrated by epidemiological studies, and it is admitted by each defendant in this case that chrysotile can cause mesothelioma. The mere fact that chrysotile fibres are less potent than amphibole fibres does not assist the resolution of causation in this case where exposure to amphibole fibres is taken into account by the medical and industrial experts.
64. Although Professor Berry, the defendants' expert epidemiologist, said that a 1983 study of 13,500 workers in a manufacturing plant producing friction materials with chrysotile asbestos detected no increased incidence of mesotheliomas, he did not argue that this study proved that chrysotile did not cause mesothelioma. Epidemiology draws its conclusions from studies of large populations.
65. The evidence is entirely to the contrary of the proposition that, because some chrysotile fibres liberated from brake linings remained bound in resin, the balance of fibres are non respirable.
66. There is accumulating evidence, to which I will later refer, that short fibres may produce lung disease.
Epidemiological Evidence
67. Epidemiological studies have demonstrated that exposure to chrysotile asbestos increases the likelihood of contracting mesothelioma. A 1998 World Health Organisation monograph on chrysotile, entitled Environmental Health Criteria 203: Chrysotile Asbestos states expressly that chrysotile asbestos poses increased risks for mesothelioma, and that no threshold of exposure had been established. A paper published by the International Agency for Research on Cancer published in 1987 is to the same effect.
68. In the course of the trial counsel for the defendants conceded that the question of the capacity of chrysotile to cause mesothelioma was not in issue. (Transcript 210.7)
69. The authoritative paper by Hodgson and Darnton, The Qualitative Risks of Mesothelioma and Lung Cancer In Relation to Asbestos Exposure, published in the Annals of Occupational Hygiene 2000; 44:565-601 reported that a cumulative exposure of 1 fibre/ml/years to chrysotile asbestos yields a lifetime "best estimate" risk of about 5/100,000 mesothelioma deaths.
70. The defendants rely upon 19 epidemiological studies published in the international peer reviewed literature upon the incidence of mesothelioma in automotive mechanics. Three meta-analyses, by Wong, Goodman et al, and Laden et al have combined the results from several studies to produce what is said to be a more precise estimate of the risk.
71. Wong concluded that: "… clearly there is no evidence to support or even to suggest an association between an increased risk of mesothelioma and exposure to brake linings On the contrary garage mechanics mesothelioma risk is similar to that in the general population. None of the six studies reported any increased mesothelioma risk among auto mechanics".
72. Goodman et al stated that the epidemiological data showed that: "Employment as a motor mechanic does not increase the risk of developing mesothelioma".
73. Laden et al stated that "… the consistent pattern that emerges from this research indicates no increase of risk of… mesothelioma, and that "automobile mechanics are not at an elevated risk of… mesothelioma from their occupation."
74. Professor Berry, commenting on the analyses of Wong and Goodman, said that the studies were sufficient to demonstrate that there was no large increase in the risk of automotive mechanics contracting mesothelioma from exposure to asbestos fibres liberated from brake linings, but that they could not demonstrate that there was no small increase in risk. He did not refer to the paper by Laden et al.
75. One obvious criticism of the studies combined into these meta-analyses is that the cohort studied were variously described as "motor mechanics", "garage workers", and "vehicle mechanics". In the same manner as persons described as "carpenters" may have been heavily exposed to asbestos fibres released from asbestos cement, or not at all exposed, the average exposures of "motor mechanics" may have little in common with the particular exposure of Mr Booth.
76. Dr Leigh, who is trained in epidemiology, gave cogent evidence criticising many of these studies upon the basis of weak case reference design, and low statistical power. He said that the standard text by Breslow and Day, Statistical Methods in Cancer Research Volume 2, table 7.7 required a power of 80 per cent before a study may be declared negative, and that none of the studies upon which the defendants rely achieved that power.
77. Specifically the power of the study by Welsh to detect a relative risk of 1.5 was 9 per cent. The power of the study by McDonald to detect a relative risk of 1.5 was 18 per cent. The power of the study by Woitowitz to detect a relative risk of 1.5 was in the order of 37 per cent; the power of that study to detect a relative risk of 1.2 was only 8 per cent.
78. At a relative risk of 1.2, for every 10 persons who may contract mesothelioma from background risks, an additional 2 will contract the disease because of occupational exposure as an automotive mechanic. The statement by Wong that: there is no evidence to support or even to suggest an association between an increased risk of mesothelioma and exposure to brake linings is correct but misleading.
79. Professor Berry said of the Wong paper that; "… one can say with 95 per cent confidence from this study that a relative risk bigger than 1.23 is excluded but the relative risk between one and 1.23 is a possibility".
80. Professor Berry also said that the study by Goodman was not capable of detecting small increases in risk. The unqualified statement by the authors that the epidemiological data showed that: "Employment as a motor mechanic does not increase the risk of developing mesothelioma" is not justified by the data.
81. Dr Leigh argues that much of the data does support a strong correlation between exposure to asbestos as an auto mechanic and the contraction of mesothelioma. I do not propose to canvass his evidence on this matter, nor do I think it necessary to repeat the persuasive detail contained in the thorough written submissions prepared by counsel for Mr Booth.
82. I am not persuaded that the epidemiological evidence specific to automotive mechanics is adverse to the submission that causation has been proved in this particular case.
Quantification of Exposure
83. Professor Berry agreed that there was no threshold of exposure to asbestos below which mesothelioma could not be contracted, and with the proposition that; "there are some very small risks but given enough people some of those risks will come home".
84. Without reliance upon the controversial epidemiological studies canvassed above, Professor Berry chose to express his opinion upon the basis of accepting the quantification by the defendants' occupational hygienists, Mr Pickford and Mr Rogers, of Mr Booth's reported exposure, and comparing that fibre burden with conclusions drawn from general epidemiological studies.
85. Professor Berry's assumptions are set out in the following table.
Asbestos Type Pickford Rogers
- Home Renovations Mixed 0.0017 f/ml/yrs 0.001 f/ml/yrs
- Brake Repair Chrysotile 0.26 f/ml/yrs 0.18 f/ml/yrs
- Loading Trucks Chrysotile and/or amosite and/or crocidolite 0.23 f/ml/yrs 0.02 f/ml/yrs