This Court was left with the impression that these boundaries were deliberately blurred in the presentation of the case. It causes great difficulty for the Court in being sure that it has resolved all the issues which were legitimately able to be raised on the appeal. This unsatisfactory state of affairs has resulted from the conduct of the appeal by the appellant Board, a statutory authority the members of which are appointed by the Minister: Dust Diseases Act , s 5(1). The respondents to the appeal, whose interests are entitled to be taken into account in identifying the proper course to be taken in the proceedings, are the widows of workers who may have claims, not to some largesse dispensed by the Board, but to the statutory entitlements created by the Act and administered by the Board.
17 In each case ground 1 alleged error in the construction of s 8 of the Dust Diseases Act. Precisely how the trial judge was said to have erred will be considered below, but the application of s 8(1)(b) was a factor addressed by her Honour and identifiable error in that respect will fall within the legitimate scope of the present appeals.
18 The second ground of appeal involved a number of limbs, with differing legal significance. The ground read as follows:
"2. The Trial Judge erred in law in making, or purporting to make, findings:
(a) in the absence of evidence to support the finding;
(b) in the absence of providing adequate reasons for making the findings;
(c) in making findings in the context of the application of an incorrect legal test;
(d) on the basis of evidence wrongfully admitted;
(e) wrongly relying upon expert evidence."
19 Perhaps curiously, given the formulation of this ground, the principal submission was that her Honour had failed to make particular findings, namely findings in each case of the effect of heavy smoking over extended periods. The respondents did not complain as to this approach, no doubt because it was understood to be a different way of expressing the primary complaint, namely that it was not open to her Honour to infer, on the evidence properly before her, that exposure to asbestos dust materially contributed to the lung cancer from which each of the workers died: ground 2(a). However s 142N(1) is construed, a ground complaining that there was no evidence to support an ultimate finding may fall within the scope of the statutory appeal if it could be said that her Honour determined, whether expressly or by implication, that no evidence was needed of a particular fact, or that evidence which did not in truth bear upon the fact was available to support it.
20 Grounds 2(c) and (d) (although not particularised) potentially fell within the scope of an appeal under s 142N. Ground 2(b), concerning the adequacy of the reasons of the trial judge, may be problematic, but the jurisprudential problems are not critical because the substance of the ground is not made out, as will be explained below. Paragraph 2(e) may or may not have involved a decision by the trial judge in point of law: it was not separately addressed in the course of argument and may be put to one side.
21 The third ground of appeal alleged that error could be "inferred" from the delay between the hearing of the case in the District Court and the delivery of judgment (a period of 18 months). The relevance of delay in an appeal of this kind will need further consideration when her Honour's reasons have been considered in detail.
22 Apart from the constraints imposed on the appellant by the limited nature of the appeal (there having been no attempt to rely upon judicial review powers of the Court pursuant to s 69 of the Supreme Court Act 1970 (NSW)), the core of the appellant's case turned on the availability of inferences in relation to the question of causation. In each case the premise was that the lung cancer should have been attributed to the physical insult to the workers' lungs from one of two carcinogens, namely tobacco smoke and asbestos dust. The appellant contended that the likelihood of the lung cancer having resulted from smoking was many times that of exposure to asbestos dust and, accordingly, none of the respondents could demonstrate that, on the balance of probabilities, the cancers resulted from exposure to asbestos dust. Thus, for example, if epidemiological studies demonstrated that in particular circumstances the likelihood of a cancer being attributable to exposure to asbestos dust was 20%, as compared with 80% in respect of smoking, the worker would fail to establish a probable causal connection between the disease and exposure to asbestos dust.
23 The alternative approach, adopted by the respondents, was that with exposure to both tobacco smoke and asbestos dust, it was reasonably likely that the two agents had interacted (the synergistic effect), with the result that each probably contributed to the disease in a material respect in a particular individual. Although it might be possible statistically to separate the likely contributions of each agent, that was neither necessary nor appropriate for determining a disease was due to a particular agent, in the relevant statutory context.
24 The appellant accepted that the concept of material contribution reflected at least part of the test to be applied in determining the eligibility for an entitlement under the Act. It also appears to have been assumed that the claimants needed to establish the causal connection according to the civil standard, on the balance of probabilities. This approach involved two assumptions. The first was that the claimant bore a burden of proof and the second the standard to which the court needed to be satisfied for the claimant to succeed.
25 The first assumption is doubtful. Although the appeal is said to be "against" the decision of the Board, and the Board is a "necessary party to an appeal", it does not follow that the claimant bore any legal burden. Further, no account appears to have been taken of the statutory obligation of the Court, in the exercise of its residual jurisdiction, to determine the matter "on the real merits and justice of the case", the Court not being bound "to follow strict legal precedent": District Court Act, s 142J(1). The precise operation of such provisions is obscure, particularly in circumstances where an appeal lies from a decision of the Court in point of law and from the rejection or admission of evidence: cf Qantas Airways Ltd v Gubbins (1992) 28 NSWLR 26. Nevertheless, it might well have been arguable that the claimants did not bear a legal burden of proof and that the Court did not need to be satisfied on the balance of probabilities. However, given the approach adopted at trial, it is appropriate that this Court proceed on the basis that the civil standard did apply and that the respondents bore a burden of proof.
26 It is also an open question as to whether the Board acted properly in treating the proceedings in the District Court (and in this Court) as strictly adversarial and as requiring or at least permitting it to challenge the admissibility of evidence and cross-examine extensively witnesses called by the present respondents. The Board remains a decision-making authority in relation to their entitlements, in circumstances where its conduct may have caused the claimants (or the Legal Aid Commission) to amass large liabilities for legal costs as a result of the manner in which the Board conducted the litigation: cf The Queen v Australian Broadcasting Tribunal; Ex parte Hardiman [1980] HCA 13; 144 CLR 13 at 35-36; Oshlack v Richmond River Council [1998] HCA 11; 193 CLR 72 at [12] (Gaudron and Gummow JJ).
27 It is not necessary for present purposes to consider the correct approach to be undertaken by the medical authority in determining such matters. Each of the respondents was unsuccessful before the authority, but exercised the right of appeal granted by s 8I of the Dust Diseases Act. This Court has expressed the view that the District Court, in exercising original judicial jurisdiction, is required to give weight to the expert opinion of the authority: Veksans at 241B. No such issue was raised in the present case and it may be difficult to know what weight should be given to a decision of the authority, which is not accompanied by reasons and which may be determined on the basis of material (and the experience of the members of the authority) which differ from the evidence properly before the District Court. In any event, nothing turned on that matter in the present case and it was accepted that the District Court was bound to determine the case in accordance with the material properly before it under the Evidence Act 1995 (NSW).
Statutory scheme for compensation: construction of s 8
28 The Dust Diseases Act prescribes the circumstances in which a person shall be entitled to an award from the Board and to receive compensation at prescribed rates: s 8(1). Paragraphs (a) and (b) deal separately with a person suffering a disability and a person who has died from a dust disease. In each case the "medical authority", constituted under s 7, is required to certify certain things, including that the disability for work or the death is "from a dust disease". In the present case, the relevant dust disease was "asbestos induced carcinoma": s 3 and Schedule 1.
29 That which the medical authority was required to certify in the case of s 8(1)(b) involved a number of elements, differently expressed, identified as preconditions to entitlement to compensation in the following terms:
"(b) where the medical authority certifies that a person died from a dust disease and that the person's death was reasonably attributable to the person's exposure to the inhalation of dust in an occupation to the nature of which the disease was due ….:
30 In this case, the disease in question, to qualify as a "dust disease", itself involved a causal element, namely that the cancer must be "asbestos induced".
31 It is clear that s 8(1)(b) has two limbs, the first requiring a casual connection between the death and a dust disease. The structure of the second limb is grammatically unclear. The question of law raised in the present case concerned the meaning of the words "reasonably attributable to". They envisage a connection between two factors or events, so that the first step must be to identify those two factors or events. The last nine words of the second limb identify something to which the disease was due, or more precisely, to the nature of which the disease was due. Although the words follows "an occupation" it would be awkward, given the context, to describe the disease as due to the nature of an occupation. The other relevant nouns are "exposure", "inhalation" and "dust". The ordinary meaning of that language would suggest that it was the inhalation of dust to which the disease was due but the addition of the words "the nature of" make it more likely that the factor being characterised is either the exposure or the dust. It is more likely that it refers to the exposure, as the primary purpose of the second limb appears to be to address the circumstances of the exposure, namely that it must occur "in an occupation". Domestic or recreational exposure would not do. Where the exposure may have arisen in more than situation, it is the occupational exposure (or the nature thereof) to which the disease must reasonably be attributable, in order to satisfy the second limb.
32 The legal error asserted by the appellant in respect of the construction of s 8 involved the identification of the two limbs of the provision, which her Honour was said to have elided. The first was said to involve a causal connection, or in the terms of the written submissions, "a pure question of causation". The second limb was said to involve "an additional requirement" involving a "normative component".
33 In respect of the first question, the appellant submitted that a claimant under the Dust Diseases Act must prove that asbestos "materially contributed to the contraction of the lung cancer". Although that language is taken from case-law identifying principles of causation in negligence, that approach was not disputed and the submission should be accepted. Error was asserted based on the proposition that as smoking was the predominant cause of lung cancer, it could not be said that exposure to asbestos dust did more than increase the risk of lung cancer.
34 The appellant purported to identify three reasons why, in addressing the second limb, her Honour had erred in concluding that each of the deaths in question was "reasonably attributable" to exposure to the inhalation of asbestos dust. The first was no more than a repetition of the proposition that smoking is the overwhelming cause of lung cancer. There was no suggestion that this basis of complaint involved her Honour's rejection of some additional "normative" element.
35 The second reason was that each of the workers acted "unreasonably" in smoking or continuing to smoke when the dangers associated with that conduct were well known: written submissions, par 37. That was identified as a submission made by the appellant to the trial judge explaining that the respondents could not show reasonable attributability: appeal submissions, par 36. At the hearing of the appeal, the appellant withdrew that statement: Tcpt, 19/11/09, pp 17-18. What was meant by that withdrawal was unclear; it seems unlikely that the appellant did not know what submission it had made to the trial judge. However, the purpose of withdrawing the submission was apparently so that the appellant could now assert that her Honour was in error in suggesting that the appellant had indeed put the argument below in precisely the way identified in par 37 of the submissions on appeal: Tcpt, CA 16/11/09, p 37 (20). Although counsel promised to "come back to" that alleged error, he did not. What he did do was refer to evidence of two experts which was supposedly "evidence on unreasonableness of smoking", which was "not considered": document handed up on appeal, item 10.
36 No error was demonstrated in the passage in the judgment below where her Honour rejected the concept of "unreasonable conduct" and nothing was left upon which any "normative component" could have been based. The submission that her Honour's rejection of the argument occurred "without giving reasons or referring to the evidence" was inapt and tendentious. Her Honour treated the submission as raising a question of construction which was addressed and rejected.
37 The construction point was not elucidated in oral argument. The statement of the trial judge that "the defendants' submission that continuing to smoke by the deceased workers constituted 'unreasonable conduct' which leads to the legal conclusion that disability and death were not 'reasonably attributable' to asbestos exposure", was disowned as "not the way in which the submission was framed: Tcpt, 16/11/09, p 37 (20). The Court was not assisted by reference to how the submission had in fact been framed, although the appellant accepted (written submissions par 37) that the application of the "reasonably attributable test" which had been proposed below was "that by smoking, especially by smoking so heavily, the workers were acting unreasonably". The complaint that her Honour misconceived the submission was not made good.
38 The third matter relied upon as a reason why her Honour erred in her construction of the phrase "reasonably attributable" was said to be "that each of the workers continued to smoke for long after their exposure to asbestos ceased". However, this appears to be a reiteration, in different form, of the complaint that her Honour failed to take account of the history of smoking of each of the workers. It does not attempt to identify a point of construction in relation to s 8(1)(b).
39 The phrase "reasonably attributable" involves a causal element, but in this instance the connection is between the occupation and the relevant exposure or inhalation, rather than between the disease and death. Beyond this, it is not necessary to go for present purposes. The only relevant exposure to asbestos dust was occupational, arising in the course of stevedoring activities undertaken by the workers.
40 Her Honour clearly understood the submission as to the relevance of the phrase "reasonably attributable" as an attempt to impose a more restrictive test of causation than that of material contribution. Her Honour stated at [18]:
"The question at issue therefore, in each case is whether the carcinoma from which each worker died was reasonably attributable to the person's exposure to the inhalation of [Asbestos] dust or asbestos induced . In either formulation the test is satisfied if asbestos dust materially contributed to the carcinomas from which the workers died."
41 This statement of the issues, which incorporated the relevant definition of a dust disease was sufficient for her Honour's purposes. No reference was made to the question of occupation, except inferentially by reference to "the workers". That did not reveal error in any event, because that aspect of the test was not in issue.
42 The correctness of this approach is confirmed by reference to the Dust Diseases Act in its original form, in which questions of disablement and death were dealt with in a single formula requiring the medical authority to certify that:
"(a) the worker's disablement for work, or
(b) the worker's death,
from the disease was reasonably attributable to his exposure to the inhalation of silica dust in New South Wales in an employment to the nature of which the disease was due …."
43 At that time the Dust Diseases Act, known as the Workers' Compensation (Silicosis) Act 1942 (NSW) ("the 1942 Silicosis Act"), added an additional restriction, namely that the inhalation must occur in New South Wales, referred to employment rather than occupation and, as in the present formulation, permitted consideration of the nature of the employment, rather than a measurable exposure to what was then limited to silica dust. Further, at that time there was no appeal from a determination of the medical authority, so that the language of the section was required to be applied by medical practitioners and not lawyers or judges. There is nothing in the language which suggests some causal or normative requirement of a kind more restrictive than material contribution.
44 The 1942 Silicosis Act had been preceded by the Workmen's Compensation (Silicosis) Act 1920 (NSW). That Act had empowered the Minister to establish a scheme for payment of compensation by the employers of workmen in industries "involving exposure to silica or other dust": s 2(1). Entitlement to a benefit depended upon either death or total disablement, or suffering from silicosis to such a degree as to make it dangerous for them to continue to work in the industry. In the first category, the primary basis of entitlement was that the worker had "suffered death or total disablement" from the disease known as silicosis and, in the latter, that he was found on medical examination "to be suffering from silicosis". The legislation assumed that silicosis was caused by exposure to silica. However, in each case, entitlement could also arise where the person suffered from any other disease of the lungs "caused by exposure to silica or other dust".
45 This legislative history reveals that the various concepts of death or disablement, disease, exposure to dust, in an occupation, were all present, but that uniformity of terminology suggesting causal connection, was never a feature of the legislative scheme.
46 The intention that the introduction of the phrase "reasonably attributable" gave rise to some normative element is implausible. Since 1920, the legislative scheme for compensation for dust diseases has been treated as part of the general workers' compensation scheme, with which the legislation is required to be construed. That scheme has at all times required a causal connection between the injury or disease and employment but has never depended upon any element of fault on the part of the employer: see, eg, Workers Compensation Act 1926 (NSW) ("the 1926 Act"), s 6(1); Workers' Compensation Act 1987 (NSW), s 4. It was not until 1996 that a requirement that the employment must be "a substantial contributing factor to" the injury was inserted in the current legislation: s 9A. The exclusion, in cases involving psychological injury of certain forms of "reasonable action" of the employer was introduced in 1995, but does not extend to other than psychological injury. The legislation has, throughout the relevant period, excluded compensation for injury "solely attributable to the serious and wilful misconduct of the worker" and in the case of an "intentional self-inflicted injury": see the 1926 Act, s 7(2) and (3) and the current Act, s 14(2) and (3).
47 No reliance was placed, in the course of the appeal, on the requirement that the Dust Diseases Act "shall be construed with the Workers Compensation Act 1987", nor was any reference made to the provisions of s 14 of the latter Act. Nor was it suggested that continued smoking constituted serious and wilful misconduct or an intentional self-inflicted injury: any such suggestion would have raised a factual issue for determination by the trial judge. Accordingly, accepting that the phrase "reasonably attributable" may allow for circumstances where, despite the existence of a dust disease, compensation is not payable, the possible factual basis, absence of occupational exposure, was absent in the present cases. Accordingly, the appellant's complaint of legal error in the construction of s 8(1) must fail.
Causal connection: expert evidence
48 At the heart of the appeal lay the proposition that in each case the respondents had failed to demonstrate that the death of each of the workers had been caused by exposure to asbestos dust. The appellant asserted that it was undeniable that in each case the cause of the lung cancer, and hence death, was exposure to tobacco smoke. The trial judge, the submission continued, failed to advert to that central argument.
49 To assess this complaint more fully, it is necessary to identify briefly the context in which the complaint arose. In one sense, the underlying factual premises were not in dispute. Thus, each of the workers had died of lung cancer, each having smoked cigarettes for considerable periods and in considerable numbers. Further, it was common ground that medical science could not identify in an individual case the actual cause of lung cancer. These facts, the appellant correctly contended, posed significant hurdles for each of the respondents in seeking to establish an entitlement to compensation.
50 The appellant recognised, and indeed insisted, that the question of causation could only be addressed through epidemiological studies which identified the likelihood of lung cancer being caused by one or another pathogen. These studies, upon which all parties relied, demonstrated, according to the appellant, that the likelihood of any particular lung cancer being caused by asbestos, even in cases of known exposure to asbestos dust, was minimal compared with the likelihood of the cancer being caused by smoking. The approach adopted by the experts was that summarised by Professor Geoffrey Berry and extracted by her Honour at [109]. Professor Berry wrote (in a report concerning the late Mr Barry Smith):
"It is impossible to state the cause of a condition, such as lung cancer, in an individual with certainty. This is because there are a variety of possible causes, and also cases for which no particular cause is known. For example cases occur in life-long non-smokers who have not been exposed to dusts or fibres; these cases are sometimes referred to as background cases. However, from epidemiological studies that have been conducted on groups of people, and analysed using statistical methods, it is possible to obtain information on the risk of exposures to various agents.
Risk is usually expressed in terms of the measure relative risk (RR) . This is defined as The ratio of the Risk of disease or death among the exposed to the risk among the unexposed . As an example it has been estimated that the relative risk in smokers compared with non-smokers is 15. Another example is that the relative risk of lung cancer due to asbestos exposure in a particular factory in London was estimated at 3. These are both average values and further analysis shows that the relative risk due to smoking depends on the amount smoked, and that due to asbestos exposure on the extent and intensity of that exposure. That is, for an agent that increases the cancer risk, higher exposures increase the risk more than low exposures.
Another measure used is attributable fraction among the exposed . This is defined as (RR minus 1)/RR, so that a relative risk of 15 gives an attributable fraction of 14/15 = 0.93 or 93%. An interpretation of this figure is that 93% of the lung cancers in smokers are attributable to smoking (and 7% are background cases). Note that a relative risk of 1 indicates no excess risk, so that a relative risk of 15 may be divided into 1 (background) and 14 (excess). Thus, for an individual smoker who develops lung cancer, although it is not certain that the lung cancer was caused by smoking, one can say that the probability that it was due to smoking is 93%.
A relative risk of 2 gives an attributable fraction of 50%. That is, it is equally likely that the condition was due to the exposure or not. For relative risks higher than 2 then the exposure is the more likely cause, and for a relative risk less than 2 the exposure is the less likely cause."
51 There is an attractive simplicity in the statistical proposition that only a relative risk in excess of 2 indicates that it is more probable than not that the particular exposure being measured was the cause of the disease. There is also an attractive simplicity in the appellant's contention that, in the example given by Dr Berry, where the relative risk resulting from smoking is five times that created by asbestos exposure, a person who has been subject to both cannot possibly contend on the balance of probabilities that his lung cancer was due to asbestos exposure, it being five times more likely that it was due to smoking.
52 There are, however, a number of confounding factors which diminish or dissipate those considerations. The first is the fact that relative risk will, in any particular case, depend upon the duration and intensity of exposure, both in the case of asbestos dust and tobacco smoke. In relation to smoking, the large number of known cases appears to have allowed for a degree of precision and relatively high confidence levels in the calculations of relative risk, dependent upon the number of cigarettes smoked per day, the period over which the smoking continued, but subject to significant reduction after cessation.
53 Errors in estimation are of particular significance in the case of a deceased worker whose smoking habits over a lifetime must be reconstructed from information obtained from others. Even greater difficulties arise with respect to asbestos exposure. Professor Douglas Henderson, who was called by the respondents, was a co-author of a document commonly known as "The Helsinki Criteria" which sought to establish a standard for the intensity of exposure to asbestos dust that would give rise to a relative risk of 2. The figure arrived at was a cumulative exposure amounting to 25 fibres/ml-years, being a calculation which included both the intensity and duration of exposure. However, the Helsinki Criteria themselves noted that "the relative risk of lung cancer is estimated to increase .5% to 4% for each fibre per cubic centimetre per year (fibre-years) of cumulative exposure. With the use of the upper boundary of this range, a cumulative exposure of 25 fibre-years is estimated to increase the risk of lung cancer two-fold. Clinical cases of asbestosis may occur at comparable cumulative exposures."
54 The identified range involved a factor of eight between its minimum and maximum limits, suggesting that at the lower boundary of the range, the relative cumulative exposure may be 200 fibre-years. The disparity depends primarily on the nature of the asbestos; thus, as explained by Dr Berry:
"Based on a published analysis of exposure-response relationships, a cumulative exposure of 25 fibre-years is a reasonable figure to use for a doubling of risk for exposure that is predominantly to amphibole (crocidolite and amosite) asbestos, whilst the other end of the range (doubling of risk at 200 fibres/ml years) may be appropriate for exposure to commercial chrysotile other than in textile production.
55 Accordingly, estimates of relative risk in relation to asbestos exposure depend not only upon measurements of the amount of dust in the environment from time to time, but also on the type of asbestos involved. The reference at the end of Dr Berry's comment to textile production alluded to a study of textile workers in the USA in which surprisingly high levels of asbestos-related lung cancer were detected, suggesting the circumstances of the exposure also had a bearing on the outcome.
56 The reference to asbestosis in the last sentence quoted above from the Helsinki Criteria should also be noted. There are experts who support (or have supported) the proposition that a finding of asbestosis is a precondition to a finding of asbestos-induced lung cancer (known as the precursor theory). That did not receive substantial support amongst the experts who gave evidence in the present case, and was not accepted by her Honour. However, the Helsinki Criteria suggest that the existence of asbestosis, though not a precondition to a finding of probable causation, may indicate a level of exposure to asbestos consistent with that giving rise to a two-fold increase in the risk of lung cancer.
57 Evidence of the intensity of exposure suffered by the three deceased workers in the present case was obtained from industrial hygienists, who provided evidence to the Court. The respondents' witness in that respect was Dr Eva Francis, who had investigated asbestos workplaces in New South Wales as an officer in the Health Department of New South Wales from early 1971. Dr Francis had personal experience in investigating conditions on the Sydney waterfront. Dr Geoffrey Pickford, called by the appellant, was an occupational hygienist who had lengthy experience with industrial users of asbestos from 1977 until 1988, when he became a private consultant, but had not himself carried out testing on the waterfront or in the holds of ships.
58 The trial judge said she accepted Dr Francis' estimates as being "more likely to reflect the probable exposure of the three deceased workers than Dr Pickford's, although she may have overestimated the exposure to some extent": at [165].
59 However, her Honour also appears to have accepted the evidence of Professor Henderson that the estimates of exposure provided by the occupational hygienists were both "subject to substantial imprecision, being retrospective estimates of exposures that occurred 20 or 30 years ago": Tcpt, 08/02/07, p 145 (35). Accordingly, Professor Henderson preferred to base his assessment on other factors including the work histories of the individuals and his own experience of cases of asbestosis among workers in similar situations. As her Honour noted at [92] Professor Henderson had expressed doubts in his evidence as to the scientific rigour of measurements taken by occupational hygienists, "taking into account the widely disparate estimates that I see": Tcpt, 08/02/07, p 143 (5). Professor Henderson, who was a specialist pathologist with extensive clinical experience with asbestos workers, considered it appropriate to take into account the kinds of cases of undoubted asbestos-induced disease which had arisen amongst waterside workers whose work experience was similar to that of the deceased claimants.
60 Quite independently of the difficulties in being sure of the actual exposure of individuals to asbestos dust, the great majority of the experts who expressed opinions in the present case accepted that smoking and asbestos exposure had an interactive or synergistic effect. As Professor Henderson explained (Tcpt, 08/02/07, p 110 (20)):
"I think most studies accept that there is a synergistic interactive effect between tobacco smoke and lung cancer [sic] so that the combined effect is greater than the sum of the individual effects. … The example sometimes used is that of United States insulation workers where from their asbestos exposure if they are non-smokers, they have a risk of about five. If they are smokers and not exposed to asbestos, then they have a risk of ten. The combined risk though is not adding them together and coming up with fifteen but its closer to fifty so if you look at the combined risk it's fifty in comparison to the sum of the individual risks of fifteen so you have an interactive effect which is thirty-five and by definition you cannot separate that out into the individual effects …."
61 Professor Henderson noted that the interactive effect was not medically explained, but appeared capable of theoretical explanation. He stated (p 111 (5)):
"A number of theories have been put forwards but the two for which there is good supporting evidence are that in the first place, the carcinogenic components, that is the particular fraction of tobacco smoke can be absorbed onto the surface of asbestos fibres which are airborne so that what the individual inhales is an asbestos fibre coated with tobacco smoke carcinogens and the asbestos fibre can then deliver the carcinogens in tobacco smoke plus their own carcinogenic properties into airway of epithelial cells at higher concentration than would otherwise be the case. The other model and again there is good evidence for this is that tobacco smoke impairs and partially paralyses the cilia which are involved in clearance of dust and other particles from the lungs so that the tobacco smoke actually impairs the clearance of asbestos fibres from airway tissues and Churg and Stevens found that the concentration of amosite fibres in the bronchial walls of cigarette smokers was up to six times greater than the same concentrations [sic] in similarly exposed individuals who were not smokers and the differences were even greater for chrysotile fibres, up to fifty-fold difference. So that you seem to have both a concentration of asbestos fibres in the tissues at which the cancers arise and there is evidence that the asbestos enhances the delivery of the carcinogens in tobacco smoke into those tissues as well as exerting their own carcinogenic properties."
62 In the end, Professor Henderson himself was not anxious to place too much weight upon a mechanical application of the Helsinki Criteria. The following informative exchange took place towards the end of his cross-examination (p 142 (20)):
"Q. … Do you agree with the proposition that attribution of increase of risk due to a cause is very fact sensitive in these asbestos-related lung cancer cases?
A. I think it is. I mean even if one has - if one looks at tobacco smoking alone the chance of even a heavy smoker developing lung cancer is probably one in ten, so most heavy smokers still don't get lung cancer. The chance of an asbestos exposed person getting lung cancer is also quite low. The chance of somebody getting asbestos exposure [lung cancer?] when sustaining both patterns of exposure is greater but still reasonably low. So that there are many imponderables. All one can do is to say on a common sense basis taking into account what is known about asbestosis, equivalent levels of exposure, even lower levels of exposure, it's probable … each of tobacco smoke and asbestos have made a causal contribution towards the lung cancer, plus other unidentified factors."
63 After discussing the value of reliance on estimates of exposure prepared by the occupational hygienists, Professor Henderson stated (p 145 (35)):
"Well I think both are subject to substantial imprecision, being retrospective estimates of exposures that occurred 20 or 30 years ago and therefore I've tended to base my assessment on other factors, for example the work history and my encountering cases of asbestosis among a similar workforce similarly exposed."
64 The cross-examiner further put to Professor Henderson (p 150):
"Q. If Dr Francis is wrong and the cumulative dose inhaled is less than she suggested, that means conclusions to the extent you relied upon her would need to be modified?
A. Well, if in fact the true inhaled dose were less than her estimates, then the risk associated with those cumulative exposures would be less. Equally, if the dose inhaled were more than Mr Pickford's, then the risk would be increased in comparison. And this is one of the reasons why I have simply adopted a very broad-brush approach, saying well I've done work on the basis of the work history, I've compared it with similar cases in my files and taken into account an editorial published by William Weiss recently. He basically said, 'Well the risks of lung cancer are increased in those worker groups where there are cases of asbestosis'. And I think that's a reasonable broad-brush approach."
65 Professor Henderson noted that Weiss' paper had been subject to "severe criticism" but, after giving a reference to the paper, noted that the criticism was on the basis that he had underestimated the risks: p 151(10). The cross-examination continued:
"Q. What I'm trying to do here is just understand the tests that you applied. Are you saying that because these men were waterside workers then asbestos made some kind of contribution to their contraction of lung cancer?
A. I think that it imposes a probability that that was the case provided that these people are representative of the cohort or group of waterside workers. And the argument is encapsulated in the following passage of text, Weiss argues that increased death rates or risks of lung cancer occur in cohorts where asbestosis also occurs. But this does not mean that asbestosis and lung cancer must occur seriatim in the same individual. All the data indicate is that lung cancer death rates are raised in cohorts where asbestosis occurs in some individuals not necessarily those who develop lung cancer. This observation is equally explicable by a dose response effect for both asbestosis and lung cancer without a direct fibrous to cancer linkage."
Her Honour's reasoning with respect to relative risk
66 Two issues of fact were critical to the outcome of these cases. One was the availability of an inference that each of the workers was exposed to a level of asbestos dust sufficient to achieve a relative risk of at least 2 and thus at least a 50% chance that their lung cancer was asbestos-induced. Secondly, since all three men were regular smokers over lengthy periods up until their lung cancers were diagnosed, it was necessary that there be a factual basis capable of supporting the conclusion that asbestos fibre, more probably than not, contributed to the lung cancers. The fact that there was an interactive effect was widely accepted by the experts. The preponderance of evidence accepted that it was a multiplicative effect (or close to it) so that the existence of a relative risk with respect to asbestos of 3 and a relative risk with respect to smoking of 15 would produce a relative risk approaching 45 with the combination of both exposures.
67 What was not entirely clear from the evidence was whether the synergistic effect operated universally or only in the excess of cases over that figure which would be achieved by adding the two effects (in the example, 27, being the difference between 45 and 15 + 3). However, there was no suggestion in this Court that some error arose as a result of this uncertainty. It followed that it was open to her Honour to conclude that, given the available biological and physical explanations, the two carcinogens probably combined, each making a material contribution to the individual carcinomas.
68 Her Honour noted the evidence of Dr James Leigh that, "whatever the level of smoking, smoking and asbestos exposure are indivisible in the causation of an individual lung cancer, and any asbestos exposure multiplies the risk of lung cancer due to smoking by some quantity greater than one": at [102]. Accepting for present purposes that it was open to her Honour to accept that opinion, there was material which would justify the finding that where smoking and asbestos exposure coincided, asbestos made a material contribution to the disease in each case.
69 Some of the experts sought to apportion the relative effects of cigarette smoking and asbestos, even where they worked interactively. As the mechanism of interaction was not known, that appears to have been an artificial exercise and one which Professor Henderson and others considered flawed. Indeed, as the proponent of the mathematical model, Professor Berry said in evidence, in a passage set out by her Honour at [59]:
"In fact often in my reports I put an extra sentence here and say in one sense it is impossible to do this because in the medical model they're closely linked together … but if it were required to do it for the purpose of compensation, given that two defendants don't have a joint bank account, as it were, then this is the method of doing it. But it's not a biological model."
70 The empirical basis upon which the apportionment exercise was undertaken was not explained in the evidence. Its relevance was not explained either in the evidence or in this Court. If it were thought to bear some relationship to the materiality of the contribution provided by asbestos, that contention was not relied upon in this Court, nor is its operation self-evident.
71 It may be that, underlying the appellant's argument in this Court, was the proposition that for a pathological condition to be reasonably attributable to a dust disease, the inhalation of dust must be a major or predominate cause and not merely a material contribution. However, that proposition was not expressly put and need not be addressed further.
72 This brief synopsis of the evidence and the reasons of the trial judge indicates the basic flaw in the appellant's core submission. Her Honour did not ignore the evidence of the causative effects of smoking; rather, that was not the issue to which the statute directed her attention. As she correctly identified, the statutory test required the Court to determine whether it had been shown on the balance of probabilities that exposure to asbestos dust materially contributed to the dust disease, namely in this case the lung cancers. One factor can materially contribute to an outcome even though, relative to another factor it has a minor effect. All that is required is that the effect be "material". That required an evaluative judgment on the part of the Court. Such a judgment, based on available evidence, could not readily be the subject of challenge in an appeal limited to a decision in point of law.
Admission of evidence: Helsinki criteria
73 To complete the foregoing analysis, it will be necessary to return to the reasons given by the trial judge. The appellant submitted that the reasons were inadequate in a manner which gave rise to a ground of appeal under s 142N. However, it also submitted that her Honour was in error in admitting: