Cross-examination
22In cross-examination, Professor Henderson was taxed with the proposition that available medical and scientific evidence did not enable an opinion to be given, in any particular case, as to what causal relationship any particular asbestos exposure had to an assumed lung cancer. All that could be stated, it was put to him, was that there were risk factors of which exposure to asbestos was one and that such exposure heightened the risk of cancer. One could not, it was put to him, translate that into an opinion about the causal responsibility of any particular exposure to a lung cancer. It was put to him that all that science tells us could be summarised in four propositions that are paraphrased as follows:
(1) There are cohorts of asbestos workers who were subject to substantial exposure who have been studied and who show an increased incidence of lung cancer compared to those who did not have that exposure (Joint Black Book Vol 1 of 2 p 255 P).
(2) Work has been taken further and a dose response relationship has been derived which is a linear dose response relationship (ibid p 255 Q). (In relation to that relationship Professor Henderson agreed that epidemiology has taken us to the stage of saying, RR [relative risk] equals I plus K times E, and the occupational hygienists may or may not be able to tell us in particular circumstances whether K or E can be determined with any precision (ibid p 257 G)).
(3) Asbestos is biopersistent (ibid p 257 J).
(4) Asbestos fibres have been shown to initiate biochemical processes which may lead to cell mutation and also proliferation of cells that have damaged DNA, directly or indirectly, from generation of toxic chemicals from the fibres themselves or from the fibre cell interactions particularly with macrophages (ibid p 257 K-M).
23As to the fourth proposition the following exchange took place:
Ibid p 257
"Q. And that is a not at all uncommon feature of other carcinogens. A - That is correct. For example ionising radiation also develops similar reactive chemicals and some of the carcinogens in tobacco smoke generate similar toxic chemicals like reactive oxygen species.
Q. And those toxic chemicals that you describe, can have either the direct or the indirect effect on the cells, direct in the sense that they may induce mutations in the cells. A - That's correct.
Q. Or indirect in the sense that they may interfere with the body's natural defence mechanisms, [that] ordinarily would control and eliminate rogue cells. A - Well, that may be part of carcinogenesis but it is a much more speculative one, but yes.
Q. What I have just put to you is a possibility but you would regard it as speculative. A - Well, in case of asbestos I would regard it as more speculative.
Q. But it is established in relation to other carcinogens is it. A - Well, yes, some of other carcinogens are known to depress cell immunity.
Q. But in asbestos that is not - sorry, you do not regard that as being - A - Well, I don't regard it as being one of the really important factors. The important interaction is thought to be the fibre macrophage interaction and they may well have secondary effects further down the track on lymphocytes and other arms of the immune system, but the essential factor is the fibre cell or rather fibres cells' interactions with the generation of reactive oxygen species, which are known to be damaging to the DNA."
24It was then put to Professor Henderson that that was "all that science tells us relevantly." (Joint Black Vol 1 of 2 p 257 X.) Professor Henderson did not accept this. He said:
Ibid p 258
"A. Well, I think it goes beyond that because a number of the steps in a mutational pathway towards cancer have been established, and there is now a - although the process is incompletely understood, there is now good evidence for a number of the mutational steps and one can name individual genes involved.
Q. Well, can we include all of that as falling within the general statement in the fourth proposition. A - Right.
Q. Now, understanding the propositions in those broad terms, is what I put to you correct, that those four propositions exhaust what science can tell us about the relationship. A - I don't think they exhaust it."
25Meticulous cross-examination then followed in aid of the propositions as to the limits of science identified. This included the following exchange:
Ibid pp 263-264
"Q. Now the creation of genomically unstable cells is something that happens even without asbestos exposure, correct. A - Yes, people develop mutations spontaneously.
Q. So it can happen spontaneously, correct. A - Yes.
Q. Or other carcinogens can be involved. A - Yes.
Q. Such as ionising radiation. A - Yes.
Q. Or cigarette smoke. A - Yes.
Q. And that may happen either at the initial stage when the first, and I call it, the ancestor cell which is the first genomically unstable cell was created or at any of the descendant stages. A - Well, yes, just as the asbestos fibres interact either at the first and as they accumulate the subsequent stages in cancer development.
Q. So you could have one genomically unstable cell that had been started by ionising radiation and then another at later generations that could accumulate a further mutation and that might be the produce of an asbestos fibre. A - Yes, but all the asbestos fibres then are doing is adding on to a previous mutation and furthering the development of the necessary causal chain of the mutations necessary for cancer development.
...
Ibid p 264
Q. So looking at the ultimate development of the cancer, it is possible to trace it back to a series of finite number of individual events at which first the ancestor cell has become genomically unstable and then further mutations have occurred to its descendant cells until it eventually becomes a cancer cell and then develops into a tumour, correct. A - Well, I don't know what you mean by the expression a series of finite steps. All I'd say is that when you have a deposition of inhaled asbestos fibres especially amphibole fibres those fibres will interact with otherwise normal cells, macrophages release toxic chemicals which can then impact on otherwise normally replicating bronchial epithelial cells and induce mutations and the more fibres that are inhaled and deposited the greater the number of the toxic chemicals, the greater the number of the mutations, the greater number of epigenetic events, for example, autocrine cell stimulation, which will lead to this expanded population of cells and the point is that all of these factors accumulate in a necessary obligate causal chain of precancerous events finally leading up to the final event which becomes the cancer.
...
Ibid p 271
Q. The proposition is that when one reads this report as a whole it is clear that the words on a probability basis and the sentence to which I have drawn attention connote an exercise for an individual in the application of a formula RR equals 1 plus K times E. A - Well, I just do not agree with that proposition. I would not use that equation. I would think that the attribution in an individual patient is based on a variety of considerations and including - and a work history of substantial to heavy exposure as in this case or asbestosis however diagnosed and I don't think one needs to invoke the equation RR equals 1 plus K times E. I don't see the relevance of that to this particular exercise.
...
Ibid p 274
Q. Now, I asked you some questions earlier about the biochemical processes which are thought to lead to the development of cancer. You will agree with me, will you not, that not all of the fibres which lodge in the lung and produce the adverse effects that you are referring to actually contribute to the chain of causal events which lead to the generation of the particular cancer which may later develop. A - I agree that not all of the inhaled fibres will actually participate in the process of carcinogenesis, that some of the fibres will migrate away and be translocated to pleura. But what I can say is that a proportion which is likely to be proportionate to the dose of each episode of exposure will participate in the process of carcinogenesis, so one is looking at a fraction, a proportion of the inhaled and deposited fibres which will participate in carcinogenesis.
...
Q. Well, we do not now how many steps there are or may be, how many mutative steps there are or may be between the original unstable - and I am sorry, I have forgotten your phrase - the ancestor unstable cell. A - Well, we don't know the precise number of steps."
...
Ibid pp 276-279
Q. Would you agree with me that the model that you have described involves an assumption that there is a continued accumulation through the generations of further mutations which, if the cell does not automatically die or undergo apoptosis or be eliminated by the body's defence mechanisms, eventually results in accumulating enough mutations that the cell then becomes a cancer cell capable of replicating itself and then the cancer grows from that cell. A - Well, that's a fair representation of the process, as we discussed this morning; and again, the more a person smokes cigarettes the greater the likelihood that the carcinogens in the cigarette smoke will lead to an outcome, yet not everybody who is even a heavy smoker will develop lung cancer. It is increasing the probability that the required chain of sequential causal mutational and epigenetic events will actually occur that lead to the cancer; and the point is, the more that one smokes, the more that one is exposed to asbestos, the greater the probability that this chain of events will come to its fruition, if you like. And the point is that each of the, if you like, cigarette smoke or asbestos exposures will contribute to the pool of asbestos fibres, from the first, second, third and fourth exposures, and as the fibre numbers increase the probability that a cancer will develop increases. Each adds to the likelihood that a cancer will develop and eventually that is translated, or comes home, or comes into being as a cancer.
Q. When it does, in your language, the fibre in question - that is, the fibre that has been inhaled as a whole - in your language has made a material causal contribution to the cancer which ultimately results. A - What I am saying is that -
Q. That is the sense in which you have used this phrase, 'material contribution or cause,' is it not. A - I don't think I've used the word 'material,' but if I have it has been a mistake on my part.
HIS HONOUR ...
Q. Doctor, can you reply. A - Well, I try not to use the word 'material,' your Honour. To me that is a legal term, the expressions I use are 'significant and substantial causal contribution', and the point that I am simply trying to make is that the more fibres that are inhaled, the greater the probability that the cancer will develop. So that each of - when you say there were four exposures, each of the exposures will increase the likelihood of a cancer developing. They each increase the likelihood on top of those that have gone before, so that the total likelihood at the end, when it's translated into a cancer, is the total cumulative exposure that has come home to fruition in terms of a cancer.
Q. In that each additional fibre adds to the chemical soup which is toxic. A - That's correct. Each of the exposures is adding to all of the events and chemicals and mutations which ultimately lead to the cancer, so that when you see a cancer in reality, as expressed in an individual patient, you're looking at the end result of all the risks or likelihoods imposed by each of multiple exposures.
... HIS HONOUR
Q. So that does each exposure create some additional mutations. A - Well, I don't think one can put it quite so precisely, your Honour, because if you have, say, somebody with four exposures to asbestos over, say a period of two or three years each, then the amphibole fibres from the first exposure, a proportion of those will be present in bronchial walls and lung tissue. They will persist. The second exposure takes place and that adds to that pool of asbestos fibres. So does the third and so does the fourth. But the first exposure fibres are still resident, so that the chemical soup and the mutational events are the end result of the cumulative exposure imposed by each of multiple exposures when there is more than one.
Q. So that each exposure creates some additional mutations. A - The likelihood is that each does, that each additional exposure, because it increases the number of fibres, increases the likelihood that the chemical messengers will induce one of the required mutations for the development of a lung cancer. I mean, I can only requote Professor Berry when he says, 'It would be invalid to conclude a lung cancer is caused only by one exposure. There were three other periods of exposure that would have made a contribution to the excess in risk, and there is no scientific basis for saying that only one of those periods caused the cancer.'
... WITNESS
If one has an exposure which has contributed, say, 60% to the total fibre pool and there are two other exposures, each of which has contributed 20%, I don't think one can say that the cancer which has developed is the outcome, even on a probability basis, from the 60%. It is the total 100% - the 60 plus 20 plus 20 - which is the cumulative exposure which has been brought home in terms of the development of the cancer.
MR PARKER
Q. That is the way you analyse it. A - Well, yes, it is.
Q. And you have said now many times that an additional exposure - or an individual episode of exposure - increases the risk of a cancer ultimately developing. A - Yes.
Q. But that particular exposure may not in fact play any role in the development of the particular cancer that in fact develops; correct. A - I think - well, I wouldn't say - I don't believe that is correct, because I think it falls into the realm of far-fetched speculation beyond what is available in the biological and scientific evidence. I think that is entirely speculative.
Q. Well, most of the cells which develop these mutations ultimately do not go on to grow into a cancer, they either die out or are eliminated by the natural processes that we have discussed; correct. A - Well, that's correct.
Q. So it's only a fraction of those cells or indeed usually only one that will actually lead to a line which endures down the generations enough and develops the necessary mutations to turn into a cancer. That is right, is it not. A - Well, yes. The majority of the cells will either die out, the mutations will be irrelevant or they will not progress to cancer for a variety of reasons and it requires a complex series of sequential causal steps to cause the cancer but the point is that the likelihood that those essential causal steps in this casual chain will be achieved is increased by the additional asbestos exposures so that one can't point to any one exposure and say well this one on a probably basis has not contributed. That to me is speculation.
Q. Nor can one point to any particular individual one and say on a probability basis this one did contribute. A - Well, as I say one cannot point to one of, say, four exposures and say that is the exposure responsible, the other three played no role. One cannot equally point to one exposure and say well that played no role it's the other three. The point is, it's all of the exposures in an individual which are ultimately translated into the development of a lung cancer.
Ibid p 279
Q. You have expressed yourself in your report and in your evidence a number of times as saying all the exposures make a substantial contribution to any cancer which ultimately develops or you have said all the exposures cumulatively cause the cancer which ultimately develops. A. And this is in accordance with current theories on carcinogenesis.
Q. That is the way you have expressed yourself and in expressing yourself you mean that all of the exposures increase the risk in the way that you have described in your evidence to me. A. That's correct.
Q. And nothing more. A - Well, I think it means more when the cancer has finally developed because the risk has come home in the form of a cancer.
HIS HONOUR
Q. But does every additional exposure increase the number of mutations. A - We can't count them because in humans one can't come back and look at the mutations. The point here is, your Honour, that even the first exposure will produce a series of ongoing mutations. The next exposure will increase the number of mutations and increase the likelihood that one of those mutations is relevant to the development of cancer and so would a third and so would a fourth. One can't neatly fractionate mutations according to each of, say, four exposures because the mutations - the fibres are long resident in lung, new fibres are added and the mutations are ongoing process over 20 to 30 years."
(Emphasis added.)
26From the totality of the written and oral evidence of Professor Henderson, illustrated by the above extensive extracts one can see the following:
(1) The consistent and careful attempts by the cross-examiner to have Professor Henderson accept that his expressed views as to necessary causal relevance of retained asbestos fibres in an asbestos induced cancer were no more than hypotheses of heightened risk; and that scientific knowledge did not permit any conclusions in the case of an individual cancer of the causal relevance of any particular exposure.
(2) The rejection by Professor Henderson of those propositions and his opinion for the reasons he gave that scientific knowledge did permit and support his opinion that upon a cancer occurring that could be attributed to asbestos (as here), the retained asbestos fibres were all necessary or obligate parts of the causal chain.
27In so expressing the matters in (2) Professor Henderson was drawing upon his specialised knowledge. It may be that the better scientific view of the pathology or aetiology of asbestos induced cancer is another quite different hypothesis. For instance, the medical evidence that formed the basis of the findings of fact in Fairchild v Glenhaven Funeral Services Ltd [2002] UKHL 22; [2003] 1 AC 32 as to the cause of mesothelioma was summarised by Lord Bingham of Cornhill at 43 [7] as follows:
"... The mechanism by which a normal mesothelial cell is transformed into a mesothelioma cell is not known. It is believed by the best medical opinion to involve a multi-stage process, in which 6 or 7 genetic changes occur in a normal cell to render it malignant. Asbestos acts in at least one of those stages and may (but this is uncertain) act in more than one. It is not known what level of exposure to asbestos dust and fibre can be tolerated without significant risk of developing a mesothelioma, but it is known that those living in urban environments (although without occupational exposure) inhale large numbers of asbestos fibres without developing a mesothelioma. It is accepted that the risk of developing a mesothelioma increases in proportion to the quantity of asbestos dust and fibres inhaled: the greater the quantity of dust and fibre inhaled, the greater the risk. But 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. So if C is employed successively by A and B and is exposed to asbestos dust and fibres during each employment and develops a mesothelioma, the very strong probability is that this will have been caused by inhalation of asbestos dust containing fibres. But C could have inhaled a single fibre giving rise to his condition during employment by A, in which case his exposure by B will have had no effect on his condition; or he could have inhaled a single fibre giving rise to his condition during his employment by B, in which case his exposure by A will have had no effect on his condition; or he could have inhaled fibres during his employment by A and B which together gave rise to his condition; but medical science cannot support the suggestion that any of these possibilities is to be regarded as more probable than any other. There is no way of identifying, even on a balance of probabilities, the source of the fibre or fibres which initiated the genetic process which culminated in the malignant tumour. It is on this rock of uncertainty, reflecting the point to which medical science has so far advanced, that the three claims were rejected by the Court of Appeal and by two of the three trial judges."
28If the induction of lung cancer were better seen as reflected by the evidence as to mesothelioma as described by Lord Bingham (as the legal submissions of the appellants asserted) that could form the basis of the rejection of Professor Henderson's evidence. But there was no contrary evidence. There was (relevantly) only that of Professor Henderson. I am unable to characterise Professor Henderson's evidence as inadmissible to prove the causal relationship between all these exposures and the lung cancer. In my view, the material crosses the line, by some measure, at which lay analysis can discern any inadequacy of the requirements of s 79 discussed by the joint judgment in Dasreef v Hawchar.
29There was some discussion at the appeal about the statement of opinion on p 9 of Professor Henderson's report of 31 August 2010 as to the latency period:
Joint Blue Book Vol 5 of 5 p 2179
"Provided that the latency interval is appropriate (i.e. more than 10 years following the beginning of any exposure), each of any identified above-background exposure makes a causal contribution towards the induction of the lung cancer or mesothelioma, the proportional causal contribution being modified by the three factors mentioned in the preceding sentence. Therefore, it follows that when there are multiple exposures with an appropriate latency interval, each one of those exposures makes a causal contribution towards lung cancer induction. It also follows that one cannot point to any one exposure as being responsible for the lung cancer entirely, with exculpation of the others."
There was no suggestion in the evidence of any dispute or issue concerning these views about the latency period. No submission or cross-examination was directed to this part of Professor Henderson's report. It is not necessary for a witness to dilate upon issues that are not in contest or give explanations that are not necessary.
30The evidence of Dr Bryant and Dr Yates may well have been bad in form in the way it simply rolled up agreement with Professor Henderson. That objection, however, was not the burden of the debate. I did not understand any submission to be put that if Professor Henderson's evidence was admissible and adequate to found the Tribunal's conclusions, any defect in the evidence of Dr Yates and Dr Bryant would make any difference to the orders on appeal.
31The acceptance that Professor Henderson has rationally explained his opinion by reference to facts, assumptions and his specialised knowledge, and the acceptance that Professor Henderson was not expressing an opinion about heightened risk makes irrelevant any criticisms of his analysis based on cases such as Bendix Mintex Pty Ltd v Barnes (1997) 42 NSWLR 307 or what I said in Evans v Queanbeyan City Council [2011] NSWCA 230. Thus, a response to the historical exegesis in the appellants' submissions of cases such as Bendix, EM Baldwin & Son Pty Ltd v Plane (1998) 17 NSWCCR 434, Seltsam Pty Ltd v McGuiness [2000] NSWCA 29; 49 NSWLR 262, Fairchild, Barker v Corus UK Ltd [2006] UKHL 20; [2006] 2 AC 572 and Sienkiewicz (Administratrix of the Estate of Enid Costello Deceased) v Greif (UK) Ltd [2011] UKSC 10; [2011] 2 AC 229 becomes unnecessary.
32Reliance was placed by the appellants on the scholarly works of Professor Stapleton such as "Factual Causation and Asbestos Concerns" (2010) 126 Law Quarterly Review 351. A reading of Professor Stapleton's work on causation in relation to asbestos, such as the above article and "Two Causal Fictions at the Heart of US Asbestos Doctrine" (2006) 122 Law Quarterly Review 189 reveals the view that New South Wales Courts have been inconsistent in their treatment of causation. Professor Stapleton noted that after there was a rejection of mere increase in risk as causally sufficient in cases such as Bendix, there was a persuasion of courts to accept expert evidence that every exposure to asbestos contributes to the triggering of the process. Professor Stapleton wrote in 126 Law Quarterly Review at 355:
"This approach seems to outstrip the limits of medical knowledge depicted in Fairchild, yet when unsuccessful defendants, attacking such evidence, applied for special leave to appeal ... they too were rebuffed: Jsekarb Pty Ltd v Plane [1999] HCATrans 368."
33Professor Stapleton is undoubtedly correct that the evidence accepted by the Tribunal in mesothelioma cases goes beyond what was accepted in Fairchild. That may have been a product of errors of fact of the Tribunal in the weighing of expert evidence, though I do not assert that. The point for present purposes is that the appeal to this Court from the Tribunal is limited by s 32. A mere error of fact, however critical, is unappealable. The question here is whether Professor Henderson's views, which, in the context of mesothelioma, have been the foundation of the Tribunal's factual findings, are admissible in so far as he proffers them in respect of lung cancer. For the reasons that I have expressed, I think they are. They may be wrong. The experience and multidisciplinary training of others, scientists and legal scholars included, may suffice beyond a lay analysis to criticise the acceptability of Professor Henderson's views. With that I do not quarrel. But that was not attempted by the appellants. His views do not suffer the characterisation capable of being made by a judge without expert assistance of unreasoned ipse dixit.
34The proposition also put forward that Professor Henderson cannot give expert evidence on causation is, with respect, incorrect. As a pathologist, if he otherwise has the basis to express an opinion, he is concerned with the science of the causes and effects of diseases. In this respect I agree with what was said by Nettle JA, Ashley JA and Redlich JA in Amaca Pty Ltd v King [2011] VSCA 447 at [110] ff; and see also Amaca Pty Ltd (under NSW Administered Winding up) v Booth [2011] HCA 53; 283 ALR 461 at 475 [49] per French CJ.
35It is true that the opinions were expressed in language that is employed in legal analysis in causation, but the expressions used were factual phrases capable of expressing meaning in the contexts in which they were used. There was no cross-examination to the effect that these were not Professor Henderson's views but the words given to him by lawyers.
36In my opinion, Professor Henderson's opinions were admissible and no error was displayed by the Tribunal in admitting them.