Amaca Pty Limited (Under NSW Administered Winding Up) v Booth & Anor; Amaba Pty Limited (Under NSW Administered Winding Up) v Booth

[2011] HCATrans 276

[2011] HCATrans 276

IN THE HIGH COURT OF AUSTRALIA

Office of the Registry
  Sydney  No S219 of 2011

B e t w e e n -

AMACA PTY LIMITED (ACN 000 035 512) (UNDER NSW ADMINISTERED WINDING UP)

Appellant

and

JOHN WILLIAM BOOTH

First Respondent

AMABA PTY LIMITED (ACN 000 387 342) (UNDER NSW ADMINISTERED WINDING UP)

Second Respondent

Office of the Registry
  Sydney  No S220 of 2011

B e t w e e n -

AMABA PTY LIMITED (ACN 000 387 342) (UNDER NSW ADMINISTERED WINDING UP)

Appellant

and

JOHN WILLIAM BOOTH

First Respondent

AMACA PTY LIMITED (ACN 000 035 521) (UNDER NSW ADMINISTERED WINDING UP)

Second Respondent

FRENCH CJ
GUMMOW J
HAYNE J
HEYDON J
CRENNAN J

TRANSCRIPT OF PROCEEDINGS

AT CANBERRA ON TUESDAY, 4 OCTOBER 2011, AT 2.15 PM

Copyright in the High Court of Australia

____________________

MR J.T. GLEESON, SC:   May it please the Court, in the Amaca Pty Limited matter I appear with MR N.J. OWENS for the appellant.  (instructed by Holman Webb Lawyers)

MR G.M. WATSON, SC:   May it please the Court, I appear with MR J.C. SHELLER for Amaba Pty Limited matter.  (instructed by DLA Piper Australia)

MR D.F. JACKSON, QC:   May it please the Court, I appear with my learned friend, MR S. TZOUGANATOS, for the first respondent in each matter.  (instructed by Turner Freeman Lawyers)

FRENCH CJ:   There is a submitting appearance for the second respondent in each matter.  Thank you.  Yes, Mr Gleeson.

MR GLEESON:   Your Honours, the starting point, we submit, for the appeals is that it is common ground here, as below, that the question of factual causation is to be determined under ordinary principles of onus of proof in a civil suit for damages.  There is no contention there should be some special or different rule.  We accept causation may be robust and pragmatic, but no more.  In terms of the nature of the proceedings, the proceedings were under the Dust Diseases Act and the question for the Court of Appeal involved one of law. We have provided a copy of the provision and that question, as we frame it, is whether there was evidence from which factual causation was capable of being made out. It is section 32 of the Dust Diseases Tribunal Act 1989 (NSW).

Your Honours, in relation to an understanding of the possibilities at least concerning Mr Booth’s injury, it may be convenient to consider his exposures to risk in three or perhaps four periods.  The first period would run from his birth in 1937 through until approximately 1953 and during that period he faced the general background risk that all Australians do and did for most of the 20th century in relation to asbestos fibres which are in the atmosphere as well as a particular exposure from two episodes of home renovations.  The second period which concerns particularly my client running from 1953 to 1962 continued as always general background risk, included a very brief exposure as a truck driver to bags which were exploding with asbestos.  It included exposure to my client’s brake linings and to other manufacturers’ brake linings.

The third period we identified as running from 1963 to, say, 1983.  The say 1983 is that in that period, apart from general background risk, there was exposure to Mr Watson’s client’s brake linings and exposure to other brake linings.  There is perhaps a fourth period, of course, which is from 1983 through to, say, 1998, Mr Booth continued to face general background risk.  I say 1998 because his diagnosis was in 2008 and the evidence was to the effect that there was a minimum latency period for asbestos of about 10 years; page 687.

Your Honours, the negligence which is not an issue before this Court was a failure to warn and that gave rise to a causation question at two levels.  The first, which is not before this Court, is whether, had a proper warning been given, the particular plaintiff would have so avoided exposure to the defendant’s asbestos as to not be capable of contracting the disease.  The second before the Court is whether, in fact, exposure to Amaca asbestos caused the disease.

Your Honours, before I come immediately to our analysis of the expert evidence, we do submit it assists in the appeal to consider two groups of matters which should not be too controversial.  The first are those matters known about mesothelioma in general which provide the context in which the particular issue can be decided, and that is proposition five, and proposition six is the legal structure of the plaintiff’s case in order to establish factual causation. 

As to proposition five, we would put that one of the puzzles of medical knowledge is this, that very small exposures to this fibre can lead to this terrible disease.  As one piece of evidence, could I ask your Honours to go to volume 2 at page 759.  This is in the report of Dr Leigh.  At the foot of that page over to page 760, first paragraph, he catalogues exposures of a very minor level, including as short as a day, which have led to mesothelioma.  That is at one end.  At the other end of the puzzle, many people can face large and sustained exposures and never contract mesothelioma.  If your Honours could go to page 687, which is in the report of Professor Henderson, he correctly makes the point at line 40 that:

Mesothelioma occurs in only a minority of asbestos‑exposed individuals ‑

even after heavy exposure to amphibole asbestos.  That is the nasty or the more nasty type including crocidolite and amosite.  The asbestos involved in brake linings is the less nasty type, if I can use that crude expression, chrysotile.  Professor Henderson says that that fact might be explained in a number of different ways and, really, we simply do not know.  It may be due to chance events, it may be due to a number of other possibilities he mentions on that page and over the next page.  That is the second general matter which is clear. 

The third general matter is that chrysotile, as involved in the present case, is the least potent form of asbestos.  Your Honours can see that from page 681 of this report in the first bullet point.  The literature varies, but taking the three types from worst to least worst, crocidolite, amosite and chrysotile, one can see chrysotile is somewhere between 15 and 100 times less potent than amosite and somewhere between 30 and 500 times less potent than crocidolite.  Your Honours, the fourth background fact which is clear is that some workers involved in brake linings have contracted mesothelioma, but most have not. 

If your Honours could go to the Australian Mesothelioma Register, which commences at page 717 – this was published in May 2002.  That appears from 712 and at that stage the register had been operating since 1986.  That is page 717, line 35.  At that stage, there were 5,500 notifications of mesothelioma in Australia.  Your Honours will see on that page that, dropping down to paragraph (d) at line 42, about 90 per cent of those cases could be related to a work exposure, two per cent were related to non‑work exposures and nine per cent could not be classified.  The nine per cent is what is sometimes described as “background risk” where no particular exposure can be identified or at least recalled by the person.

The point about brake linings appears from page 740 at line 40.  Over this period of 15 years there were in total 78 persons who had reported an involvement with brake linings who had suffered the disease.  The total number of workers with brake linings is obviously massive.  One estimate, at page 750 ‑ ‑ ‑

FRENCH CJ:   That heading “Single exposure” means exposure only to asbestos from that designated source, does it?

MR GLEESON:   Yes.  Then 19 identified that plus another source to make the 78.  While your Honours have that page, I will be coming back to home renovations, but you might notice under the heading “Asbestos dwelling/fence – built/renovated” and “Asbestos dwelling – lived in”, which would include but not be exhausted by home renovations. there are 85 and 38 in total.

The number of brake mechanics in Australia is massive.  One estimate is given by Dr Leigh at page 756.  At line 20, he quoted the ABS figure for 1997, there being 83,000 persons in the category of vehicle mechanic which would include but not all be brake linings and he works out an average rate for persons in the vehicle mechanics group of 21.8 per million person per year.  That is in a population of a million persons involved in motor vehicles in a year one would see 21.8 with the disease and he observes that would be 20 times greater than the background rate where one would see one per million person year.  He does some calculations further down that page and your Honours might observe at about line 35 he calculates that a lifetime risk if you are a vehicle mechanic would be a quarter of one per cent. 

In this list of matters which are non‑controversial, could I next come to general background risk.  Professor Henderson explained that well at page 685, lines 30 to 50, and in terms of the position that we all face, he said at line 35:

As a consequence of the inhalation of airborne asbestos fibres in the ‘environment at large’, virtually all adults in either urban or rural environments and without a history of either occupational or non‑occupational exposure to asbestos [have] asbestos fibres in their lung tissue (up to 1,000,000 fibres/g dry lung tissue –

Then he refers to the figure of one to two mesotheliomas per million persons per year which converted to a lifetime risk, assuming an average life of 70 years, gives a figure which is seen in some of the material that everyone has a 70 in 100 million chance of contracting mesothelioma simply from background. 

The next preliminary matter is that the exposures to asbestos which Mr Booth faced in our category A, that is, between 1937 to 1953, were capable on their own or in combination of causing mesothelioma.  If I could indicate that in respect to the background exposure, that is because of the material we are now looking at.  In relation to the home renovations, that was specifically dealt with at page 667 from lines 20 onwards where Professor Henderson described what is involved in the release of asbestos fibre when home renovations are occurring and he correctly emphasises at line 30 that the dust often remains in the home or the environment after the work has been done and at line 40 he observes 85 total cases of home renovations attributed mesothelioma in the register that I have been to. 

The other matter he notes about home renovations at the foot of that page and over is that the earlier the exposure, everything else being equal, the greater its power in risk terms.  So for the given exposures which Mr Booth faced, around eight, his risk was two to three times greater for an exposure of the same level which occurred later in life.  Another aspect is to consider the types of asbestos in home renovations which were of the more dangerous types.  Dr Leigh, at page 759 in the passage I have been to, also referred to these brief exposures being capable of causing asbestos. 

In relation to his work on the truck, if I could just refer to page 659 where there is a description between lines 20 to 30 of what occurred, and at page 666 at about line 25 Professor Henderson considered, given what is known, that the type of asbestos he was there exposed to may have been the worse amphibole type.  Your Honours, they are the matters that we consider to be relatively non‑controversial which set the stage for debate.

In our proposition six, we take up a point which was addressed in our submissions which was, what was legally involved in a finding of causation given the exposures in different periods and to different types of asbestos?  We would submit that the plaintiff’s case needed to involve, in order to obtain a judgment against both defendants, these three propositions.  The first proposition was that his two sources of exposure prior to 1953 did not in fact realise their individual and cumulative capacities.  Had they done so, that is, had they achieved their capacities and by 1953 he was a person who irreversibly would suffer the disease as and when he did, any later exposure would not be causative in law, he was already fully injured.  So that was a proposition implicit in the case, necessarily implicit.

The second, pursuing it chronologically, is in the 1953 to 1962 period which concerns my client.  The plaintiff’s case involved the proposition that some of the fibres to which he was exposed in that period played a necessary role in his subsequent contraction of the disease and those fibres either were or included Amaca’s fibres as opposed to being solely attributable to other sources.

The third matter in order to sustain a verdict against both defendants was that as of 1962 Mr Booth was a person potentially but not actually injured in the sense that the changes in his body up until then had put him on the path to the disease, but there needed to be a further contribution from Mr Watson’s client post‑1962 for the disease to manifest in 2008.  If that were not true, then Amaba could not have been held liable.

Your Honours, the next matter that we put, which is proposition seven, just before I come to the two critical experts, which is at the heart of this case, is that no proof or opinion was offered as to when the plaintiff contracted the disease.

FRENCH CJ:   What do you mean by “contracted the disease”, because there is pretty much a process with a whole lot of things happening, some of which go in one direction, others go in the other direction.

MR GLEESON:   Yes, “contracted” is a shorthand for that process has reached the point where irreversibly he will suffer the disease as and when he did.  One of the features of this case is that no expert, and there was no other evidence to this effect, identified that question, and might I add to that a related absence.  There was no evidence as to the length or time of the period in which the process actually occurred within Mr Booth, that is, the harmful process which, from beginning to end, made his disease irreversible.

FRENCH CJ:   Is it right to say that a lot of that process is, short of biopsy, undetectable until you start getting breathlessness?

MR GLEESON:   Yes, and what none of the experts did was to say, even on a matter of probability or usual case or average, that process will take X years from beginning to end or when it is likely to have occurred in Mr Booth, save for one matter which is in relation to the latency period.  The evidence was that, in general, the latency period is between 10 and 75 years.  Your Honours will see that latency period on page 687, lines 30 to 40.

HAYNE J:   Leaving aside what you have said most recently about the latency period, does the series of submissions you have just made about what the plaintiff’s case must have been proceed from assumptions about an understanding of the process which culminates in a patient presenting with mesothelioma?

MR GLEESON:   It certainly proceeds from an assumption that each of the exposures he faced were capable, individually or in combination, of playing a role in a process leading to mesothelioma.  It assumes that much and I have made that explicit.  As to whether it makes assumptions about what is involved in the process, I do not believe it does.  It simply says that as at 1953, it must be the case for them to succeed that you were not then injured.  Your Honour might say, what do I mean by injured?  I mean enough changes have occurred in your body where it is irreversible that you will manifest this disease as and when you do.

HAYNE J:   Do you accept that the relevant legal question is whether the defendant’s negligence was a cause of the plaintiff’s injury?

MR GLEESON:   Yes. 

HAYNE J:   You seek, do you not, to impose upon that question a series of further questions or propositions of the kind you have described, namely, that the plaintiff must demonstrate, for example, that he would irreversibly suffer the disease at a particular point, and the question is, is this imposition of the further framework which you seek to erect either permissible or helpful?

MR GLEESON:   Well, your Honours, there is a difference between what we offer in proposition six and seven.  Six, we would submit, is necessary and therefore is also helpful.  Six involves some propositions of law underpinning it which we would submit are uncontroversial.  The first is you cannot be causally liable in negligence if a person has already suffered irrevocably the relevant injury before your conduct affects them.  That underpins proposition six a. 

Proposition six b is that there must have been something happening in the period where Amaca asbestos came in contact with Mr Booth which, whether on its own or with other causes, was a necessary step in the ultimate disease.  Proposition six c I have sought to explain, that Amaca can only be liable if at the end of 1962 Mr Booth was not a person irreversibly going to suffer the injury. 

As to what is in Proposition seven, your Honour, it is in a little different category.  It may not be necessarily in all cases fatal to Mr Booth if there is no opinion or proof of the matters I have referred to, that is, when it was irrevocably suffered and over what period of time, but if there is such a gap, it may prove to be highly critical, as it did in this case.

HAYNE J:   The basic proposition I think I am putting to you, Mr Gleeson, might be expressed as follows, that the imposition of the timeframe or time constraints which you seek to introduce through these propositions assumes, perhaps justifiably, perhaps not, that it is both relevant and helpful but at least relevant to speak in terms of irrevocable contraction of the disease.  Now, that itself is a proposition, namely, irrevocable contracting of the disease is a proposition that seems to proceed from an understanding of the medical development of the disease which I thought you began by telling us was relevantly unknown.

MR GLEESON:   Yes.  Most of it is unknown.  I believe the best way I can attempt to proceed further with your Honour’s questions is, I have set up the framework and your Honour is posed to challenge as to whether that part of it is useful.  I now need to come squarely ‑ ‑ ‑

HAYNE J:   Relevant and.

MR GLEESON:   Relevant and.

HAYNE J:   The real sting is in the “relevant”, is it not, Mr Gleeson, yes?

MR GLEESON:   I always try to be useful, your Honour, even if not relevant.  I would like to come now squarely to the way in which the plaintiff did seek to prove causation, whether it be expressed in the one line proposition or whether it needed to face the hurdles we have erected, and that brings us centrally to two key witnesses, Professor Henderson and Dr Leigh, which I wish to deal with in that order.  We are now coming to the central issue of whether their evidence spoke of anything more than an increase in risk.  If it did not, then we would submit Mr Booth’s case ought to have failed. 

Your Honours, with Professor Henderson, the order in which I would like to deal with that is this; firstly to look at his report, then his oral evidence in‑chief, in cross‑examination and then some evidence he gave in other proceedings which was tendered in this case.  His first and main report commences at page 681 – I am sorry, the report itself commences a little earlier at page 661.  I pass over his simple medical report at 644.  At page 653 he was asked three questions:

Can chrysotile asbestos cause mesothelioma?

He ultimately answered that question, “Yes.”  Secondly:

Is there a recognised safe level of exposure to chrysotile –

He ultimately answered that question, “No.”  We do not raise issue with those ultimate questions and answers.  The reasoning has an issue I will come to.  The critical one is the third question:

Was Mr Booth’s exposure to asbestos from brake linings . . . [as assumed] sufficient to make a ‘material’ contribution to the development of his mesothelioma?

He said, “Yes”, and that is where the question arises.  On page 666, lines 30 to 50, and then at the top of 667, he says – one should read Appendix A and Appendix B to find his generic discussion on the scientific basis for causation of plural malignant mesothelioma by asbestos.  He goes on to say:

In particular, I emphasis that the risks and causal contributions from absolute exposure towards the development of malignant mesothelioma are dependent upon [three matters] –

This issue between “risk”, what he means by that, and “causal contributions”, what he means by that is the matter I will seek to address.  All that is discussed at length in appendix A.  We see at the top of page 667 indistinctly that the purpose of appendix B is to narrow the question to asbestos containing brake materials.  If I could ask your Honours to go to appendix A on 681.  He starts by making five summary points which he argues for in the paper.  I have referred to the first.  The second is that there is, “No lower threshold level of exposure” that is unrelated to an increase in risk – we emphasise “risk”.  The third, he refers to:

the Peto model and its modifications –

and this is the centrepiece of his work –

the risk of mesothelioma can be related to cumulative asbestos exposure –

which is referable to the –

intensity, frequency and duration of exposure) multiplied by time in years raised to the cubic or 4^th power) –

That leads to a formula your Honours see at the foot of the page which is not that forbidding.  “I” which he defines as risk/incidence of mesothelioma equals “ct^k”, and over the page, “I” is incidence”, “c” is the cumulative exposure which is a product of a number of matters, “t” is the time in years following exposure and “k” is a multiplication of time.

I want to make one general submission about what this model means and then try and make it good from this material.  The general submission is that this formula tells us no more than this.  It tells us the number of cases of mesothelioma one would expect to see within a population of persons who bear the characteristics of exposure and latency period reflected in the formula.  What it would tell you, for instance, is that for persons suffering particular intensities of exposure over particular periods with particular latency, one might see 10 cases of mesothelioma per million persons per year.  That is what it tells you.  It is a measure, and that is why he uses both risk and incidence together.  It is a measure of observed cases within a population. 

That is the general proposition I want to try and make good and can I supplement it with this general proposition, that the whole basis of Professor Henderson’s work is either that, what I have just described, or that figure expressed as in a relationship to a control group being persons who have merely background exposure.  The whole of this report is designed to reflect that material.  If your Honours look at page 682 through to 685, he says at line 25:

No minimum threshold dose of inhaled asbestos has been delineated below which there is no increase in risk of mesothelioma, as indicated by the following –

He then goes through a whole series of studies.  All of them are reflecting the incidents of mesothelioma in a population of defined characteristics either absolutely or relative to a control group who face only background risk.  To take one example, if your Honours go to the bottom of 682, there is a report speaking of persons who have:

a decreased risk of an SIR [standardized incidence ratio] of less than 0.50 –

So farmers, for example, would show a 0.5 risk relative to persons in an urban area with ordinary background risk who would have a risk of 1 when framed in this fashion.  If your Honours look at page 683, in the second bullet point he talks about an analysis in terms of relative risks, again doing the sort of comparison I have mentioned.  The next bullet point talks about an odds ratio and so on, over the next page.  At the top of page 685 he pulls it together to some extent by saying that all of these analyses of:

relative risks (RRs), odds ratios (ORs) . . . represent cases in excess of any ‘background’ risk from ‘background’ exposures –

Now, your Honours know one of the issues in the case that we are agitating is whether Professor Henderson when he says “risk” and “causation” is saying anything about legal causation.  All he is really saying is, in a population of persons with defined characteristics this is the number you would expect to see suffer this disease.  On page 686 he describes the same point in the first couple of paragraphs and at 687 at the foot of the page, which I mentioned, he says the reason that some people only get it could depend upon a range of factors and it might be genes, and he speaks of genes over on page 688. 

Now, that is the entire analysis and that has led to the conclusion at page 689, foot of the page, which is the concept of cause being used by Professor Henderson that the courts below have said is adequate for legal cause.  What he says is from that discussion the:

attribution of mesothelioma to asbestos exposure requires fulfilment of two essential criteria –

The first is that the person has worked in an environment with elevated concentrations of fibres, he says especially amphibole fibres, that is not the present ones:

with a cumulative exposure in excess of any exposure derived from the general environment.

The next paragraph:

In other words, causal attribution of mesothelioma to antecedent asbestos exposure(s) requires evidence that the exposure(s) constituted cumulative exposures in excess of so‑called ‘background’ –

That is the first condition.  The second condition over the page is an appropriate latency interval.  In the case of this plaintiff and each plaintiff where this type of evidence is relied upon, that is, save for one matter I will come to, as good as it gets.  That is, that some work which has been done observing what occurs in given populations is used as the basis for saying, “We can attribute cause.”  For public policy or public health issues there is obviously good sense in the notion that is being applied.  Legally it does not meet the test for causation under the law for this reason, that what this theory does not do is provide a reason or rational basis for concluding which, if any, or in combination of the various cumulating exposures have in fact played a role in the disease process of the relevant person, or when they have done so.  Your Honours, if I could move to appendix B which deals with the specific brake position commencing at 695.

HAYNE J:   Before you part from the proposition just articulated, the theory at 689, you say, does not provide a basis for concluding which, if any, or in combination of cumulative exposures played a role in the disease process of the relevant person.  Is that more or less the proposition advanced?

MR GLEESON:   Yes.

HAYNE J:   Is that a proposition also that assumes that the disease process is known?

MR GLEESON:   I would have thought it is a proposition true, whether the process is known or unknown.  The only facts we know about Mr ‑ ‑ ‑

HAYNE J:   If the disease process is not known, I think the question may be radically different.  If the disease process is not known, is it more probable than not that X was a cause of Y?  It may yield a different form of analysis from the analysis that is required where you know what relates X to Y.

CRENNAN J:   So in other words, possibly the irrevocable suffering point is one where questions of relative risk and so on are perhaps less important than individual factors specifically known in relation to this person’s irrevocable suffering point being known.  I am just picking up your language of course.

MR GLEESON:   Yes.  The distance Professor Henderson has travelled is to say that in a population of persons who face a given exposure pattern, this is the number of cases I would expect to see who suffer the disease.  He then makes the point, correctly, that the risk which any individual within that population faces may be greater or lower than the result the population suffers.  That will depend upon factors which starts to take us into the unknown area as to exactly why it is that of the very many people who suffer the same exposure most do not contract the disease and some do.  They are the sorts of matters that he had identified at the foot of page 687 as matters upon which there is no resolution. 

So he makes the point correctly that if we are moving from population in general to the risk faced by an individual in advance, it would be influenced by individual specific factors about which we do not know enough.  But the path that we are challenging is that instead of facing that bedrock of uncertainty candidly and squarely, he is using the language of cause to say I will jump to the opposite extreme and say if you are one of the very small minority where the disease has come home, I will attribute a causal relationship between each and every exposure you faced and the disease and I will do so without knowing what it was that actually happened within your person which caused any one or more of those risks to come home. 

Now, your Honour Justice Hayne asked me about is there a radical difference if nothing is known about the process to a case where there is something known about the process.  This case, and it is the qualification I referred to earlier, falls somewhere in the middle.  It is closer to the end of the unknown than the known, but the one element that I have not yet taken the Court to which is said to provide some insight into the process is a biological statement that where fibres are taken in to the person, we know at least this much; that some fibres will be expelled, some fibres are less likely to travel to the lung, and that includes our type of fibre, some fibres are less likely to travel to the pleura, and that includes this type of fibre, fibres need to travel to the pleura before they can be involved in the “process”. 

What is happening at that point becomes more difficult to know, but the possibilities seem to include; that some fibres can be involved in what is called initiation, actually the process of doing something nasty to a cell which starts to change its character, some can be involved in a process of proliferation after a cell has started to change its character, sometimes cells can restore themselves from the dead, sometimes there can be more attack upon cells and the process can occur in what is described as a multigenerational phase. 

FRENCH CJ:   Yes, but there is a possibility of repeated initiations, that is not a single cell event.

MR GLEESON:   There is the possibility of that as well.  That is the one piece of evidence that I will come to almost shortly, and that is what is known in the Australian medicine and courts about the process.  That being known, we are not quite in a case where it is a complete ignorance situation, but that being known, what these experts are saying is without pinpointing the period in which that process took place in a given individual, without pinpointing when the damage became so great that one could not turn back, we will assign a causal relationship between every exposure over a period of 70 years and the end result in the unlucky person who contracts the disease, whereas of course, by definition in the person who does not contract it, no cause has occurred.  It is that leap, we submit that is a leap, which each of the experts make and that is the centrepiece of our appeal.

FRENCH CJ:   Do you accept that the epidemiological evidence, perhaps considered by itself and perhaps also in conjunction with the causative model which you have just outlines, leaves open the possibility or the inference that cumulative exposure increases the risk of contracting the disease in the sense of moving to an irreversible point?

MR GLEESON:   Yes, and the amount by which it does that is then a question which can be investigated.

FRENCH CJ:   So one might, for example, have on that basis an exposure which imposes a burden within a timeframe which taken by itself would not lead to the, as it were, irreversible onset, the other mechanisms which we can – you have outlined some of them and perhaps there may be speculation about others, might prevent that happening in a particular individual, but a first burden added to by a second burden together impose a sufficient burden on the system to lead to, in this particular individual, the contraction of the disease?

MR GLEESON:   We accept that is capable of occurring.

FRENCH CJ:   In other words, the necessary causal connection between one particular product manufacturer and the disease does not have to be established by reference to some sort of irreversible state reached at the point at which the person ceases to be exposed to that manufacturer’s product.

MR GLEESON:   In principle we must accept that and we have sought to frame it that, in the case of Amaca, there needs to be a basis to conclude that exposures to its product between 1953 and 1962, whether individually or cumulatively, have had a role in the process which is only dimly known which has led to a manifestation in 2008.  Your Honours, where I wish to go to is to ‑ ‑ ‑

CRENNAN J:   That is a role in relation to the interaction between fibres and the cells?

MR GLEESON:   Yes.  Where I wish to go to is to complete Professor Henderson as a whole, as I have embarked on that task, and then I have to come to the references to the biology which I have sought to briefly summarise, and then I will try and draw it together.  His appendix B at page 695 considers the particular position with brake linings, and at 696, at about line 25, he was considering the publications epidemiological which purported to show zero increase in risk for automotive mechanics over the background risk.  That is what he was dealing with.  At 697, at the foot of the page, he gives a further explanation of relative risk versus individual risk.  I might just ask your Honours to read that, but my submission is that it bears out that he is using incidence and risk in the manner I have outlined.  He says at the foot of the page the reason that risk is not merely theoretical is that:

it represents the ratio of the incidence rates derived from the actual number of observed cases relative to the control/reference group.

He would prefer “rate ratio” as a term.  It is an average across a group.  It will not correspond with the individual risk.  That will vary from person to person.  His ultimate conclusion on brakes as a risk area is at pages 705 to 707 and, really, he placed heavy reliance upon the register that I have taken the Court to say, well, look, if there are 78 cases in there of brakes, even if 78 out of a much larger population of motor mechanics, that suggests, looked at as a whole, an increased risk over mere background.  So his conclusions are then on 707, lines 20 to 30.  It is an appropriately cautious but ultimately affirmative conclusion that while the epidemiological data is inconclusive on brake lining specifically, there is enough data on chrysotile generally in terms of capacity to draw a conclusion that exposure to brake linings probably has a capacity to influence the development of mesothelioma.  Finally in that report, your Honours, perhaps at page ‑ ‑ ‑

GUMMOW J:   How would that proposition at line 30 differentiate your client from Mr Watson’s client?

MR GLEESON:   It does not.  They are in the same field.  They are both with chrysotile.

GUMMOW J:   Well, does he ever come to that sort of situation?

MR GLEESON:   No, never has he descended beyond capacity in general.  You released some fibre with chrysotile which studies have shown – not on brakes specifically, but on chrysotile generally – might see a higher incidence in a population to what happened with Mr Booth.  Your Honours, at 708, finally on this report, there is a section between 30 and 40 which we would submit shows that any reference by Professor Henderson to causation is not in a sense the law would adopt.  Causation for a mesothelioma is a sum of risks for firstly what he calls “true spontaneous”.  That is the category the experts accept that there appear to be some people who contract it without any asbestos exposure recalled or unrecalled, together with – it sounds a little bit like Donald Rumsfield – the known no exposures together with the known exposures where the mesothelioma is in excess of general environmental, and so on.  You add them all up.  Causation is a sum of risks.  There is no threshold.  Every exposure adds to risk that has gone before and is incremental upon the spontaneous risk. 

The effect of that is, on that theory, if you ask the question what caused Mr Booth’s mesothelioma, on Professor Henderson’s construct, it was caused by everything in proposition three of our document.  Everything caused it because everything contributed to a cumulative risk. 

HAYNE J:   There are three distinct questions which may need to be kept separate.  One, what caused Mr Booth’s mesothelioma?  That is one question which may be medically important to observe.  Second, does asbestos exposure cause mesothelioma?  That is a question that might invite attention to epidemiological studies.  The legally relevant question I would have thought is, was the negligence of this defendant a cause of this man’s injury?

MR GLEESON:   Yes, we accept that, your Honour, and the negligence here being failure to warn involves the proposition that on the assumption factually that given a warning he would have reduced his exposure to Amaca asbestos to nil or as good as nil, therefore, we would pare it down to, were the fibres released from Amaca products a cause of the disease which manifested itself in 2008?

HAYNE J:   The question, what caused Mr Booth’s mesothelioma admits of answers at several levels.

MR GLEESON:   Yes.

HAYNE J:   One, exposure to asbestos.  Two, exposure to asbestos released from brake linings.  The legally relevant question is, was it the defendant’s?

MR GLEESON:   Yes, and there is nothing in the model that I have taken the Court to so far or in the biology I am coming to which allows for any distinction between different sources of asbestos in attributing legal cause.  The cross‑examination is in volume 1, the examination and cross‑examination.  At page 154 at the top in‑chief ‑ ‑ ‑

HEYDON J:   Why do we have a lot of examination in‑chief when we have had a very detailed and scholarly report?

MR GLEESON:   Objection was taken to the entire attempt to expand the case in‑chief.  Questions were asked by Mr Semmler which were designed to expand upon the so‑called cumulative exposure theory for the reason that it had a massive flaw at the heart of it.  They were objected to and the trial judge said, “Sit down, Mr Watson.”

HEYDON J:   That is really additional to the report.  It is further evidence permitted by a form of leave.

MR GLEESON:   Yes.  Mr Watson stood back up again and objected and he was told to sit down twice.  He is trying to stand up now.  I will only to what in‑chief is material today.  At 154, the point between lines 10 to 15 was that an explanation was given for why the chrysotile is seen to be less potent and it is partly because of its shape and its size and the fact that it has a much better half life.

FRENCH CJ:   That is the crocidolite has the longer half life?

MR GLEESON:   I put that the wrong way around, your Honour, it has a shorter half life.  Page 157 is important because this is the key passage that the trial judge and the Court of Appeal said was conclusive of proof of causation.  The question was asked at 156, line 40, and one can understand why Mr Watson objected to it; even though experts can be asked leading questions, it is perhaps the most leading rolled up conclusory question in the history of the law.

HAYNE J:   That is a very large proposition that one.

MR GLEESON:   Well, if your Honour looks at the question, your Honour might even on this occasion agree with me.

All asbestos exposure within an acceptable latency period causes or materially contributes to mesothelioma.  Do you agree –

So, objection.  The question is allowed, and at page 157, line 30, the expert says, “I agree” and says something about his agreement.  Then in the next question and answer when he is asked to refer to what he is describing in his report, that is page 15 is page 666 of the appeal book, he says ‑ ‑ ‑

FRENCH CJ:   Sorry, he is understanding that question in the sense of if a person gets mesothelioma which is caused by asbestos, it has been contributed to by all asbestos exposures.

MR GLEESON:   Yes, and that is what he is seeking to assert, but even in his answer at about line 35 he says:

So that is cumulative exposure increases, so does the risk of mesothelioma –

We must accept that, and here I point out, and we have seen this type of evidence before –

risk is not a theoretical construct, but rather it is rate of the number of cases of mesothelioma one will see in the exposed populations.

So we have seen there within just those two questions and answers that the cause he is speaking of is not the legally relevant question whether the negligence of a particular defendant cause was a cause of the mesothelioma of a particular plaintiff.  Now, the Court of Appeal – I will just give the reference – at page 1226 to 1227 proceeded on the basis that if an expert says that ‑ ‑ ‑

GUMMOW J:   Page 1226?

MR GLEESON:   Page 1226 to 1227.  This particular answer is at the top of 1227.  The answer at lines 30 to 35 is quoted.  The court does not quote the qualification at lines 35 to 40.  Justice Basten says, well, if that evidence is in, there is a basis for finding legal causation and an appeal court on an appeal under a question of law has nothing more to do.  That is why this case is so significant to the entire process of these matters in the Dust Diseases Tribunal.  So that is that part of his evidence.

Then, your Honours, at the bottom of 158 to 159 he is asked about the childhood exposures, and this is his only attempt to discriminate between exposures.  He says there, at the lower end of low dose, the truck was at the lower end of low dose and the brake linings over 25 years, so that is rolled up both defendants, would fall into the low dose range and, in his theory, all of those are to be treated as causes.  Your Honours, at the foot of page 160 he is asked by reference to his report:

What is the basis of your assertion . . . [about the Peto] model, or otherwise, that when there are multiple asbestos exposures each contributes to cumulative exposure and to risk and causation –

Mr Watson objects that this should have been in the report.  It is allowed.  The answer is at the top of 162, and that is the answer the Court of Appeal has relied upon at page 1226 and this is the answer that it is thought that various things are going on together.  At about line 20 he says:

the more fibres there are the greater number of fibres there will be interacting with mesothelial cells which themselves undergo proliferation . . . so that the ultimate development of mesothelioma and its probability of development –

he is back to probabilities –

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 –

and this is all well accepted.  That is one version of what I call the biological evidence about the process, and that is as far as it goes.  Nothing there allows one to say that the particular fibres of Amaca between 1953 and 1962 have in fact played a role in any such process which may or may not have been occurring during those years.  That is the evidence which the Court of Appeal says once that is in, that is available to prove causation without more.  In the cross‑examination of Professor Henderson at page 179 at the bottom there is an explanation of how fibres ‑ ‑ ‑

GUMMOW J:   I thought what the witness was doing at 162 was displacing what he calls the “one fibre” hypothesis, was he not?

MR GLEESON:   Yes, your Honour is correct.  What he was not doing relevantly to our case was providing a basis in science or knowledge or thinking for saying that in Mr Booth’s case some of the or all of the Amaca fibres in the period I have mentioned in fact played a role of this character.

HEYDON J:   When he says “probability”, what does he mean?  Does he mean more than a 50 per cent chance, or does he mean some ‑ ‑ ‑

MR GLEESON:   No, he simply means in the sense of, what number of cases will I see in a population facing this type of exposure and if I add extra elements of exposure, one might think of three populations.  Population one is the control group, background risk.  Population two, are persons with background risk plus a certain amount of home renovations.  Population three, background plus home renovations plus a certain amount of brakes.  He is saying, as I move from population one to two to three, I would expect to see more cases.  That is all he is saying, in our submission.  He is here giving a reason why you might see more cases, that you can have these sort of interactions between fibres and cells.  To take your Honour Justice Gummow’s question, part of his point is that if the single fibre theory was an explanation for the majority of cases, it may still be true for some cases, but if it explained the majority of cases, you may not expect to see these different results between populations.  In that sense, one can see the point he is making.

FRENCH CJ:   But does it translate to the proposition that the probability that any person will develop the disease is a function of cumulative exposure, inter alia, other variables being the time and so forth, over which that exposure occurs or those exposures occur?

MR GLEESON:   Yes.

GUMMOW J:   What the Court of Appeal then seems to be doing at paragraph 52 on 1227 is to hook this up with notions of material contribution from the case law.  What do you say is wrong with that?

MR GLEESON:   What is missing is a basis in medicine or science for being able to conclude more probably than not that at least some of the fibres released by each and every exposure have in fact played a role, a material contribution, in a process within a given plaintiff which has led to a result.  That is the missing element.  These are the aspects of the cross‑examination I wish to refer to.  At 179 at line 40 he indicates the matters that are known and not known about the process of transmission of the fibres within the body.  At 180, line 27, the proposition about increase in risk is put to him and his answer is risk – we have seen this, it is not a theoretical construct, it is based on the:

numbers of cases which result from that type of inhalation.  And . . . risk is a bad term but everyone uses it. 

My answer to Justice Heydon about what probability meant is reflected here.  As one reads on in the paragraph, he is asked about some evidence he gave in another matter where he used a term “stochastic” and he said, well, that is “the same as probabilistic” and it all just refers back to how many cases you will find in a given population.

FRENCH CJ:   He is using risk as a synonym for probability of bad outcome?

MR GLEESON:   Yes, as observed, in a given population either absolutely or relatively to a control population.  That is all it is.  His unease with risk is his point that if you were trying to ascertain the true risk ex ante for an individual, it will vary up or down from the population risk by reference to your individual factors which we do not known enough about.  The point at 182 to 183, the point of that cross‑examination was that he accepted that each of the earlier exposures, the childhood renovations, the truck, et cetera, were capable on their own of causing the mesothelioma in Mr Booth, but because of the way his model works, one sees at, for example, 183 at the top, he says that although this was one of the cumulatively lowest doses he has encountered, the childhood exposure contained:

amphibole asbestos so I would’ve said that it made a small but I would think significant causal contribution, incremental upon any background risk –

So the way he uses cause, Mr Booth’s mesothelioma was caused by everyone’s. 

FRENCH CJ:   Your complaint is there is no differential aetiology?

MR GLEESON:   Yes.

FRENCH CJ:   It would not matter whether Mr Booth had, instead of having done brake linings, for example, had worked in a factory for your client alone for 30 years and been exposed to high concentrations of asbestos dust throughout that time?  That would not exclude the possibility that his disease was initiated and put on the irreversible path by his background exposure of helping his father with home renovations?

MR GLEESON:   Yes, and the model, the construct can accommodate, investigate or allow findings on the various possibilities and the result of the construct is that if it is correct, the law says in every case brought, for instance, in New South Wales in Dust Diseases Tribunal, provided you prove that an exposure increased risk above background, you need prove nothing more, you find that defendant liable, provided it is within a 75 year latency period – how it deals with issues of contribution between tortfeasors is a further problem, but you simply do not ask anything more, you do not discriminate.

HAYNE J:   In the case of where there is but a single party that has exposed the plaintiff to a high dose, it would be possible in at least some cases, would it not, to move from the observations about the populations to the conclusion that it is more probable than not that the exposure by the one defendant was a cause?

MR GLEESON:   Your Honour’s question includes “in some cases”, and one technique by which that has been done is this.  If one treats your population base risk as, say, one based on general background exposure, if the dose is such as to increase that risk to a dramatically higher figure, say, two or more, there has been one form of reasoning approved in various tribunals, that allows an inference to be drawn more probably than not that the increment or the addition over what would be a non‑tortious risk was so substantial that, for example, one would be on the path to causation.  So, your Honour, I do not rule out the possibility of that and in some of the cases – and in England there is a great deal of discussion that if you have doubled the true risk, whether that allows a finding on the balance of probabilities that you must have made a material contribution, although of course in England it is now over overlain by a different legal test.

FRENCH CJ:   So within the framework of the expert evidence we have in this case, your submissions accommodate the possibility of liability for a single high dose exposure?

MR GLEESON:   It would be possible, but it would require an investigation of those matters.  One of the points Mr Watson is going to deal with, I foreshadow, tomorrow is that to the extent that this trial judge actually made findings on the extent to which the risk was increased, the finding he in fact made in relation to my client was that the risk was increased by not a factor of two, but by 10 per cent.  So that, put simply, what the judge actually found was if the background risk is 70 cases per million persons over a lifetime, which is a low estimate, he measured that the Amaca increase in risk might be an extra seven cases per million over a lifetime measured across a whole population and he treated the home renovations risk as somewhere between 0.5 and 4.

So that if that were to be the alternative approach which could be possible, we would submit that the present case would not allow it.  The references for what I have just put to the Court are found in volume 3 at page 1144 in paragraph 166 near the end.  He concluded that the Amaca increase in risk was “10 per cent of the additional fibre burden beyond background”.  Amaba he said was an additional 20 per cent.  There is a problem with the mathematics, which Mr Watson will point out, but even on the face of it, that is the type of material, and he got to that because of what is found on pages 1136 to 1137. 

At 1136 at paragraph 136 he noted that Professor Berry assumed the background was 70 per million in a lifetime.  That is the bottom end of Professor Berry.  The top end is in paragraph 139.  What he has found is that there was an increase of 10 per cent or seven cases per million per lifetime measure on a population basis.  The figure for the home renovations your Honours see in the table in 133.  Depending what was in it, the increase was between 0.6 and 4.  The other matters I wanted to take the Court to in the cross‑examination of Professor Henderson are at page 184 of volume 1.  At about line 15 his Honour was trouble and asked this question:

I take it doctor when you say it caused an increase in risk, that was an increase of risk at the time.

His Honour thought it was risk ex ante.  Professor Henderson said:

No, an increase in risk subsequently, your Honour.  There is no increase in risk at the time the fibre is inhaled but –

it is when certain things occur.  Risk is a bad term –

because you can say, okay from this he is at risk but the risk is not – does not eventuate until the mesothelioma develops.  And risk is always based on the numbers of cases in the exposed versus unexposed populations.

That is what risk and cause means.  Then the next answer:

In the case of Mr Booth, are you able to say whether or not that particular risk of the last exposure came home.

That is presumably being asked about the Amaba exposure.  Answer, “No.”  He cannot speak specifically.

I’d say particularly the risk from all of his exposures came home because –

That is what the model tells me ‑

the model which I adopt is that of a cumulative exposure dose response, so I think that all of the asbestos fibres that he’s inhaled, or at least a proportion of them –

we have drawn attention to that ‑

will contribute to the risk and to the ultimate development –

The next question is probably the high point of the cross‑examination:

you are also saying is this, that individually you cannot say whether any of these risks . . . came home, you can only say it was an increment to the risk.   A---That’s right.

That is the best that the evidence got for the defendants.  Your Honours, there was one other matter of Professor Henderson I wished to show which was that in volume 2 at page 570 some evidence he had given in another case was tendered as admissible evidence here and if I could go in particular to 580, there is a passage about lottery tickets which we submit shows the problem with this theory as a matter of a legal causation.  It is between lines 25 to 35 and he is being asked some questions about risk and increase in risk and in relation to this particular plaintiff he says:

in my opinion a significant increase in risk but a small risk, and it would be a small risk incremental . . . and if one goes back to the analogy with lottery tickets, if one says that for example his background exposure has given him, say, three lottery tickets out of 100,000 ‑

or 30 out of a million –

towards winning the prize, then his home handyman exposure may have given him an additional two or three tickets, but the point is that the prize is not for any one ticket –

and this is where the analogy breaks down –

The prize of mesothelioma is for all the tickets. 

That illustrates what is going on with this model and we submit it does not match the legal test ‑ ‑ ‑

FRENCH CJ:   Is that saying anything more than that the probability of winning increases the more tickets you have and thus the probability of getting the disease increases the more exposures you have.

MR GLEESON:   That much we can agree with.  What he seems to be saying by saying that you get the prize for all the tickets, he is trying to there make the leap and say if you have got the disease, instead of attributing it to what is in fact the winning ticket, because we do not know what the winning ticket is, we will just assume all tickets are winners.

Your Honours, could I then come to the second main witness, the only other one I will deal with, which is Dr Leigh.  His evidence from his other proceedings is also quite illuminating.  It commences at page 525 and at 535 he gives, from line 30 onwards, evidence of the biology, and if I may respectfully say in Mr Booth’s case, this is probably as detailed as the biological explanation gets.  This is the most that can be known about the process.  It runs from 535 over to 537.  Could I draw attention to this on 536?  He is asked at line 20, why is it that all cumulative exposure are considered to play some part.  Why would that follow?  Answer:

That’s because the later exposures may be involved in promotion rather than initiation.  They may also be involved in and get more initiation [going] . . . You have got a dose of carcinogen, a number of fibres if you like, acting on a number of cells in a probabilistic way.

We come back to that probabilistic term, which I have sought to explain –

Not every fibre acts on every cell and at different points in time some cells are suffering genetic damage, some cells that have already suffered genetic damage are being promoted into clones of abnormal cells and becoming tumours.

Then he refers to repair processes and the like.  At line 20 on 537 he comes back to this stochastic or probabilistic concept in that:

the probabilities of fibre cell interaction depend on the number of fibres and the number of cells, so simplistically the more fibres –

and he speaks of free radicals and they are explained.  Coming down to line 40:

Well, simplistically, the more fibres – I have used the analogy in court cases . . . it’s like sperm and ova.  I mean, only one sperm actually fertilises the ova but there’s millions sent out to do the deed, so the more there are the more chance of one being hit.

Then he is asked about the number of fibres acting on cells:

is one fibre sufficient or is it possible that one fibre could initiate the changes in the cells?---Ultimately one fibre does initiate the change in the cell, but it’s because it’s been given a big chance by being one of a huge force –

So although these experts are rejecting the single fibre theory, they are considering that in terms of initiation it is likely that it is one of the army which has had the effect, and he says that at page 538:

It’s a bit like the army, if you have a lot of soldiers you’ve got more chance of hitting somebody.

So coming back to your Honour the Chief Justice’s question, it really is simply about more fibres, everything else being equal, more chance of the ultimate contraction of the disease.  If your Honours could go to page 547, between lines 30 to 35, he puts the background risk at 10 to 30 per cent, and at 549 in cross‑examination the question at line 45 is this:

You see, medical science doesn’t permit us now to say that in the case of [the particular plaintiff] he would not have got mesothelioma except for the specific period of home handyman exposure [in issue] he has described.  Do you agree?‑‑‑What I say is that the specific periods of home handyman exposure added to his overall risk.  I’m not necessarily saying that that tipped him over the line but it certainly added to his risk. 

So we are simply back to risk.  Then at page 550, at line 20, Mr Watson puts to him that it is just a matter of risk and increase of risk, and the answer is:

Well, it’s a matter of the fact that he’s got it and he had this exposure, so that you have to assume, you know, from the end point that all the exposure must have had something to do with it, whatever the risk‑creating potential was.  You have to assume that some of those fibres had something to do with it.

Now, that is really back to the bedrock of uncertainty.  You are making an assumption that some fibres, who knows which, had something to do with it.

HEYDON J:   There was a possibility that the disease could be obtained without any exposure at all.

MR GLEESON:   And there is a possibility it could be obtained without any exposure at all.  He acknowledges that at page 546, line 30.  Just to conclude this, at 551 he is asked a question at the top and he refers to the Peto model, so he is basing himself on that as well, and the trial judge again needed clarification of an answer and asked this question, line 25:

Doctor, what does it mean in a context to say they were causally more potent and statistically more potent?‑‑‑It is statistically because you can’t actually say, you know – there is no direct way of knowing which fibre did what to which cell at which time.  That’s what I mean by stochastic or statistical.  . . . it’s just statistical.  It is probability, I think, it’s probability.

And finally at page 557 at line 30, he was pressed:

Why must it have had something to do with it?

That is the exposure being sued upon.  Answer:

Well, you can’t say that it didn’t because they were additional fibres.  As I said, the whole process is probabilistic.  There must have been some probability that those additional fibres had something to do with it.  You can’t exclude that possibility.

And then the next question:

If a single fibre may initiate the . . . [process] is it necessary that there be further fibres to promote the process?‑‑‑That’s a good question.  I would say yes.  Certainly there needs to be some more – some agents . . . Whether they are further fibres or something else I don’t know but I would say yes.

And if one or more fibres have initiated the process commencing with the cell change will the inhalation of further fibres necessarily play some part in the promotion . . . ?‑‑‑You can’t exclude the possibility that they do.

Now, that is where it ends up.  So the position we have reached is that even the witness who gave the most detailed evidence available on any possibility of biology is ultimately in a position of saying it is most probably a single fibre that has done the initiation.  The more soldiers in the army more chance in the battle.  Once the first soldier has breached the wall, others may have a role in what continues, you cannot exclude it, there we are.

Your Honours, in relation to Leigh, his other evidence is found in two places.  If I could just give the reference.  His main report is found in volume 2 at pages 751 to 766.  The high point, which by now is very familiar, is on page 754 at the bottom.  At 757 at about line 17 he is talking about the studies and he talks about odds ratio again, the same concept as Henderson was using.  Perhaps at line 35 we see the essence of his reasoning which we criticise, that the:

inability to demonstrate epidemiologically a statistically significant increase in risk . . . does not negate in any way a causal inference in an individual case where the only asbestos exposure, above general background environment, was incurred in that occupation.

Why he concludes that it is the incremental exposure rather than the background which had the effect is not borne out.  Biology he talks about on 758 to 759 and the probabilistic approach is found on 759.  In terms of his oral evidence, if I can conclude Leigh on that point, it is in volume 1.  Evidence in‑chief followed a familiar pattern of him being asked to supplement his report, page 210.  You will see at the top of 211 this same concept of all these things are going on:

at different points in time, at different rates, so you have to assume that the fibres are doing something –

At 213 to 214 – this is still in‑chief – he is asked at the bottom about asbestos as a complete carcinogen and he describes it as an initiator and promoter:

Q.By the process of that which you said in your earlier longer answer.   A‑‑‑Yes.

Then over the page he is led to two answers:

Q.And does that apply to all fibres.

Well, that is – I am embarrassed myself, the second worst question –

A‑‑‑Yes.

Q.Can you exclude any.   A‑‑‑No.

So we are back to this concept, the reason I say everything is involved is simply because I am unable to exclude individual ones.  Just beneath that he is asked:

Q.Now the explanation that you gave . . . [is in a book is it not?]  Dodson & Hammar.   A---Yes.

. . . 

Q.And is your understanding of the mechanism consistent with what’s set out in that chapter.   A---Yes.

Dodson & Hammer, I believe I am correct, is probably the only medical or scientific article bearing on the point which is in the trial and in the appeal books.  Your Honours will find it in volume 2 at page 469.  It discuses in detail the way the processes might work.  The summary may be enough on page 489 and while it is consistent with the possibility of multiple fibres having roles to play over a process which takes some time, it does not support the notion that fibres from every exposure over the entire latency period, more probably than not, play a role in the contraction of the disease in a particular person.  So that is the one report he referenced. 

In his cross‑examination he was asked, at page 260 at about line 30 about what he says about the various exposures, and his position is that every exposure, the garage, background, home renovations, bags, everything makes a material contribution, that has the absence of reasoning in it that I have identified earlier.

FRENCH CJ:   Does the lesser potency, as they call it, of the chrysotile translate into a higher cumulative exposure for the same risk as, say, a lesser load of crocidolite would incur?  Does that emerge from the evidence?

MR GLEESON:   That follows from the evidence for the same load.  If it be crocidolite, the cumulative exposure and risk therefore will be greater.  One of the reasons why, when I showed your Honours that the trial judge had calculated the Amaca increase in risk as only 10 per cent, your Honours might have thought that seems a little low for a lot of years doing brakes, that is a function of the weightings that were applied to a less potent cause.  So he has used the language of material contribution and then he has pressed on that at the bottom of 261 – there is a great deal of objection but finally he gives this answer at the foot of the page:

any one of these exposures singly or in subgroups plus the background would have made a material contribution to causation.  You don’t need any single one, if you have one you don’t need the other three.

A bit further down the page, about line 28, he says does not dismiss any exposure as making a contribution:

Q.       So a person walking at a distance of 50 metres from a building site where asbestos cement sheets are being cut up [and you inhale the fibre]  . . . you would not dismiss that.   A---No.

Why?

Because that single fibre would have increased the risk.

So every fibre causes mesothelioma if it increases risk.  That is evidence, for instance, that a single fibre can, he says, have the effect.  The final reference I wish to go to is this.  At page 338 at line 40 a bold question was put that you could not find any literature which supported the proposition:

All cumulative exposure to asbestos in an individual case must be considered to play some part in causation.

No one has ever said that.  His answer initially was there was a monograph.  He then withdrew that answer at 339, at the top, and he was given an invitation at 35 to find any such literature and that was never taken up.  Your Honours, that has taken me through to proposition eleven.  I propose to invite Mr Watson to deal with twelve and thirteen as part of his address.  What that leaves me to do, apart from relying upon what is in fourteen and fifteen, is just to indicate the key parts of the Court of Appeal judgment where we say the error occurred.

GUMMOW J:   Well, how about starting with the trial judge?

MR GLEESON:   Yes, the trial judge, I will start there, your Honour.  Firstly, if your Honours go to 1108, the evidence of ‑ ‑ ‑

FRENCH CJ:   Incidentally, do you accept those statements of matters not in dispute at paragraph 22 of his judgment?

MR GLEESON:   Yes.  The essential complaint is that what his Honour has done is simply set out a part of the evidence of these experts, has not set out the balance of the material that I have taken to Court to which explains what these experts mean and has then given it a meaning that it equals material contribution.  So with Henderson, you see the material set out at 25 and at 26 and, in effect, his Honour has said that is enough, plaintiff wins based on that evidence.  What his Honour has not dealt with is the fact that Professor Henderson is clearly speaking about the probability of cases being seen in an exposed population, that Professor Henderson has never provided a theory which would allow one to discriminate and attribute to the fibres coming from the tortfeasor an actual role in the contraction of the disease.

I will leave Musk and Heiner to Mr Watson.  Coming to Dr Leigh at 1111, paragraph 34 might be accepted that asbestos can be involved in the initiation phase and in subsequent phases.  Paragraph 35 contains the logical leap:

It is because of this capacity of asbestos fibres to be involved at several stages of tumour development that Dr Leigh considers that, in an individual case, all cumulative exposure to asbestos fibre must play some part in the causation. 

The leap is self‑evident.  Paragraph 36 does not provide a reason to treat risk as the same as cause.  Paragraph 37 records some of the concessions of Dr Leigh and we would have thought that 38 which dismissed those concessions is a failure to deal with the legal issue posed by causation.  One then passes over to 1119 where in paragraph 59 one sees the summary conclusion which lacks the appropriate basis in the evidence. 

HEYDON J:   You attack paragraph 52 as well, I think.

MR GLEESON:   Yes.  Then if one goes to 1126, paragraph 93, the finding that has already been made that all “asbestos fibres act accumulative to cause mesothelioma” influences the entirety of this part of the judgment. I will leave that to Mr Watson.  Going then to page 1136, there are the calculations of the incremental risk and one passage I want to specifically deal with is page 1142, paragraph 162, which might appear to be an alternative or softer basis upon which to find causation.  His Honour describes this as an inference which is overwhelming.  Can I give our response to the four facts.  The first fact is “mesothelioma was caused by the inhalation of asbestos fibre.”  The answer to that is more probably than not that is true.

FRENCH CJ:   That was one of the points not in dispute in paragraph 22.

MR GLEESON:   Yes.  More probably than not that is true.  The second matter:

Mesothelioma very rarely occurs in persons who have not been exposed to asbestos fibres beyond the background level that pervades urban environments.

True.  Add, it also very rarely occurs, but slightly less rarely, in persons who are exposed to asbestos fibres beyond background.  I have been to that material.  Proposition three is troublesome.  It says, what I can do is take into account the combined burden of exposure from both defendants without discriminating between them which added to his burden.  The first problem with that is it has not taken into account a fact discriminating appropriately between not only the two defendants but the other brake exposure which is not sued upon in the case.  That is the first matter.

The second matter is, as you would read that, it infers that is some very substantial additional exposure.  I come back to the questions from the Chief Justice and Justice Hayne, the actual increment for Amaca is no more than “10 per cent”.  That is the figure on paragraph 166.  The third matter is that it has simply passed over the entire question of why is one to find more probably than not that within the period 1953 to 1962 changes occurred within his body attributable to Amaca asbestos or changes occurred after that date, again attributable to that asbestos which caused the disease.

Proposition four, the previous exposure was trivial in comparison – the previous exposure I have shown at paragraph 133 – for the home renovations, at least, could be an additional four cases per million per lifetime which would not be trivial, relative to the additional seven cases for Amaca.  So that our proposition is to the extent that is said to be an alternative or softer inferential approach to causation which does not have the problems of the experts, causation was not capable of being established.  In terms of the Court of Appeal ‑ ‑ ‑

GUMMOW J:   Well, just before you leave that, so that a net result at page 1162 is this judgment against both defendants in the one sum, is that right?

MR GLEESON:   Yes.

GUMMOW J:   Were they joint tortfeasors?  What is the basis for that?

MR GLEESON:   It is not spelt out whether they are joint or several because there is no analysis of whether their so‑called causal contributions in any way overlapped in time.

GUMMOW J:   Yes, at paragraph 172.

MR GLEESON:   Yes.  That is as far as it is taken.

HAYNE J:   Well, one reading of paragraph 162 would be that on the balance of probabilities, it is more probable than not that exposure to asbestos at work with brake linings rather than exposure to asbestos by way of background, by way of home renovation or by way of truck loading was a cause of the disease.

MR GLEESON:   I would attack that as being available, but if that were the finding ‑ ‑ ‑

HAYNE J:   That is an understanding of what is said there.

MR GLEESON:   Yes, that has still stopped us a step short of an inference as to a causal connection between the negligence of Amaca and the plaintiff’s injury.  Taking up your Honour’s question, if we are to read paragraph 162(3) as a combined finding about all brake exposures, as it literally appears, 166 tells us that his Honour has found a figure of 44 per cent of an excess accumulation of fibre burden from all brake exposures over background, but then when he breaks it down, that becomes 10 per cent Amaca, 20 per cent Amaba, and presumably 14 per cent other people.  It still has the problem that it has glossed over all timing issues as to when it is said that processes actually occurred within Mr Booth which were relevant to the disease.  It has not in any way addressed that, but it also has passed over the fact that it is said to be at most a 10 per cent incremental burden.

Your Honours, in the Court of Appeal the only parts I need to go to are these.  At 1219, paragraphs 23 to 25 is Justice Basten’s assessment of what is available on an appeal on a question of law.  We also refer to the decision of Kostas v HIA in this Court, which is not referred to here.  At 1226 to 1227 I made the submission in relation to paragraphs 50 to 52 that on an appeal on a question of law it is insufficient for the Court of Appeal to simply read those words and say if an expert says that, it is open to the trial judge to find causation and there is nothing further for us to consider.  At 1239 to 1241 the argument put at paragraph 85(b) was wrongly rejected by the court in 86 and it seems the court in 86 is harking back to what it said in 52.  Professor Henderson’s report is then set out again over at 1240.  Nothing in that report goes beyond increase in risk, and paragraph 89 has the same errors involved in it of accepting opinion which uses risk and cause interchangeably without analysis. 

GUMMOW J:   .....in a way might, as the Chief Justice points out, may start with a statement of claim itself, might it not?  Paragraph 6 on page 3 the two companies seem to be sued as joint tortfeasors from what I can work out.

MR GLEESON:   Yes, that is so, your Honour.

GUMMOW J:   Paragraph 6:

The cause of the Plaintiff’s pain, injury, loss and damage was the negligence of the First and Second Defendants.

MR GLEESON:   Yes, and then they are just rolled up together.

GUMMOW J:   Yes.  Was there ever any complaint about that?  You pleaded to it, did you not?

MR GLEESON:   Could I ask Mr Watson to deal with that tomorrow, your Honour, on that question.  He will know the answer to it. 

GUMMOW J:   Yes, all right.

MR GLEESON:   The last bit I wish to just mention in the Court of Appeal is the passage at 1251 that was discussed on the special leave application.  It is paragraphs 118 to 119 of the judgment.  The evidence of Henderson was set out at 118 which had the words in it “or at least a proportion”.  The court does not set out his following answers which I have been to this afternoon which show what he was really saying.  But 119 in the end seems to be why Justice Basten says you can reason from risk to cause and the analogy, it is always dangerous, is if I am in a room with asbestos and I inhale it, I am risk of various things happening and the risks could proceed through various paths and if the risk materialises, one can infer cause.  The obvious problem with this dangerous analogy is that a more appropriate analogy would be, at various periods of time I am in a number of rooms and sometimes I am in more than one room.  They are my bundle of cumulative risks.  If I win the lottery ‑ ‑ ‑

FRENCH CJ:   I think it is Schrödinger’s cat.  You are in superposed states.

MR GLEESON:   He told me to say that, your Honour, and I knew ‑ ‑ ‑

HAYNE J:   Only silk can be in two rooms at once, Mr Gleeson.

MR GLEESON:   If I said that you would ‑ ‑ ‑

FRENCH CJ:   That might be a good time to stop, Mr Gleeson.

MR GLEESON:   ‑ ‑ ‑interrogate me about my knowledge of it and I would be found faulty.  Your Honours, that is what we wish to put in‑chief.  Could I indicate from my personal perspective, I am required to be Melbourne tomorrow.  If the Court will forgive that, if there any matters of reply, Mr Owens would deal with them.

FRENCH CJ:   Yes, very well, Mr Gleeson.

MR GLEESON:   Thank you.

FRENCH CJ:   The Court will adjourn until 10.15 tomorrow morning.

AT 4.18 PM THE MATTER WAS ADJOURNED
UNTIL WEDNESDAY, 5 OCTOBER 2011