Amaca Pty Ltd v Ellis & Ors

[2009] HCATrans 296

[2009] HCATrans 296

IN THE HIGH COURT OF AUSTRALIA

Office of the Registry
  Perth  No P13 of 2009

B e t w e e n -

AMACA PTY LTD (ACN 000 035 512)

Appellant

and

TERESA ELLIS AS EXECUTOR OF THE ESTATE OF PAUL STEVEN COTTON (DEC)

First Respondent

THE STATE OF SOUTH AUSTRALIA

Second Respondent

MILLENNIUM INORGANIC CHEMICALS LTD (ACN 008 683 627)

Third Respondent

Office of the Registry
  Perth  No P14 of 2009

B e t w e e n -

THE STATE OF SOUTH AUSTRALIA

Appellant

and

TERESA ELLIS AS EXECUTOR OF THE ESTATE OF PAUL STEVEN COTTON (DEC)

First Respondent

AMACA PTY LTD (ACN 000 035 512)

Second Respondent

MILLENNIUM INORGANIC CHEMICALS LTD (ACN 008 683 627)

Third Respondent

Office of the Registry
  Perth  No P12 of 2009

B e t w e e n -

MILLENNIUM INORGANIC CHEMICALS LTD (ACN 008 683 627)

Appellant

and

TERESA ELLIS AS EXECUTOR OF THE ESTATE OF PAUL STEVEN COTTON (DEC)

First Respondent

THE STATE OF SOUTH AUSTRALIA

Second Respondent

AMACA PTY LTD (ACN 000 035 512)

Third Respondent

FRENCH CJ
GUMMOW J
HAYNE J
HEYDON J
CRENNAN J
KIEFEL J
BELL J

TRANSCRIPT OF PROCEEDINGS

AT CANBERRA ON WEDNESDAY, 4 NOVEMBER 2009, AT 10.16 AM

Copyright in the High Court of Australia

__________________

MR G.M. WATSON, SC:   May it please the Court, I appear with MR J.C. SHELLER for Amaca Pty Ltd in each of the three appeals.  (instructed by Minter Ellison Lawyers)

MR M.L. ABBOTT, QC:   May it please the Court, I appear with my learned friend, MR S.J. DOYLE, for the State of South Australia in each of the three appeals.  (instructed by State Solicitor for Western Australia)

MR D.F. JACKSON, QC:   May it please the Court, I appear with my learned friend, MR N.J. OWENS, for the appellant, Millennium, in the appeal which is P12 of 2009 and for the third respondent in each of the other two matters.  (instructed by Lavan Legal)

MR B.W. WALKER, QC:   May it please the Court, I appear with my learned friend, MR J.R.C. GORDON, for the first respondent in each of the appeals.  (instructed by Slater & Gordon)

FRENCH CJ:   Mr Walker, before we hear from Mr Watson, just to have a sense of the parameters within which this debate is to be conducted, we look to 63 and 90, I think, in your submissions in P12 and ask whether it is your case that the asbestos exposure – it is put on the basis that the asbestos exposure materially contributed to Mr Cotton’s disease and it is within that framework we are operating?

MR WALKER:  Yes.

FRENCH CJ:   Yes, all right.

GUMMOW J:   At paragraphs 63 and 90 of your written submissions, is that right?

MR WALKER:   Yes.  I hope 63 makes it clear that is an attempt to frame a question that we say is the relevant issue – was the relevant issue.  It follows that my answer to the Chief Justice’s question is emphatically, yes, that it has always been run.  It is certainly our position here that the courts below were correct to find that the conduct of the defendants in exposing my client’s husband to asbestos in breach of their duties of care materially contributed to his lung cancer.

GUMMOW J:   It just becomes – I say “just becomes” – but it becomes an evidentiary dispute, does it?

MR WALKER:   Evidentiary and the related issue of the inferences that ought to be drawn on the relevant standard of proof, yes.

FRENCH CJ:   We are not just talking about an enhancement of risk?

MR WALKER:   No.  In due course I will attempt to persuade your Honours that that is a red herring.

FRENCH CJ:   Thank you, Mr Walker.  Yes, Mr Watson.

MR WATSON:   Your Honours, in most, nearly all, tort cases there is direct evidence establishing the causal connection between the breach and the injury so that in the ordinary case you have the blow, the bony fracture, the x‑ray, et cetera.  The situation is different when medical science cannot explain the biological processes.  In the field of tort, that kind of situation is becoming more common and that is what this case is about.  Your Honours, may I explain briefly where I intend to go with my submissions.  There are three broad areas. 

The first, I propose to deal with the test for causation which was applied by the majority in the Court of Appeal.  As part of that, your Honours, I will show that the departure from the orthodox occurred based upon authorities used by their Honours inappropriately.  The second part of the submissions will deal with the effect of the failure to separate the two periods of exposure.  We have called those the South Australian exposure and the Millennium exposure.  The third part of the submissions will deal with the issue of the supervening or intervening cause, that is, the smoking and, more particularly, the continuing to smoke after the South Australian exposure ceased.

Your Honours, I will go to the first issue; that is the causation test.  Your Honours, as is a general rule, when medical science cannot provide direct evidence of a causal connection, some other evidence, circumstantial evidence, is necessary.  That other evidence must be, so the authorities say, sufficiently strong and coherent to support a definite inference of causation.  May I just give an example of that kind of evidence.  In some cases the timing and the sequence of the events is critical.  May I remind your Honours of the old case of Adelaide Stevedoring Company Ltd v Forst. 

The coronary thrombosis which was suffered by the worker in that case followed very soon after an episode of heavy physical exertion and, hence, the inference was able to be drawn linking a possibility with a particular body of evidence where, your Honours, in these proceedings timing and sequence cannot assist.  What is more, every investigation, whether it was clinical, whether it was radiological, pathological or the like, every investigation failed to identify any factor which might indicate a particular cause for Mr Cotton’s lung cancer. 

Your Honours, it is in those circumstances that in this case we submit that the plaintiff properly went to the epidemiological evidence and we submit further it was the only evidence available to the plaintiff.  May I say this generally about that in this case, that is, not to disparage the value of the epidemiological evidence.  This was an unusual case insofar as the evidence was given by two leading masters of the field, Professor de Klerk and Professor Berry.  Their evidence was of a particularly high standard and it provides a proper basis for the findings which we will ask your Honours to make in due course. 

The problem for the plaintiff was that the epidemiological evidence established that it was extremely unlikely that any asbestos, or at least any asbestos from which Amaca could be held liable, had any role at all in the development of Mr Cotton’s lung cancer.  The evidence – we have detailed this in our written submissions – established, we say, with respect, clearly that it was smoking and, for the purposes of the law, smoking alone which caused Mr Cotton’s lung cancer. 

Your Honours, there is another more legally accurate of way of putting that same proposition.  We submit that the plaintiff failed to discharge the burden of proof to demonstrate that Amaca’s asbestos caused the lung cancer.  Of course, the majority in the Court of Appeal arrived at a different conclusion and I now propose to move to demonstrate, if I can, that point of error.  As your Honours know, it lies at the heart of our submission that the majority was applying an unorthodox test for causation and it is one which we say led the majority to conclude that causation is established by proof of a mere increase of risk and, I will add, in this case by proof of a very small increase in risk.  Can I show your Honours two examples from appeal book 4. 

If your Honours go to page 1507 – it sounds intimidating when I read out that number – your Honours, on page 1507 there is paragraph 315.  I am going to come back to this paragraph in some detail, your Honours, but at the moment I just wish to show your Honours the final two sentences.  About halfway though the paragraph your Honours will see a sentence “Further, a period of exposure”.  If your Honours read that, we say that that plainly contemplates fixing liability on the basis of an increase in risk and even, although that increase in risk – and pausing there, that is, the exposure to asbestos – did not cause the injury, that is, the lung cancer.  I just draw your Honours’ attention to the final sentence and the reference to “low threshold”, but I promise will come back to that in a little more detail. 

Your Honours, on our submission, the legal principle which the majority tried to encapsulate in the third sentence in that paragraph would correctly be stated along these lines.  An exposure to asbestos can only be found to have made a material contribution where the injury would not have been suffered without the exposure.  As I say, I will come back to paragraph 315, but can I take your Honours to page 1513 for a moment.  The first sentence of paragraph 338 we say is another example.  I will not read it out to your Honours.  We say that that explicitly contemplates fixing liability even although the breach of duty did not cause the injury.

I want to explain to your Honours how this departure from the orthodox came about, if I may.  I will take your Honours back to paragraph 315 on page 1507.  Your Honours will see that that paragraph commences with a reference to their Honours’ earlier judgment in Hannell.  Your Honours, I do not contend that the next sentence is wrong in principle.  We would accept it as legally accurate, but we would ask your Honours to look at the authorities which are cited for the proposition.

The two cases, Krakouer and Franklin, are criminal cases.  They are criminal cases dealing in each instance with criminal liability for murder.  Your Honours, those decisions we say are authority for principles inapplicable here and the reference to them explains, at least in part, the test applied by the majority.

GUMMOW J:   What was the issue in Krakouer?

MR WATSON:   We will deal with it.  We did have copies of the unreported decision of the Western Australian Court of Appeal in Krakouer v The State of Western Australia [2006] WASCA 81 provided to your Honours. Krakouer was a murder case and it came about in really quite gruesome circumstances.  Krakouer and his victim got into a fight.  A third man got involved in the fight.  That third man delivered the victim the most terrible blow with a mallet.  There was medical evidence that that blow was such that it may have killed the victim either instantly or at least eventually. 

Meanwhile, Krakouer armed himself with a stake, which was near the scene of the fight, and he delivered another terrible blow to the victim and that was a potentially lethal blow in its own right.  So there was an issue about who killed the victim.  Was it Krakouer or was it the other man?  Or even if the other man had not killed the victim instantly, whether he would have died in any event?  A question arose in the context as to whether or not a conviction of Krakouer for murder could stand.

Your Honours will see that the Western Australian Court of Appeal comprised President Steytler, Justice Wheeler and Justice McLure.  Justice Wheeler agreed with President Steytler, so did Justice McLure, who also delivered some further reasons on this issue of causation in the context of the criminal law.  The doctrine at stake in Krakouer – this applies equally, your Honours, to Franklin incidentally – was that a doctrine which is usually called substantial contribution or is sometimes called significant contribution, that is, whether or not a person who did not actually carry out the killing can be held liable for the murder. 

Justice Gummow, can I remind you of the case of Osland in which your Honour participated which was one where a woman induced her son to kill her husband and the question was, whether that being so, murder could be found.  So the doctrine here at stake in Krakouer is substantial contribution and the result of the application of that doctrine is this; that one does not need to show for establishing criminal liability that the death, the particular injury central to a finding of murder, was carried out by the accused.  Your Honours, could I say no matter that it resembles in a general way a test for material contribution, it is quite different material contribution at common law as it is applied in the field of tort.

HAYNE J:   Well the premise in Krakouer and in Franklin is that each event, each cause was a cause?

MR WATSON:   Yes, that would be part of it.

HAYNE J:   That is the question at issue in this case.

MR WATSON:   It is different because to determine whether or not, for the purposes of criminal liability for murder, the contribution is pitched at a much lower level.  I did mention that in its own terms it is described as significant or substantial.

HAYNE J:   But leaving aside that difference which in itself is important reason to look at the cogency of the authority, both injuries in Krakouer were or contributed to the death, did they not?

MR WATSON:   They did.

HAYNE J:   And that is the question at issue here.  Was exposure to asbestos a cause of the injury sustained, namely, lung cancer leading to death?

MR WATSON:   That is true, and that is where the test to be applied in cases like Krakouer resembles the material contribution at common law but also the differences are so significant.  For example, in Krakouer, medical evidence was called to attempt to establish that it had been the third man’s blow which had been the killing blow, and there were different questions of burden of proof and the like which were necessary to consider in that context.  But what I would respectfully submit to your Honours is that knowing that that is the basis for Krakouer and, for that matter, Franklin, that does explain what their Honours say in the third sentence of paragraph 315 where their Honours say that it is open to conclude cause even though the injury would have occurred in any event.  In other words, Krakouer could be found liable even though the third man’s blow would have killed the victim in any event.

FRENCH CJ:   So that if one exposure, in this case to tobacco, is a sufficient cause of the disease and subsequent death, does that answer the question whether exposure to asbestos can be said to make a material contribution?

MR WATSON:   It does.

FRENCH CJ:   And say that the death could be explained by the smoking?

MR WATSON:   There have to be findings, but if in probability the lung cancer was caused by smoking, that is sufficient to exculpate the asbestos.  That is the common law position.

HAYNE J:   That is to search for single cause, is it not?

MR WATSON:   No, because if the death was going to come about in any event, then that would exculpate the other causes.

HAYNE J:   But do you accept that searching for single cause is a false step?

MR WATSON:   Of course I do, I accept that your Honour.

HAYNE J:   The relevant question is whether asbestos was a cause of the injury, is that right?

MR WATSON:   That is true.

HAYNE J:   The observation at line 22 on 1507, “a period of exposure to asbestos fibres can make a material cumulative contribution” may or may not be factually controversial.  Assuming it not to be factually controversial, the controversy in this case was whether asbestos fibres did make a material contribution.

MR WATSON:   That is true.  Your Honour’s focus is slightly different to that of the Chief Justice’s questions.  If the smoking was going to cause the lung cancer in any event, then that would exculpate the asbestos, but I accept, Justice Hayne, that the inquiry is to look at the asbestos to see whether it is a cause, not the cause, and also the same inquiry is appropriate in respect of the smoking.

HAYNE J:   But the answer you give denies one of the fundamental premises for the debate, I think.  The fundamental premise for this debate is that medical science cannot tell you what it was that led to the deceased contracting lung cancer.

MR WATSON:   That is very true.  That is why we have said and we have acknowledged that other evidence, in this case circumstantial evidence supplied by the epidemiology, would be available to a plaintiff who sought to prove that in the absence of the direct evidence.

HAYNE J:   But the hypothetical that it is relevant to inquire whether smoking would have done this or asbestos would have done that must not be permitted, I think, to mask the premise from which the debate proceeds – no one knows what caused the cancer.  The question ultimately is, is it proved that asbestos was a cause?

MR WATSON:   I respectfully accept that, your Honour.

FRENCH CJ:   That is not answered by characterising the tobacco exposure as a sufficient cause?

MR WATSON:   No, that is determined by the evidence.  Your Honours, this exchange leads seamlessly to the next case to which I wish to take your Honours.  It is cited as authority for the proposition in the third sentence of paragraph 315, and that is Bonnington Castings [1956] AC 613. Just as your Honours acquire the authority, could I remind your Honours that this particular decision, Bonnington Castings, was very important to the majority in this case and it was very important to the majority in their earlier decision in Hannell.  They referred to it several times in both cases.

Your Honours, can I remind your Honours about the facts in Bonnington Castings.  Mr Wardlaw suffered from a lung condition called pneumoconiosis.  Pneumoconiosis can be caused by the inhalation of silica dust.  While he was at work Mr Wardlaw inhaled a great deal of silica dust.  Some of that dust emanated from pneumatic hammers and some of the dust emanated from swing grinders.  The dust Mr Wardlaw inhaled from the grinders but not from the hammers was as the result of the negligence or a breach of statutory duty of his employer.  Mr Wardlaw had succeeded and this case is before the House of Lords as an appeal by the employer.  Can I take your Honours to the speech of Lord Reid at page 618.

GUMMOW J:   I think you will get better if you go to the speech of Lord Keith at the bottom of page 626, about six lines from the bottom of the page, which I think picks up what Justice Hayne has been putting to you.  Lord Keith says:

and I think the national inference is that had it not been for the cumulative effect the pursuer would not have developed ‑

et cetera.  So it is a “but for” situation.

MR WATSON:   Yes.

GUMMOW J:   If you are going to understand the case, you have to begin with that.

MR WATSON:   Yes.  Your Honours, may I show you Lord Reid’s speech.  It is quite fair to say that their Honours, in this case and in Hannell ‑ ‑ ‑

GUMMOW J:   Lordship’s, I think.

MR WATSON:   I am sorry, his Lordship’s speech, at page 618.  I will show you briefly that his Lordship set out the statute upon which the statutory count was to be based.  I show your Honours that because at page 620 in the first paragraph Lord Reid had to resolve what was the first issue in the appeal.  The intermediate appeal court had, in the context of the statutory count, reversed the onus of proof.  Lord Reid said that that was error and corrected it.  I wish to show your Honours, about six or seven lines from the bottom of that paragraph, that in resolving that issue his Honour said what we take to be a statement of orthodox and what we would respectfully submit is different to the test relied upon by the majority:

In my judgment, the employee . . . in civil actions:  he must make it appear at least that on a balance of probabilities the breach of duty caused or materially contributed –

We say that the majority in citing Bonnington Castings at the conclusion of the third sentence is actually, with respect, misapplying it.  At the top of page 621 there is a very important reference to the nature of the disease which was being dealt with.  There a reference to the medical evidence establishing that:

pneumoconiosis is caused by a gradual accumulation in the lungs of minute particles of silica inhaled over a period of years.  That means, I think, that the disease is caused by the whole of the noxious material inhaled and, if that material comes from two sources, it cannot be wholly attributed to material from one source or the other.

Your Honours, may I just pause there and say that is a classical description in the law of an injury or disease which is both cumulative and divisible and there is some significance to that in the context of the way that the majority used it.  The finding by Lord Reid as to the medical nature of the problem was, in effect, that each lungful of the dust inhaled by Mr Wardlaw was a small separate injury, a kind of micro-injury.  So that, your Honours, the hammers inflicted one injury and the grinders inflicted another injury.  They both, in effect, were accumulating into one injury but it was divisible between the two. 

Your Honours, I will come back in a moment to places where that has been discussed or that interpretation has been given to Bonnington Castings, but I wanted to show your Honours something further about seven lines down.  It becomes important in the appeal.  It is a statement by Lord Reid that:

A contribution which comes within the exception de minimis non curat lex is not material –

et cetera.  That is something relied upon by the plaintiff at trial in the Court of Appeal and here and I am going to have to return to that later at the appropriate moment.

HEYDON J:   You challenge that?

MR WATSON:   Yes, I do, your Honour.  I should say this, your Honour, I will also attempt to explain it.  I believe that Lord Reid may have been dealing with another issue.  He may have been dealing with the fact that he was talking about two separate injuries.  The laws always recognise that one cannot sue in tort for an injury which is so small that it would be regarded as de minimis, hence explaining the whole of the phrase “the law is not concerned with trivialities”.  It could well be that Lord Reid had in mind the different injuries which emerged from the grinders and the hammers, but I will come back to that, I promise, or a threat. 

Your Honours, the key to it is that Bonnington Castings is not a case about an indivisible injury.  This is referred to by the author of the article to which the Court refers.  That is Tse, Tests for factual causation (2008) 16 Torts Law Journal 249.  This particular issue is discussed by the author at page 254.  I hope that your Honours will accept that this is a convenient shorthand way of supporting our submission about the divisibility of the injury in Bonnington Castings.  In 254, the author refers to the fact that Bonnington Castings had been cited in an earlier Canadian decision.  I will not read any of that to you.  It is more or less what I have been saying.

What I wanted to show your Honours was something on page 255.  In the second new paragraph it said that, “Courts have also been willing”, et cetera, in the discussion about “cumulative, or dose-related injuries” and there is a footnote 17.  Inn 17 there is a catalogue of the classical English cases on the divisibility issues:  Thomson, a decision of Justice Mustill sitting at first instance; Holtby, an asbestos case; and Hatton, a complex psychiatric case.  Your Honours will see that here the author, Tse, refers to the fact that in Hatton and Holtby the judges in those cases explained the result in Bonnington Castings that it was a point probably not taken that if the employer had said “Well, I only wish to pay the damages attributable to that portion of my negligence”, that that finding would have been made.  That is divisibility.

Your Honours, finally in this first part of my submissions, in attempting to demonstrate error by the majority in principle it is necessary, I think, to look at their Honours’ earlier decision in Hannell.  Before I take your Honours to the reported decision, it is probably helpful to look at how their Honours used Hannell here. If I take your Honours to appeal book 4, page 1505 at paragraph 307 your Honours will see that the majority begin to deal with causation. Their Honours refer to their earlier judgment in Hannell and to Bonnington Castings, et cetera.  I show your Honours that and it follows at paragraph 309 with the assertion – and this is presumably based upon Bonnington Castings – that, “a contribution is material if it is something more than de minimis”.

GUMMOW J:   It is the second sentence at paragraph 309 which is the problem.

MR WATSON:   Your Honour, yes.  Your Honours will note that in Hannell and this case the majority used Bonnington Castings on the basis that it was an authority applicable in the area of indivisible injuries.  Mr Sheller has pointed out to me that I should have shown your Honours something else in Bonnington Castings, for which I have mixed feelings of gratitude and otherwise, but I should have shown it to your Honours.  Can we go back briefly to Bonnington Castings.  At page 623 of the report there is another statement in the speech of Lord Reid which we say shows that the test in Bonnington Castings was nothing but the orthodox.  Just before the end of his Lordship’s speech:

In my opinion, it is proved not only that the swing grinders may well have contributed but that they did in fact contribute –

et cetera.  That becomes important because I will show your Honours in due course that here it was thought, at least by the primary judge, or it appears to have been thought by the primary judge the fact that asbestos is capable of contributing is sufficient.  I should have shown your Honours something else on page 1505 of the Court of Appeal book.  Their Honours set out a long quote from their own decision in Hannell in the second paragraph quoted.  Their Honours in Hannell had said:

The approach to causation in Bonnington Castings is conventional and has been approved by the High Court in March v Stramare at 514, 532; Bennett at 419, 428; Chappel v Hart at [27].

With respect, that may not be so.  It depends which proposition upon which their Honours rely that Bonnington Castings establishes.  For example, in each of those cases Bonnington Castings has been cited as authority for the proposition that all that a plaintiff need prove is that a breach was a cause, not the cause, which we would accept to be the conventional approach.  But nowhere in those cases is it suggested that it be used in the way that it has been used by the majority here, which is that it is not necessary, in fact, to show that the breach caused the injury.

At long last could I take your Honours to the reported decision in Amaca v Hannell (2007) 34 WAR 109. The Bench was similarly comprised, Chief Justice Martin, President Steytler and Justice McLure. There was a joint judgment by President Steytler and Justice McLure. I want to take your Honours just to part of it which deals with causation. If your Honours go to page 192.

Paragraph 387 comes under the heading “Causation principles”.  I just want to touch on this ever so lightly to get into what we say, with respect, is an exemplification of error or at least going too far on the state of the authorities.  Your Honours will see on the next page, 193, that paragraph 390 is mainly devoted to a discussion of McGhee v National Coal Board.  That case has proved controversial, not just here, but also in the United Kingdom.  It was explained one way by Lord Bridge in Wilsher’s Case, but more recently Fairchild has come to accept that McGhee is an early form of Fairchild.

Their Honours quote from Lord Wilberforce’s speech in McGhee and then in paragraph 391 move into a discussion relating to the Fairchild decision.  As paragraph 390 ‑ ‑ ‑

GUMMOW J:   I do not think Mr Walker advocates Fairchild.

MR WATSON:   I understand that, but I believe – I am sorry I should not put it that way.  I understand that, your Honour, but it is my submission that the majority in the Court of Appeal in this case and in Hannell were advocating Fairchild and may have even been applying it, in one way or the other.  In paragraph 392, their Honours in the majority said that members of the High Court had relied upon McGhee and then quoted the paragraph from Bennett by Justice Gaudron.  Your Honours Justice Gummow, Justice Hayne and Justice Heydon recently had a look in the case of Roads and Traffic Authority v Royal at a very similar passage in a judgment of Justice Dixon in Betts v Whittingslowe and looked at the issues which were there raised and whether or not it stood as the proposition for some kind of reverse of onus or the like available in limited circumstances.

Your Honours, I will take you to that judgment later in the argument, but it is very similar to that statement by Justice Gaudron in Bennett and, indeed, her Honour based that statement upon Betts v Whittingslowe.  If your Honours then go to page 198, the intervening pages being taken up with some discussion of the evidence, on page 198 the majority in paragraph 412 – that is the part that they quote in their judgment in this case, your Honours – paragraphs 412 and 413 and then if your Honours go to page 199, paragraph 417 there is a discussion, which I will not read to your Honours because it is lengthy, but it concludes with a statement that:

The application of the Bennett test –

Presumably referring back to Justice Gaudron’s statement:

in those circumstances produces the same result as in Fairchild.

GUMMOW J:   I do not think that is what Justice Heydon was saying in Chappel v Hart.

MR WATSON:   Paragraph 420 ‑ ‑ ‑

GUMMOW J:   There are cases in which the “but for” causation is made out, but the law says you need something more.  This is a case where it seems “but for” is not made out.  The question is what less will do?  But I do not think Mr Walker advocates the something less.  He does not advocate Fairchild and I do not think he advocates the Canadian idea of injury falling within the ambit of risk created by the breach of duty.

MR WATSON:   Yes, again, if I may say so.  But, your Honours, what I am ‑ ‑ ‑

GUMMOW J:   I am not sure in the end what this case is about, other than the evidentiary question of whether there really was an evidentiary basis for saying “but for causation” in the sense of a sufficient, not necessarily sole, cause was made out.

MR WATSON:   That is so.  What I am trying to demonstrate is that – I will be robust about it – the surprising result at which the majority arrived can be explained by the test which the majority was applying, and the only other reference that I want to give in relation to this part of my submissions is to paragraph 420 where it seems there that the majority were saying that a Fairchild exception can apply under existing Australian law.  Your Honours, we would respectfully submit that that part of ‑ ‑ ‑

HAYNE J:   I think the explanation for the majority conclusion lies in that second sentence in paragraph 309 at page 1506, and on the face of things there seems to be in internal contradiction within it.  If there is an internal contradiction within it, then that may have consequences.  If there is not, I cannot at the moment see how it is resolved.  But that we will hear.

MR WATSON:   What I wanted to do, and this is the end of the first part of my submissions, is attempt to establish error on the part of majority.  They are the submissions that I wish to put on that point, and I wish now to move to the second matter if I may and that is the failure by the majority to evaluate – for the purposes of determining causation – the role of the two separate periods of exposure.  We would respectfully submit that this is an error symptomatic of an error in approach, and in any event, in practical terms by itself constitutes an error and such that we would succeed on this point alone.

I am going to start, if I may, by taking your Honours to the judgment of Chief Justice Martin who gave a particularly careful judgment on this point.  It is in appeal book 4, page 1452.  When I say “careful”, it is also lengthy.  This portion of the judgment runs for 16 pages.  It starts in paragraphs 164 and 165, with Chief Justice Martin saying that the primary judge had directed himself toward the correct question, that is, where there were two periods of exposure.  I will call it “two defendants” which just makes it more simple in the circumstance, that the primary judge had to make findings in each case that there breach of duty case caused the injury.

Chief Justice Martin sets out sections of the primary judge’s judgment where the primary judge acknowledges that that is the question, but for the next 15 pages, Chief Justice Martin exposes the fact that the primary judge then failed to do so.  If your Honours kept turning over page after page, there are quotes and then interpolations by Chief Justice Martin demonstrating that the primary judge simply declined to carry out this exercise.

The primary judge expressed it in different ways.  He declined to carry out the exercise because he thought it was inappropriate.  He thought that it was inappropriate because this was a cumulative risk.  He thought that it was inappropriate because there was evidence that the two periods of risk could enhance each other, et cetera.  It is detailed there.

At page 1461, there is a passage to which I wish to take your Honours, just below line 30.  Chief Justice Martin is quoting from the primary judgment, paragraph 513.  I am going to come back to this paragraph and how it was utilised by the majority, but at this stage can I show your Honours that what the primary judge had said at the start was it was important that the two periods of exposure were capable of combining.  Then there is a reference to some of the evidence, and then the primary judge said, and this was the finding:

the periods of exposure to asbestos . . . are, in my view, capable, either alone, or more probably in combination, of causing or contributing -

Your Honours, that is not a finding of material contribution from either period, or even both periods.  In paragraph 182 at the foot of that page, Chief Justice Martin expresses some concern over the way in which the primary judge had put paragraph 513.

FRENCH CJ:   I wonder if that was nothing more than a rather loose way of referring to risk.

MR WATSON:   I think that is, with respect, correct, your Honour and I am going to come to that and how the majority used it because the majority actually took up that paragraph 513 and said “That is it, that is the finding”, and it seemed to be a finding of some sort of biological process was involved of causation, but I am getting there, if I may.  Could I just move ahead and show your Honours that at paragraph 193, Chief Justice Martin declared this portion of the primary judgment to be in error, and in paragraph 194 discussed the implications of correction of that error.  For example, on one view of it, because the primary judge had simply declined to deal with the issue, Chief Justice Martin said it could be a matter for a retrial or remitter, but he came to the view that that was unnecessary.

Now, can I show your Honours how the majority dealt with this.  It is at page 1514.  In our written submissions, we put in writing carefully and with respect that it is not easy to see what the majority actually did with this issue.  If your Honours look at paragraph 340, the last sentence of it suggests that their Honours concluded the primary judge had made separate findings.  I will not take you there, I have read those paragraphs in the primary judgment carefully, and they could be construed to do that, but the majority then immediately go on to say that:

the trial judge did not attempt to determine the quantitative extent of the risk ‑ ‑ ‑

Chief Justice, that may reinforce your feeling on the matter – the primary judge did not determine the quantitative extent of the risk from each exposure.  Could I just pause there and say, with great respect, it is very hard to see how the primary judge could have arrived at a conclusion, a satisfactory conclusion, on the issues described at the second sentence of paragraph 340.  If that quantitative analysis of risk had not been undertaken, then the majority in the first sentence in paragraph 342 refer to the fact that the trial judge considered whether or not it was appropriate to have regard to both periods as they were combined, and as the majority says, that was an issue at trial.

Your Honours, pausing there, I would respectfully submit that the best interpretation of what the majority had to say about the primary judgment there was that it was in error on this point, but from here it is not clear what the majority did with it.  On page 1515 there is a quote.  Their Honours introduce it by saying “the trial judge continued”.  Your Honours, it is the same paragraph, 513.  Chief Justice French drew attention to the fact that this may be speaking of risk, and may I just show to your Honours it must be and I am going to take your Honours to a little evidence to show that it must be.

More importantly, in my view, there were two periods of exposure, the second capable of combining . . . I accept the opinion of Professor Musk that discrete periods . . . are capable in combination of causing or contributing to the cause or progress of the disease.  This too, I am satisfied, is the opinion of Professor de Klerk.  This opinion appears to me to be consistent with the literature –

although that is not identified, and this conclusion:

Accordingly, the periods of exposure . . . are, in my view, capable, either alone, or more probably in combination, of causing -

In paragraph 343 their Honours say something which is not available from that paragraph.  Their Honours said that the primary judge had found –

that the asbestos fibre exposures in the successive periods operated cumulatively ‑ ‑ ‑

It is that word “operated” which seems to have been a movement from risk to cause, something which happens in the judgment seamlessly many times.

GUMMOW J:   The word “cumulatively” is obscure, too.

MR WATSON:   It is, your Honour, in this context, as I am going to make a submission in due course that it is better understood if every time the words “cumulative injury” are seen, they are read as though their Honours said “cumulative risk”.  But, your Honours, may I show at paragraph 344 what their Honours made of it:

The finding in [513] that the successive asbestos exposures operated cumulatively led to the further finding that each period . . . materially contributed –

That is not what the primary judge found, with respect.  I think this is a moment when perhaps I should depart and speak of what it might have been when the majority described the lung cancer as being a cumulative injury.  Could I say at the outset, if one is to speak of a cumulative injury, one is almost certainly speaking of biological processes, very similar to the way that Lord Reid spoke of the injury in that case.

FRENCH CJ:   There is nothing to link.  There was evidence as to the distinction between the initiation and promotion in the aetiology of cancer, but there was nothing to link the asbestos exposures to any particular stage.

MR WATSON:   That is correct, your Honour, and I do not know of any expert who actually used terminology such as to suggest that lung cancer is a cumulative injury.

FRENCH CJ:   In other words, there is nothing to link this to a biological theory?

MR WATSON:   Nothing, and there is a little evidence I am going to take your Honours to in a moment which takes it away from it.  Really, I have already foreshadowed this.  If your Honours look at it every time the word “risk” appears, especially in the phrase “cumulative risk”, if the – sorry, I have that the wrong way around – every time the phrase “cumulative injury” is used, if it is exchanged with “cumulative risk”, then the judgment makes sense on the basis of the evidence.

May I remind your Honours that that paragraph 513, which the primary judge had delivered and which had been commented upon by the majority, referred to two things.  One was the evidence of Professor Musk.  Professor Musk is a leading medical practitioner.  The other evidence was that of Professor de Klerk.  He was an epidemiologist and biostatistician and was not commenting upon biological processes.  Hence, Chief Justice French, could I say with respect, is right.  That paragraph was directed at risk, not cause.

Could I show your Honours some of the evidence from Professor Musk, that being the last basis for this kind of assertion.  In appeal book 1 at page 64 at line 10 there are four questions and answers:

You were asked about causation and you spoke about causation . . . Yes.

In that context were you speaking about causation as reflecting an increase in risk?‑‑‑Yes.

And factors such as smoking cigarettes or inhaling asbestos which might increase a risk?‑‑‑Yes.

Because it’s not possible to speak with medical scientific certainty about the causation of a cancer.  It has to be done really as a matter on the best available statistical evidence?‑‑‑For the probability, yes.

I am not sure the evidence upon which the primary judge was relying when making the finding at paragraph 513, but the primary judge did ask some questions of Professor Musk.  We would respectfully submit they point in the direction opposite to the primary judge’s conclusion.  They figure commencing at page 80 of the same book.  These are questions by the primary judge at the conclusion of evidence.  Some of them are a little long.  I hope I fairly paraphrase them at times.  The first is at about line 15.

The present case . . . seems to involve . . . a question of whether an acceptable conclusion can be reached as to whether smoking or asbestos exposure or both contributed . . . Do the papers or discussions to which you have been referred –

deal with that?

I believe so, yes.

And what can be drawn from the state of knowledge ‑

Answer:

I think we can get some idea of the relative contribution to the risk that he had from those exposures and work out from them what the attribution ‑

Dr de Klerk has done so.  Then skipping a question and answer – not that it harms us – at the foot of the page:

Am I also correct in assuming that . . . there were no clinical or pathological indications from which a conclusion could be drawn . . . No.  The smoking history ‑

So there is nothing from the clinical or pathological indicators.  The top of the next page is important.  This is his Honour’s question.  It does not provide a basis for the finding about Professor Musk’s evidence.  Mr Cotton’s condition:

His condition not involving mesothelioma, the cancer could presumably have been due to any of the potential causes of lung cancer?‑‑‑Yes.

The next question even acknowledges the background risk.  I am sorry to jump around like this, your Honours, but could I take you back to the majority judgment on this point at paragraph 350 on page 1517.  This is in the context of resolving this issue, which I can assure your Honours was an important issue at trial and on appeal, of separating these two periods.

Paragraph 350 commences with rejecting the primary judge’s judgment on a particular point.  The primary judge had suggested that simply because scientists had not yet defined a safe low threshold, that precluded the finding of no causation.  Her Honour said that was wrong.  But then there is this statement:

However, the fact that exposure to very small amounts of asbestos is capable of causing lung cancer is a relevant factor to be taken into account –

Just pausing there, I suppose the words “very small” could mean different things in different contexts.  I am unfamiliar with any evidence in the proceedings where any expert had said that very small doses could cause lung cancer.  It seems that their Honours were falling into the same error that the trial judge had fallen into and which their Honours set out to correct – that is, simply because there was no safe threshold, that is relevant to causation.  With respect, that is not so.  Your Honours can see now what their Honours mean by “low threshold” in terms of this causation.

Paragraph 351 is important because Professor Musk carried out an apportionment for the two periods.  When Professor Musk did that, he carried out the apportionments on the precise elevation in risk found by the primary judge.  The primary judge found a relative risk of 1.1 to 1.2 and between three and eight per cent of the risk was attributable to the South Australian exposure.  This is hard evidence of the nature and extent of the risk.  I will foreshadow my submission in relation to smoking.  Nowhere will your Honours find a comparison between that number and the 1400 per cent increase due to smoking.

I show your Honours, briefly, 352, to show that the findings of Professor Musk enjoy corroboration, as it were.  Professor de Klerk carried out the same exercise on a slightly higher relative risk.  Once account is taken of the slightly higher relative risk, the results are substantially identical.  In other words, two leading experts have come at the same result, which suggests that this is valuable, genuine assessment of the risk.  Yet, at the foot of page 1517, this is in effect the whole of the judgment on this point, the last two lines:

As to the qualitative –

I think their Honours might have meant “quantitative” –

evidence of the extent of the separate employment exposures, we rely on the findings made by the trial judge which we uphold for reasons given below.

That is one thing.  That would be, in other words, the findings which supported Professor Musk’s calculation of three to eight per cent.  But their Honours went on and said this:

However, even if the findings were flawed it is clear Mr Cotton was exposed to very significant levels of respirable asbestos . . . sufficient to justify a finding –

Your Honours, what that means is their Honours were prepared to find causation a level lower, perhaps much lower, than the three to eight per cent risk.  We say, your Honours, that in the end there are four problems with this portion of the judgment.

The first problem is that nowhere is there any comparison or evaluation of a three per cent increase in risk or, for that matter, an eight per cent, but bearing in mind where the onus lay, a three per cent increase in risk with the increase of risk for smoking of 1400 per cent.  Just pausing there, that figure of 1400 per cent is derived from the primary judge’s findings not challenged in the Court of Appeal.  Your Honours, surely in reaching the point required by the common law, that according to Briginshaw is actual persuasion or, according to Luxton v Vines, the basis for an actual indefinite inference, surely there had to be some comparison carried out between the asbestos, small, and the smoking, large.  All of that is exacerbated, if their Honours were still prepared to make a finding as they foreshadowed, at a level much lower than three per cent to eight per cent. 

The second problem is that the findings of the majority take no account of the separate position of the parties.  Your Honours, simply by saying that some effect is the result of the cumulative process, assuming that to be correct, does not provide a legal basis for finding one party liable for the acts of another.

FRENCH CJ:   Just going back to that sentence you took us to at 1518, paragraph 353, is that anything more than an inference of fact based upon the evidence that asbestos can have a causative effect, but not based upon any particular level of risk assessment?

MR WATSON:   That is all it is, your Honour.

FRENCH CJ:   So when they speak of significant levels, they are speaking of, obviously, simply what was put in evidence and I suppose simply saying they are not de minimis.  They are associated with some sort of risk, but they are not getting any quantification at all.

MR WATSON:   I think it must be the de minimis reference.  Yes, I will agree with your Honour, but certainly they do not engage in the qualification at all.

GUMMOW J:   This sentence at paragraph 353 that each made a material contribution links back to paragraph 309 which you took us to at page 1506 where they say:

‘but for’ . . . not required when a factor makes a material cumulative contribution.

What does that mean, other than some notion of risk?

MR WATSON:   It has got to be risk.  It has got to be a finding like Fairchild, with respect.  It says that if there is a material contribution, it does not really matter whether it caused it or not.  Liability can be fixed on the party for increasing that risk.

HAYNE J:   That is using contribution in a very particular sense and I do not know what it is.

MR WATSON:   Yes.  Your Honours, I was at the point where I was suggesting that the effect of what the majority did was to say, because it is a cumulative injury, the party, my client, first in time is also fixed with liability for the acts of another party later in time.

No consideration was actually given to this matter by the majority.  No theory was propounded upon which liability could be fixed upon the South Australian exposure defendants for this.  Your Honours, the subsequent exposure at Millennium was, according to the primary and appeal findings, a tort.  By definition, the conduct was unreasonable.  It follows that Amaca and, for that matter, South Australia, are, in effect, being found liable for the tort of another party.  It is a new variety of vicarious liability which has derived from the idea of a cumulative injury, whatever that may be.

HAYNE J:   Cumulative injury seems to be given some content by this last sentence in paragraph 513 of the trial judge’s reasons reproduced at 1515, where his Honour concluded that “the periods of exposure . . . alone, or more probably in combination” as though the biological processes were of the same kind as pneumoconiosis.

MR WATSON:   Yes, that is true.  That is what that would mean, with respect.  That is not the case here.  Chief Justice Martin spent a bit of time on this.  The primary judge had used the terminology “divisible” and “indivisible” incorrectly and reversed it.  It meant nothing to the way that his Honour approached the principles, but Chief Justice Martin does discuss the idea of divisibility at a point, but your Honour is quite right.

HAYNE J:   Was there any evidence that asbestos disease is associated with biological processes of the same kind as were encountered with pneumoconiosis?

MR WATSON:   Yes, there was.  There was specific evidence and the disease was asbestosis and the reason why that evidence was led was to distinguish the nature of asbestosis from lung cancer.

FRENCH CJ:   There was something about certain classes of lung cancer which are more likely to be associated.  Lower lobe cancer, is that right?

MR WATSON:   There was a discussion about it but it really, could I say, I hope I did just the explicit ‑ ‑ ‑

FRENCH CJ:   There was no finding for that, though.

MR WATSON:   No finding, and it really came to nothing.  There was some debate about whether or not lower lobe was more common than upper lobe.  There was also some reference to a cell type of cancer, small or non‑small.  But Professor Musk actually scotched that sort of thinking quite early and I do not think it ever arose as being something which might be able to be useful here.  Your Honours, I have made my point about what we say is the second problem.  It is a kind of vicarious liability.  The third problem is of a different kind and I step here warily.  With respect, the result is one which defies common sense.  Can I just rely upon those figures of the three per cent risk and the 1400 per cent risk.

Your Honours, it is now clear that common sense by itself could never and will never provide an appropriate all round test for causation, but it certainly might provide an appropriate filter.  For example, a conclusion on causation should not defy common sense or, if you want to put it the other way, a conclusion on causation should conform with common sense.  We would respectfully submit that that did not happen here.

GUMMOW J:   Are we not really in the realm of evidentiary inference?

MR WATSON:   Yes.

GUMMOW J:   Is that not the stage at which you start to inject notions of common sense?

MR WATSON:   Yes, but, your Honour, that is really my submission.

GUMMOW J:   I am not saying that critically.

MR WATSON:   My submission is that one would then sit back and take a deep breath and say that is three per cent compared to all of this other risk.

CRENNAN J:   But three per cent is not sufficient for the - does not support drawing the inference.

MR WATSON:   It cannot, your Honour, it is just nowhere near it.

FRENCH CJ:   The question is what is the process that is working here where we are dealing with risk?  Is the process a process of inference along the lines of exposure, plus associated risk, plus disease outcome supports inference of some causative involvement, which we call a material contribution?

MR WATSON:   Yes.

FRENCH CJ:   Or is it exposure, plus risk, plus associated injury leads to imposition of liability and we call it material contribution?

MR WATSON:   Yes, your Honours, we frankly acknowledge that this case could be proved if one was able to establish a sufficiently large increase in risk of the inference ‑ ‑ ‑

FRENCH CJ:   So you can support the inference if the risk is high enough in the formula I just put?

MR WATSON:   Yes.  We gave an example in writing.  If Mr Cotton had set out to establish that his ‑ ‑ ‑

GUMMOW J:   You would want to know what went into the statistical method to produce the notion of risk, would you not?

MR WATSON:   Yes, of course, your Honour, and could I say that is why I said near the outset this was an unusual case insofar it was not like a typical personal injuries case.  These were genuine leaders.  These were not the students of the literature.  These were the authors and masters of the area – de Klerk and Berry and this ‑ ‑ ‑

GUMMOW J:   Well, they may be, but the question is what techniques do they use?

MR WATSON:   There is a description in papers and the like and could I say this, if it is any comfort to your Honour, that all of the witnesses felt that these apportionment models were appropriate.  I know that there is some particular reliance placed upon the evidence of Dr Leigh, but Dr Leigh gave some specific evidence that the modelling methods were appropriate and, in particular, Professor Berry’s conduct of the modelling was appropriate.  I wrote a reference to that.  I will just give it to your Honours.  I am going to take you there, but I will just refer to it.  It is in appeal book 1 at page 247.

FRENCH CJ:   They are all based on population studies. 

MR WATSON:   They are based upon population studies, but the populations are ‑ ‑ ‑

GUMMOW J:   Not upon biopsy?

MR WATSON:   No, because I should say this.  I answered the first question by the Chief Justice incorrectly.  The studies were of a variety of different kinds.  They select what group to follow and study.  Sometimes they study a group because they know that they have been exposed and they watch and see what happens to them.  Sometimes they do it post‑mortem and the like and the design of that is a very great skill in its own right, and that is the skill of an epidemiologist.  Professor Berry – his curriculum vitae is produced in the appeal books – is a world leader, not just in this field of asbestos‑related diseases, but in epidemiology generally and the design of these studies and their interpretation.

GUMMOW J:   Yes, I know, but we have to know what is the purpose of embarking on these studies?  It is matters of public health, is it not?

MR WATSON:   Yes.

GUMMOW J:   It is not affixing legal liability to anybody.

MR WATSON:   That is correct, but the results of them are still useful for the purpose that we have here.

KIEFEL J:   They are studying patterns, are they not, in outcomes of exposures in various groups within the population?

MR WATSON:   That is correct, your Honour.

KIEFEL J:   Did anyone here dispute the extrapolation from the epidemiological studies to probabilities?

MR WATSON:   Not only was it not disputed, acceptance of that was a part of the plaintiff’s case at trial and I will take your Honours to that evidence in just a moment.

HAYNE J:   Because it had to be; because this was the only evidence the plaintiff had, was it not?

MR WATSON:   Exactly, your Honour.  I am going to come to that evidence now.  Thank you, your Honour.  There was evidence about these figures.  I would like your Honours, if you would not mind, to have appeal book 4 open at paragraph 351.  That is page 1517 and then if your Honours would also obtain access to appeal book 1 and, in particular, at page 391.  The reason I have asked your Honours to keep both open is to justify the assumptions put to Professor Berry in a question at line 40:

Could I just ask you in terms of two assumed relative risks in the case of Mr Cotton, would you assume that he had a relative risk due to smoking of 10 –

I remind your Honours that the actual finding by the primary judge was a relative risk of 15, so it was higher.  The second assumption is a relative risk due to asbestos of 1.08.  Your Honours can see that comes straight out of paragraph 351.  So it has taken the upper end of the South Australian exposure and a figure which is too low for smoking.  In other words, the result which is about to emerge is favourable to the plaintiff.  The question is how many times more likely is it that Mr Cotton’s lung cancer was caused by cigarette smoking than asbestos inhalation?  At the top of the page it is answered.  Professor Berry was doing some maths in his head but out loud, but when you get to the end of it, the last two lines:

and the ratio of those is approximately 100, so it’s about odds of 100:1.

That is not all that is on that.  This is an answer to Justice Kiefel’s question.  Could your Honours also go to page 395.  Your Honour Justice Kiefel, this is cross‑examination of Professor Berry and in some ways it is encapsulating the plaintiff’s case at trial.  Your Honours will see that at the top of page 395:

Would you agree that nothing that you have told his Honour . . . excludes that inhalation of asbestos as being a cause of Mr Cotton’s lung cancer?---Yes.

I am just going to pause there and refer generally, if I may, to a decision of Justice Hope delivered while his Honour was in the New South Wales Court of Appeal in a case called Sydney County Council v Furner.  It is referred to from time to time as being authority for the proposition that one does not establish causation by simply saying a factor cannot be excluded.  The second question on that page is:

And perhaps that small risk translated in effect to the entire risk; in other words, was the sole cause of the lung cancer Mr Cotton suffered?---Well, yes, again that’s a question of probability.  I mean, I answered a question a few moments ago when I said the odds are 100 to 1.

I do not think Professor Berry knows much about gambling.  If he did, he might be the man to know.  The third question, and this is the plaintiff’s case:

You answer it as a question of probability?---Yes.

But in fact it’s a question of what goes on within the person’s body, isn’t it?---It may well be a question of what goes on inside the person’s body but I don’t think we have any evidence . . . 

We never can have that evidence at a cellular level, can we?---No.

Then if your Honours go down two or three questions:

Epidemiology would be a very blunt instrument, if I could put it that way for determining the cause of disease in an individual case.  Would you agree with that?---Well, it’s an instrument that can only use – because it relates to groups and individuals are members of groups, then any particular individual can only be approached on the epidemiological viewpoint through probability.

FRENCH CJ:   Coupled with the previous statement, you do not need to go this far, I suppose, but it is almost a statement that we are in the territory of dealing with inherent uncertainty as to the actual process that occurred in a particular disease aetiology.

MR WATSON:   Yes, that would be a way of putting it.

FRENCH CJ:   So you can only speak probabilistically.

MR WATSON:   Yes.  Your Honours, at this stage I want to come back – and Justice Heydon asked me a question about this – to the majority’s application of the low threshold or de minimis test.  We say that these findings that we have now shown your Honours, this 100 to 1 factor, they probably reflect the majority’s application of a low threshold and there is no doubt that that came from Lord Reid’s reference to de minimis in Bonnington Castings.  With respect, that is not the law of Australia.  By itself establishing that some contribution was not de minimis, does not establish causation. 

Justice Gummow has looked at that second sentence of that particular paragraph 309.  That is why, because there are other questions which are at stake.  Contrary to submissions by the plaintiff, that statement by Lord Reid has never been picked up by this Court and it is now 53 years old.  In her submissions at paragraph 75 in the Millenium appeal – I will not take your Honours to it, but I will just identify it – the plaintiff submitted that this de minimis test was approved in the case of March v Stramare, and they cite in that submission page 532.  With respect, that is not so.  Could I take your Honours very briefly to March v Stramare (1991) 171 CLR 506. I know your Honours have looked at this case once or twice. The page cited by the plaintiff in her submissions is page 532 and there is true ‑ ‑ ‑

GUMMOW J:   That is only a statement by one Judge.

MR WATSON:   It is not only that.  If read in context with the bottom of page 531, it is Justice McHugh discussing contending theories of causation around the world and, with respect, quite deliberately not solving them.  That statement of de minimis has never been accepted in Australia.  It cannot sit with the “but for” test which makes it unlikely that Justice McHugh had in mind that it was an appropriate test for causation.  I briefly touched on this potential explanation of what Lord Reid had in mind when saying that.  I will repeat it because I dealt with it out of turn. 

It may well be that Lord Reid was considering the idea that the hammers and the grinders had each created separate injuries and neither of those injuries in the eyes of tort law were de minimis so that a plaintiff could sue upon them.  If that is not an adequate explanation for what Lord Reid meant, then, we respectfully submit, that your Honours should disapprove of it as being part of the law of Australia.

GUMMOW J:   The assumption still is that it was a cause, is it not?

MR WATSON:   That is the assumption which is underpinning it all the time.

HEYDON J:   Do you agree with this – to say something is material is to say it is not sole, and maybe it is not substantial, but it has some materiality, some significance.  It seems to me there is a huge distance you have to go before you get down to the point of which you move into something that is de minimis.  Is your submission in accord with that line ‑ ‑ ‑

MR WATSON:   It does.  Your Honour, it is as simple as this.  There are many things which may not be de minimis, which when you evaluated them, you would not regard as material.  There is a long gap between our test for causation and that statement of Lord Reid regarding de minimis if it was directed at causation.  Your Honours will be pleased to know I have nearly finished.

The fourth problem with that part of the judgment of the majority is that it fails to evaluate the arguments regarding supervening cause, and your Honours, that is the third and final part of my submissions.  Your Honours, nearly all of Mr Cotton’s risk of contracting lung cancer came from his smoking after the South Australian exposure.  The finding in the Court of Appeal by the majority and also by Chief Justice Martin in this respect, was that had Mr Cotton ceased to smoke at the end of the South Australian period, his risk of contracting lung cancer due to tobacco smoke would have reduced almost to that of a non-smoker.

I will not take your Honours to it, I will just give your Honours the reference to the majority.  It is in appeal book 4, page 1567 at paragraph 493.  Moreover, your Honours, there were findings and in quite strong terms that by taking up smoking in the first place – I will remind your Honours that warnings were already on the packets when Mr Cotton took up smoking – that by taking up smoking in the first place, and certainly by continuing to smoke over the years, Mr Cotton’s own conduct was unreasonable.

Those findings provided the basis for contributory negligence, but they are relevant to the issue with which I am now dealing.  Again, I will not take your Honours to it, I will just give your Honours the references to the findings.  They are both in appeal book 4, Chief Justice Martin, page 1501 at paragraph 292, and the majority at page 1568 in paragraphs 494 and 495.  Your Honours, we set out a good deal of the detail about the history of warnings on packs of cigarettes.  It was all proved at trial.  It is in our written submissions and I will not repeat it.

Your Honours, may I respectfully submit that in some ways this case resembles issues at stake in the recent decision of this Court in Roads and Traffic Authority v Royal (2008) 82 ALJR 870. The particular portion I wanted to take your Honours to, and this is so recent I am sure it is fresh in your Honours’ minds, it is at page 878 where in the plurality judgment, there was a discussion commencing at paragraph [31] dealing with the further arguments of the defendant. In paragraph [31] there is a discussion of Betts v Whittingslowe and what it means in context.  Then in paragraph [32], there is a discussion of the matter relevant to the argument I am currently mounting and it refers back to March v Stramare and the superseding, intervening or supervening cause ‑ ‑ ‑

GUMMOW J:   What is said in paragraph [33] is important too, is it not?

MR WATSON:   I was going to come to that.  Paragraph [33] is, in a like manner, dealing with those issues.  Your Honour Justice Gummow sees that the words there were that there was an assumption of a chain of causation.  Once your Honours have looked at that I will take you to what the majority had to say.  It is almost identical to that.

If your Honours go to appeal book 4, paragraph 354 at page 1518 the whole of this argument is dealt with in a paragraph.  It records that the submission was put and the submission was rejected.  We would respectfully submit because it is again proceeding, as your Honours can see in the last lines, in respect of an assumption of causation.  But, your Honours, I cannot resist pointing out to your Honours that their Honours in the majority have seamlessly moved back into the other field of discourse.  All of a sudden we are talking about risk, not cause.  Your Honours, we say that that is an error.  I can put it briefly as to why that is so.  The continuation of smoking after the South Australian period of exposure ‑ ‑ ‑

FRENCH CJ:   By the way, they speak of increasing the risk of lung cancer from smoking.  Is that simply a way of referring to the so‑called multiplicative effect on overall risk of a combination of smoking and asbestos exposure?

MR WATSON:   That might be what their Honours had in mind.

FRENCH CJ:   There is nothing in the evidence, is there, to suggest a biological mechanism by which asbestos exposure increases the risk associated with smoking.

MR WATSON:   That is so.  That is correct.  Perhaps their Honours are talking about some use of the epidemiology but still that paragraph would constitute error in those circumstances because of what I am about to put.  The continuation of the smoking after the cessation of exposure to asbestos in South Australia should properly, we would respectfully submit, be seen as constituting by itself a cause.  If that means that there was – and we do not accept that there was – some sort of multiplicative effect which could explain any of this your Honours could see that multiplicative effect being almost entirely created by the unreasonable act of continuing to smoke post that period.  Your Honours, those are my submissions.

FRENCH CJ:   Thank you, Mr Watson.  Yes, Mr Abbott.

MR ABBOTT:   May it please the Court, we adopt and rely on all that my learned friend Mr Watson has said.  I do not propose to go to the same cases, other than Bonnington’s Case very briefly, nor to cite or refer to the same passages that my learned friend has.  I take it as read.  Our submissions on behalf of the appellant, South Australia, logically formed three parts.  In part one we deal with the findings of the majority in relation to causation and to their conclusion that Mr Cotton’s lung cancer was caused or materially contributed to by asbestos inhalation.  That concerns what essentially is found in book 4 from paragraphs 303 to 339.

In part two we address the conclusion by the majority that the trial judge did not err in failing to separate the role of any asbestos inhaled during his employment with EWSD and Millennium respectively and the majority dealt with this from book 4, paragraph 340 to paragraph 353.  Finally and briefly in part three of our submissions we will address some discrete matters arising out of some of the written submissions, but very briefly.

Let me turn then to what this case was about.  It was obviously, so far as this appeal is concerned, a causation case and there were two steps which the trial judge was required to take, firstly, making a finding of general causation whether the relevant agent – in this case asbestos – more probably than not – was capable of causing or materially contributing to the disease, namely the lung cancer and secondly, a finding of specific causation, whether the disease, lung cancer, more probably than not was, in fact, caused or materially contributed to by the relevant agent, in this case asbestos.

As we have heard there was no medical evidence of cause and what there was was epidemiological evidence which, in our respectful submission, may enable a court to determine general causation because the interpretation of the epidemiological evidence and the data which it throws up said to provide a nexus between exposure to the agent and contraction of the disease, may lead to certain conclusions.  Such evidence is, as everyone has acknowledged in this case, probabilistic evidence.  It is evidence of possible causes and, of course, having said that it may assist the Court in coming to a finding of specific causation after considering all the evidence.  So the central theme of our submissions, as indeed my learned friend Mr Watson’s, is that specific causation under our legal system requires more than a mere possibility and although an inference ‑ ‑ ‑

FRENCH CJ:   The term “possibility” covers a range of probabilities, does it not?

MR ABBOTT:   Yes, it does.

FRENCH CJ:   I mean you can have a possibility which is associated with a very low probability and a possibility which is associated with a high probability.

MR ABBOTT:   In this case there was a very low probability and a very low possibility.  Although an inference of causation may be drawn by a court, even when the scientific evidence will not do so, and there are some cases where that has been done, a court would not, in our submission, draw such an inference of specific causation when there is only a mere possibility and would only use a mere possibility after assessing all the evidence and all the probabilistic evidence.

So the cases to which my learned friend has already referred show that this Court and other courts have on occasions considered and required in addition to evidence of general causation and evidence, of course, of breach of duty as a starting point further evidence of an increase in foreseeable risk of injury or disease, the actual eventuation of that injury or disease, a proven likelihood that such increase in risk was causative of that disease and the absence of any other likely cause.

I stress the last two points:  a proven likelihood that such increase in risk was causative of the disease and the absence of any other likely cause.  In this case it is our submission that the respondent had failed to produce any evidence to prove a likelihood that an increase in risk from asbestos fibre ingestion caused Mr Cotton’s cancer, let alone from the South Australian exposure.  As the respondent had to concede, there was another overwhelmingly likely cause – tobacco smoking.

FRENCH CJ:   Risk itself is a statement about the probability of asbestos exposure causing the disease.  When you speak about increase in risk having a causative effect, I wonder whether you are not really conflating two concepts there.  The increase in risk tells us something about the increase in the probability that asbestos exposure will cause the disease.  The question surely is whether there is an increase in risk that enables you to infer that asbestos caused the disease.

MR ABBOTT:   That is true.  Chief Justice Spigelman in Seltsam v McGuiness said that the increase should be to the order of 50 per cent, so one gets to the more probable than not situation.  I think the increase in risk in that was about 1.3, which he said was not in accordance with the “but for” situation.

At the heart of my submissions on parts one and two is the meaning and significance of the concept of cumulative causes as used by the majority in their reasons.  We say this because, in our submission, it is through the use of the terminology of “cumulative” when appended to causes that the majority have converted what we say was, on the evidence, a case about mere increase in risk to a finding of material contribution and that they have done so without there being any additional evidence which would enable such a conversion to occur.  In short, we say, by employing the term “cumulative” the majority has moved from increase in risk to a finding of causation of injury when the evidence did not permit that step to be taken.

A starting point for that is our contention that in the judgment of the majority they appear to have proceeded on the basis that the terms “interdependent”, “multiplicative”, “synergistic” and “cumulative” all somehow meant the same thing, or at least were to a degree synonymous with each other, that those four terms were to be contrasted with “independent” and “additive” and that those terms were indicative of a cause of injury, not as the evidence when properly examined discloses, an increase of risk of injury only at its highest.

The starting point, in our submission, for this examination is at appeal book 4, page 1504, paragraph 305, where the majority said at line 38:

It was accepted by all parties that the risk created by exposure to both tobacco smoke and asbestos is greater than the addition of the two; the enhancement of risk created by their combination is either multiplicative or close to multiplicative.  This is referred to as the multiplicative or synergistic effect.

The reason why it was accepted by all parties that the risk in the sense of likelihood of risk was greater than the additive was due to the fact that all the epidemiological experts undertook an epidemiological exercise either in their reports or in their evidence, or both, and to a very great extent all agreed that there was an additional risk which was greater than the risk created by adding the risk created by exposure to asbestos to the risk created by smoking.

At paragraph 306 at page 1504 the majority evaluated the epidemiological evidence and continued with their analysis of causation.  Their starting point at paragraph 306 was the relative risk analysis, and they said that:

In order to calculate the RR it is necessary to estimate the cumulative dose of the relevant carcinogen (in this case tobacco smoke and asbestos fibres) to which the claimant has been exposed.

The notion of a cumulative dose is referred to on more than one occasion in paragraph 306, not only on page 1504, but also over on page 1505, and it can be no more than a step in assessing the increased risk of contracting lung cancer as a result of exposure to both carcinogens.  But on one view of what follows, it could be said that the majority have already assumed that even at this early stage, that whenever both carcinogens are present, they are both acting on the cells to produce the cancer, rather than merely being capable of acting in that way, because as we know, again, there was no medical evidence for the actual cause.  All the evidence from every source at its highest was that the there was a risk that the two carcinogens might or could have acted together at the same time to produce, or to cause or contribute to Mr Cotton’s lung cancer.

KIEFEL J:   At some convenient point would it be possible for you to provide some transcript and appeal book references to the evidence which the parties accepted that the risk created by exposure to both is greater than the addition of the two?

MR ABBOTT:   Yes.

KIEFEL J:   Does that come directly from the reports?

MR ABBOTT:   Yes, it does.  It comes from the evidence of Professor de Klerk, Professor Berry, and I can find those references.  Those to my left will find the references expeditiously and we would make them ‑ ‑ ‑

KIEFEL J:   But you say it appears clearly enough in the reports, it is not part of the examination of those experts by the trial judge?

MR ABBOTT:   Yes, this is summarised by – my learned junior has referred me to appeal book 4, page 1469, paragraph 197 in the judgment of his Honour, Chief Justice Martin where he said:

The consistent evidence of all the experts was to the effect that asbestos fibre and tobacco smoke are both carcinogens which might each cause lung cancer . . . The consistent evidence of the experts was also to the effect that if a person is exposed to both tobacco smoke and respirable asbestos fibre, the effect of the two carcinogens, working together, is not merely additive but multiplicative in the sense that the total risk of contracting lung cancer to which such a person is exposed is not the sum of the risks occasioned by exposures to the carcinogens, but rather the multiple of those risks -

Then there is a collection of references, which I think is probably all the ones that I would have put to your Honour.

At appeal book 4, page 1505, the majority in paragraph 308 then refer to their joint judgment in Hannell, and it is significant that they pray in aid Hannell for the recitation of the fact that in Hannell they found that the exposure of respirable asbestos from all sources operated cumulatively.  That is to be found in the passage in line 5 of paragraph 308:

The majority in Hannell concluded on the evidence that the exposure to respirable asbestos from all sources operated cumulatively -

The words are “operated cumulatively”.  Again, it is our submission that at this stage, the majority are proceeding on the basis that carcinogens which act cumulatively, by definition act causatively because they operate cumulatively to cause the cancer.  Of course, Mr Hannell lost but on foreseeability grounds.

Our submission from Hannell and the majority’s reference to Hannell is reinforced by what follows, because we say that on a fair reading of paragraph 308, the majority are proceeding on the basis from here on that a cumulative dose, as referred to in their previous paragraphs, which is sufficient to be, in their view, a material contribution, could be inferred somehow from the evidence and therefore a finding of causation made.

FRENCH CJ:   They are dealing here, are they not, with asbestos as though it is just the only relevant exposure?

MR ABBOTT:   Yes, they were.  In Hannell it was the only relevant exposure.

FRENCH CJ:   It is in that sense that “cumulative” is being used.

MR ABBOTT:   Yes.

FRENCH CJ:   You get one bit, another bit makes things worse, another bit makes them even worse and so forth.

MR ABBOTT:   Yes, but they transpose the word “cumulatively” and continued to use the word as though it was causative, not merely indicative of increase in risk.  They then move from, in their discussion of causation principles, they move from the concept of cumulative doses to a slightly different concept at paragraph 311 on page 1506, line 28, where they say:

Causes of an indivisible injury or disease are cumulative if they operate inter-dependently to produce the injury or disease.

In our submission, by that stage they have then moved to proposing a test of causation by a finding of interdependence and/or a finding that they act cumulatively.  We say that in making this statement the majority are referring to a category of case in which the interdependent agents have not simply operated to increase the total risk, which does not get a mention in paragraph 311, but rather have operated cumulatively to cause or contribute to the disease or injury.

We say that from paragraph 311 onwards, with respect, the majority have proceeded in their reasons on the basis that the interdependent or synergistic effect of asbestos and smoking inevitably means that they must be cumulative causes or contributors to the lung cancer from which Mr Cotton died.  We say that, at the very least for us, paragraph 311 is the point where the majority have moved from increased risk of contracting the disease to causation of the disease by conflating the notion or by applying the notion of cumulative causes when they should have been talking ‑ ‑ ‑

GUMMOW J:   Is Wilsher v Essex [1988] AC 1074 an authority on anyone’s list?

MR ABBOTT:   No, your Honours.

GUMMOW J:   I have an idea it is referred to in Fairhaven.

MR ABBOTT:   We do have Wilsher. I can return to that in a minute. It is our contention that by paragraph 311 the interdependent operation of carcinogens, if they are found to be interdependent, equals cumulative causes. This is demonstrated further by what they then said at paragraph 315 at appeal book 4, page 1507. At the end of paragraph 315, a passage to which my learned friend has already taken the Court, they say:

As previously noted, that is consistent with the low threshold for what can constitute a ‘material’ contribution where causes are cumulative.

There must be therefore, in our respectful submission, of, what some commentators have referred to, jump the evidential gap by finding that causes are cumulative because they are interdependent they thereby make a material contribution.  If this is not clear or not as clear as it could be at this stage, it is certainly clear by paragraph 319 on page 1508 at line 19 where they mention the evidential gap.  They say in the second sentence:

However, it is clear from the trial judge’s reasons as a whole that he accepted the medical evidence, reflected in the acknowledged synergistic effect of tobacco smoke and asbestos, that tobacco smoke and asbestos fibres operated inter‑dependently and thus cumulatively to cause to cause Mr Cotton’s lung cancer.

FRENCH CJ:   That is a statement almost about biological processes.  It is not a statement about risk, is it?

MR ABBOTT:   It is not a statement about risk at all.  That is my point.  All that the trial judge, with respect, could have said – as I go on, it is clear that the majority endorsed that summary of the trial judge’s.

FRENCH CJ:   The problem is, I suppose, this term “cumulative” can invite slippage between cumulative use to describe the biological processes – one dose of fibres is bad for you and an additional dose is worse in terms of biological processes – to cumulative as enhancing risk.

MR ABBOTT:   They get to the notion of cumulative risk, cumulative in the sense of enhancing risk, by employing the interdependence, that is, the multiplicative or synergistic effect.  That, in one sense, gives a cumulative risk but it does not give a cumulative cause.

HAYNE J:   Can I just interrupt you and go back and see whether I understand the sequence you say the majority are taking.  As I understand it, you begin at 305 where you are concerned with measurement of risk, is that right?

MR ABBOTT:   Yes, your Honour.

HAYNE J:   No regard at that point to the size of the risk.  You simply are concerned with the mechanics of measurement of risk, in particular, the case where someone is both a smoker and exposed to asbestos.  That is step one.  Step two you say is seen variously but amongst other places in 308, 309 where you move from method of calculating risk to a conclusion about cause without regard to the size of the risk that has been measure in a particular fashion, is that right?

MR ABBOTT:   Yes, your Honour.

HAYNE J:   Is the argument that you have advanced thus far any greater than the two steps I have identified?  Is there a third or fourth step that I have not identified in what I have said?

MR ABBOTT:   I do not think so, your Honour.  I could use more words to describe it, but I think it is the ‑ ‑ ‑

HAYNE J:   That is what I feared, Mr Abbott.

HEYDON J:   There is a further step, is there not?  In paragraph 319 on page 1508, the assertion that there was a cause, whether you call it an evidentiary gap or a logical gap, it is just an assertion.  It does not demonstrate what is being asserted.

MR ABBOTT:   No.  The end result justifies the beginning of the sentence.  We say that from this point on, at the very least, the majority have proceeded on the basis that interdependent possible causes of lung cancer they have found to have acted synergistically to produce a cumulative cause which, in the view, of the majority inevitably leads to the conclusion that the cumulative cause caused the lung cancer.  This was, in their reasoning, in our submission, an essential step because they have then found that the likelihood that such a cumulative cause was greater than any risk, which risk was based on epidemiological evidence, their cumulative cause finding was not, in our respectful submission, based on epidemiological evidence.

I think it is fair comment, if I may say this about what they have said so far, that there has been a confusing use by the majority of the label “cumulative” and it is not readily apparent on a first or even a 20th reading of their judgment as to how they made the transition from a finding of increased risk by reason of the synergistic effect of the interaction, so the epidemiological evidence said, of asbestos and smoking to a finding of cumulative causes in this particular case.

The best I can proffer by way of explanation is that their Honours, with great respect, appear to assume that the evidence of a synergistic effect was sufficient for them to take this step.  So at the heart of our section of this appeal, of the appellants’ case, it is our contention that the evidence did not permit a conclusion that the synergistic effect meant that the asbestos and smoking acted as a cumulative cause in this particular case.

KIEFEL J:   Are you going to deal with the evidence about what was meant by synergistic effect?

MR ABBOTT:   Yes, I am.  Rather, the evidence as to the synergistic effect did not permit anything more than a conclusion of a very small increase in the total risk as distinct from cause and nor did the rest of the evidence permit any jumping of the evidential gap or, indeed, a resolution of the evidential gap that Mr Cotton’s lung cancer was materially contributed to by asbestos fibre inhalation.  The majority had previously contrasted the case of Hannell at 314 at pages 1506 to the top of 1507, line 2, as a case:

where there were multiple sufficient concurrent cumulative causes of an indivisible disease.

They contrasted Mr Cotton’s case as being a case where the asbestos exposures were “successive”, but, of course, the tobacco smoking and the asbestos were concurrent.  In Hannell and their reference to Hannell as it related to Mr Cotton’s case, they are obviously talking at line 2 of causes of lung cancer which, in Mr Cotton’s case, they found were interdependent and, therefore, cumulative.  We say that it is obvious that what they are talking about are not causes, but risk factors because proof of cumulative interaction, interdependency, synergistic effect, whatever you like, cannot per se be proof of cause.  It can only be proof of an increase in risk from which an inference of causation may, in some circumstances, be drawn on the whole of the evidence. 

Chief Justice Martin took that approach and found there was no basis for such an inference.  He found, to the contrary, that the evidence supported a conclusion that it was overwhelmingly likely that the smoking was the cause of Mr Cotton’s lung cancer.  The majority then continued at paragraph 320 at appeal book 1508 to refer to the trial judge’s conclusions in these terms:

The trial judge’s conclusions that the separate carcinogens (tobacco and asbestos) and successive exposures to the same carcinogens (asbestos) operated cumulatively –

that is not “could operate” but “did operate” –

are reached in the course of the trial judge’s analysis of the statistical evidence.

Two comments can be made about that.  The first, it is clear that in that statement the majority are saying that the separate carcinogens and successive exposures to one of the carcinogens were found by the learned trial judge to have operated cumulatively and, therefore, causatively in the sense of causing Mr Cotton’s cancer. 

Secondly, they note that the trial judge had reached this conclusion as a consequence of his analysis of the epidemiological evidence.  At this point, I must refer very briefly to the epidemiological evidence because central to the ‑ ‑ ‑

HAYNE J:   Just before you do, does the proposition which your side of the record advances come down to three points:  the risk of developing this kind of lung cancer from asbestos is small; the risk of developing this kind of cancer from asbestos is larger if you smoke, but it is still small; the risk of developing cancer from smoking is very large?

MR ABBOTT:   And always very large, whether compared to any ‑ ‑ ‑

HAYNE J:   Does it boil down to those three propositions?

MR ABBOTT:   Yes.  I am not going to deconstruct the epidemiological evidence, but the majority and the trial judge relied very heavily on Dr Leigh, and as we will see, rejected the conclusions of the epidemiological evidence on the basis that it was predicated on a fallacious assumption of independence of risk factors, whereas they said it should have been predicated on interdependence of risk factors.

I will deal with Dr Leigh’s evidence very briefly.  We have actually set out in our written submissions what we want to say about Dr Leigh.  It is contained in the written submissions of South Australia, page 15, paragraphs 85 through to 88, which concludes at page 17, and rather than take up the Court’s time by reading those or referring to those pages, I invite the Court in due course to read what we have said about Dr Leigh and the way in which we say Dr Leigh’s evidence may have been misunderstood or misconstrued.

Very briefly, as we say in our submission at page 15, paragraph 85, we cite the evidence where Dr Leigh says a passage on which the majority and the trial judge extensively relied:

While the precise mechanism of interaction between asbestos and tobacco smoke in causing lung cancer is not known, it is not possible in my view to separate their effects in the individual case when both have acted and it is thus –

As we say at paragraph 87, he makes the assumption that both have acted, and of course, what follows by the use of the words “thus more probable than not” is really highlighting no more than the first statement, which is an assumption that both have acted, but this passage is used by the majority and indeed by the trial judge as proof of an expert that both did act rather than what we say it can only be used for is Dr Leigh is adverting to a situation, not where it has been proved that both have acted, but is merely putting forward a situation where he assumes that both have acted.

Dr Leigh’s evidence was epidemiological.  Although he had a medical qualification, his medical qualification was not directed towards supplying a medical cause for the lung cancer suffered by Mr Cotton.  His evidence was entirely directed to epidemiological evidence.

KIEFEL J:   Is that entirely correct because at some points in his report, does he not appear to speak from experience rather than actually drawing upon the models that he footnotes?

MR ABBOTT:   Of course he draws from his experience, yes.  A fair summary of his evidence, in our submission, is that he says it is unclear as to what the mechanism is.  He does not proffer an explanation as to what the evidence is, nor does he give a medical opinion that lung cancer is caused by X, Y or Z.  I now want to turn to the basis on which the majority, after considering Dr Leigh, rejected or said that one could put aside the epidemiological evidence.  The epidemiological evidence, the majority’s dealing of it, runs from paragraphs 321 at appeal book 1508 through to 326 at appeal book 1510.  At paragraph 326, after dealing with the epidemiological evidence, the majority say – and in our submission this is, with great respect, a completely wrong statement:

Thus, the statistical multiplicative model assumes that asbestos and tobacco smoking are independent carcinogens and the figure of 0.20 represents the probability of the two carcinogens acting independently to both cause the disease at the same time.

HEYDON J:   You say it is wrong, but is it not internally contradictory?  If they are acting in ‑ ‑ ‑

MR ABBOTT:   Yes.  The statistical multiplicative model assumes not that asbestos and tobacco smoking are independent carcinogens but they are interdependent carcinogens and the figure of 0.20 represents the probability of two carcinogens acting interdependently to both cause the disease at the same time.  Again we run into a problem of definition and the use by the majority and, indeed, by the trial judge of the words “interdependent” and “independent” and the contrast between those two becomes fairly crucial from now on in this judgment.

In our submission, the fact of the matter is, on the whole of the evidence, that when the epidemiological evidence spoke of multiplicative or the multiplicative model or multiplicative action between tobacco and asbestos they were all proceeding on the basis that the two carcinogens were somehow acting interdependently and not independently.  Put shortly, in our submission, the evidence was that on the assumption that two carcinogens acted independently, the expert evidence was that you applied an additive model.  On the assumption that the two carcinogens acted interdependently, you applied the multiplicative model.  So it is our submission that the statistical multiplicative model referred to in paragraph 326 of the judgment of the majority did produce a result premised on interdependence, not mere independence of two carcinogens.

The references to that – and I will not read from them – are Professor de Klerk at book 2, pages 827 to 828; Professor Berry at appeal book 2, page 860; and Professor Musk, at appeal book 1, page 8 and following.  The reason – or at least it appears from the judgment that the finding at paragraph 326 was an essential part of the reasoning of the majority because the paragraphs that then follow, but not exactly, thereafter proceed on the basis that there is a fallacy and that the epidemiologists, all of them, have fallaciously assumed in their calculations that the carcinogens acted independently rather than interdependently.

The error of this seems to have arisen from a discussion which the trial judge had with Professor de Klerk, which is set out at application book 1, pages 371 to 373.  I take the Court to book 1, 371 to 373.  This seems to have been the genesis of what we say is error on the part of the trial judge, which error was taken up by the majority and used to discard or put to one side all the epidemiological evidence.  It starts by the trial judge saying, halfway down the page:

Dr de Klerk, there is something about this mathematics which has got me puzzled, I must say.  I have heard evidence from a number of specialists, chest physicians, including Dr Musk, to the effect – a proposition which is challenged by the defendants in this case – that where there is an incidence of developing lung cancer by a person who is a smoker and where there is an incidence of the risk of developing lung cancer due to asbestos exposure if an individual is exposed to asbestos and is a chronic smoker in his or her case the effect of the two exposures is in some way to enhance the individual effect of the other.  It has been referred to as synergistic or multiplicative or a variety of way[s] but the substance of the evidence has been that if you are both a smoker and exposed to asbestos then your risk of developing lung cancer would be greater than if you had been exposed simply to asbestos alone or to smoking alone.  Is that a prevalent view among the consultants?---Yes.  Your actual risk would be increased.

He was then asked to look at some calculations.  I will not read that out.  At page 372, line 11, he is taken through by the trial judge in these terms:

You then, in your exercise, to work out the probability of the lung cancer due to the two carcinogens acting together, multiply P1 by P2?---Yes.

Each of them being less than 1, and you must get a figure which is less than P1 or P2?---Yes.

So the calculation will inevitably produce the probability of the combined effects which is less than either P1 or P2?---Yes.

That must be so, if you multiply two fractions.  The trial judge, however, cannot accept that.  He says at page 373, line 1:

That seems to run counter to the evidence that they have an increasing effect –

With respect, the trial judge is ignoring that multiplication is only referable to the amount of increase in risk, not to the totality.  Professor de Klerk says:

I think that’s again a sort of quirk . . . 

Can I just put something else to you for consideration?  When it comes to assessing the probabilities of different causes for an effect, isn’t there some doctrine that whether you multiply or add the causes depends upon whether they are truly independent?---Yes.

Does your calculation assume that these causes are independent?---Yes.

FRENCH CJ:   That is Bayes’ theorem, is it not?

MR ABBOTT:   Bayes’ theorem, yes.  Sir Richard Eggleston’s book was the leading text on that.  We say, with respect, that Professor de Klerk makes a wrong answer there.  In fact, his calculations that he had just been through have been to multiply and to assume that the causes are interdependent.  Then there follows a discussion, which I will not read out, but, in our respectful submission, that is the highlight of the evidence that would give the majority and, indeed, the trial judge any basis for what now follows in the decision of the majority.  They are paragraphs that I now intend to turn to.

FRENCH CJ:   If you apply Bayes’ theorem, which applies to probabilities of independent events – the simplest example is tossing a coin, the probability of one coin coming up heads is 1 on 2, the probability of the next coin coming up heads is also 1 on 2, but the probability of both of them coming up heads is 1 in 4.  I suppose if Bayes’ theorem were applied on the assumption that the probability that the event that smoking causes the cancer is independent of the event that asbestos causes the cancer, then the probability that smoking causes the cancer and asbestos causes the cancer is going to be smaller than either of the component probabilities.

MR ABBOTT:   It has to be.  I will deal with that very briefly when I come to the relative risk scenarios.  We say the error on the part of Professor de Klerk has been cited by the majority at the foot of page 1509 and used for their conclusion at page 1510, paragraph 326.  This is an important point in their judgment because from here on they proceed on the basis that the work that was being done by the epidemiologist is of only very limited assistance and, worse still, they assume that if the right model had been done on the assumption of interdependent carcinogens, not independent carcinogens, then the result that would have been obtained would be much, much higher than what was obtained by all the epidemiologists in the course of their evidence.

The conclusion of the majority at 326 is then used for the purpose of condemning or, to use a non‑pejorative word, describing the epidemiological evidence as suffering from a major and significant fallacy.  The majority, in our respectful submission, at paragraph 334 cite, we say obviously with approval, at pages 1511 and 1512 the evidence of the trial judge where he rejected the epidemiological evidence that had been done, we say correctly done, using a multiplicative model which presumed interdependence, not mere independence, of the two risks.  In particular, the majority referred to, or at least part of the passages at page 1512, line 20, where the trial judge said:

I therefore regard it as a major, and significant, fallacy in this litigation for the defendants to be contending that these mathematical results (correct for the precise application to which they must be limited) mean or support a conclusion that in cases of lung cancer with combined exposure to smoking and asbestos, it is only members of the smallest category of that group who have had their cancers caused by the combined effect of both carcinogens.  This fallacy is due, as both Professor de Klerk and Professor Berry accepted, to failing to recognise that the mathematical models which their proponents adopted are only appropriate for the combined effect of independent causative agents acting simultaneously but not for dependent or related causes acting in combination.

The majority then observe at paragraph 335:

It is apparent from these paragraphs and confirmed elsewhere in the reasons . . . that the trial judge accepted that tobacco smoke and asbestos operated cumulatively.  The medical evidence of Professor Musk ‑

was to the same effect.  They then set out Professor Musk and refer to Dr Leigh.  They then refer to the evidence of Dr Leigh that I have already criticised.  I will not read it out again.  They then come to the conclusion which we say is again a wrong conclusion because it enabled them to put to one side the epidemiological evidence.  At 336 on page 1513:

Once it is accepted that smoking and asbestos are not independent but rather cumulative causes of lung cancer, the epidemiological evidence has no direct application to the question of causation at law because it is based on a false assumption.

GUMMOW J:   What was the majority left with?

MR ABBOTT:   What was the majority left with?  Nothing.

GUMMOW J:   They seem to be destroying themselves.

MR ABBOTT:   With great respect, they then proceeded on the false assumption ‑ ‑ ‑

GUMMOW J:   Were they left with Dr Leigh?

MR ABBOTT:   They were left with Dr Leigh and only with Dr Leigh and on the assumption, which I will show the Court they then made, that if the correct epidemiological formula had been adopted the figures would have been much higher, unquantifiably.  They never quantified how much higher.  They say in 336 on that basis:

It was unnecessary for the trial judge to go through the process . . . of determining which statistical causation category applied in this case.  Once it is determined that tobacco smoking and all asbestos exposures operated cumulatively ‑

and remember this is in terms of risk ‑ ‑ ‑

HAYNE J:   We have gone from “can” to “are”.

MR ABBOTT:   Yes; exactly.  They have gone from “risk” to “cause”.  The only remaining issue is whether each asbestos exposure made a material contribution, which is the second part of my submissions.

We say that what has happened here is unfortunately a misapprehension and a misunderstanding because the risk contribution of two carcinogens acting together, that is, synergistically, is the product of the individual risk contributions, and that is the exercise for, on the assumption of interdependent carcinogens, but it will always be the case in this particular case that because the tobacco alone risk was very high, and the asbestos alone risk was very small, the effect of multiplying the two was to give a combined risk is to be a much smaller risk than that of tobacco alone, and not greater, certainly it could never be greater than tobacco alone.  But the majority and the trial judge seemed to be wanting to say at all times, if you combine the two, you have to get a risk which is higher than tobacco alone.  That is the problem that they could not get over.

CRENNAN J:   I think it was referred to by the trial judge as enigmatic. 

MR ABBOTT:   Enigmatic, yes, I am just coming to that.  I can just very briefly give the Court the passages where they reject or do not accept the epidemiological evidence.  At 336 I have repeated the false assumption.  The false assumption was, as we know, the multiplicative method only dealt with independent and not interdependent.  At 334 they say the basis for this fallacy – sorry, I have referred the Court to the passage where the trial judge gave the reason for the fallacy at the end of paragraph 334 on page 1512.  But the trial judge had already said much more in the same vein.  If the Court goes to appeal book 3, page 1198, paragraph 324 it talks about the cross‑examination of Mr Rogers.  I will not read it out, but the last sentence of the trial judge’s views of Mr Roger’s evidence is in these terms:

It follows, in my respectful opinion, that there must be an unspecified fallacy in these calculations which failed to report the chance of developing lung cancer from a combined exposure to tobacco and asbestos.

He then said just above that, his conclusion was:

the instance of cancer due to a combination of asbestos exposure and smoking, among people exposed to asbestos, must be greater than the incidence attributable to smoking alone, or at least involve an earlier onset.

That, in his eyes, gave rise to the unspecified fallacy.  At paragraph 517, page 1277, book 3, the last two sentences at the bottom of the page:

As Professors Leigh and Berry each acknowledged, this is a mathematical approach appropriate only for calculation of the effects of independent causes, rather than interdependent causes which have a synergistic effect such as occurs with exposure to tobacco and asbestos together.  The employment of such a method –

That is, the multiplicative method as used by the epidemiologists –

involves a mathematical fallacy if the product were to be treated as measuring the combined chance of developing a lung cancer as the result of exposure to both asbestos and tobacco.  The synergistic nature of the relationship, and the evidence of the statisticians Dr Leigh and Professor Berry on this issue, demonstrates clearly that the chance of developing lung cancer from exposure to both asbestos and tobacco must be greater than the chance of developing asbestos from exposure to either carcinogen alone.

FRENCH CJ:   If you regard tobacco and asbestos as independent causative agents, or potentially causative agents, then you can understand the multiplicative effect in the context of what I put to you earlier, in that you have, as it were, one bit of bad luck if the tobacco exposure causes a cancer and two bits of bad luck if the asbestos exposure causes a cancer and two bits of bad luck is less probable than one bit of bad luck.  I am putting it very simplistically, but that is really the essence of the use of a multiplicative approach to independent events.

MR ABBOTT:   Your Honour, I can apply it to what happened in this case because, in truth, there is no fallacy, mathematical or otherwise, because all the figures demonstrate is that when the risk for asbestos is small and the risk from tobacco great, the increase due to the synergistic effect, the multiplicative effect is likewise small.

FRENCH CJ:   Synergistic is something different, is it not, from what I just described?

MR ABBOTT:   They called it synergistic ‑ ‑ ‑

FRENCH CJ:   That is where there is an interaction between the two, they are not independent events.

MR ABBOTT:   They equated synergistic with multiplicative, so one takes the multiplicative exercise ‑ ‑ ‑

FRENCH CJ:   Well, there is a conceptual difficulty.

MR ABBOTT:   Yes.  If you took an example, if the relative risk, and we have seen figures of relative risks, for example, taking Professor de Klerk’s figures at page 1509 – if you took Professor de Klerk’s figures and said that the RR, relative risk of smoking was say, 20, and they are not the figures that he has here, and the relative risk of asbestos was 1.1 – he has taken it as 1.3, I am using a simple example – the combined effect of both, multiplying the two, would give a result of 22, which is an increase of only two in the combined relative risk of both carcinogens and this is much smaller, of course, than the relative risk of smoking alone on the example I have posited, but if you applied to ‑ ‑ ‑

FRENCH CJ:   The relative risk is not the probability, the attributable fraction is the probability.

MR ABBOTT:   No, the attributable fraction is the probability.  You can see this demonstrated that if the relative risk for smoking was, say, 20 on Professor de Klerk’s figures and the relative risk for asbestos was the same, 20, then multiplying these risks would give 400, giving an increase of 360, which translated into percentage terms in terms of the attributable fraction would give a huge increase.  So, I mean, it works.  The multiplicative model takes into account interdependency.  It is just as I said once but I will say for the last time, where the risk from tobacco is very great and the risk from asbestos is very small, multiplicative model gives a result which the learned trial judge could not comprehend or was not prepared to comprehend.

FRENCH CJ:   That might be a convenient time.  We will adjourn till 2.15.

AT 12.46 PM LUNCHEON ADJOURNMENT

UPON RESUMING AT 2.16 PM:

FRENCH CJ:   Yes, Mr Abbott.

MR ABBOTT:   As I said before the Court rose, because a majority rejected the multiplicative model, which, on our submission, the epidemiologists had used and which did allow for the interdependence of the two carcinogens, as a result they either rejected or put to one side the epidemiological evidence and it therefore followed, on their analysis of the interaction of the two carcinogens, that tobacco smoking and asbestos inhalation always operated cumulatively.  “Cumulatively”, on their definitional terms, always meant greater than each and “cumulatively”, on their terms, always meant that the smoking and asbestos together caused the cancer.

In our submission, that must be and can only be the effect of what the majority said at page 1513 of book 4 at paragraph 336.  The sentence I have already taken the Court to, the third sentence in that paragraph, reads:

Once it is determined that tobacco smoking and all asbestos exposures operated cumulatively, the only remaining issue is whether each asbestos exposure made a material contribution.

They have assumed causation because cumulatively is arrived at as a consequence of them having acted interdependently.

In our submission, on a close analysis there were two strands to the majority’s decision in relation to ground 1, on both of which we take issue.  The first strand I have just mentioned – that the epidemiological evidence proceeded on the basis of independent carcinogens and not interdependent carcinogens and that the results therefore obtained by the epidemiological evidence must be lower, and that it could somehow be inferred that asbestos exposure when combined with smoking made a material contribution, and a material much greater than that attributable to smoking alone.  That was one way.  The second way was that the two carcinogens were capable of acting independently and if they acted interdependently as well as independently then the sum total was cumulative.  Cumulative equalled causative in the sense that a material contribution must have been made.

The problem with all of this, as I will turn to very briefly in part two of my submissions, is that it ignores any assessment on any view of how much greater any of this additional contribution, rightly or wrongly arrived at or inferred rightly or wrongly by the majority and the trial judge would be in relation to the South Australian exposure.  As we said in our written submissions at paragraph 51 on page 9, there is a further flaw in this.

We have said that Chief Justice Martin referred to further passages from the trial judge’s reasoning in relation to the synergistic effect, explaining that the logical flaw in this reasoning was the failure to appreciate that while the incidence of lung cancer within the community as a whole will be greater for those exposed to both carcinogens than to only one, that tells one nothing about the proportion of people within that group who have contracted the disease but who would have contracted it irrespective of their exposure to one or other of the carcinogens.  That assessment required an evaluation of the sufferer’s relative exposure to each carcinogen and the likely consequences of each.  The footnote to the judgment of Chief Justice Martin refers to that.

In short, the majority were able to disregard the evidence, proceed on an erroneous basis and conclude that the contribution made by the asbestos exposure must have been, in some unknown way, material because the total risk must have been, in some unknown way, higher by which process a material contribution was established.  There are three other matters that they mentioned which I must very briefly mention which they may have taken into account.  It is not clear that they did.  Those are dealt with in our written submissions at page 18, paragraphs 95 to 98. 

We say in those paragraphs and we make the point in paragraph 94 that in dealing with ground 1 the majority left it up in the air in the section that deals with ground 1 and perhaps were intending to return to discuss matters that more properly or could have been included in ground 1 when they dealt with grounds 2 and 3 in the second part of their reasons, because, as we say in paragraph 95, the majority’s conclusion in that section of the reasons that the aggregate asbestos exposure materially contributed to the lung cancer appears to have been based upon three things.  Firstly, the acceleration or early onset of Mr Cotton’s cancer, secondly, Mr Cotton’s exposure to intermittent high short‑term exposures of asbestos fibres and, thirdly, the lack of any safe threshold level of asbestos.

In paragraphs 96, 97 and 98 we say why this Court should reject those as reasons.  I need not trouble the Court by reading paragraph 96.  In paragraph 97, again the majority acknowledged that it was not suggested that this might affect the risk and, thus, of the three reasons which they set forth, it seems, as we say in paragraph 98 of our written submissions, the majority placed significant reliance upon the acceleration or early onset of Mr Cotton’s lung cancer and whilst it may be accepted that he developed lung cancer earlier than most with a history of smoking, Chief Justice Martin pointed out he was still within the normal range, albeit at the lower end.  More importantly, this case was never run as an acceleration case. 

So the conclusion that we come to of the majority in relation to ground 1 was that they found on the basis of an indivisible disease the actual cause of which, unlike Bonnington, was unknown, possible causes having been identified, they found both causes acted in a cumulative way in the sense which they defined “cumulative”, and they found that each cause operated to cause or make a material contribution to the disease, namely, the lung cancer and they failed to consider the separate contributions, having come to that conclusion, but at the same time purported to apply Bonnington, as my learned friend, Mr Watson, has said, to the effect that they found that material contribution was any contribution which was not de minimis and, as a result of that, came to the conclusion that liability should attach to both the EWSD South Australian exposure and the Millennium exposure.

I now want to deal then with part two which deals with ground 2, the failure of the majority to deal with the contribution of the individual exposures separately.  We have set out some facts in our submissions at pages 3 and 4 which are relevant to this consideration.  Our submissions at page 3, paragraphs 9 and following deal with the facts which we say are relevant.  We deal with the relative risk scenarios in paragraphs 10 and following and at paragraph 15 on page 4 we refer to the fact that various of the witnesses carry out an analysis of the attributable fractions or probabilities for a population of lung cancer sufferers exposed to the levels of asbestos and smoking that Mr Cotton was exposed to.

We then note that their evidence divided the total risk into four scenarios as the possible sources of risk and the experts provided differing probabilities for the four scenarios, due mainly to the differing assumptions they made about the level of Mr Cotton’s exposure to asbestos and smoking.  The most favourable for the respondent, or for Mr Cotton, was Professor de Klerk, who used relative risk of 1.3 for asbestos and 7.7 for smoking and that gave a probability of 67 per cent for smoking only, three per cent for asbestos, 20 per cent for both and 10 per cent for background.  As we have said, in other words, asbestos was only an acting or operating agent in 23 per cent of cases, of which three per cent it was probable that it acted on its own, and a further 20 per cent of cases in combination with smoking, which was the third scenario.

We have given figures there in paragraph 18 for Dr Leigh and Professor Berry.  We have then referred to the fact that – in the last sentence in paragraph 20 of our submissions - it would be safe to assume that the percentage attributable to the South Australian exposure alone would be less than one per cent.  So we are talking about, on the body of evidence that was produced in this matter, a very low probability that the South Australian exposure was in any way likely as a risk factor.

In our written submissions we briefly dealt with this at page 19, paragraphs 101 and 102 and it is those submissions that I want to enlarge on.  I adopt, without reading, paragraphs 101 and 102 of our submissions and I also adopt the submissions of my learned friend this morning who dealt with this very point, but from Amaca’s perspective.

We want to make some additional points, if the Court pleases.  We complain that neither the trial judge nor relevantly the majority determined, or had due regard to, the true nature and extent of the South Australian exposure and the significance of that true nature and extent to the issue of causation.  It is certainly correct that the majority, nor the trial judge assessed separately the contribution, if any, of the South Australian exposure to the contraction of Mr Cotton’s lung cancer.

There was a total failure to find what contribution, if any, the South Australian exposure made, other than it was said to be by the majority a material contribution.  Secondly, there was a failure by the majority to conduct what we say they recognised they had to conduct, namely a separate evaluation of the South Australian contribution and, as my learned friend, Mr Watson, has said this morning, their approach means that the EWSD contribution is liable for Millennium’s contribution on that scenario, even if on a true construction of the evidence the South Australian contribution made no material contribution to Mr Cotton’s lung cancer and, of course, vice versa.

Even a finding, if it could be made, which we say it was not, that they were capable of making a material contribution does not mean that they did, in fact, make a material contribution.  A finding that each made a contribution does not also mean that each contribution was material.  The majority at paragraph 340, page 1514 of book 4 recognised that the trial judge’s task had been to determine whether each exposure had caused or materially contributed to the contraction of Mr Cotton’s lung cancer.  That so much is clear.  At 341 on page 1514 the majority also recognised that the trial judge had failed to apportion what the majority described in paragraph 341 in the last sentence, as:

the cumulative dose or RR as between the exposures at EWSD and Millennium.

That phrase is telling:

did not apportion the cumulative dose or RR –

The cumulative dose cannot be the relative risk.  It shows that they are confabulating or confusing relative risk with causative dose when they use a cumulative dose or RR interchangeably.

So putting to one side the question of latency, which has got nothing to do with us, it is clear that the trial judge had proceeded on the basis, as the majority say at paragraph 342:

It is also the case that the trial judge repeatedly considers and answers the question whether it was appropriate to have regard to the combined exposure to asbestos at each of EWSD and Millennium in determining whether it caused or materially contributed to Mr Cotton’s condition.  However, that was an issue at trial.

The majority, at 343, however, after citing the paragraph that my learned friend has already taken the Court to, at the end of paragraph 342 at page 1515, as my learned friend has already said, fall into error with respect, because they characterise a statement by the judge of capability, that is, the possibility of exposure, and they translate that into the fact of causation in saying:

In this paragraph the trial judge finds that the asbestos fibre exposures in the successive periods operated cumulatively to cause lung cancer (in addition to the individual periods of exposure being sufficient to cause the disease).

In our submission, that error is an error which thereafter infects their entire process of reasoning for the balance of this section of their judgment.  The effect of what they have done, obviously, is to translate a finding of the trial judge as a potential contribution to risk into a finding of actual contribution of injury in this particular case and we say this is the key error which Chief Justice Martin exposed in his reasons which run from, as my learned friend took the Court to this morning, paragraph 166 at appeal book 1453 right through to paragraph 193 at appeal book 4 page 1468.  Chief Justice Martin’s starting point – and I am only going to read a couple of paragraphs of this section of his judgment – is paragraph 166.  His Honour said:

Accordingly, consistent with established and conventional principle, it was necessary for the trial judge to make specific findings with respect to the extent of Mr Cotton’s exposure to respirable asbestos fibre while he was employed at EWSD, and then to determine whether, on the balance of probabilities, that exposure caused or materially contributed to his lung cancer.

There would be no contention that that was indeed the task of the judge.  The Chief Justice then concludes at paragraph 193 at page 1468, the passage my learned friend took the Court to, which is really the answer to this at line 1:

But the only question addressed and resolved by the trial judge was whether the aggregate exposure experienced by Mr Cotton during both periods of employment caused or materially contributed to his condition.  That was not the question which the trial judge was required to resolve.

The more relevant passages - and I will not read them out – I ask the Court note that in our view the more relevant passages where the Chief Justice is properly critical of the trial judge are at paragraphs 167 on page 1453; 168 over the page and then 181 where his Honour said:

These paragraphs lend further support ‑

His Honour is continually referring back to the trial judge’s evidence and 182 which I must read because ‑ ‑ ‑

HEYDON J:   It has been read already.

MR ABBOTT:   Which has been read already by my learned friend.  We say it is significant that although the majority often stated their disagreement with the observations and views of Chief Justice Martin and paragraphs, for example, 337 and 338 of their judgment at appeal book page 1513 and 338 on the same page are passages where they state that they respectfully disagree with the views and observations of the Chief Justice.

Nowhere in dealing with grounds 2 and 3 from paragraphs 340 onwards do they refer to Chief Justice Martin’s views and observations, whether critically or otherwise.  His views seem to have been, if not ignored by the majority, then put to one side.  Certainly nowhere do they otherwise explain how they made the transition from the trial judge’s finding of potential contribution to risk to a finding of actual contribution to injury.  So they concluded at paragraph 353 at the foot of page 1517, line 37:

we are satisfied that it was open to the trial judge to conclude, as he did, that the asbestos exposures at each of EWSD and Millennium made a material contribution to the contraction of lung cancer by Mr Cotton.

Our complaint is that there is no reasoning that supports that view.  It was in the face of evidence that did no more than demonstrate an increase of risk occurring, not that it did occur.  The passage that my learned friend, Mr Watson, has already taken the Court to this morning which then follows we say this seems to be the majority perhaps having some misgivings about some of the trial judge’s conclusions, with respect.  They say at page 1518 at the end of paragraph 353:

However, even if the findings were flawed it is clear Mr Cotton was exposed to very significant levels of respirable asbestos fibres over each employment period ‑ ‑ ‑

FRENCH CJ:   That is the sentence you began with, I think.

MR ABBOTT:   Yes.  That is the assertion of fact with which I conclude this section.  Nowhere in their reasons do they give us the train of logic which led to that view.

We say the only causal link that is proffered is the accelerative link that I have already referred to but, as we know and as Chief Justice Martin said in the passage I have already referred the Court to, this case was not run on acceleration basis.  So we say and submit that in relation to ground 2 there was a dearth of evidence and no basis for the conclusion of the majority and that the majority erred in upholding the decision of the trial judge in this respect. 

That brings me to the third part which is very brief.  I wanted to say something about Bonnington Castings v Wardlaw which is perhaps different from what my learned friend, Mr Watson, has said this morning, and to offer a couple more comments in relation to Bonnington Castings v Wardlaw because this is a decision on which the respondent, in her submissions, relies and is relied on for the proposition that a material contribution, that is, a contribution which is more than de minimis, is sufficient to make out causation.  Importantly, in the context of this appeal, Bonnington is a case where there was a proven material contribution to injury itself, not merely a material contribution to the risk of injury, which is what we have if we have anything here.

GUMMOW J:   This notion of de minimis may come from the argument at page 617 about ten lines from the bottom of the page:

Of the dust inhaled the amount contributed by the swing grinders was not negligible or inconsiderable.

MR ABBOTT:   Yes, it may have, your Honour.

GUMMOW J:   The last sentence of that paragraph is important too:

The result of the appellants’ contentions would be that in order to succeed the respondent would have to eliminate all innocent sources.

MR ABBOTT:   That is very significant.

GUMMOW J:   That seems to be the setting in which the House of Lords then gave their reasons.

MR ABBOTT:   Yes, for, as we have heard, the exposure to silica dust had two sources, a tortiously responsible source and a non‑tortiously responsible source.  Lord Reid at page 620 held that it was not enough to show that it was possible that the injury was caused by the dust from the swing grinder, that it was necessary to find on the balance of probabilities that the dust from the swing grinder caused or materially contributed to the injury.  So we say that Bonnington Castings is authority for the proposition that you still need to prove a material contribution to the injury, not merely a risk of contribution to the injury.  On the facts of Bonnington, the plaintiff was able to discharge the onus on it.  Because of the nature of the plaintiff’s injuries, it could be shown by medical evidence that both sources of dust operated cumulatively in the case of Mr Wardlaw to cause his injury.  At page 621, Lord Reid explained at the top of the page:

The medical evidence was that pneumoconiosis is caused by a gradual accumulation in the lungs of minute particles of silica inhaled over a period of years.  That means, I think, that the disease is caused –

I emphasise “caused” –

by the whole of the noxious material inhaled and, if that material comes from two sources, it cannot be wholly attributed to material from one source or the other.

HAYNE J:   What is said by his Lordship in that part of his speech is to be understood also in light of the earlier statement of facts by his Lordship, which is reproduced at 614 from the last 10 or 12 lines, which seems to be taken entirely from the speech of Lord Reid and explains the report at 618, commencing:

LORD REID stated the facts and continued -

Thus, the de minimis reference, to which some attention has been focused, may better be understood having regard to his Lordship’s statement of the facts as recorded.

MR ABBOTT:   I am grateful, your Honour, for directing me to that passage on 614.  Lord Keith was, in our submission, to a similar effect at page 626, but I will not read out that part of his judgment.  It has already been discussed.  Bonnington, in our submission, is readily distinguishable from the present case.  Here the medial evidence was unable to supply or identify a cause.  Not even Dr Leigh could do that.  In Bonnington, the medical evidence did supply a cause and the medical evidence enabled a finding that the operating agent was silica dust from both sources.  The only issue left was the materiality of the proven cause -– that is, the proven contribution of the dust from the swing grinders.

In relying upon Bonnington, the majority and the respondent in her submissions assume that the asbestos was the operating agent.  They do not proffer evidence to prove that it was the operating agent, whereas proof that it was the operating agent is the very issue which needs to be determined in this case and was not determined.  The medical evidence shed no light on the question of whether or not asbestos or tobacco smoke was the operating agent.

The epidemiological evidence did not allow a finding to this effect either.  The synergistic effect did not allow or require a finding that the asbestos and tobacco smoke operated together in every case.  At most, the results of the epidemiological evidence permitted a finding that sometimes they acted ‑ ‑ ‑

KIEFEL J:   At some point I think you had promised to take us to the evidence about what the synergistic effect was actually meant to mean – not in the reasons of the judges but in the expert evidence itself.  Can I say, from my point of view, it is not entirely clear to me what you say.  If once the errors shown in the Court of Appeal are sufficient to cast doubt upon their reasoning, we are nevertheless left with the decision of the trial judge which, in relation to materiality, seems to be based in large part upon this synergistic effect creating some greater risk, although it does not seem to have been quantified in a particular way.

MR ABBOTT:   No, it is unquantified.

KIEFEL J:   But it is mentioned a number of times in his Honour’s conclusion, such that one infers it was of importance.  What was the evidence about the synergistic effect and what do you say his Honour was saying about it?

MR ABBOTT:   Professor Musk, at appeal book 1, pages 8 and following he is asked this at line 12:

Firstly, do you have a view as to the association between asbestos and cigarette smoking? ‑ ‑ ‑Yes.  In our data from the Wittenoom people the multiplicative model pretty well fits the data best.

Do you maintain that as your view? ‑ ‑ ‑Yes, I think that fits the data well and that’s a convenient way of looking at it.  A multiplicative model is the model that I would favour, not that I think it’s critically important clinically or anything.  That’s the model I favour.

Returning to my earlier question, how is it thought that asbestos fibres and the carcinogens in cigarette smoke interact in this way? ‑ ‑ ‑ The production of cancer is thought to be due to a sequence of changes in the DNA of the cell, a sequence of mutations, and it’s thought that cigarette smoke and asbestos act at different stages of those changes, different stages in the process so that if one has increased the risk by five and the other one is there too, well, the risk attributed to that is superimposed on the risk of five so it multiplies that risk rather than just adds to it, but that’s a sort of empirical observation that the multiplicative model fits and the interpretation of that is a convenient sort of hypothesis to proceed on.

GUMMOW J:   At page 9, about line 10 there is a clear explanation of the mesothelioma situation.

MR ABBOTT:   Yes, in contrast to lung cancer.  So we say, in answer to your Honour’s question, no one could explain the biological mechanism for the interaction, only that, to use Professor Musk’s words, “the multiplicative model pretty well fits the data best.”

KIEFEL J:   His Honour is talking about the interaction as an explanation of why the model he has chosen is acceptable, is that right?

MR ABBOTT:   Yes, your Honour.

KIEFEL J:   Is there any further discussion by the experts as to a particular effect synergy and interaction which somehow has one agent promoting the other, which seems to be implied in his Honour’s approach?

MR ABBOTT:   No, your Honour.  The additive model was put as the mere addition of one to the other.  It was said that the multiplicative model equalled a synergistic effect.

KIEFEL J:   Only because the two of them are interacting.

MR ABBOTT:   Only because it is multiplicative. 

HAYNE J:   Well, you say there is no other evidence.  What about Dr Leigh’s report at page 900?  In volume 3, page 900 needs to be read also with page 904 and 905.

MR ABBOTT:   At page 900 he said they act “multiplicatively” at approximately line 10.

KIEFEL J:   Line 35 “a synergistic effect”.

MR ABBOTT:   Yes.  That may be where their words “synergistic effect” comes from.  Over on page 901, just below the middle of the page, is the famous passage that is referred to in the judgment.

HAYNE J:   That is a passage, is it about “when both have acted” at ‑ ‑ ‑

MR ABBOTT:   Yes, exactly, that is the “when both have acted”.  The multiplicative effect is referred to at page 904 in the last paragraph.

FRENCH CJ:   The reference to a multiplicative use – use the term multiplicative in this context – is not used, I think, with mathematical precision, it is just to contrast with – another way of saying synergistic in the sense that it is greater than the sum of the parts.

MR ABBOTT:   Exactly, your Honour.  So far as transcript references are concerned, Dr Leigh, at page 212, appeal book 1, referring to an article by “Vanio and Buffetta” at the top of the page, gave a long answer beginning at line 5 about the development of cancerous cells and then what tobacco did and at ‑ ‑ ‑

CRENNAN J:   At the bottom of the page there is a reference to creating a synergy, so the total risk is greater than the sum of its parts.

HAYNE J:   What is meant by the witness by that is apparent from page 210 of the book at 43, is it?

MR ABBOTT:   Yes.  Finally, the last reference I can proffer is at page 257 of the same book, line 18.  In re-examination another concept is introduced of “supramultiplicative”:

My learned friend asked you some questions about the multiplicative effect and said there were a range of views . . . From what to what does the range extend?‑ ‑ ‑The range extends from additive to supramultiplicative, or even slightly less than additive to supramultiplicative.

Supramultiplicative meaning what?‑ ‑ ‑More than multiplicative.  The combined effected is even more than multiplying them together; multiplying them and then adding some more.

Then he is asked:

Is there in fact a biological explanation for the multiplicative effect?‑ ‑ ‑Yes, there are a number of biological hypotheses or proposed mechanisms that are listed in papers or cited in the original report or again in the more recent paper, the Vainio and Boffetta list, the four mechanisms.  I can read them out but they’re in there.

Are they, to your mind, convincing hypotheses?

Damning them with faint praise, he says:

They’re all plausible, and in some cases experimental basis to them.

You have read the various papers.  Where do you stand . . .  As I said, I believe that the general consensus, in my opinion, is that it’s approximately a multiplicative effect in the majority of cases.

We say that is a fair assessment of the evidence at its highest.

GUMMOW J:   Is there any evidence of the role of genetics in this?

MR ABBOTT:   Do you mean predisposition via genetic, or the effect of these carcinogens on a gene?

GUMMOW J:   No, predisposition.

MR ABBOTT:   There is a mention, and I cannot bring it to mind, about it is yet unknown as to what the cause is or the likely cause of why people ‑ ‑ ‑

FRENCH CJ:   The family history in this particular case did not figure in the evidence?

GUMMOW J:   It did, did it not?

FRENCH CJ:   It was mentioned, but ‑ ‑ ‑

MR ABBOTT:   Not that we are aware of.  Some of experts proffered genetic predisposition as one possible factor which might impinge on the impact of why some people got lung cancer when exposed to more than one carcinogen, and why some people did not get cancer when exposed to the same amount of carcinogens over the same time.

GUMMOW J:   What is page 257 talking about?

MR ABBOTT:   Page 257?

GUMMOW J:   Yes, the first two paragraphs.

MR ABBOTT:   The passage I have just read from, Dr Leigh being asked about multiplicative effect?

GUMMOW J:   No, page 257, the top of the page.

MR ABBOTT:   I assume it is a reference to Mr Cotton’s family history and the possibility of some genetic ‑ ‑ ‑

FRENCH CJ:   He refers on the previous page to having noted that family history.

MR ABBOTT:   Yes, the report.  I must say, I have not read that report.

GUMMOW J:   Do these epidemiological studies take this sort of thing into account ‑ ‑ ‑

MR ABBOTT:   Yes, I think it is a question of which epidemiological ‑ ‑ ‑

GUMMOW J:   ‑ ‑ ‑ as a matter of scientific method when they are looking at populations?

MR ABBOTT:   I cannot answer that, I am sorry.  Having said that I cannot answer that, is my last answer.  I have finished my submissions, if the Court pleases.

FRENCH CJ:   Thank you, Mr Abbott.  Yes, Mr Jackson.

MR JACKSON:   Your Honours, may I say that we rely on our written submissions, of course, and we adopt what has been said by those before us.  There are number of matters with which I wish to deal relatively briefly.  Your Honours, Mr Cotton was, of course, a smoker for 26 years and he died of lung cancer.  Of course, there is nothing surprising about that in the sense that lung cancer is a possible, indeed, a likely result of smoking and for a long‑term smoker lung cancer will, in effect, get you in the end if nothing else has in between and done so first.  That is the evidence of Professor Musk at volume 1, page 14, lines 12 to 21.

Your Honours, if one is looking for causes which are alternatives to smoking and in the case of a smoker who has died of lung cancer or contracted cancer, there is a need to do so because litigation against the persons who induced the smoking is likely to be difficult because of identification of persons responsible over a long period and other matters, including the question of contributory negligence and perhaps, in places where it is available, Valente and a greater emphasis now on the ability to obtain 100 per cent, as it were, contributory negligence in some jurisdictions.

That means that it is necessary to look for other circumstances which can be causes of lung cancer – and one possibility is exposure to asbestos.  We would accept that, on the evidence, three things were established in relation to asbestos.  One was that exposure to asbestos fibres can be a cause of lung cancer – I say a cause of lung cancer.  The second is that the evidence suggests that if a smoker – and by that I mean a regular long‑term smoker such as the deceased – has an exposure to asbestos the risk of contracting lung cancer from that cause is increased.  The third is that, to the extent that one can engage in the mathematics or quasi‑mathematics of things the increase in the risk is not merely in the summation, adding the two together as it were.  There is an element, though not a full element, of multiplication.  That is a matter that your Honour the Chief Justice was discussing a few moments ago with my learned friend.

Your Honours, all that, in our submission, refers to an increase in risk.  In our submission, try as one may in this case, the evidence – I am going to come to the evidence in a little more detail in a moment – does not demonstrate more than that the risk of lung cancer was increased and that the exposure to asbestos may have played a part in the lung cancer.  It does not tell you what part.

Now, your Honours, may I deal first with the contention that the evidence demonstrated that there was a medical cause that one could identify.  That is the view which appears to have been medical as distinct from an increase in risk.  That is the view that appears to have been taken by the majority and it is also relied on here by the respondent.

What I wanted to do, your Honours, if I could indicate where I am going on this, is to go to the various passages of evidence which in our submission indicate that the evidence demonstrated that there was an increase in risk but it did not demonstrate more than that.  Could I go first to the reference which one sees in volume 4 at page 1512 to which your Honours have been taken more than once, and that is to the passage from Dr Leigh’s evidence to which the majority referred at the bottom of page 1512 and the top of page 1513.

That evidence has been the subject of considerable attack by our learned friends from South Australia and I shall not repeat what they have said.  But there is a further factor in relation to his evidence, and it is that it makes it apparent in our submission that to determine the part played by exposure to asbestos for legal reasons it is appropriate and necessary to go to the epidemiological studies.

Your Honours will see that at a reference that was mentioned by your Honour Justice Hayne a few moments ago, and that is in volume 3, the report of Dr Leigh.  The passage quoted is at page 901 in the second new paragraph on the page, but when one goes from that to page 904, the last paragraph on the page, what your Honours will see is that Dr Leigh then says:

Whilst it can be argued that asbestos exposure multiplies the risk of lung cancer, whatever the level of smoking, that smoking and asbestos exposure are indivisible in the causation of an individual lung cancer, and that any asbestos exposure multiplies the risk of lung cancer due to smoking by some quantity greater than one, it is nevertheless possible, if required for legal or administrative reasons, to partition attributabilty to smoking and asbestos under a variety of mathematical risk models.

What the doctor is saying there, your Honours, is that when one moves to try to put a figure on it, as it were, one goes to the epidemiological studies.  Your Honours, if I could go to two further references in his oral evidence in volume 1, you will see at page 210, at the bottom of the page, when coming to explain what he meant by the synergistic effect of asbestos with tobacco in causing the lung cancer, about line 40 on page 210, he spoke in terms of risk and, your Honours, he said:

What I mean is that tobacco and asbestos, in my opinion, act in some way together to cause lung cancer in an individual exposed to both in that in some way – there are a number of hypotheses discussed . . . but basically a person exposed to both has a higher risk than the sum of the two risks added together.  They combine to create a synergy, so the total risk is greater than the sum of its parts –

Your Honours will see that expanded a little on the top of the next page.  So, your Honours, the observations that he is making are observations which in the end come down to questions of risk.  Could I refer also, your Honours, to page 214 and in the passage commencing about line 11 Dr Leigh was asked:

notwithstanding all of this information, the precise mechanism of interaction is not known.  Therefore, what conclusion do you draw from that –

And your Honours will see the conclusion expressed as being:

in the individual case when both agents are there, they must both have had something to do with the tumour development.

Well, your Honours, they must have had something to do, but if one is looking to see what that means, and in the earlier passage to which reference was made at page 210, what he seems to be saying is that they increase the risk of developing lung cancer. 

FRENCH CJ:   Is it right to say that the evidence as to the existence of a synergistic effect is entirely based upon the epidemiological studies and that the question of a biological mechanism by which that might occur is simply a matter of hypothesis on the evidence, I think.

MR JACKSON:   Yes, your Honour, that is what we contend the evidence says.  Now, your Honour, I accept that the passage from Dr Leigh that comes from page 901 in his report, and this is at page 335, is one that has an element of ambiguity about it.  Your Honours will see, as does to a degree what he says at page 214 in the sense when both agents are there and he uses slightly different expression in the passage from page 901, he said “when both have acted”.  What is apparent is that it is not possible to say how they have acted.  What is being said is that you have a situation where both are there and the possibility in terms of risk of the development of lung cancer is increased.

Your Honours, I was going to go next to the reliance also placed by the majority, if I could go back to paragraph 335 in the majority’s reasons at page 1512 in volume 4.  You will see at about line 39, or really throughout the paragraph, that in addition to what was said by Dr Leigh, reliance was also placed by the majority on what was said by Professor Musk.  There is a reference there at about line 41 to the original transcript at page 392. 

I will come to that passage in just a moment, your Honours, if I may, but I just wanted to say this about it if I could.  If one goes to the full passage of the evidence of Professor Musk, one will see two things.  One is that he says that the exact consequences are not known, but the other is that he too is speaking in terms of risk.

May I take your Honours to that.  In volume 1, your Honours - page 7 in volume 1 is page 392.  Could I go to the bottom of page 6 and you will see at the bottom of page 6 about line 42 he was asked:

So is the means by which carcinogens cause cancer not known to medical science?---At a biological level, no.

Then the next question he was asked:

Can you tell his Honour what are the causal implications for a cigarette smoker who was occupationally exposed to asbestos?

Your Honours will then see that he says:

Well, cigarette smoke contains carcinogens also and cigarette smoke is by far the most important cause of lung cancer in the community.  The same type of genetic damage –

Your Honours, may I stop at those words for a moment, because this little bit about genetic damage and the same type of genetic damage is the actual part referred to by the majority in the Court of Appeal in that passage to which I have just referred.  However, Professor Musk goes on to say on page 7:

The same type of genetic damage is seen although the exact sequences in the DNA chain aren’t known but asbestos and cigarette smoke both can cause cancer and in combination the effect or the risk, the effect is more than additive, it being thought that they multiply the effects of each other, but some studies suggest that the multiplicative model may be a bit of an overestimate of the combined risk of the two agents, but it’s certainly more than additive.

Your Honours, what we would say about that is that he is speaking about, we would say, risk, but the fact that he is speaking about risk is suggested also, in our submission, by the fact that he goes on to say that the relative contribution of the possible causes can be determined or is to be determined from the epidemiological exercise, and you will see that at page 80 in volume 1 and page 81 also.  At page 80, your Honours will see about line 15 he was asked:

Do the papers or discussions to which you have been referred in the course of evidence today deal with a case where it it’s necessary to distinguish between potential dual causes such as asbestos and smoking?---I believe so, yes.

The next answer, commencing at about line 23:

I think we can get some idea of the relative contribution to the risk that he had from those exposures and work out from them what the attribution was in terms of proportions and that has been done mathematically.  I know Dr de Klerk did it in his report and that gives us a sort of a number to hang our hat on, although the numbers are troubled by the imprecision of the information being put in.  For instance, we haven’t discussed what forms of asbestos –

et cetera.  Your Honours will see then at the bottom of page 80, he agreed – and this is the fourth last line on the page – that:

there were no clinical or pathological indications from which a conclusion could be drawn on those factors alone about the cause of the tumour –

and he went on to say, to put it shortly:

The smoking history was from the history provided and the exposure history was similarly from the history provided –

Then your Honours will see at the top of page 81 that he agreed that the condition:

the cancer could presumably have been due to any of the potential causes of lung cancer –

Your Honours will see the last two questions and answers on page 81:

So in this case the conclusion which you have reached that the cancer was due to smoking and asbestos exposure is based entirely on the occupational history?---And a smoking history.

And a smoking history?---Yes.  So we’re applying general observations ‑ ‑ ‑

Your Honours, he refers to elimination of radiation.  The reason for saying that is that in one of the reports someone said it might have been caused by radiation.  Your Honours, no one suggests that, nor were people from Mars anywhere around at the time either, but he goes on to say that –

we recognise from his history that he has been exposed to two agents which are known to cause cancer and we know from our general observations from the medical literature that they are dose related effects and therefore we can apply those relative risks from the literature to the patient to compute –

Your Honours will see, I will not read it out, but the remainder, in effect, of that answer.  Your Honours, could I just say also it is the evidence of those two witnesses that form the core of the reasoning at paragraph 335 to which I referred earlier and, in our submission, they are consistent only with their being an increase in risk.  Also, your Honour, and I will come to this in just a moment, what they do in the case is that the experts upon whom the majority in the Court of Appeal placed such reliance themselves thought that the way to resolve the question of which might be responsible for what was to go to the epidemiological evidence and, as I am going to demonstrate, your Honours, scant regard was in fact paid to that by the majority in the Court of Appeal, but, your Honours, may I postpone that for just a moment. 

The feature I also wanted to mention, your Honours, was that in addition to the evidence of those two witnesses, reliance is placed by our learned friends in their submissions in response to us, paragraph 110, upon some other passages in the evidence.  May I take your Honours to those very quickly.  The first of those concerns Professor Wan and in his evidence in volume 2 at page 893, in his report – you will see his report starting at page 892.  You will see then, your Honours, the answer to question one commencing about line 38.  He said that “occupational exposure” is “capable of causing lung cancer”  You will see in answer 3, page 895, that he said:

Exposure to asbestos alone over many years in the absence of smoking might marginally increase the relative risk, but where such asbestos exposure is combined with cigarette smoking, the risk could be extraordinarily changed so that the relative risk of the combined exposure may approach 100 times that in the general population.  The exact relationship is uncertain but is certainly far grater than merely an additive risk.

Your Honours, no reliance seems to have been placed upon Professor Wan’s evidence in the majority in the Court of Appeal and the reasons for that are attacked by our learned friend, Mr Watson, in his written submissions.  Your Honours, I will not go into the detail, but your Honours might well take the view that what was being said by Professor Wan was based on considerations which were incorrect.

Your Honours will see also that there was reliance placed on the evidence of Dr Kendall which is in volume 1 at page 272.  At about line 15 he was asked to explain his reasoning as to the causes of the lung cancer.

FRENCH CJ:   Sorry, what was that page reference?

MR JACKSON:   I am sorry, page 272 in volume 1, your Honour.

FRENCH CJ:   Thank you.

MR JACKSON:   It is about line 15.  He was asked to explain to the judge his reasoning as to the causes of Mr Cotton’s lung cancer.  He said:

I think in general terms the literature supports lung cancer being associated with cigarette smoking in a fairly consistent manner even in terms of a dose response manner such that people that smoke heavier are more likely to get lung cancer than the people who smoke lighter or for less time so that there’s a strong association between cigarette smoking and lung cancer.

Your Honours, none of that, one would think, would come as a great surprise.  He then goes on to say:

There’s a less obvious but well‑documented association of lung cancer with people who are exposed to asbestos and so that was the basis for my statement that the lung cancer is likely to be contributed to both, by smoking and by asbestos exposure.

It seems to be simply saying that both of them are possible causes, therefore, if you encounter both possible causes the lung cancer is likely to be contributed to by both.  You will then see, your Honours, if one goes to about line 32 or 33 he said:

You still have a problem to deal with.  I think we rely a lot on epidemiological data which really helps if one’s looking at a population.  If one’s looking at an individual patient, it doesn’t necessarily help to say that because their smoking might be less than some others that have lung cancer or the asbestos exposure might be less than in some others with lung cancer, it doesn’t mean to say that the person hasn’t got lung cancer due to those factors.  That’s the difficulty I think.

Your Honours, one might say exactly the reverse of that as well.  I should say, your Honours, there is a reference at that page to his report.  If one is looking to see the report, it is in volume 2 at page 841.  That is what he was being asked about.  Finally in relation to this, this is not something that is relied on by our learned friends, but your Honours will see the report of Dr Berry, which is in volume 2 commencing at page 857.  He speaks of the “Combined effect of asbestos exposure and smoking”.  You will see a reference immediately preceding that to his views about “The increase in risk of lung cancer following asbestos exposure”.  He goes on to say at about line 30 what is meant by it being:

approximately multiplicative; it is certainly more than additive but possibly not as much as multiplicative. 

He goes on then to subdivide, in the next paragraph, the risk “into components representing the percentage contributions of the different risks”.  Your Honours will see the way in which that works out:  92 per cent due to smoking alone; due to asbestos alone, 0.1 per cent; smoking‑asbestos combination, 0.9 per cent; and a background risk of seven per cent and says, as is apparent from those figures, that:

The risk due to smoking is much greater than that due to asbestos. 

Then on the next page, your Honours, at the top of page 861 he goes on to say, “The problem is how to subdivide component (c)”, which your Honours will have seen is “Due to smoking‑asbestos combination”, the 0.9 per cent, and goes on to indicate the two methods of doing it.  That is in the first of two paragraphs on page 861 and he expresses his views in the summary about line 22 on that page.

Your Honours, the point is if one were to quibble about a percentage here or there, but the reality is that the relative scales of likelihood, your Honour – that is an ungainly expression I know – but are demonstrated as being ones where the probability, if one has to look at things in realistic terms, in our submission, is that the lung cancer was caused, as it so often and sadly is, by smoking.  I say sadly because smoking is, of course, addictive.  

Now, your Honours, what the evidence demonstrates, it is submitted, is that the evidence that is relied on is really evidence which relates in truth to risk and, secondly, that that means that it is necessary to go to other evidence if one is attempting to work out the part actually played by exposure to asbestos.  That takes one to the issue of whether the contribution made by asbestos was material in the present case.  Your Honours, we would submit that there really is no other way of dealing with that issue than by reference to the epidemiological evidence.  Your Honours, we have set out that contention more fully in our submissions in reply in paragraphs 4 to 12.  Your Honours, I will not read them out, but that is the essence of what we say. 

Your Honours, if one does go then to that evidence, its effect is summarised in a number of places, but may I take your Honours to one place that your Honours have already been to so that your Honours will not have to go to a significant number of different places, and that is in the submissions in‑chief on behalf of South Australia in paragraphs 10 to 20 to which your Honours were taken a little while ago.  Now, if one goes to paragraphs 10 and 11 what one sees is that the – and your Honours the references are given – if one looks at the risk of smoking, looks at the risk occasioned by smoking, the result was that that was an increase by about 1400 per cent, from a relative risk in one you go to 15.  If one goes to paragraph 11, the relative risk from the two exposures, asbestos, is between one and two, so that we are talking about an increase in risk of between 10 and 20 per cent. 

Your Honours, one does not see in the majority in the Court of Appeal’s reasoning any consideration of a comparison of that nature.  It is a very stark one, with respect, very stark indeed, 1400 per cent as against the 10 to 20 per cent.  Your Honours, I am going to come back to that in just a moment, but could I say this, that instead, what one sees in the reasons of the majority in the Court of Appeal is, with respect, the rather bland observation at paragraph 336, page 1513.  Your Honours have been to this paragraph quite a bit, I know, but your Honours will see in the first sentence of it that what is being said is that:

the epidemiological evidence has no direct application to the question of causation at law because it is based on a false assumption.

Well, now, your Honours, that is rather a funny thing because you will see that that was not the view of the witnesses to whom I have referred so far.  It was not the view of Dr Leigh, it was not the view of Professor Musk, both of whom are the persons relied on in the immediately preceding paragraph.  When I say it was not the view, what I mean by that is that they said if you want to work out the relative importance of the causes, you go to the epidemiological evidence.  Of course, the other witnesses to whom I have referred, were to the same effect.

GUMMOW J:   If you are right about this, Mr Jackson, in your criticisms of the Court of Appeal majority, and that decision falls over, where does that leave the primary judge’s decision?

MR JACKSON:   Well, your Honour, it really, in our submission, leaves the primary judge’s decision as one itself that should have been set aside.  I am putting that a little too compactly.  What I mean by that is that you will see that what is said at paragraph 335 in the majority is, in effect, to pick up what was said and accepted in, for example, the passages of the primary judge which are quoted at paragraph 334 in the majority in the Court of Appeal.  You will see, your Honours, the last sentence quoted on page 1512 between lines 25 and 30 the primary judge had appeared to adopt a rather similar view to that adopted by the majority in the first sentence of page 336. 

The point I am seeking to make, your Honours, is that the evidence which appeared to commend itself, for example, Musk and Dr Leigh, to both those courts, if I can put it that way, was evidence which carried within itself the notion that if one moved from the theoretical to the practical to work out what was the cause for legal purposes, you did go to the epidemiological studies.  If one went to those, what they demonstrated, in our submission, was that there are a number of ways one might express it.  But the difference in scale between the contributions that the two causes were likely to have made were dramatic. 

Your Honours, the difference in the scale was really quite extraordinary.  Your Honours, I say that because your Honours will see that if one goes back to paragraph – I am sorry, I did not quite finish what I should have said in response to your Honour.  The answer would be, in our submission, that the appeal to the Court of Appeal should have been allowed.  The consequence of that should have been that the case against the asbestos defendants was dismissed.  Now, your Honours, I just want to add one further thing about paragraph 336.  The last sentence of paragraph 336 at page 1513 says that:

The RR figure for asbestos and its derivative attributable fraction may at best serve as a general guide in answering the question whether the asbestos exposure was material in determining contribution between tortfeasors.

Now, your Honours, “general guide” may perhaps be not the most felicitous selection of terms but, your Honours, to describe something that compares 1400 per cent with 10 to 20 per cent as giving a general guide and then taking, in effect, no notice of it seems, with respect, an unusual course to follow.

Could I just say, your Honours, I said I would go back to those paragraphs of the written submission on behalf of South Australia.  All I want to say further about it – and I am referring to page 3 of the submissions in-chief of South Australia and in particular to paragraphs 12 and 13 – that they demonstrate that the South Australian exposure was a bit less than ours, but whether one adds them together or takes ours separately they are all small, and, your Honours, we would say in the scale of matters miniscule. 

Now, your Honours, if I could just pause at that point, your Honours.  What we would seek to say is this.  In the proceedings the short fact was that it was incumbent on the respondent to demonstrate that the exposure to asbestos was a cause of the lung cancer.  In reality what was shown was that it increased the possibility of lung cancer.  The extent to which it increased the possibility had to be considered in a context where there was another very likely, very likely indeed, cause, and the evidence showed a basis – indeed really, in our submission, the only basis for quantifying the part played by the exposure to asbestos, and, in our submission, that it was minimal.

Your Honours, the majority, if I can go back to their reasons – this time still at page 1513 but paragraph 337 - the majority seem to have recognised, and I would refer to the second sentence of paragraph 337, they appear to have recognised that not every “contribution made by exposure to asbestos is material”.  So that appears to assume, your Honours, to put it the other way, that there may be exposure.  Exposure has the potential of increasing the risk, but not every increase in risk is material. 

Now, if one were looking for a case in which one would draw that conclusion then, in our submission, this would be such a case.  Your Honours, could I say this.  Where is there any consideration of that issue in real, as distinct from theoretical, terms by the majority in the Court of Appeal?

GUMMOW J:   Did they not have to focus on – given the epidemiological evidence as the primary facts, if you like – what it was legitimate to infer from that in terms of deciding causation?  You say you cannot legitimately use it to infer that result.

MR JACKSON:   Yes, your Honour.  Could I just say why we say that.  If I can just go back one point, it is that that is the evidence, one assumes.  The evidence demonstrates – there are possible little shades of difference in numbers, perhaps – that the overwhelming possibility is that lung cancer is caused by smoking.  It demonstrates also that there is a possibility of getting lung cancer from exposure to asbestos.  It demonstrates also, I think it right to say, that there is a possibility, and the evidence would seem to support it, as I submitted at the start of our submissions, that there is some increase in risk by virtue of the possibility that the two may operate in some way together.

But one sees the figures that are the possible result, the percentages – I referred to them a moment ago – of the two acting together.  They are small indeed in the way in which they can be distributed.  But the result of it all, your Honours, is if one is saying did exposure to asbestos, was it a cause of the cancer – one cannot say, first of all, that it is more likely than not that it was.  If that is the test, it was not so.  If one is saying that there was an increased risk and the risk was – and I will come back to this in a moment – not something which was de minimis but was greater than that, how is it possible on the evidence to say that the risk was one which was established to be one that one could say was made a material contribution to the contraction of the disease?

FRENCH CJ:   This is really along the lines, I suppose, of what I was putting to Mr Watson earlier on.  The question is whether one can use the conjunction of a probability of a bad outcome, which is caused by an exposure, together with that outcome to infer causal connection.  It may be that it simply depends upon the level of risk whether one is entitled to draw that kind of inference.

For example, if you had, say, a 10 per cent risk that exposure to asbestos could lead you to cause lung cancer but there are competing risks of 75 or 80 per cent with respect to tobacco, the question then is when you have the exposure to asbestos, you have the competing exposure to tobacco, you have the event of disease and death, the question is whether you are justified in drawing the inference from that level of risk and that outcome that there was a causative contribution by the exposure to asbestos.  It seems to me you are not saying much more than that, whatever you are entitled to infer at the higher levels of risk.  This does not get anywhere near there.

MR JACKSON:   Your Honour, that is what I am saying.

FRENCH CJ:   You are not saying that you can never make an inference of causal connection from epidemiological evidence?

MR JACKSON:   No, I am not, your Honour.  Could I explain what I am seeking to say in that regard, but do so by starting from perhaps a simple example.  If Telstra or someone who makes holes in the streets forgets to put the lid back on and at night time someone walks into the hole and injures themselves, there is a chance that someone will do that.

If someone is a courier working at night, as they sometimes do, riding a bicycle around a city and the bicycle goes in there it may be that one cause is some excessive speed or a lack of care on behalf of the bike rider, but another cause is the fact that the bike rider fell down a hole.  Now, one can say, your Honours, that there was a chance that people would fall down the hole, particularly if it was unlit and at night and that, although 20 people might not, one of 21 might do so.  Now, even though there is only perhaps statistically a five per cent chance, then one could say that it was obviously a cause.  So, your Honours, a simple enough case.

When one comes to competing causes in this area and when, your Honour, I say “this area” relating to lung cancer particularly because different considerations may apply to the other forms of asbestos caused diseases, some of which are cumulative, some of which are not, but when one comes to lung cancer, what you will see is that the epidemiological evidence considerations are based on, for example, things such as the length of exposure to asbestos, things of that kind.  That is where the figures that may result will derive from a combination of things. 

If you have a person who is exposed to asbestos for a long time in a heavy dose situation, but smokes only a little, then it will be easy enough to work out – your Honour, I am not saying that every case ends up this way or ends up the way we suggest.  What I am saying is that every case turns fundamentally on the evidence, of course, but if the approach taken by the majority in the Court of Appeal appears to have been to say that once you determine that the two causes operate cumulatively, whatever that means in

the context, then except in the cases not further elaborated that are referred to in the second sentence of 337, then there is liability on the part of the persons responsible for the exposure to asbestos.

It is a significant question, your Honours, because what it does mean is that you are likely to have someone, a plaintiff or plaintiff’s representatives, who do not have an effective cause of action.  I use the expression “effective” to indicate the prospect of success or getting money out of it against the persons responsible for the smoking addiction, but they do have a cause of action on this theory against the asbestos companies.  Now, of course, some asbestos dealing companies like Amaca are ones that are, in a sense, winding up the past, but some, like ourselves, are companies that are continuing an industrial operation, differently dealt with no doubt from the past, but ones that have to keep going and they become the targets for these classes of action.

Your Honour, I do not mean that people should not sue.  I am just saying that is one of the things that follows from it.  Your Honours, what I was going to say further was this, that there remains, of course, the question of the individual liability of the asbestos defendants.  I would adopt, as our learned friends, I think, recognise, that we can say about them what they say about us, why are we responsible for Amaca or South Australia?  Why are they responsible for us?

Your Honours have been taken to the reasoning of Justice Heenan in volume 3 at page 1276, paragraph 513, and the reasoning of the majority in volume 4 at page 1517, around paragraph 345.  The reasoning of the majority appears inherently contradictory, with respect, and no satisfactory reason is given why, if there is liability, the task of division‑up or exemption from liability should not have been carried out.  Your Honours, those are our submissions.

FRENCH CJ:   Thank you, Mr Jackson.  Yes, Mr Walker.

MR WALKER:   Your Honours, may I start by trying to make clear matters for which we do not contend; secondly, matters that may appear to be that of mere nomenclature, but go beyond that, that we will not seek, as it were, to defend in the Court of Appeal majority reasons, though of course defending not merely the outcome, but in truth the reasoning expressed by some unfortunate language and identify immediately that some of the unfortunate language is the not useful and ambiguous term “cumulative”.  It is explained by their Honours in a way which, with great respect, permits us to support their reasoning, but it is not a happy word.

The second and most obvious unfortunate expression is that which one finds in paragraph 336 “epidemiological evidence”.  I have a deal of reconstruction to do on that, but I can and can thereby support their argument.  The third unfortunate expression is found in an important paragraph which we will seek to confront in all its implications, namely paragraph 309, and the unfortunate expression there is the reference to the “but for” test as if it is somehow being put to one side in a case like this, or in this case.

Having noted those matters of nomenclature with which we have to deal, and I accept they may be serious conceptual matters involved in that, can I protest some of the things we are not going to do, particularly as there have been more than the passing suggestion by our opponents that our cause should be rendered unattractive by the nature of some of our supposed ambitions.

We are not asking the Court to depart from what we will call “orthodoxy” in relation to common law reasoning shown by decisions of this Court and by courts seeking to follow the rules in this Court concerning causation in negligence actions.  If I slip occasionally and call it merely causation, may I make it crystal clear it is always about causation in negligence actions.  It may or may not be exactly similar to causation in crime or causation in deliberate torts or causation in contract.  For the purposes of this argument, it is causation in negligence actions. 

We will certainly not be suggesting that there was any gap that needed jumping – if by jumping is meant doing something which judges ought not to do, as opposed to a more dignified step – if there was no gap to be jumped, there were steps to be taken and they could all be taken, and they were all taken when the reasons are read, as I submit, they ought to be read but, most particularly, we are today anti-comparativists.  We are not going to be urging on your Honours anything from England and Wales or Canada which overtly says let us jump a gap in a way the common law has hitherto not permitted, that is, frank law making by the judges, so as to overcome in particular what are supposed by some to be the unreasonable strictures in cases of this kind imposed by the “but for” test.

That brings me to my next protestation of what we are not doing.  We are not going to join any chorus suggesting that the “but for” test is atavistic or inappropriate.  With great respect, the reference to it as a negative criterion, supplying a necessary screen by this Court in March v Stramare is entirely, with great respect, appropriate and of current usefulness.  How could it be otherwise in an area which, after all, concerns compensatory remedy in the course of the administration of justice, not arbitrary rules, where there has been wrongdoing?  How could it be right to say to somebody you are to compensate the plaintiff, though your actions made no difference to the position, that is, your actions fail a “but for” test?

GUMMOW J:   I take it from what you have been saying that you do not seek to enter into the US decisions as discussed by Professor Stapleton, 122 Law Quarterly Review 189?

MR WALKER:   That is right.  I am bound to say there may be return to that in another case next week, but for the purpose of this argument the United States and Canadian approaches – they are different and they are different within the United States – do not provide material which any exigency that this case raises would make useful for this Court’s consideration of some change to the law.  We are not urging change to the law.

We do not characterise this as a case that requires change to the law.  In particular, in relation to Resurfice Corp v Hanke, the Supreme Court of Canada decision, [2007] 1 SCR 333 in the reasons of the Chief Justice at pages 343 and 344 in the course of paragraphs 24 and 25, things are said which, in our submission, do not translate or transpose readily to what is necessary to determine this case. I will return to those particular parts of the Chief Justice’s reasoning, but I will not be saying that they supply a statement of principle which readily or probably at all should find any place in this country’s law.

The next thing that we will not be doing, as I said when asked about this at the outset of the hearing this morning, is I will not be submitting that without more, and those are two very important words, that without more proof of increased risk in the sense that the epidemiology can demonstrate, risk in that sense is enough as an abstract or general proposition in favour of plaintiffs to discharge the burden of proof on the balance of probabilities of causation.  That is not a large concession because we submit that it is a very rare case indeed where it could be truly said if a case that gets to both trial and decision that there is really nothing more than that.

FRENCH CJ:   There is generally the event.

MR WALKER:   Well, I hope I will be able to supply more than the event.

FRENCH CJ:   But that is at least an additional factor.

MR WALKER:   It is, because without the event there would not be anything to complain about, although I should warn your Honours that in other jurisdictions, perhaps in jurisdictions for which your Honours are the apex, there will be claims for something in the nature of justiciable damage simply because of an increase in risk where there has not been something eventuated.

GUMMOW J:   You are being elliptical, Mr Walker.

FRENCH CJ:   You need not talk about loss of chance here.

MR WALKER:   No, I am not talking about loss of chance here.  Now, clearly enough, widespread community perception of an increase in risk has already given rise to some claims, none of which have reached this Court and maybe none will, that they themselves cause a form of compensable damage in the form of worried or pathological extent and that obviously will have to be dealt with sooner or later.

We are not saying that where the event, which is the event about which the risk has been measured, where that has come about, we are not saying that without more, demonstration of the pre‑existing risk is enough.  However, nor are we saying that the epidemiology falls away for all purposes after it has been used to demonstrate either the natural history or the accepted scientific view that a particular – I will call it “exposure” because of the facts of this case – can produce – in the sense of can biologically lead to – the outcome, in this case a disease.

One of the most obvious reasons, given the issues joined and the way in which the arguments have been presented, as to why I will not be giving that away, is that the principal plank in all the arguments against us is that the risk of smoking was that which eventuated in this case and which ought to be held to preclude any finding on the balance of probabilities of a material contribution by the exposure to asbestos.

The argument against us, and we do not say it is flawed on this account – simply on this account, there are other reasons it is flawed – the argument against us starts with the proposition, look at the risk figures for smoking.  Look at the risk figures for asbestos.  Admittedly, I am going to say there is a third set of risk figures which they do not talk about much, but I am going to talk about much more, namely look at the risk figures for tobacco and asbestos combined.  But the argument against us is to say, look at the risk figures for smoking, that should lead to an inference that it is smoking that caused – they do not have to prove anything of course, but they say they have, and thereby have rebutted any inference or prevented any inference from being drawn on the balance of probabilities that exposure to asbestos materially contributed to the lung cancer.

We stress that there is nothing illegitimate in itself in parties where there are multiple putative causes.  Again, if I slip and say causes I accept that they are all only putative causes.  In a case of multiple putative causes it is appropriate to use the extent of the evidence which the state of scientific knowledge permits, and in this case histology or molecular science or microscopy will not give you anything to distinguish between the exposures.  Where the state of scientific knowledge means that the extent of the evidence is, for example, epidemiological observation backed up by laboratory studies lending biological plausibility to the statistical associations being causal, as is the case here, for both exposures and the combined exposure, then, in our submission, of course it will be appropriate to an extent to play the numbers, if I can put it that way, but not, we submit, by means of the so‑called attributable fraction method carefully considered by the trial judge and rejected for cogent reasons, rejected somewhat less elaborately by the majority of the Court of Appeal and, in our submission, wrongly, that is, illogically from a legal point of view – I stress from a legal point of view – pursued by the Chief Justice in the Court of Appeal. 

Now, the numbers that ought to be, however, considered are numbers which will certainly support what my learned friend, Mr Jackson, said in his closing, particularly in response to the Chief Justice’s point, and I hope we have made this clear in our written submissions.  Of course, it is the case that in a combined effect, such as the epidemiology and the clinicians and the laboratory work very strongly suggests beyond contest in this case is true of tobacco and asbestos, it may be in a particular plaintiff’s case that the role of the asbestos was so slight that it could not be held, on the balance of probabilities, to have made a material contribution.

Ultimately, that is something that might, in an appropriate case – I stress in an appropriate case, not this one – be demonstrable or testable by relatively precise arithmetic calculation.  But while I have referred to numbers and to the legitimacy of something in the nature of numbers being used in contests of the present kind, it should not be supposed that we accept that the numbers that have been peppered through the record in this case and referred to in particular in the submissions and addresses against us are an appropriate heuristic tool for this Court in this case – and for a reason plainly identified by the trial judge on the basis of concessions from experts and upon consideration of lay evidence recollecting matters at the workplaces, and a matter well and truly adopted and for, in our respectful submission, impeccable reasons by the majority, namely, garbage in, garbage out.

The data for exposure to asbestos was, one would say laughably if a fatality was not in question, woefully inadequate.  They lent themselves to perfectly good faith, perfectly honest differences of estimation by persons whose competence was not in doubt during the trial of a kind that is attributable to one obvious factor.  This case is being argued on causation at a point when two anterior steps have been established.

The anterior step of duty – and I should say both these were fought, and hard – has been determined against the appellants.  That means, of course, something in the nature of foreseeability which in turn obviously turns upon, to use an English word, risk or danger.  The risk or danger, relevantly, is of something like lung cancer from exposure to asbestos.  The second thing that has been determined is negligence, that is, the content of the duty being rather more than doing nothing there was a failure to take the reasonable care that the duty imposed by doing the various things which could have been done and which on the probabilities have been held would have been such likely to have avoided these fatal exposures, if they were fatal.  Which brings me to next question, causation.

We therefore have people with duties who broke them, concerning exposures to a very toxic substance, asbestos.  They were responsible for the exposures, even Amaca in its own way.  It cannot be said that the late Mr Cotton had any responsibility whatever for the fact that exposure data, that is, measurements and records of monitoring of the workplace exposure to this known dangerous substance, it was absent from the record, that the State had such woeful paucity of material by which something more reliable could be given with a more workable range lending some plausible reliability to estimates of exposure.

Every number that comes out that compares asbestos to tobacco in this case – every number that comes out – is the result of arithmetic performed by models.  The models were competing in the sense that there were schools of thought about them but this is not a case, your Honours will be pleased to know, that requires you to decide which school of thought to follow about the arithmetic modelling.  The arithmetic is not in question, but the data that goes into the arithmetic being performed is in every case to be derived from material which I have described as garbage.

Both at first instance and in the Court of Appeal that was one of the main reasons why great caution was expressed echoing the caution that you will see in the various experts to which we will come about anything in the nature of the, we say, spurious position linked to estimates of the importance of the asbestos exposure by numbers.

GUMMOW J:   Are we not – I think you will probably accept this – in the area of inference to be drawn from this?

MR WALKER:   Yes, absolutely.

GUMMOW J:   And the criteria by which the law assesses inferences?  It is always left a bit obscure, to my mind.

MR WALKER:   The first and last requirement ‑ ‑ ‑

GUMMOW J:   I do not ask you to do it on the spot, but it just seemed to me to be a problem.

MR WALKER:   The beginning and end has to be logic.

GUMMOW J:   Logic itself is a house of many mansions.

MR WALKER:   It is.  In some cases syllogistic reasoning will suffice but certainly not in every case.

HAYNE J:   It is drawing a conclusion about historical significance in the simplest case by reference to experience.  In a case of this kind where we are not concerned with matters of common experience it has to be an informed process.

MR WALKER:   Yes.

HAYNE J:   Informed by the evidence?

MR WALKER:   It has to be, yes.

HAYNE J:   And thus you place some emphasis on what you describe as the GIGO proposition.  On whom does that risk fall?  It was for your side of the record, I fear, to prove the case.

MR WALKER:   Yes, I am not going to suggest ‑ ‑ ‑

HAYNE J:   We have heard a lot this afternoon about what your case is not, Mr Walker.  I wondered whether before 4.15, you might give us the slightest glimpse of what it is to be.

MR WALKER:   Certainly, your Honour.  I am happy to ‑ ‑ ‑

KIEFEL J:   May I ask you, in that regard, are you suggesting or arguing by reference to difficulties in problems in relation to background data which might have assisted your client that a slightly different approach ought to be taken either to the inference that is drawn, or to the level of proof that is required?

MR WALKER:   Not in terms of onus, and certainly not in terms of standard.  It is still more likely than not that we have to satisfy.

KIEFEL J:   More readily draw the inference, something of that order?

MR WALKER:   Only in the familiar way that one judges evidence according to the capacity of parties to adduce it, and exposure data lies peculiarly within the realm of those who, the finding of duty and breach indicate should have been doing rather better in their own workplaces concerning measurement and monitoring of this substance, asbestos, and that is only a familiar fundamental proposition about evidence, namely one evaluates the nature of the evidence according to, among other things, the capacity of the parties to have adduced it.

KIEFEL J:   You might be taking us into a comparative area then, if that is the approach you are taking.

MR WALKER:   We say that is the common law in this country, to evaluate evidence by features which include the capacity of the respective parties to have knowledge about the subject matter in question that can be seen to underlie a number of different approaches, one of them – not relevant in this case – is Jones v Dunkel, obviously.  Your Honours, we adduced evidence of exposure.  It attracted the epithet in the Court of Appeal “qualitative”, another word might be “impressionistic”.  It is not a misprint for “quantitative”, it is “qualitative”, and that is because there were people, colleagues of the late Mr Cotton, who came and talked about what it was like to be working in these trenches, in this factory, et cetera.

They were descriptions which simply did not permit dismissing the exposure as not sufficiently proved to have been at a level which medical science shows is capable of causing lung cancer.  It did not lend itself to numbers.  Numbers were necessarily done in order to get some handle on the comparison between asbestos and smoking, and if I may in the minute remaining to me answer Justice Hayne’s question thus?  What Mr Cotton was actually exposed to was his self‑inflicted tobacco and the defendant‑inflicted asbestos.

He was not exposed only to his tobacco or only to one or other of the defendant’s asbestos.  What his physical organism experienced was the combination.  The medical science shows, and it is really beyond contest pace some of the matters in South Australia’s address, is that that is, of all the candidate possibilities in this case, the most dangerous exposure for him, tobacco and asbestos.  I hope it is not seen as simply tendentious.  We have, in order to try and clarify our use of that expression, hyphenated it in our written submission, because tobacco and asbestos is the subject of study.  Your Honours have been taken to a part and the main parts of the evidence about it already. 

So it was the most dangerous exposure if you are comparing it with the other two candidates which, for reasons of argument advanced by the defendant not the plaintiff, were in question in the case, namely, tobacco alone and asbestos alone.  Mr Cotton was not tobacco alone or asbestos alone, he was tobacco and asbestos.  So our proposition is this.  Turning, in effect, some of the arguments against us against themselves.  The great confidence, the, as it were, self‑demonstrating assertion made against us that we would accept that the tobacco is a very dangerous substance, that

most certainly can cause lung cancer, when you add the asbestos to it, the exposure is even more dangerous than exposure to tobacco.  That easily passes the threshold necessary under the “but for” test, but for the tobacco and asbestos, given the elimination of other matters, given the very young age of the onset, but for the tobacco and asbestos he would not have suffered his lung cancer.  There is the necessary role of the “but for” test.

But in order for the defendants to be liable they must have made a material contribution to his lung cancer.  They are not responsible for the tobacco any more than a defendant who hits a person is responsible for an eggshell skull.  But they are responsible for the asbestos and so the question comes down to this.  Did the asbestos in the tobacco and asbestos combination play a material part?  Did it materially contribute to the outcome?  The short answer is we are here comparing dangerousness.  It is the only way in which one an reason in medical science about putative causes.  When you have eliminated, by the circumstances, factual, rather than expert of a particular case – get rid of radiation, get rid of other chemicals, et cetera – what you are left with in this case is an exposure which, according to the medical science, is by a considerable margin, more dangerous than the other very dangerous exposure, namely tobacco.

It is not by fractions, it is by the difference that we have referred to in our written submissions and which is produced by material relied upon against us.  Hence, his lung cancer would not have been caused but for tobacco and asbestos.  Asbestos made a material contribution to tobacco and asbestos.  Therefore, the plaintiff has succeeded in showing that her damage was, more likely than not, due to the negligence of the defendants.

FRENCH CJ:   Yes, all right, Mr Walker we will adjourn until 9.30 tomorrow for a pronouncement of orders and 10.15 for the resumption of this matter.

AT 4.19 PM THE MATTER WAS ADJOURNED
UNTIL THURSDAY, 5 NOVEMBER 2009