Amaca Pty Ltd v Ellis ; The State of South Australia v Ellis; Millennium Inorganic Chemicals Ltd v Ellis [2010] HCA 5
HIGH COURT OF AUSTRALIA
FRENCH CJ,
GUMMOW, HAYNE, HEYDON, CRENNAN, KIEFEL AND BELL JJ
Matter No P13/2009
AMACA PTY LTD (ACN 000 035 512) APPELLANT
AND
TERESA ELLIS AS EXECUTOR OF THE ESTATE OF
PAUL STEVEN COTTON (DEC) & ORS RESPONDENTS
Matter No P14/2009
THE STATE OF SOUTH AUSTRALIA APPELLANT
AND
TERESA ELLIS AS EXECUTOR OF THE ESTATE OF
PAUL STEVEN COTTON (DEC) & ORS RESPONDENTS
Matter No P12/2009
MILLENNIUM INORGANIC CHEMICALS LTD
(ACN 008 683 627) APPELLANT
AND
TERESA ELLIS AS EXECUTOR OF THE ESTATE OF
PAUL STEVEN COTTON (DEC) & ORS RESPONDENTS
Amaca Pty Ltd v Ellis
The State of South Australia v Ellis
Millennium Inorganic Chemicals Ltd v Ellis
[2010] HCA 5
3 March 2010
P13/2009, P14/2009 & P12/2009
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2.
ORDER
In each matter:
1. Appeal allowed with costs.
2. Within 14 days of the date of this judgment the appellant should file and
serve any proposed amended notice of appeal.
3. Within 28 days of the date of this judgment either the parties should file
agreed minutes of the consequential orders they seek to have this Court
make, or, in default of agreement, each party should file, and serve on the
opposite party, written submissions setting out the consequential orders
which that party submits that this Court should make, together with any
submissions which the party makes in support of, or in opposition to, any
proposed amendment of the notice of appeal.
On appeal from the Supreme Court of Western Australia
Representation
G M Watson SC with J C Sheller for the appellant in P13/2009, the second
respondent in P14/2009 and the third respondent in P12/2009 (instructed by
Minter Ellison Lawyers)
M L Abbott QC with S J Doyle for the appellant in P14/2009 and the second
respondent in P13/2009 and P12/2009 (instructed by Crown Solicitor for the
State of South Australia)
D F Jackson QC with N J Owens for the appellant in P12/2009 and the third
respondent in P13/2009 and P14/2009 (instructed by Lavan Legal)
B W Walker QC with J R C Gordon for the first respondent in each appeal
(instructed by Slater & Gordon)
Notice: This copy of the Court's Reasons for Judgment is subject to
formal revision prior to publication in the Commonwealth Law Reports.
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CATCHWORDS
Amaca Pty Ltd v Ellis
The State of South Australia v Ellis
Millennium Inorganic Chemicals Ltd v Ellis
Negligence – Causation – Balance of probabilities – Deceased was a smoker –
Deceased exposed to respirable asbestos fibres in course of employment –
Deceased died of lung cancer – No scientific or medical examination can say
whether deceased's lung cancer caused by inhalation of tobacco smoke,
respirable asbestos fibres, both, or neither – Use of epidemiological evidence –
Whether epidemiological evidence founded inference of causation –
"Synergistic" effect of smoking and exposure to asbestos fibres – Whether
proved that exposure to asbestos more probably than not caused or contributed to
deceased developing lung cancer – Relevance of material contribution.
Words and phrases – "epidemiology", "material contribution", "more probable
than not", "relative risk", "synergistic effect".
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1 FRENCH CJ, GUMMOW, HAYNE, HEYDON, CRENNAN, KIEFEL AND
BELL JJ. Paul Steven Cotton died of lung cancer. He was a smoker, and it is
well established that smoking can cause lung cancer. Breathing in asbestos fibres
can also cause lung cancer. The determinative issue in each of these three
appeals is whether the plaintiff (the executor of his estate) had established at trial
that it was more probable than not that exposure to respirable asbestos fibres was
a cause of Mr Cotton's cancer. Although a respondent to each of the appeals in
this Court, it will be convenient to continue to refer to Ms Ellis, the executor of
Mr Cotton's estate, as the plaintiff.
2 No scientific or medical examination can say why Mr Cotton developed
lung cancer. His cancer was not, as some are, a cancer peculiarly associated with
exposure to asbestos. The evidence at trial showed that most sufferers of lung
cancer have smoked, some have been exposed to asbestos, some have smoked
and been exposed to asbestos, and some have neither smoked nor been exposed
to asbestos. The evidence also showed that not everyone who smokes, not
everyone who has been exposed to asbestos, and not everyone who has smoked
and been exposed to asbestos, will develop lung cancer.
3 Mr Cotton had smoked on average somewhere between 15 and 20
cigarettes a day for a bit over 26 years before he was diagnosed with lung cancer.
4 Mr Cotton had been exposed to respirable asbestos fibres in the course of
his employment, first with the Engineering and Water Supply Department of the
State of South Australia ("the EWSD") between 1975 and 1978, and later, with
Millennium Inorganic Chemicals Ltd ("Millennium") between 1990 and his
death in 2002. His exposure to asbestos when working with the EWSD resulted
from working with asbestos cement pipes manufactured by Amaca Pty Ltd
(formerly James Hardie & Coy Pty Ltd – "Amaca").
5 When, as here, medical and scientific examination cannot say whether
exposure to respirable asbestos fibres was a cause of Mr Cotton's cancer, the
medical practitioner and scientist have little choice but, as one witness said at
trial, to "take it into consideration in looking at what might have caused his lung
cancer". In their inquiries, the uncertainty about cause means that they cannot
"exclude it from the end result".
6 The courts' response to uncertainty arising from the absence of knowledge
must be different from that of the medical practitioner or scientist. The courts
cannot respond to a claim that is made by saying that, because science and
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French CJ
Gummow J
Hayne J
Heydon J
Crennan J
Kiefel J
Bell J
2.
medicine are not now able to say what caused Mr Cotton's cancer, the claim is
neither allowed nor rejected. The courts must decide the claim and either dismiss
it or hold the defendant responsible in damages. As Dixon J rightly said1, albeit
in a context very different from this:
"There are few, if any, questions of fact that courts cannot undertake to
inquire into. In fact it may be said that under the maxim res iudicata pro
veritate accipitur [a thing adjudicated is received as the truth] courts have
an advantage over other seekers after truth. For by their judgment they
can reduce to legal certainty questions to which no other conclusive
answer can be given." (emphasis added)
The plaintiff recognised that the courts were asked in this case to reduce to legal
certainty a question of causation to which no other conclusive answer can be
given.
7 The plaintiff sued the State of South Australia (in respect of the alleged
defaults of the EWSD), Amaca and Millennium in the Supreme Court of Western
Australia. Each defendant was an appellant in this Court.
8 At trial, each of the State of South Australia, Amaca and Millennium was
found2 by the trial judge (Heenan J) to have been negligent and to have breached
a duty or duties owed to Mr Cotton and his dependants. All three were found
liable in negligence. South Australia and Millennium were also found to have
breached terms implied in the contract of employment each had made with
Mr Cotton and to be in breach of statutory duty. The terms implied in each
contract (and the relevant statutory duty) obliged each employer to take
reasonable care for the safety of Mr Cotton. Judgment was entered for the
plaintiff against each of South Australia, Amaca and Millennium.
9 By majority (Steytler P and McLure JA, Martin CJ dissenting), appeals to
the Court of Appeal of Western Australia by each of South Australia, Amaca and
1 Bank of NSW v The Commonwealth (1948) 76 CLR 1 at 340; [1948] HCA 7.
2 Ellis v The State of South Australia [2006] WASC 270.
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French CJ
Gummow J
Hayne J
Heydon J
Crennan J
Kiefel J
Bell J
3.
Millennium, against the judgments entered at trial, were dismissed3. By special
leave, each of South Australia, Amaca and Millennium appeals to this Court.
10 Neither the existence of duty nor breach of duty was in issue in this Court.
Argument of the appeals in this Court proceeded, for the most part, on the
assumption that the relevant claims were framed in negligence. The central
question was whether it had been shown to be more probable than not that
exposure to asbestos was a cause of Mr Cotton's death. More particularly, in
each case, had it been shown to be more probable than not that the negligence of
the defendant in question was a cause of Mr Cotton contracting lung cancer?
11 It was the plaintiff's case in this Court (and in the courts below) that
causation was to be decided by applying a "but for" test: would Mr Cotton have
contracted lung cancer but for the negligent exposure to asbestos?
12 The plaintiff expressly disavowed any argument in these appeals that
demonstrating only that the exposure to asbestos increased the risk of contracting
lung cancer was sufficient to establish causation. It was the plaintiff's case in this
Court, as it had been in the courts below, that she could succeed only if she
showed that Mr Cotton's exposure to asbestos had caused or contributed to (in the
sense of being a necessary condition for) his developing lung cancer. This being
the way in which the case was presented, it will be neither necessary nor
appropriate to consider issues of the kind considered by the House of Lords in
McGhee v National Coal Board4, Fairchild v Glenhaven Funeral Services Ltd5
and Barker v Corus UK Ltd6 or by the Supreme Court of Canada in Resurfice
Corp v Hanke7.
13 These reasons will demonstrate that each appeal should be allowed.
Causation was not established in the plaintiff's case against any defendant. The
3 South Australia v Ellis (2008) 37 WAR 1.
4 [1973] 1 WLR 1; [1972] 3 All ER 1008.
5 [2003] 1 AC 32.
6 [2006] 2 AC 572. See also Sienkiewicz v Greif (UK) Ltd [2009] EWCA Civ 1159.
7 [2007] 1 SCR 333.
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French CJ
Gummow J
Hayne J
Heydon J
Crennan J
Kiefel J
Bell J
4.
evidence did not establish facts which positively suggested that it was more
probable than not that the negligence of any defendant was a cause of
Mr Cotton's cancer.
14 To support that conclusion it will be necessary to examine what evidence
was led at trial, what the trial judge decided and what the majority in the Court of
Appeal decided. It will also be necessary to examine the way in which, in
argument in this Court, the plaintiff sought to describe what was held in the
courts below, and sought to analyse the evidence. Those steps will necessarily
require examination of detail. But in the end, the plaintiff's case, that it was more
probable than not that Mr Cotton's being exposed to respirable asbestos fibres
was a cause of his cancer, fails because no more was established than that,
although exposure to asbestos may have been a cause of his cancer, it was not a
probable cause.
Proceedings at trial
15 The plaintiff's case at trial was, and at all subsequent stages of this
litigation has been, that resolution of the issue of causation in her claim against
each defendant depended on inference. Her case was that the evidence founded
the inference that it was more probable than not that the negligence of each of the
defendants was a cause of Mr Cotton's lung cancer. That is, the plaintiff's case,
that causation should be inferred, depended upon establishing one or more facts
which "positively suggest[ed], that is to say provide[d] a reason, special to the
particular case ... for thinking it likely that in that actual case ... a specific state of
affairs existed"8. The "specific state of affairs" alleged to exist in this case was
"but for" causal connection between the relevant defendant's exposing Mr Cotton
to respirable asbestos fibres and his contracting the lung cancer from which he
died.
16 The evidence relied on as establishing the facts which "positively
suggest[ed], that is to say provide[d] a reason ... for thinking it likely" that the
defendant's negligent exposure of Mr Cotton to respirable asbestos fibres was a
cause of his cancer was evidence of epidemiological studies, which recorded and
drew conclusions from the results of studies of large groups or populations.
8 Jones v Dunkel (1959) 101 CLR 298 at 305; [1959] HCA 8.
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Bell J
5.
17 Epidemiological evidence was adduced from Professor Musk (a
respiratory physician), Professor de Klerk (an epidemiologist), Dr Leigh (a
consultant occupational physician and epidemiologist) and Professor Berry (an
epidemiologist and biostatistician). All four witnesses had longstanding interest
and experience in the study of asbestos-related diseases.
18 The evidence of four other witnesses, Professor Wan, Dr Kendall,
Mr Kottek and Professor Fox was specifically mentioned by the trial judge in his
consideration of causation. Professor Wan gave evidence directed principally to
the levels of Mr Cotton's exposure to asbestos and the connection between
asbestos exposure and lung cancer. Dr Kendall, a respiratory physician, gave
evidence of his opinion about the causes of Mr Cotton's cancer. Dr Kendall said
that he could not say whether or not Mr Cotton's cancer was due to smoking or
inhalation of asbestos products or some other cause. "Rather", he said, "I think it
is a combination of all three." Mr Kottek, an occupational and environmental
health consultant, gave evidence about the levels of Mr Cotton's exposure to
asbestos when he was working, concluding that he "would have faced at least
some increase (certainly more than minimal) in the risk of lung cancer over and
above that which he would have faced from smoking alone". Professor Fox, of
the Department of Clinical Haematology and Medical Oncology at the Royal
Melbourne Hospital and the University of Melbourne, gave evidence of his
opinion about the cause or causes of Mr Cotton's cancer.
19 Although expressly relied on by the trial judge, little reference was made
on the hearing of the appeals in this Court to the evidence of Professor Wan,
Dr Kendall, Mr Kottek or Professor Fox. Attention was focused upon the
epidemiological evidence of Professor Musk, Professor de Klerk, Dr Leigh and
Professor Berry.
The epidemiological evidence at trial
20 Reduced to its essentials, the epidemiological evidence showed that many
sufferers of lung cancer had smoked tobacco, a few had been exposed to
asbestos; some of those who had been exposed to asbestos had also smoked;
some had been neither smokers nor exposed to asbestos. The observations made
about the relationship between exposure to the known carcinogens of smoking
and asbestos and the development of lung cancer were used and interpreted by
epidemiologists in a number of different ways.
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6.
21 First, the data were used to provide measures of "relative risk". Relative
risk was defined by Professor Berry (by reference to a Dictionary of
Epidemiology9) as the "ratio of the risk of disease or death among the exposed to
the risk among the unexposed". The measures of relative risk given in evidence
described the size of the increase in the risk that a healthy person would contract
lung cancer that was to be attributed to exposure to smoking, to asbestos, or to
both smoking and asbestos. Second, the data were used to provide a measure of
the extent to which the exposure to asbestos increased the chance that a smoker
who was exposed to asbestos would contract lung cancer. Third, the data were
interpreted as showing that the numbers of lung cancer sufferers who were
smokers and had been exposed to asbestos were higher than would have been
expected if the incidence of lung cancer in smokers was added to the incidence in
those exposed to asbestos. This last observation was expressed as tobacco and
asbestos having "a synergistic effect" and as asbestos exposure "multiplying" the
risk of lung cancer due to smoking by a quantity greater than one.
22 These short descriptions of the ways in which the epidemiological data
were used should not be understood as denying the complexity of the analyses
that yielded the results described. Nor should the brevity of the descriptions be
permitted to obscure the level of detail at which the data were analysed and
expressed. To take but one example of that detail, account was taken in the
relevant analyses not only of the extent to which Mr Cotton had smoked but also
of the levels of exposure to respirable asbestos fibres that were to be expected in
each of his particular employments.
23 There were, of course, differences in the ways in which the several
witnesses expressed their opinions. There were differences between them about
the particular values that should be given for the various measures of risk and
probability about which they spoke. But neither the differences in expression,
nor the differences in values stated, should obscure the very substantial measure
of agreement between the witnesses on matters which bore upon the question of
causation.
24 Professor de Klerk, Professor Musk, Professor Berry and Dr Leigh all
gave evidence about the relative risk of exposure to smoking, to asbestos, to both
smoking and asbestos, and to neither smoking nor asbestos. From values of
9 Last (ed), A Dictionary of Epidemiology, 3rd ed (1995) at 145.
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7.
relative risk it was possible to derive, and Professor de Klerk, Professor Berry
and Dr Leigh did derive, measures of the "attributable fraction" among the
exposed. The "attributable fraction" among the exposed (usually expressed as a
decimal or as a percentage) expressed the probability that the cancer in question
was caused by exposure to the carcinogen or carcinogens in question.
25 The relative risk assigned to exposure to smoking or to exposure to
asbestos varied with the level of exposure. Because the witnesses used different
levels of exposure in their calculations, they derived different relative risk values.
Those different values were as follows:
Relative risk from Relative risk from
smoking exposure to asbestos
Professor de Klerk 7.7 1.3
Professor Musk 20 1.1 to 1.2
Professor Berry 15 1.1
Dr Leigh 8 1.16
It will be observed that each witness gave a relative risk from smoking that was
many times greater than the relative risk from exposure to asbestos.
26 Using the figures for relative risk that he adopted, it was Professor
de Klerk's opinion that the probability that Mr Cotton's lung cancer was due to
smoking only was 0.67 (or 67%); the probability that cancer was due to asbestos
only 0.03 (or 3%), due to asbestos and smoking 0.2 (or 20%), and due to neither
smoking nor asbestos 0.1 (or 10%).
27 Professor Musk offered no written opinion assigning equivalent
probabilities or attributable fractions and was not asked to offer an opinion on
those matters in his oral evidence.
28 Professor Berry calculated the probabilities as:
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Crennan J
Kiefel J
Bell J
8.
"(a) Due to smoking alone 92%
(b) Due to asbestos alone 0.1%
(c) Due to smoking-asbestos combination 0.9%
(d) Background risk 7%."
Dr Leigh expressed the view that, if it were necessary "to partition attributability
to smoking and asbestos", an approximate apportionment of 2 to 12% (or 5 to
20% if higher cumulative exposures were taken to account) should be made to
asbestos.
29 One aspect of the epidemiological evidence that was given at trial must be
kept at the forefront of consideration. Although there were differences between
witnesses, all who gave evidence at trial about relative risks due to exposure to
asbestos and due to smoking agreed that the risk due to smoking was much
greater than the risk due to exposure to asbestos.
30 None of the four witnesses mentioned assigned a probability greater than
23% to the chance that Mr Cotton's cancer was caused by his exposure to
asbestos, with or without his also being exposed to smoking. All assigned a
much higher probability (not less than 67%) to the cancer being caused by
smoking alone. Professor Berry described the relationship between the two risks
by saying that it was about 100 times more likely that Mr Cotton's lung cancer
was caused by smoking than by asbestos inhalation. While the witnesses differed
about the figures, all witnesses agreed that the risk from smoking was many
times greater than the risk from asbestos inhalation.
31 It is necessary to say something more about the synergistic or
multiplicative effect of smoking and asbestos. That is necessary because an
essential premise for the conclusions reached by the trial judge and the majority
in the Court of Appeal10 was that the acknowledged synergistic effect of tobacco
smoke and asbestos showed that tobacco smoke and asbestos fibres operated
interdependently to cause Mr Cotton's lung cancer. A proposition not different in
any fundamental respect lay at the heart of the plaintiff's argument in this Court.
10 (2008) 37 WAR 1 at 82 [319].
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Crennan J
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Bell J
9.
The synergistic or multiplicative effect of smoking and asbestos
32 It is convenient to examine the evidence that was given about the
synergistic effect of tobacco smoke and asbestos inhalation by first examining
the evidence of Dr Leigh. Argument in this Court proceeded on the footing that
no other witness gave evidence that was more favourable to the plaintiff's
arguments about synergistic effect.
33 Dr Leigh gave evidence about research into the possible biological
mechanisms for the synergistic effect, and noted that some research suggested
that tobacco smoke and asbestos act at different stages of the development of
cancer. He expressed the opinion that:
"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 more probable than not, that in this situation, the lung
cancer was the singular result of the two factors acting together. It is
however true that exposure to either factor alone is capable of causing
lung cancer." (emphasis added)
34 The meaning and effect of this passage of Dr Leigh's report was much
debated in the course of the argument of the present appeals. In terms, the
proposition advanced by Dr Leigh in this passage of his opinion was that when
both smoking and asbestos cause cancer, the cancer is "the singular result of the
two factors acting together". That proposition, if taken literally, would not
address the question in issue in these cases. The question for decision in these
cases is whether asbestos was a cause of the cancer.
35 Reading his opinion as a whole, it is evident that Dr Leigh did not express
the view that, if a smoker has been exposed to asbestos and develops lung cancer,
the asbestos exposure is, or is probably, a cause of that cancer. Dr Leigh
expressly acknowledged not only that the precise mechanism of interaction
between asbestos and tobacco smoke is not known, but also that it remains
possible (for what he described as "legal or administrative" reasons) "to partition
attributability to smoking and asbestos under a variety of mathematical risk
models". To read the passage from his evidence about "singular result of the two
factors acting together" as saying that, if a smoker has been exposed to asbestos
and develops lung cancer, the asbestos exposure is necessarily (even probably) a
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10.
cause of the cancer, would not be consistent with his acknowledgement that the
probability of causal connection can be divided ("partition[ed]") between the two
carcinogens. As noted earlier, he assigned to asbestos a probability of causal
connection of 2 to 12% (or 5 to 20% if higher exposure levels were taken).
36 Two further points reinforce the conclusion just described. First, and most
importantly, the plaintiff did not submit that Dr Leigh's evidence should be
understood in some way different from the understanding just described.
Secondly, reading Dr Leigh's opinion as not going so far as to say that asbestos
exposure is, or is probably, a cause of Mr Cotton's cancer is not only consistent
with his dividing attribution of cause between the two carcinogens, it explains the
way in which he stated the premises for making that division. Dr Leigh
acknowledged that there is an argument that smoking and asbestos exposure are
indivisible in the causation of an individual lung cancer. But he did not adopt
that argument as his opinion. He said that:
"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 ... to
partition attributability". (emphasis added)
37 Dr Leigh's approach to the matter was consistent with that of Professor
Musk, who accepted in cross-examination that, in considering what might have
caused lung cancer in a person, "a medical and scientific way of approaching the
question" was that "if there is a carcinogen present, then don't exclude it from the
end result", "take it into consideration in looking at what might have caused [the
patient's] lung cancer". But as explained earlier in these reasons, the courts'
response to the uncertainty that results from absence of knowledge must differ
from that of the medical practitioner or scientist.
Causation at trial
38 The trial judge identified the relevant question in a way which did not
direct attention to whether the negligence of a particular defendant was a cause of
Mr Cotton's cancer. The trial judge said11 that the plaintiff would succeed:
11 [2006] WASC 270 at [641].
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11.
"if the evidence establishes that it is more probable than not that
Mr Cotton's lung cancer was caused by asbestos arising from one or both
of his periods of occupational exposure to that mineral or if it supports the
conclusion, on the probabilities, that his cancer was caused to a material
extent by the combined effects of his periods of asbestos exposure with the
effects of his chronic smoking". (emphasis added)
Not only did this framing of the question not distinguish between defendants, it
assumed (by its reference to "one or both" periods of exposure) that cumulative
exposure to asbestos, by the negligence of more than one defendant, would be
sufficient to establish the relevant causal connection between a defendant's
negligence and the damage suffered.
39 Having thus identified the question to be answered, the trial judge
restated12 it by asking whether, "on the probabilities, Mr Cotton's two sequential
periods of occupational exposure to asbestos, acting in combination with his
habit of smoking, contributed to the development and/or progress of his fatal
tumour". In his Honour's opinion13, there was "really no answer to the evidence
of Professors Musk, Wan, Dr Kendall, Professor de Klerk, Dr Leigh and
Professor Berry that a not insignificant contribution to the combined causative
effect was due to this asbestos exposure" (emphasis added). The conclusion that
both periods of occupational exposure to asbestos made a "not insignificant" or
"material" contribution to the onset or the development of Mr Cotton's cancer (or
both its onset and development) was said14 to be supported by "the probabilities
[being] that the toxic effect of the carcinogens of tobacco and asbestos had
synergistic effect, and that their effects were also cumulative upon previous
exposures".
40 To approach the matter in this way diverted attention from whether
individual defendants were to be found liable. It treated the relevant question as
being: why did Mr Cotton develop lung cancer? But as pointed out earlier in
these reasons, the relevant question, to be asked separately in respect of each
12 [2006] WASC 270 at [687].
13 [2006] WASC 270 at [687].
14 [2006] WASC 270 at [689].
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12.
defendant, was: is it more probable than not that the negligence of the defendant
was a cause of Mr Cotton's cancer? The difference between the questions is
important. The litigation sought to attribute legal responsibility for Mr Cotton's
cancer and death. Asking why Mr Cotton developed lung cancer could be
understood as asking what aspects of his history would be considered significant,
for their purposes, by a clinician, an epidemiologist, or an occupational health
expert.
41 No separate attribution of responsibility as between defendants was made
by the trial judge. Attempts made by some of the witnesses (particularly
Professor Musk, Mr Kottek, Dr Leigh and Professor Berry) to estimate the
proportions "by which each exposure may have contributed to the final fatal
result" were dismissed15 by the trial judge as "rather superficial and
approximate". The trial judge concluded16 that, because there were no
proceedings between defendants seeking contribution or apportionment, it was
unnecessary and undesirable to attempt to estimate those proportions.
42 As Martin CJ rightly pointed out17 in his dissenting opinion in the Court of
Appeal, the absence of contribution or apportionment proceedings was not to the
point in considering the question of causation. The trial judge was required to
decide the plaintiff's claim against each defendant by deciding whether the
negligence of that defendant was a cause of Mr Cotton's cancer. Deciding only
whether the aggregate exposure to asbestos was a cause of Mr Cotton's cancer
did not answer the question about the particular responsibility of each defendant.
Causation in the Court of Appeal – the majority opinion
43 The hinge about which the reasoning of the majority turned was their
acceptance18 that the trial judge had found that "the medical evidence, reflected in
the acknowledged synergistic effect of tobacco smoke and asbestos, [showed]
that tobacco smoke and asbestos fibres operated inter-dependently and thus
15 [2006] WASC 270 at [690].
16 [2006] WASC 270 at [690].
17 (2008) 37 WAR 1 at 52-53 [193].
18 (2008) 37 WAR 1 at 82 [319].
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13.
cumulatively to cause Mr Cotton's lung cancer". The majority of the Court of
Appeal examined what they described19 as "the statistical evidence" led at trial,
including the evidence of Professor de Klerk, Dr Leigh and Professor Berry. But
to the extent to which that evidence sought to identify the probability that
asbestos was a cause of Mr Cotton's cancer, the majority appear to have treated
the evidence as not to the point. Their Honours said20 that:
"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."
Rather, their Honours continued21:
"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."
44 The proposition made by the majority in the Court of Appeal, that the
epidemiological evidence had no direct application to the question of causation,
proceeded from the premise (explored in the immediately preceding and
succeeding paragraphs of the reasons22) that Mr Cotton's smoking and his
exposures to asbestos had operated "cumulatively" to cause his cancer. This, the
majority concluded23, had been established at trial by the evidence of Dr Leigh.
Their Honours said24:
19 (2008) 37 WAR 1 at 82 [319].
20 (2008) 37 WAR 1 at 86 [336].
21 (2008) 37 WAR 1 at 86 [336].
22 (2008) 37 WAR 1 at 85-86 [335], 86 [337].
23 (2008) 37 WAR 1 at 86 [337].
24 (2008) 37 WAR 1 at 86 [337].
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"Whether or not potential causes operate cumulatively is a matter of
medical science. Only Dr Leigh [of the witnesses called at trial] is a
specialist physician and epidemiologist. The other epidemiological
experts do not have medical qualifications."
The plaintiff's arguments in this Court
45 Many of the issues which were agitated at trial, and determined by the trial
judge, were not in dispute in this Court. In particular, it is not necessary to
examine the controversies at trial, further considered in the Court of Appeal,
about such matters as the extent to which Mr Cotton was exposed to respirable
asbestos fibres25, or whether concentrated exposure to fibres over small periods is
more toxic than sustained exposure to smaller levels over longer periods26.
Rather, as noted at the outset, arguments in this Court were confined to the issue
of causation.
46 In arguing the appeals to this Court, counsel for the plaintiff did not
support the first step in the reasoning of the majority in the Court of Appeal: that
"the epidemiological evidence has no direct application to the question of
causation". On the contrary, the arguments on behalf of the plaintiff in this Court
depended in critically important respects upon the epidemiological evidence.
47 The whole tenor of the plaintiff's argument in this Court (as it appears to
have been at trial and on appeal to the Court of Appeal) was first, that causation
was established as a matter of inference not direct proof, and second, that the
inference of causation was to be drawn from a proper understanding of the
epidemiological evidence. Framing the argument in this way entailed rejecting a
critical step in the reasoning of the majority in the Court of Appeal. It was not
the plaintiff's argument in this Court that Dr Leigh's evidence (or the evidence of
any other witness) should be understood as offering an opinion that, independent
of epidemiological analysis, it could be concluded that exposure to asbestos was
a cause of Mr Cotton's cancer.
25 (2008) 37 WAR 1 at 9-34 [32]-[141] per Martin CJ.
26 (2008) 37 WAR 1 at 18-20 [74]-[78].
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48 The plaintiff submitted that the majority's use of the word "cumulatively"
(in the expression "tobacco smoke and asbestos fibres operated inter-dependently
and thus cumulatively") was "unfortunate". In particular, so the plaintiff
submitted, it should not be understood as a reference to the kinds of process that
lead to a condition like boilermakers' deafness or other forms of progressive
disease or injury. Rather, the plaintiff submitted, "cumulatively" should be
understood as a reference to an interdependent (because synergistic or
multiplicative) operation of the two carcinogens to which Mr Cotton was
exposed – tobacco smoke and respirable asbestos fibres.
49 The proposition that there was an interdependent operation of the two
carcinogens was an essential premise for the plaintiff's arguments in this Court.
It was a premise that was said to be established by the epidemiological evidence.
The proposition was reached by the following steps:
(a) Mr Cotton had been exposed to two carcinogens, tobacco smoke and
respirable asbestos fibres.
(b) In ways that are not now known, tobacco smoke and asbestos work
together to cause cancer "in the usual case".
(c) They must work together because more people who are exposed to both
carcinogens contract lung cancer than would be expected from the
incidence of lung cancer in those exposed only to smoking and the
incidence of lung cancer in those exposed only to asbestos.
From this proposition about interdependence, the plaintiff's argument proceeded
to the conclusion that causation was to be inferred by taking three further steps:
(d) There was no alternative explanation or differentiating factor suggested by
the medical, social or personal history for Mr Cotton.
(e) The only two explanations for Mr Cotton developing cancer that need to
be considered are that his smoking was the sole cause of his cancer, or that
the combined effect of asbestos and smoking caused his cancer.
(f) Because exposure to both tobacco smoke and asbestos is more dangerous
than exposure to one or the other, it is more probable than not that
exposure to both was the cause of his cancer and his exposure to asbestos
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was a not insignificant cause of (made a material contribution to) his
developing cancer.
50 The plaintiff sought to draw some support for the conclusion that asbestos
was probably a cause of Mr Cotton's cancer by pointing out that the age at which
he developed cancer was at or near the start of the range of ages at which cancer
might be expected to develop in a person who had smoked to the extent he had.
But given that Mr Cotton fell within the range of ages (albeit at the younger end
of that range) the observation does not support the conclusion asserted.
Causation not established
51 The question to which the plaintiff sought to have an affirmative answer
inferred was, in each case: is it more probable than not that the negligence of the
defendant was a cause of Mr Cotton's cancer? Observing only that exposure to
asbestos may have been a cause does not answer that question affirmatively.
52 Three steps in the plaintiff's argument require close consideration: first,
that smoking and asbestos must work together; second, that the only two
explanations of Mr Cotton's cancer that need be considered are smoking as the
sole cause and the combined effect of both smoking and asbestos; and third, that
because exposure to both is more dangerous than exposure to one or the other,
exposure to both was probably the cause of Mr Cotton's cancer.
Smoking and asbestos must work together?
53 The proposition that smoking and asbestos must work together to cause
cancer was not a proposition established by opinion evidence. As explained
earlier, Dr Leigh accepted that the proposition was one that "can be argued", but
he did not adopt it as his opinion. We were taken to no other opinion evidence to
the effect that, if there has been exposure to the two carcinogens, and a person
develops lung cancer, the two must have worked together.
54 It may be accepted (at least for the purposes of debate) that the synergistic
or multiplicative effect suggests that in some cases the two carcinogens will have
contributed to the development of an individual patient's cancer. But the
proposition which the plaintiff advanced was an absolute proposition of universal
application: smoking and asbestos must work together and they must have
worked together in this case. That proposition was not established.
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Consider only smoking or combination of smoking and asbestos?
55 The second of the plaintiff's propositions requiring close consideration is
that the only two relevant explanations of Mr Cotton's cancer that need be
considered are smoking as sole cause, and the combined effect of both smoking
and asbestos. The plaintiff submitted that all other possible causes of
Mr Cotton's cancer were to be dismissed from consideration as improbable. This
confinement of the field for consideration was said to follow from the way in
which the case had developed and been argued at trial.
56 It may greatly be doubted that argument at trial can be understood as
having confined the field for debate in the manner asserted. Rather, the plaintiff's
assertion is better understood as no more than an observation that the evidence of
epidemiological studies established that most who developed lung cancer had
been smokers and that the next highest group was formed by those who had been
both smokers and exposed to asbestos. But if conclusions are to be drawn from
population studies, all of the results obtained for all possible causes of the cancer
must be considered. To consider whether one of two circumstances is more
"dangerous" than another must not be permitted to obscure examination of the
relative dangers of all causes.
57 Observing that by far the largest number of a population of lung cancer
sufferers had been either smokers, or smokers and exposed to asbestos, does not,
without more, provide a foundation for an inference about the probability that
asbestos exposure was a cause of Mr Cotton's cancer. The plaintiff sought to
provide that foundation by the third of the steps to which close attention must be
given: that because exposure to both smoking and asbestos is more dangerous
than exposure to one or the other on its own, it follows that it is probable that
exposure to asbestos was a cause of Mr Cotton's cancer.
"More dangerous"?
58 The basis on which the description "more dangerous" was attached to
exposure to both smoking and asbestos was not identified in argument. At least
in part it seems to have been used as a qualitative description of the synergistic
effect examined earlier in these reasons. But the critical question is whether the
exposure to asbestos was a cause of Mr Cotton's cancer.
59 To the extent to which the plaintiff's description "more dangerous" was
intended to reflect some quantitative measure of the probability that one
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carcinogen rather than another was a cause of cancer, it was a proposition not
supported by the evidence. None of the witnesses whose evidence is examined
earlier in these reasons assigned a probability greater than 23% to the chance that
Mr Cotton's cancer was caused by exposure to asbestos (whether alone or in
combination with smoking). Professor Berry put that probability as low as 1%;
Dr Leigh put it at between 2 and 12% (or 5 and 20% if higher exposure figures
were used). Professor de Klerk considered the probability that Mr Cotton's
cancer was due to asbestos exposure alone was only 3% and due to exposure to
both was 20%. The witnesses who expressed an opinion on the matter agreed
that the probability that Mr Cotton's cancer was caused by smoking alone was
high (Professor de Klerk said 67%; Professor Berry said 92%).
60 If the description of exposure to smoking and asbestos as "more
dangerous" than exposure to one or the other was intended to reflect a
quantitative comparison of risk, it is a description that did not accurately reflect
the evidence given by the witnesses about the relative risks of smoking compared
with the relative risks of exposure to asbestos. And if the description "more
dangerous" was intended to convey no more than that those who were exposed to
both smoking and asbestos were at greater risk of developing cancer than those
who were exposed to only one of those carcinogens, it is necessary to bear
steadily in mind that the evidence did not establish that smoking and asbestos
must work together.
61 This third step in the plaintiff's argument was not made good.
62 As explained at the commencement of these reasons, there being no direct
evidence about what actually caused Mr Cotton's cancer, it was the plaintiff's
case that the epidemiological evidence established facts which "positively
suggest[ed], that is to say provide[d] a reason ... for thinking it likely"27 that, in
exposing Mr Cotton to respirable asbestos fibres, the negligence of each
defendant was a cause of his cancer. To draw an inference about causation from
what was established by the epidemiological studies, it would be necessary to
decide whether the particular case under consideration should be treated as
conforming to the pattern described by the epidemiological studies. Absent
evidence which suggests that the individual may stand apart from the ordinary,
there may be sufficient reason to assume conformity, but whether or not that is
27 Jones v Dunkel (1959) 101 CLR 298 at 305.
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so, it is important to recognise that the first step that must be taken, if an
inference is to be drawn from epidemiological studies, is to relate the results of
studies of populations to the particular case at hand. That step is not inevitable28.
63 In this case, even if it were decided that Mr Cotton's case was not atypical,
application of either the relative risk or the probability analyses given in evidence
does not found the inference that the plaintiff sought to have made. The
probabilities and distributions recorded in the epidemiological studies would
point away from the conclusion urged by the plaintiff.
64 Although the witnesses differed about the particular values that should be
assigned to the relative risks and probabilities derived from epidemiological
studies, it is not necessary in this case to choose between them. It is enough to
recognise that, whichever figures are taken as the best expression of the results of
epidemiological studies:
(a) the relative risk of Mr Cotton developing his cancer from exposure to
respirable asbestos fibres (whether alone or in combination with smoking)
was much lower than the relative risk of his smoking as he did;
(b) the probability of Mr Cotton developing his cancer, if exposed to asbestos,
was much lower than the probability of his developing his cancer from
smoking as he did.
If the relative risks and probabilities derived from epidemiological studies were
to be treated as revealing what was a probable explanation of what caused
Mr Cotton's cancer, those analyses support two conclusions. First, it is more
probable than not that smoking was a cause of (in the sense that it was a
necessary condition for) Mr Cotton's cancer. Second, the risks and probabilities
associated with asbestos, whether alone or in conjunction with smoking, are low
and not sufficient to found the inference which the plaintiff sought to have made:
that it is more probable than not that exposure to respirable asbestos fibres was a
cause of Mr Cotton's cancer.
65 It was not shown to be more probable than not that asbestos was a cause
of (a necessary condition for) his cancer. It was not shown that exposure to
28 State Government Insurance Commission v Laube (1984) 37 SASR 31 at 32-33.
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asbestos made a material contribution to his cancer. Material contribution was
not shown because a connection between Mr Cotton's inhaling asbestos and his
developing cancer was not demonstrated.
The relevance of material contribution
66 The plaintiff made a deal of reference to the decision of the House of
Lords in Bonnington Castings Ltd v Wardlaw29 and, in particular, the statement
of Lord Reid30 that:
"What is a material contribution must be a question of degree. A
contribution which comes within the exception de minimis non curat lex is
not material, but I think that any contribution which does not fall within
that exception must be material."
Particular attention was given to what was meant by saying that any contribution
that was not de minimis must be material.
67 It is important to recognise the context in which this statement was made.
The issue in Bonnington Castings was whether exposure to silica dust from
poorly maintained equipment caused or contributed to the pursuer's
pneumoconiosis, when other (and much larger) quantities of silica dust were
produced by other activities at the pursuer's workplace. Those other activities
were conducted without breach of duty. As Lord Reid rightly pointed out31, the
question in the case was not what was the most probable source of the pursuer's
disease: dust from one source or the other. The question was whether dust from
the poorly maintained equipment was a cause of his disease when the medical
evidence was that pneumoconiosis is caused by a gradual accumulation of silica
particles inhaled over a period of years.
68 This description of the issue of causation in Bonnington Castings shows
how different it is from the issue of causation in this case. The issue in
Bonnington Castings was whether one source of an injurious substance
29 [1956] AC 613.
30 [1956] AC 613 at 621.
31 [1956] AC 613 at 621.
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contributed to a gradual accumulation of dust that resulted in disease. The issue
here is whether one substance that can cause injury did cause injury. Or, to adopt
and adapt what Starke J said in Adelaide Stevedoring Co Ltd v Forst32, was
Mr Cotton's cancer "intimately connected with and contributed to" by his
exposure to asbestos? Questions of material contribution arise only if a
connection between Mr Cotton's inhaling asbestos and his developing cancer was
established. Knowing that inhaling asbestos can cause cancer does not entail that
in this case it probably did. For the reasons given earlier, that inference was not
to be drawn in this case. Questions of what is a material contribution do not
arise.
A paradoxical result?
69 It was submitted that the conclusion that causation was not established in
this case entailed a paradox. If consideration of the results of the population
studies described in evidence in this matter does not permit the inference that
Mr Cotton's cancer was caused or contributed to by exposure to asbestos, no
claim by an individual in Mr Cotton's position could succeed. And yet, the
argument continued, the population studies showed that exposure to asbestos was
a cause of cancer in some cases. How then could it be right to reach a result that
entailed the corollary that all individual claims would fail?
70 The answer to the question can be expressed in several different ways. All
depend upon the basic and unpalatable fact that no scientific or medical
examination can now say, with certainty, what caused Mr Cotton's cancer or lung
cancer in any other particular case. As explained at the outset of these reasons,
despite this uncertainty, the courts must, and do, "reduce to legal certainty [a
question] to which no other conclusive answer can be given"33. The courts do
that by asking whether it is more probable than not that X was a cause of Y.
Saying only that exposure to asbestos may have been a cause of Mr Cotton's
cancer is not a sufficient basis for attributing legal responsibility. Observing that
a small percentage of cases of cancer were probably caused by exposure to
asbestos does not identify whether an individual is one of that group. And given
the small size of the percentage, the observation does not, without more, support
32 (1940) 64 CLR 538 at 567; [1940] HCA 45.
33 Bank of NSW v The Commonwealth (1948) 76 CLR 1 at 340.
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the drawing of an inference in a particular case. The paradox, if there be one,
arises from the limits of knowledge about what causes cancer.
Conclusion and orders
71 For these reasons each appeal should be allowed with costs.
72 Each appellant's notice of appeal in this Court seeks orders setting aside
only the orders of the Court of Appeal made on 26 September 2008. By its
orders of 26 September 2008 the Court of Appeal dismissed the appeals to that
Court by the State of South Australia and Millennium, but stood over for further
consideration the making of orders dealing with Amaca's appeal and the making
of orders dealing with the costs of all three appeals to the Court of Appeal.
Those matters were dealt with by orders made on 29 January 2009. In addition,
each appellant's notice of appeal in this Court seeks the setting aside of orders of
Heenan J made on 8 December 2006 but no other order made at first instance.
The orders of 8 December 2006 provided, in effect, for judgment for the plaintiff
but reserved the costs of the action. The papers made available to this Court do
not show whether any later order was made at first instance dealing with those
costs.
73 If an appellant seeks consequential orders which deal with orders in the
courts below, other than the orders of the Court of Appeal made on 26 September
2008 and the orders made at first instance on 8 December 2006, that appellant
will require leave to amend its notice of appeal.
74 Each appellant should now have an opportunity to consider whether it
wishes to seek leave to amend. And in any event, all of the parties to the appeals
should now have an opportunity to consider what further orders this Court should
make beyond allowing each appeal with costs. There should be orders in each
appeal in the following terms:
1. Appeal allowed with costs.
2. Within 14 days of the date of this judgment the appellant should file and
serve any proposed amended notice of appeal.
3. Within 28 days of the date of this judgment either the parties should file
agreed minutes of the consequential orders they seek to have this Court
make, or, in default of agreement, each party should file, and serve on the
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opposite party, written submissions setting out the consequential orders
which that party submits that this Court should make, together with any
submissions which the party makes in support of, or in opposition to, any
proposed amendment of the notice of appeal.
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