JUDGMENT
Sienkiewicz (Administratrix of the Estate of Enid
Costello Deceased) (Respondent) v Greif (UK)
Limited (Appellant)
Knowsley Metropolitan Borough Council
(Appellant) v Willmore (Respondent)
before
Lord Phillips, President
Lord Rodger
Lady Hale
Lord Brown
Lord Mance
Lord Kerr
Lord Dyson
JUDGMENT GIVEN ON
9 March 2011
Heard on 26, 27 and 28 October 2010
Appellant (Greif) Respondent (Sienkiewicz)
Jeremy Stuart-Smith QC Christopher Melton QC
Charles Feeny Richard Pearce
(Instructed by Hill
Dickinson LLP)
(Instructed by Norman
Jones Solicitors)
Appellant (Knowsley) Respondent (Willmore)
Jeremy Stuart-Smith QC David Allan QC
Charles Feeny Simon Kilvington
(Instructed by Berrymans
Lace Mawer LLP)
(Instructed by John
Pickering & Partners LLP)
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LORD PHILLIPS
Introduction
1. Mesothelioma is a hideous disease that is inevitably fatal. In most cases,
indeed possibly in all cases, it is caused by the inhalation of asbestos fibres.
Unusual features of the disease led the House of Lords to create a special rule
governing the attribution of causation to those responsible for exposing victims to
asbestos dust. This was advanced for the first time in Fairchild v Glenhaven
Funeral Services Ltd [2002] UKHL 22; [2003] 1 AC 32 and developed in Barker v
Corus UK Ltd [2006] UKHL 20; [2006] 2 AC 572. Parliament then intervened by
section 3 of the Compensation Act 2006 further to vary this rule. The rule in its
current form can be stated as follows: when a victim contracts mesothelioma each
person who has, in breach of duty, been responsible for exposing the victim to a
significant quantity of asbestos dust and thus creating a “material increase in risk”
of the victim contracting the disease will be held to be jointly and severally liable
for causing the disease.
2. These two appeals involve cases where the defendant was the sole known
source of occupational exposure to asbestos dust. In each case the extent of the
exposure found was very small. In each case, the Court of Appeal, applying the
special rule, held the defendant liable for causing the disease.
3. In Willmore v Knowsley Metropolitan Borough Council the Council
contends that the trial judge erred in finding that it was responsible for exposing
Mrs Willmore to sufficient asbestos dust to cause a material increase in risk. The
appeal involves an attack on findings of fact by the judge, which were upheld by
the Court of Appeal, but no issue of principle, albeit that it nicely illustrates the
effect of the special rule of causation. I agree that this appeal must be dismissed for
the reasons given by Lord Rodger and I have nothing to add to these.
4. In Sienkiewicz v Greif (UK) Ltd (“Greif”) the respondent is the daughter of
Mrs Enid Costello and sues as administratrix of her estate. The appellant, Greif,
raises two separate, albeit interrelated, grounds of appeal. The exposure for which
the judge found Greif to have been responsible only increased the total amount of
exposure which Mrs Costello would have experienced as a result of environmental
exposure to asbestos, that is exposure to asbestos in the atmosphere, by 18%. Greif
submits that in these circumstances the respondent failed to prove on balance of
probability that Greif caused Mrs Costello’s mesothelioma; to do this she would
have had to prove that the exposure for which Greif was responsible had more than
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doubled the environmental exposure. This submission raises the following
important issue of principle. Does the special rule of causation that applies in cases
of mesothelioma leave any room for applying a test of balance of probability to
causation? It also raises a general issue as to the applicability as proof of causation
in personal injury cases of a test usually applied to epidemiological evidence that I
shall call the “doubles the risk” test. Shortly stated this test attributes causative
effect to any factor that more than doubled a risk that would otherwise have been
present of the injury that occurred.
5. Greif’s alternative submission is that occupational exposure to asbestos dust
will only constitute a material increase in risk for the purpose of the special rule of
causation if it more than doubles the environmental exposure to such dust to which
the victim was subject. It did not do so in the case of Mrs Costello.
Methods of proving causation
6. Most claims for death or personal injury result from accidents. In such cases
the cause of death or personal injury will seldom be in issue. A body of knowledge
which I shall call “medical science” will enable a witness, expert in that science, to
describe the precise mechanism by which the accident brought about the death or
injury. I shall describe this as the “biological cause” of death or injury. It is
sometimes referred to by the more general description of the “cause in fact”. In
some cases, however, medical science will not yet have identified the precise
mechanism by which an injury gives rise to a particular physical consequence. In
such cases it may be possible to deduce that there was a causative link between the
two by evidence of what usually happens. Epidemiological evidence that a
particular injury or disease usually follows a particular type of bodily insult may
enable a court to conclude in a particular case, on balance of probability, that the
former was caused by the latter. “Post hoc ergo propter hoc”. A finding of
causation based on such evidence is sometimes described as “the cause in law”.
7. Where the court is concerned with a speculative question – “what would
have happened but for a particular intervention” it is likely to need to have regard
to what normally happens. A good example of such a situation is the task of
estimating the loss of expectation of life of a person whose death has been caused
by negligence or breach of duty. In such a situation the evidence upon which the
court will reach its conclusion is likely to be provided, at least in part, by a
statistician or an epidemiologist. Medical science will identify whether the
deceased had any physical characteristic relevant to his life expectancy.
Epidemiology will provide statistical evidence of life expectancy of the group or
cohort to which the deceased belonged. With this material the court answers the
hypothetical question of the length of the life that the victim would have enjoyed
but for the breach of duty of the defendant.
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8. Epidemiology can also provide a court with assistance in deciding what
actually happened, when the cause of a disease or injury is not clear. For one
remarkable example of the use, and ultimate rejection, of epidemiological evidence
see Loveday v Renton [1990] 1 MLR 1. Another remarkable case, to which I shall
make further reference was XYZ v Schering Health Care Ltd [2002] EWHC 1420
(QB); 70 BMLR 88.
9. When a scientific expert gives an opinion on causation, he is likely to do so
in terms of certainty or uncertainty, rather than probability. Either medical science
will enable him to postulate with confidence the chain of events that occurred, ie
the biological cause, or it will not. In the latter case he is unlikely to be of much
assistance to the judge who seeks to ascertain what occurred on a balance of
probability. This reality was expressed by Lord Prosser in Dingley v The Chief
Constable, Strathclyde Police 1998 SC 548, 603 with a clarity that merits
quotation:
“In ordinary (non-lawyers’) language, to say that one regards
something as ‘probable’ is by no means to say that one regards it as
‘established’ or ‘proved’. Yet in the civil courts, where we say that a
pursuer must prove his case on a balance of probabilities, what is
held to be probable is treated as ‘proved’. I do not suggest that any
lawyer will be confused by this rather special meaning of the word
‘proved’. But speaking very generally, I think that the civil
requirement of a pursuer – that he satisfy the court that upon the
evidence his case is probably sound – would in ordinary language be
regarded as very different from, and less stringent than, a
requirement that his case be established or proved. More importantly
in the context of such a case as the present, the fact that the two
concepts are distinct in ordinary language, but the same in this legal
context, seems to me to give rise to a risk of ambiguity or
misunderstanding in the expressed opinions of expert witnesses. And
this risk will be increased if the expert in question would normally,
in the exercise of his profession, adopt an approach to such issues
starkly different from that incumbent upon a court. Whether one uses
the word ‘scientific’ or not, no hypothesis or proposition would be
seen as ‘proved’ or ‘established’ by anyone with any form of
medical expertise merely upon the basis that he had come to regard it
as probably sound. (Indeed, I think even the word ‘probable’ would
be reserved for situations where the likelihood is thought to be much
more than marginal). And even if, in relation to any possible
proposition or hypothesis, such an expert even troubled to notice that
he had come to the point of regarding it as not merely possible but on
balance ‘probable’, then I think he would regard that point as one
from which he must set off on further inquiry, and by no means as
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being (as it is in the courts) a point of arrival. Mere marginal
probability will not much interest him. But it must satisfy a court.”
10. The issue in Dingley was whether the development of multiple sclerosis had
been caused by physical injury sustained in a motor accident. Medical science was
not able to demonstrate the connection between the two, and reliance was placed
on epidemiological evidence. Lord Prosser, at pp 604-605, had this to say about
this method of proof:
“I am not much impressed by one argument advanced for the
defender to the effect that the pursuer’s argument is essentially ‘post
hoc, ergo propter hoc’, and therefore unsound. Plainly, one will
more readily conclude that B is caused by A, or probably caused by
A, if one can identify, or at least envisage, some kind of mechanism
whereby B might be caused by A. Equally, if one simply cannot
identify or envisage such a mechanism, the mere fact that on one
occasion B happened after A (and perhaps very quickly after A)
would not, in the absence of other indications, lead one easily to
conclude that B was caused by A. But no one, certainly in this case,
suggests that such a single coincidence is to be interpreted as
involving a causal relationship. And once one moves from single
coincidence to a number of occasions when B follows (perhaps
quickly) upon A, dismissiveness of ‘post hoc, ergo propter hoc’
reasoning seems to me to become less and less appropriate. Indeed,
unless and until one can identify or envisage a connecting
mechanism, countless conclusions as to causal relationship are
reached precisely upon a form of ‘post hoc, ergo propter hoc’
reasoning: if B is observed never to occur except shortly after A, the
conclusion may be relatively easy – but if B is observed to occur
frequently after A, then even if each sometimes occurs without the
other, the frequency with which B occurs after A may nonetheless
well justify a more or less firm conclusion that A, in certain
circumstances, causes B. I do not regard such conclusions as based
on false (or indeed simple) logic. The approach is in my opinion
inherent not only in conclusions drawn from one’s general
experience or ‘anecdotal evidence’. It is inherent also in much
experimental research, and also, as it seems to me, in epidemiology.
And while it may always seem somewhat insufficient, until one can
find an identifiable possible mechanism, as a basis for claiming that
the causal link is proved or established, in either ordinary or
scientific terms, that feeling of insufficiency strikes me as much less
appropriate if one stops short of such claims and contents oneself
with saying that the causal relationship is marginally probable (or is
proved or established only as required in civil litigation).”
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11. Knowledge about mesothelioma is based in part on medical science and in
part on statistical analysis or epidemiology. These appeals raise the question of
whether, and if so to what extent, the court can satisfactorily base conclusions
about causation on the latter, both in mesothelioma cases and more generally.
Principles of causation in relation to disease
12. Many diseases are caused by the invasion of the body by an outside agent.
Some diseases are caused by a single agent. Thus malaria results from a single
mosquito bite. The extent of the risk of getting malaria will depend upon the
quantity of malarial mosquitoes to which the individual is exposed, but this factor
will not affect the manner in which the disease is contracted nor the severity of the
disease once it is contracted. The disease has a single, uniform, trigger and is
indivisible.
13. The contraction of other diseases can be dose related. Ingestion of the agent
that causes the disease operates cumulatively so that, after a threshold is passed, it
causes the onset of the disease. Lung cancer caused by smoking is an example of
such a disease, where the disease itself is indivisible. The severity of the disease,
once it has been initiated, is not related to the degree of exposure to cigarette
smoke.
14. More commonly, diseases where the contraction is dose related are
divisible. The agent ingested operates cumulatively first to cause the disease and
then to progress the disease. Thus the severity of the disease is related to the
quantity of the agent that is ingested. Asbestosis and silicosis are examples of such
diseases, as are the conditions of vibration white finger and industrial deafness,
although the insults to the body that cause these conditions are not noxious agents.
For this reason it is important to distinguish between asbestosis and mesothelioma
when considering principles of causation.
15. Mesothelioma is an indivisible disease. As I shall explain there is
uncertainty as to whether its contraction is related to the amount of asbestos fibres
ingested.
16. It is a basic principle of the law of tort that the claimant will only have a
cause of action if he can prove, on balance of probabilities, that the defendant’s
tortious conduct caused the damage in respect of which compensation is claimed.
He must show that, but for the defendant’s tortious conduct he would not have
suffered the damage. This broad test of balance of probabilities means that in some
cases a defendant will be held liable for damage which he did not, in fact, cause.
Page 7
Equally there will be cases where the defendant escapes liability, notwithstanding
that he has caused the damage, because the claimant is unable to discharge the
burden of proving causation.
17. There is an important exception to the “but for” test. Where disease is
caused by the cumulative effect of the inhalation of dust, part of which is
attributable to breach of duty on the part of the defendant and part of which
involves no breach of duty, the defendant will be liable on the ground that his
breach of duty has made a material contribution to the disease – Bonnington
Castings Ltd v Wardlaw [1956] AC 613. The disease in that case was
pneumoconiosis. That disease is divisible. The severity of the disease depends
upon the quantity of silica inhaled. The defendant did not, however, argue that, if
held liable, this should only be to the extent that the dust for which it was
responsible had contributed to the plaintiff’s symptoms. It was held liable for
100% of the disease. There have, however, been a series of cases at first instance
and in the Court of Appeal in which it has been recognised that where there has
been a number of exposures of a claimant to bodily insults that have cumulatively
caused a divisible disease, responsibility should be apportioned so that an
individual defendant is liable for no more than his share of the disease. This
apportionment may necessarily be a rough and ready exercise: see Mustill J’s
analysis in Thompson v Smiths Shiprepairers (North Shields) Ltd [1984] QB 405 at
pp 437-444 and the cases cited in McGregor on Damages, 18th ed (2010) at 8-010
to 8-016
What is known about mesothelioma
18. The special rule of causation applied to mesothelioma was devised because
of ignorance about the biological cause of the disease. It was accepted in Fairchild
and Barker that this rendered it impossible for a claimant to prove causation
according to the conventional “but for” test and this caused injustice to claimants.
It is not possible properly to consider the issues raised by this appeal without
reference to what is known about mesothelioma. This has been summarised in
many cases, and much of my own summary in Bryce v Swan Hunter Group plc
[1988] 1 All ER 659 of what was known 25 years ago remains true today. The
cases under appeal did not involve the introduction of detailed evidence of what is
known today about mesothelioma, proceeding on the basis that findings in
previous cases could be taken as read. There was, however, introduced in evidence
a case control study by Peto and Rake, published in 2009 by the Health and Safety
Executive, on “Occupational, Domestic and Environmental Mesothelioma risks in
Britain” (“the Peto Report”), which is said to be the first representative study to
quantify the relationship between mesothelioma risk and lifetime occupational and
residential history in this country.
Page 8
19. In these circumstances I have turned to recent judicial authority in order to
augment the information contained in Peto and Rake’s study. It has not been
necessary to look further than the collation of data about mesothelioma set out by
Rix LJ in his judgment in the series of appeals collectively described as
Employers’ Liability Insurance “Trigger” Litigation [2010] EWCA Civ 1096. I
shall set out in an annex to this judgment details of the current knowledge about
mesothelioma that I have obtained from these sources. I can summarise the effect
of the material in the Annex as follows:
i) Mesothelioma is always, or almost always, caused by the inhalation
of asbestos fibres.
ii) A significant proportion of those who contract mesothelioma have no
record of occupational exposure to asbestos. The likelihood is that in
their case the disease results from inhalation of asbestos dust that is
in the environment. There is, however, a possibility that some cases
of mesothelioma are “idiopathic”, ie attributable to an unknown
cause other than asbestos. Mr Stuart-Smith QC for Greif submitted
that the Peto Report indicates that this is more than a possibility, but
I do not so read it. I do not, however, think that it matters whether
some cases of the disease are idiopathic.
iii) The more fibres that are inhaled, the greater the risk of contracting
mesothelioma.
iv) There is usually a very long period between the exposure to asbestos
and the development of the first malignant cell. Typically this can be
at least 30 years.
v) There will be a lengthy period between the development of the first
malignant cell and the point at which the disease can be diagnosed.
At the time of Fairchild this was thought to be 10 years, but is now
thought to be at least 5 years. During this period, further exposure to
asbestos fibres will have no causative effect.
vi) The mechanism by which asbestos fibres cause mesothelioma is still
not fully understood. It is believed that a cell has to go through 6 or 7
genetic mutations before it becomes malignant, and asbestos fibres
may have causative effect on each of these.
vii) It is also possible that asbestos fibres have a causative effect by
inhibiting the activity of natural killer cells that would otherwise
destroy a mutating cell before it reaches the stage of becoming
malignant.
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20. These propositions are based in part on medical science and in part on
epidemiological studies. They represent the current understanding of a disease
about which much remains to be discovered.
The development of the special rule of causation that applies to mesothelioma
21. The starting point in tracing the development of the special rule of causation
is the decision of the House of Lords in McGhee v National Coal Board [1973] 1
WLR 1, an appeal from the First Division of the Court of Session. The pursuer
claimed against his employers for dermatitis which he alleged had been caused by
breaches of their common law duties. He was employed in a brick kiln, where he
got covered in brick dust. This, so it was held, involved no breach of duty on the
part of the defenders. They were, however, held in breach of duty for failure to
provide a shower which would have enabled him to wash off the dust as soon as he
finished work. He had to cycle home covered in dust and sweat. Two medical
experts were called. The effect of their evidence was that the brick dust caused the
dermatitis but that the precise mechanism whereby it did so was not known. It was
agreed, however, that the risk of contracting the disease would have been reduced
had the pursuer been able to wash off the dust before he cycled home. The cycle
ride home in his unwashed state increased his risk of getting dermatitis.
22. Lord Reid at p 4 summarised this evidence as follows:
“The medical evidence is to the effect that the fact that the man had
to cycle home caked with grime and sweat added materially to the
risk that this disease might develop. It does not and could not explain
just why that is so. But experience shows that it is so.”
23. The nature of the evidence of that experience is not apparent. It does not
appear to have been based on epidemiological research. Neither witness was able
to quantify the extent to which failure to wash increased the risk, and one said that
it was not possible to do so. If epidemiological data had existed it might have been
possible to make a quantitative assessment based upon it of the extent to which
delay in washing off brick dust increased the risk of dermatitis.
24. On the very limited evidence available it was possible that the dermatitis
had already been triggered by the time that the pursuer stopped work. It is equally
possible that the additional exposure while he cycled home caked in dust had a
critical incremental effect in triggering the disease. The defenders’ failure to
provide showers increased the hazard posed to their workforce by brick dust and it
was impossible on the evidence to determine whether this increase in hazard was
Page 10
or was not the critical factor in causing the pursuer’s dermatitis. Thus the facts of
McGhee were not on all fours with those of Bonnington. In Bonnington it was
possible to say that the inhalation of the silica attributable to breach of duty had
contributed to causing the plaintiff’s pneumoconiosis. In McGhee it was not
possible to say whether or not the lack of a shower had in fact contributed to the
contraction of the dermatitis.
25. I have not found it possible to identify in McGhee reasoning that is common
to all members of the House. The analysis of the decision that is now generally
accepted is that the majority of their Lordships adapted the approach in
Bonnington to the facts of McGhee by equating contribution to the risk of
contracting dermatitis with contribution to the disease itself. They did so in
circumstances where it was impossible to say whether, on balance of probability,
the absence of shower facilities had been critical. What four of their Lordships did
not consider was what the position would have been if there had been
epidemiological evidence that gave a negative answer to that question. Lord
Salmon did, however, expressly confront this question at p 12. After observing that
the expert evidence did not enable one to place a percentage figure on the extent to
which the lack of shower facilities had increased the risk of contracting dermatitis,
he added:
“It is known that some factors materially increase the risk and others
materially decrease it. Some no doubt are peripheral. Suppose,
however, it were otherwise and it could be proved that men engaged
in a particular industrial process would be exposed to a 52 per cent
risk of contracting dermatitis even when proper washing facilities
were provided. Suppose it could also be proved that that risk would
be increased to, say, 90 per cent when such facilities were not
provided. It would follow that if the decision appealed from is right,
an employer who negligently failed to provide the proper facilities
would escape from any liability to an employee who contracted
dermatitis notwithstanding that the employers had increased the risk
from 52 per cent to 90 per cent. The negligence would not be a cause
of the dermatitis because even with proper washing facilities, ie
without the negligence, it would still have been more likely than not
that the employee would have contracted the disease – the risk of
injury then being 52 per cent. If, however, you substitute 48 per cent
for 52 per cent the employer could not escape liability, not even if he
had increased the risk to, say, only 60 per cent. Clearly such results
would not make sense; nor would they, in my view, accord with the
common law.”
26. In the example given by Lord Salmon the lack of shower facilities did not
quite double the risk of contracting dermatitis. Thus, if one applies the “doubles
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the risk” test, the lack of shower facilities could not be shown to be the cause of
any individual workman’s dermatitis. I can understand why Lord Salmon
considered that to base a finding of causation on such evidence would be
capricious, but not why he considered that to do so would be contrary to common
law. The balance of probabilities test is one that is inherently capable of producing
capricious results. Nor do I understand his cryptic comment:
“I think that the approach by the courts below confuses the balance
of probability test with the nature of causation”.
The “doubles the risk” test is one that, as I shall show in due course, has been
adopted in subsequent cases as a valid method of deciding causation on balance of
probabilities, and one which Mr Stuart-Smith has sought to apply on these appeals.
27. In Hotson v East Berkshire Area Health Authority [1987] AC 750 causation
again caused a problem. The plaintiff, aged 13, had fallen out of a tree and
sustained injury which reduced the flow of blood to cartilage in his hip joint. In
breach of duty the defendants failed to diagnose this for five days. He suffered
permanent disability of the hip joint. The issue was whether the injury itself was so
severe that the subsequent disability of the hip joint was inevitable or whether, but
for the five day delay, it would have been possible to prevent that disability. The
medical evidence was that there was a 75% likelihood that the former was the
case, but a 25% possibility that the delay in treatment was critical. At first instance
[1985] 1 WLR 1036 Simon Brown J held that the defendant’s breach of duty had
robbed the plaintiff of a 25% chance of avoiding the disability. The House of
Lords held that this analysis was erroneous. The plaintiff was not robbed of a
chance of avoiding the disability. The die was cast as soon as he had sustained his
injury. Either the disability was inevitable or it could, with due skill and care, have
been avoided. On balance of probability, estimated at 75/25, the former was the
position, so the plaintiff had failed to prove causation.
28. The particular interest of Hotson in the present context is the consideration
given by Lord Mackay of Clashfern to McGhee, a case in which he had appeared
as leading counsel for the employers. Like Lord Salmon, he took an
epidemiological example. He said, at p 786:
“In McGhee v National Coal Board [1973] 1 WLR 1 this House held
that where it was proved that the failure to provide washing facilities
for the pursuer at the end of his shift had materially increased the
risk that he would contract dermatitis it was proper to hold that the
failure to provide such facilities was a cause to a material extent of
his contracting dermatitis and thus entitled him to damages from his
Page 12
employers for their negligent failure measured by his loss resulting
from dermatitis. Material increase of the risk of contraction of
dermatitis is equivalent to material decrease in the chance of
escaping dermatitis. Although no precise figures could be given in
that case for the purpose of illustration and comparison with this case
one might, for example, say that it was established that of 100 people
working under the same conditions as the pursuer and without
facilities for washing at the end of their shift 70 contracted
dermatitis: of 100 people working in the same conditions as the
pursuer when washing facilities were provided for them at the end of
the shift 30 contracted dermatitis. Assuming nothing more were
known about the matter than that, the decision of this House may be
taken as holding that in the circumstances of that case it was
reasonable to infer that there was a relationship between contraction
of dermatitis in these conditions and the absence of washing facilities
and therefore it was reasonable to hold that absence of washing
facilities was likely to have made a material contribution to the
causation of the dermatitis.”
29. In contrast to Lord Salmon’s figures, Lord Mackay’s figures demonstrate
that, statistically, the lack of washing facilities more than doubled the risk of
contracting dermatitis. Had evidence supporting such figures been given, it would
have enabled the House, by application of the “doubles the risk” test, to conclude
that the lack of shower facilities had, on balance of probabilities, caused Mr
McGhee to contract dermatitis. I do not at this stage comment on whether or not it
would have been appropriate for the House to apply that test.
30. Lord Mackay went on to comment:
“Although neither party in the present appeal placed particular
reliance on the decision in McGhee since it was recognised that
McGhee is far removed on its facts from the circumstances of the
present appeal your Lordships were also informed that cases are
likely soon to come before the House in which the decision in
McGhee will be subjected to close analysis. Obviously in
approaching the matter on the basis adopted in McGhee much will
depend on what is know of the reasons for the differences in the
figures which I have used to illustrate the position. In these
circumstances I think it unwise to do more than say that unless and
until this House departs from the decision in McGhee your Lordships
cannot affirm the proposition that in no circumstances can evidence
of loss of a chance resulting from the breach of a duty of care found
a successful claim of damages, although there was no suggestion that
the House regarded such a chance as an asset in any sense.”
Page 13
Once again I find this comment cryptic. Lord Mackay seems to be treating
epidemiological evidence as evidence of “loss of a chance”, but it is not clear
whether he is suggesting that such evidence might lead to a partial recovery rather
than a full recovery in a case such as McGhee.
31. The next step in the story is Wilsher v Essex Area Health Authority [1988]
AC 1074. A baby boy, born three months prematurely, developed a condition of
the retina which rendered him blind. There were five possible causes of the
condition. One was the negligent administration of an excessive quantity of
oxygen. The other four involved no fault on the part of the defendant’s medical
staff. The expert witnesses were unable to say which caused the disease. The Court
of Appeal, purporting to apply the principle in McGhee, held in favour of the
infant. Mustill LJ expressed the principle, as he understood it, as follows [1987]
QB 730, 771-772:
“If it is an established fact that conduct of a particular kind creates a
risk that injury will be caused to another or increases an existing risk
that injury will ensue; and if the two parties stand in such a
relationship that the one party owes a duty not to conduct himself in
that way; and if the first party does conduct himself in that way; and
if the other party does suffer injury of the kind to which the risk
related; then the first party is taken to have caused the injury by his
breach of duty, even though the existence and extent of the
contribution made by the breach cannot be ascertained.”
32. This analysis of McGhee was principled and coherent, but it was of wide
general application and fundamentally rewrote the law of causation. It opened the
floodgates and, I suspect, this may, in part, be the reason why it was subsequently
rejected.
33. In Wilsher, Sir Nicolas Browne-Wilkinson V-C, dissenting in the Court of
Appeal at p 779, did not accept Mustill LJ’s analysis:
“To apply the principle in McGhee v National Coal Board [1973] 1
WLR 1 to the present case would constitute an extension of that
principle. In the McGhee case there was no doubt that the pursuer’s
dermatitis was physically caused by brick dust: the only question
was whether the continued presence of such brick dust on the
pursuer’s skin after the time when he should have been provided
with a shower caused or materially contributed to the dermatitis
which he contracted. There was only one possible agent which could
have caused the dermatitis, viz, brick dust, and there was no doubt
Page 14
that the dermatitis from which he suffered was caused by that brick
dust. In the present case the question is different. There are a number
of different agents which could have caused the RLF. Excess oxygen
was one of them. The defendants failed to take reasonable
precautions to prevent one of the possible causative agents (eg
excess oxygen) from causing RLF. But no one can tell in this case
whether excess oxygen did or did not cause or contribute to the RLF
suffered by the plaintiff. The plaintiff’s RLF may have been caused
by some completely different agent or agents, eg hypercarbia,
intraventricular haemorrhage, apnoea or patent ductus arteriosus. In
addition to oxygen, each of those conditions has been implicated as a
possible cause of RLF. This baby suffered from each of those
conditions at various times in the first two months of his life. There
is no satisfactory evidence that excess oxygen is more likely than
any of those other four candidates to have caused RLF in this baby.
To my mind, the occurrence of RLF following a failure to take a
necessary precaution to prevent excess oxygen causing RLF provides
no evidence and raises no presumption that it was excess oxygen
rather than one or more of the four other possible agents which
caused or contributed to RLF in this case. The position, to my mind,
is wholly different from that in the McGhee case [1973] 1 WLR 1,
where there was only one candidate (brick dust) which could have
caused the dermatitis, and the failure to take a precaution against
brick dust causing dermatitis was followed by dermatitis caused by
brick dust. In such a case, I can see the common sense, if not the
logic, of holding that, in the absence of any other evidence, the
failure to take the precaution caused or contributed to the dermatitis.
To the extent that certain members of the House of Lords decided the
question on inferences from evidence or presumptions, I do not
consider that the present case falls within their reasoning. A failure
to take preventative measures against one out of five possible causes
is no evidence as to which of those five caused the injury.”
34. In the House of Lords, Lord Bridge of Harwich, reversing, with the
agreement of the other members of the House, the decision of the Court of Appeal,
approved the Vice-Chancellor’s analysis. He went on to hold at p 1090 that
McGhee
“laid down no new principle of law whatever. On the contrary, it
affirmed the principle that the onus of proving causation lies on the
pursuer or plaintiff. Adopting a robust and pragmatic approach to the
undisputed primary facts of the case, the majority concluded that it
was a legitimate inference of fact that the defenders’ negligence had
materially contributed to the pursuer’s injury. The decision, in my
Page 15
opinion, is of no greater significance than that and to attempt to
extract from it some esoteric principle which in some way modifies,
as a matter of law, the nature of the burden of proof of causation
which a plaintiff or pursuer must discharge once he has established a
relevant breach of duty is a fruitless one.”
This analysis of McGhee has fared no better than that of Mustill LJ, cited at para
31.
35. Bryce v Swan Hunter Group plc [1988] 1 All ER 659 was heard after the
decision of the Court of Appeal and before the decision of the House of Lords in
Wilsher. It was a claim in respect of mesothelioma against three defendants who,
as successive employers, had tortiously exposed the plaintiff to asbestos dust. He
had had other exposure to this less than 10 years before the onset of the disease
and those responsible for this had not been joined as defendants. McGhee, as
explained by Mustill LJ in Wilsher, was applied, resulting in a finding that each of
the defendants was liable. I understand that after this decision insurers of
employers who had consecutively subjected workmen to asbestos dust tended to
accept joint and several liability for mesothelioma and to agree apportionment. At
all events, this Court was not referred to any decision where such an approach was
challenged until Fairchild.
36. Fairchild involved three separate mesothelioma claims, which had been
heard together by the Court of Appeal [2002] 1 WLR 1052. In each case the victim
had been employed by a series of employers, each of which had wrongly exposed
him to asbestos dust. No attempt had been made to prove, by epidemiology or
otherwise, that on balance of probabilities, any particular employer had caused the
victim to contract the disease. The Court of Appeal ruled against each claim on the
ground that it had not been shown on balance of probability that any defendant had
caused the disease. Reliance on McGhee was rejected on the ground that Lord
Bridge in Wilsher had held that it established no new principle of causation and
that, in McGhee, there had been no doubt that the defendant had caused the
dermatitis – the only question was whether the defendant had done so in breach of
duty. If McGhee was applied in the Fairchild situation there was a risk that a
defendant would be held liable for a disease that it had not caused at all.
37. The House of Lords reversed the Court of Appeal, holding that the principle
in McGhee was applicable. Lord Bingham at paras 21 and 22 held that Lord
Bridge had been wrong in Wilsher to hold that McGhee represented no more than a
robust finding of fact that the defender’s negligence had materially contributed to
the pursuer’s injury. The opinions of at least the majority in McGhee could not be
read as decisions of fact or orthodox applications of settled law. The House had
adapted (rather than adopted) the orthodox test to meet the problem of proving
Page 16
causation that had arisen on the facts of that case. Lord Nicholls of Birkenhead put
the matter this way at para 44:
“Given the medical evidence in McGhee, it was not open to the
House, however robustly inclined, to draw an inference that the
employer’s negligence had in fact caused or materially contributed to
the onset of the dermatitis in the sense that, but for that negligence,
the dermatitis would not have occurred. Instead, a less stringent
causal connection was regarded as sufficient. It was enough that the
employer had materially increased the risk of harm to the employee.”
38. There is room for debate, and there has been debate, as to the precise basis
upon which the House in Fairchild applied the McGhee principle to the
mesothelioma claims under consideration. I do not propose to enter that debate, for
it was overtaken by the decision of the House in Barker. At this point it suffices to
note the following.
39. The House was agreed that the application of the McGhee principle was
circumscribed by a number of conditions, though not agreed as to what these were.
Lord Bingham at para 2 identified 6 relevant factors that applied to the cases under
consideration, before going on to hold that they brought into play the McGhee
principle:
“(1) C was employed at different times and for differing periods by
both A and B, and (2) A and B were both subject to a duty to take
reasonable care or to take all practicable measures to prevent C
inhaling asbestos dust because of the known risk that asbestos dust
(if inhaled) might cause a mesothelioma, and (3) both A and B were
in breach of that duty in relation to C during the periods of C’s
employment by each of them with the result that during both periods
C inhaled excessive quantities of asbestos dust, and (4) C is found to
be suffering from a mesothelioma, and (5) any cause of C’s
mesothelioma other than the inhalation of asbestos dust at work can
be effectively discounted, but (6) C cannot (because of the current
limits of human science) prove, on the balance of probabilities, that
his mesothelioma was the result of his inhaling asbestos dust during
his employment by A or during his employment by B or during his
employment by A and B taken together.”
40. At para 7 Lord Bingham explained the shortcomings of medical science:
Page 17
“It is not known what level of exposure to asbestos dust and fibre
can be tolerated without significant risk of developing a
mesothelioma, but it is known that those living in urban
environments (although without occupational exposure) inhale large
numbers of asbestos fibres without developing a mesothelioma. It is
accepted that the risk of developing a mesothelioma increases in
proportion to the quantity of asbestos dust and fibres inhaled: the
greater the quantity of dust and fibre inhaled, the greater the risk. But
the condition may be caused by a single fibre, or a few fibres, or
many fibres: medical opinion holds none of these possibilities to be
more probable than any other, and the condition once caused is not
aggravated by further exposure. So if C is employed successively by
A and B and is exposed to asbestos dust and fibres during each
employment and develops a mesothelioma, the very strong
probability is that this will have been caused by inhalation of
asbestos dust containing fibres. But C could have inhaled a single
fibre giving rise to his condition during employment by A, in which
case his exposure by B will have had no effect on his condition; or
he could have inhaled a single fibre giving rise to his condition
during his employment by B, in which case his exposure by A will
have had no effect on his condition; or he could have inhaled fibres
during his employment by A and B which together gave rise to his
condition; but medical science cannot support the suggestion that
any of these possibilities is to be regarded as more probable than any
other. There is no way of identifying, even on a balance of
probabilities, the source of the fibre or fibres which initiated the
genetic process which culminated in the malignant tumour.”
41. Lord Bingham identified at para 23 the problem raised by the facts of
Fairchild as follows:
“The problem of attributing legal responsibility where a victim has
suffered a legal wrong but cannot show which of several possible
candidates (all in breach of duty) is the culprit who has caused him
harm is one that has vexed jurists in many parts of the world for
many years.”
He justified his decision by the following policy considerations set out at para 33:
“It can properly be said to be unjust to impose liability on a party
who has not been shown, even on a balance of probabilities, to have
caused the damage complained of. On the other hand, there is a
strong policy argument in favour of compensating those who have
Page 18
suffered grave harm, at the expense of their employers who owed
them a duty to protect them against that very harm and failed to do
so, when the harm can only have been caused by breach of that duty
and when science does not permit the victim accurately to attribute,
as between several employers, the precise responsibility for the harm
he has suffered. I am of opinion that such injustice as may be
involved in imposing liability on a duty-breaking employer in these
circumstances is heavily outweighed by the injustice of denying
redress to a victim.”
42. Lord Bingham did not expressly consider the approach to be adopted where
a claimant had been exposed to asbestos dust both from employers in breach of
duty and from sources that did not involve fault, or which involved fault on the
part of the claimant himself. At para 34 he expressly limited the special rule of
causation that he was endorsing to a situation where all six of the factors that he
had identified at the start of his speech were present. At para 22 he underlined why
the special rule did not apply on the facts of Wilsher:
“It is plain, in my respectful opinion, that the House was right to
allow the defendants’ appeal in Wilsher, for the reasons which the
Vice-Chancellor had given and which the House approved. It is one
thing to treat an increase of risk as equivalent to the making of a
material contribution where a single noxious agent is involved, but
quite another where any one of a number of noxious agents may
equally probably have caused the damage.”
43. The other members of the House did not circumscribe the special rule of
causation as tightly as Lord Bingham. In McGhee itself the causal competition had
been between exposure to dust that involved no fault and exposure that involved
fault on the part of the employers, a point made by Lord Rodger at para 153. He
also held that Mustill LJ had illegitimately extended the special causation test in
Wilsher. He held, at para 149:
“Mustill LJ’s extension of the approach in McGhee to a situation
where there were all kinds of other possible causes of the plaintiff’s
condition, resulted in obvious injustice to the defendants. In
particular, there was nothing to show that the risk which the
defendants’ staff had created – that the plaintiff would develop
retrolental fibroplasia because of an unduly high level of oxygen –
had eventuated. That being so, there was no proper basis for
applying the principle in McGhee. As [Sir Nicolas BrowneWilkinson V-C] decisively observed, a failure to take preventive
measures against one of five possible causes was no evidence as to
Page 19
which of those five had caused the injury. The reasoning of the ViceChancellor, which the House adopted, provided a sound and
satisfactory basis for distinguishing McGhee and for allowing the
appeal.”
44. Lord Rodger set out his conclusions at para 170:
“First, the principle is designed to resolve the difficulty that arises
where it is inherently impossible for the claimant to prove exactly
how his injury was caused. It applies, therefore, where the claimant
has proved all that he possibly can, but the causal link could only
ever be established by scientific investigation and the current state of
the relevant science leaves it uncertain exactly how the injury was
caused and, so, who caused it. McGhee and the present cases are
examples. Secondly, part of the underlying rationale of the principle
is that the defendant’s wrongdoing has materially increased the risk
that the claimant will suffer injury. It is therefore essential not just
that the defendant’s conduct created a material risk of injury to a
class of persons but that it actually created a material risk of injury to
the claimant himself. Thirdly, it follows that the defendant’s conduct
must have been capable of causing the claimant’s injury. Fourthly,
the claimant must prove that his injury was caused by the
eventuation of the kind of risk created by the defendant’s
wrongdoing. In McGhee, for instance, the risk created by the
defenders’ failure was that the pursuer would develop dermatitis due
to brick dust on his skin and he proved that he had developed
dermatitis due to brick dust on his skin. By contrast, the principle
does not apply where the claimant has merely proved that his injury
could have been caused by a number of different events, only one of
which is the eventuation of the risk created by the defendant’s
wrongful act or omission. Wilsher is an example. Fifthly, this will
usually mean that the claimant must prove that his injury was caused,
if not by exactly the same agency as was involved in the defendant’s
wrongdoing, at least by an agency that operated in substantially the
same way. A possible example would be where a workman suffered
injury from exposure to dusts coming from two sources, the dusts
being particles of different substances each of which, however, could
have caused his injury in the same way. Without having heard
detailed argument on the point, I incline to the view that the principle
was properly applied by the Court of Appeal in Fitzgerald v Lane
[1987] QB 781. Sixthly, the principle applies where the other
possible source of the claimant’s injury is a similar wrongful act or
omission of another person, but it can also apply where, as in
McGhee, the other possible source of the injury is a similar, but
Page 20
lawful, act or omission of the same defendant. I reserve my opinion
as to whether the principle applies where the other possible source of
injury is a similar but lawful act or omission of someone else or a
natural occurrence.”
The conundrum
45. Neither Lord Bingham nor Lord Rodger explained the nature of the
principle that justifies restricting the application of McGhee to the situation where
the competing causes of the injury suffered by the claimant involve the same or a
similar noxious substance or agency. There is, however, a more significant
conundrum raised by Fairchild which is particularly relevant to this appeal. Lord
Bingham observed (see para 40 above) that it is accepted that the risk of
developing mesothelioma increases in proportion to the quantity of asbestos dust
and fibres inhaled. If this is so why should one not determine the probability that a
particular defendant caused a claimant’s mesothelioma by analysing the extent to
which he wrongfully contributed to the exposure of the claimant to asbestos dust
and fibres? This conundrum is highlighted by the decision of the House in Barker.
Barker
46. The question that Lord Rodger had expressly left open at the end of his
speech in Fairchild was raised directly in Barker, one of three appeals that were
heard together. The claimant was the widow of a man who had died of
mesothelioma. He had been exposed to asbestos dust on three occasions in his
working life. Once when working for a company which had since become
insolvent, once when working for the defendant and once when working for
himself. On the last occasion he had failed to take reasonable precautions for his
own safety. In the courts below the defendant had been held jointly and severally
liable with the insolvent company, but the claimant’s damages had been reduced
by 20% to reflect her husband’s contributory negligence. The other two appeals
involved employees who had been exposed to asbestos dust by a series of
employers, many of whom had since been held insolvent. In the courts below the
solvent employers who had been sued were held jointly and severally liable. In
each appeal the defendants argued that the special rule of causation that the House
had applied in Fairchild should be further refined so as to render each employer
liable only for that proportion of the damages which represented his contribution to
the risk that the employee would contract mesothelioma. This submission was
accepted by all members of the Committee with the exception of Lord Rodger,
who dissented.
Page 21
47. Lord Hoffmann gave the leading speech for the majority. He dealt first
with the question of whether the Fairchild principle could apply in a case where
part of the exposure was non-tortious. At para 17 he gave a positive answer to that
question:
“The purpose of the Fairchild exception is to provide a cause of
action against a defendant who has materially increased the risk that
the claimant will suffer damage and may have caused that damage,
but cannot be proved to have done so because it is impossible to
show, on a balance of probability, that some other exposure to the
same risk may not have caused it instead. For this purpose, it should
be irrelevant whether the other exposure was tortious or non-tortious,
by natural causes or human agency or by the claimant himself. These
distinctions may be relevant to whether and to whom responsibility
can also be attributed, but from the point of view of satisfying the
requirement of a sufficient causal link between the defendant’s
conduct and the claimant’s injury, they should not matter.”
48. Lord Hoffmann then turned to deal with apportionment. He did so on the
premise that mesothelioma is an indivisible injury caused by a single exposure to
asbestos dust. The greater the overall exposure, the greater the risk of an individual
fatal exposure: see paras 2 and 26. If, under the Fairchild principle exposure had
been treated as if it had actually contributed to the disease, the conventional
approach would have resulted in all those responsible for exposure being held
jointly and severally liable for the injury caused. Lord Hoffmann did not consider
it fair to impose such liability on employers “in cases in which there is merely a
relatively small chance” that they caused the injury (paras 43 and 46). He avoided
this consequence by interpreting the Fairchild principle as one that rendered a
defendant liable for contributing to risk, not contributing to injury. The risk created
was itself the damage, albeit that the principle only applied where injury had been
caused. As risk or chance was infinitely divisible, each defendant could be held
liable for his contribution to the risk.
49. At the end of his consideration of the issue of causation, Lord Hoffmann
made the following finding as to the limit of the Fairchild principle or exception:
“24. In my opinion it is an essential condition for the operation of the
exception that the impossibility of proving that the defendant caused
the damage arises out of the existence of another potential causative
agent which operated in the same way. It may have been different in
some causally irrelevant respect, as in Lord Rodger’s example of the
different kinds of dust, but the mechanism by which it caused the
damage, whatever it was, must have been the same. So, for example,
Page 22
I do not think that the exception applies when the claimant suffers
lung cancer which may have been caused by exposure to asbestos or
some other carcinogenic matter but may also have been caused by
smoking and it cannot be proved which is more likely to have been
the causative agent.”
50. In considering how apportionment would work in practice, Lord Hoffmann
said this:
“36. Treating the creation of the risk as the damage caused by the
defendant would involve having to quantify the likelihood that the
damage (which is known to have materialised) was caused by that
particular defendant. It will then be possible to determine the share
of the damage which should be attributable to him. The
quantification of chances is by no means unusual in the courts. For
example, in quantifying the damage caused by an indivisible injury,
such as a fractured limb, it may be necessary to quantify the chances
of future complications. Sometimes the law treats the loss of a
chance of a favourable outcome as compensatable damage in itself.
The likelihood that the favourable outcome would have happened
must then be quantified: see, for example, Chaplin v Hicks [1911] 2
KB 786 and Kitchen v Royal Air Force Association [1958] 1 WLR
563.
37.These are of course cases in which there is uncertainty as to what
will be, or would have been, the outcome of a known event; for
example, the consequences of a fractured ankle, a beauty contest or a
lawsuit. The present case involves uncertainty as to the cause of a
known outcome, namely, the mesothelioma. But in principle I can
see no reason why the courts cannot quantify the chances of X
having been the cause of Y just as well as the chance of Y being the
outcome of X.”
51. He returned to this theme under the heading of “quantification” at para 48:
“But when the damage is apportioned among the persons responsible
for the exposures to asbestos which created the risk, it is known that
those exposures were together sufficient to cause the disease. The
damages which would have been awarded against a defendant who
had actually caused the disease must be apportioned to the
defendants according to their contributions to the risk. It may be that
the most practical method of apportionment will be according to the
Page 23
time of exposure for which each defendant is responsible, but
allowance may have to be made for the intensity of exposure and the
type of asbestos. These questions are not before the House and it is
to be hoped that the parties, their insurers and advisers will devise
practical and economical criteria for dealing with them.”
52. These passages raise the conundrum to which I have referred in para 45
above in an acute form. If it is possible, on the basis of responsibility for exposure,
to deduce the relative likelihood of a defendant being the employer who actually
caused the injury, why should one not resolve liability according to the normal test
of balance of probability. If one can determine that there was “a relatively small
chance” that a particular employer caused the injury, why should that employer not
be absolved from liability on the ground that he can prove, on balance of
probability, that he was not responsible?
53. Lord Scott agreed with the reasoning and the result reached by Lord
Hoffmann. He recognised, however, that the limitations on medical knowledge
rendered it impossible to say whether mesothelioma was caused by a single
exposure, and thus a single employer, or by a combination of more than one
exposures and thus, possibly, by more than one employer: para 51. His speech also
implicitly raised the conundrum. When dealing with apportionment he said this, at
para 62:
“Ascertainment of the degree of risk would be an issue of fact to be
determined by the trial judge. The issue would depend upon the
duration of the exposure for which each negligent defendant was
responsible compared with the total duration of the claimant’s
exposure to the injurious agent in question. It might depend also on
the intensity of the exposure for which the defendant was responsible
compared with the intensity of the exposure for which the defendant
was not responsible. The exact type of agent might be a relevant
factor in assessing the degree of risk. I have in mind that there are
different types of asbestos and some might create a greater risk than
others. Other factors relevant to the degree of risk might come into
the picture as well. The assessment of the percentage risk for which
an individual defendant was responsible, and therefore the
percentage of the total damage for which that defendant could be
held liable, would, as I have said, be an issue of fact to be decided on
the evidence in each case.”
Why could one not assess the probability of having caused the injury on the same
basis as that used to apportion contribution to the risk of causing the injury?
Page 24
54. The same question is raised by the speech of Lord Walker, who also agreed
with the reasoning and result reached by Lord Hoffmann. He observed, at para
109:
“A rule of law by which exposure to risk of injury is equated with
legal responsibility for that injury entails the possibility that an
employer may be held liable for an injury which was not in fact
caused by that exposure (though in the present state of medical
science, that fact can be neither proved nor disproved). This possible
unfairness cannot be eliminated, as the House recognised in
Fairchild, but it is considerably reduced if each employer’s liability
is limited in proportion to the fraction of the total exposure
(measured by duration and intensity) for which each is responsible.”
The underlying premise of all three speeches, as of the speeches in Fairchild, is
that it is not possible to determine causation unless medical science enables one to
do so with certainty. But the law of causation does not deal in certainties; it deals
in probabilities.
55. Lady Hale agreed in general with the majority, but she did not accept that
the gist of the actions was the risk created rather than the mesothelioma. To that
extent she shared the reasoning that had led Lord Rodger to dissent.
56. The result of the decision in Barker was that, where not all those who were
responsible for an employee’s mesothelioma were before the court, only a
proportion of the relevant damages would be recoverable. This was highly
significant having regard to the very long latency period of the disease, for in most
cases there was a high likelihood that there would be employers who had
contributed to exposure and who had gone into liquidation. Apportionment also
dealt with the problem of contributory negligence. The rejoicing with which the
insurance industry must have greeted this result was short lived as Parliament
intervened.
The Compensation Act 2006
57. The preamble to the 2006 Act includes among its objects “to make
provision about damages for mesothelioma”. The relevant parts of the provision
made are as follows:
“3. Mesothelioma: damages
Page 25
(1)This section applies where—
(a) a person (‘the responsible person’) has negligently
or in breach of statutory duty caused or permitted
another person (‘the victim’) to be exposed to asbestos,
(b) the victim has contracted mesothelioma as a result
of exposure to asbestos,
(c) because of the nature of mesothelioma and the state
of medical science, it is not possible to determine with
certainty whether it was the exposure mentioned in
paragraph (a) or another exposure which caused the
victim to become ill, and
(d) the responsible person is liable in tort, by virtue of
the exposure mentioned in paragraph (a), in connection
with damage caused to the victim by the disease
(whether by reason of having materially increased a
risk or for any other reason).
(2) The responsible person shall be liable—
(a) in respect of the whole of the damage caused to the
victim by the disease (irrespective of whether the victim
was also exposed to asbestos—
(i) other than by the responsible person, whether or
not in circumstances in which another person has
liability in tort, or
(ii) by the responsible person in circumstances in
which he has no liability in tort), and
(b) jointly and severally with any other responsible person.”
58. This provision has grafted onto the Fairchild/Barker principle a special rule
in relation to liability in damages that applies only to mesothelioma. The 2006 Act,
coupled with Fairchild, has draconian consequences for an employer who has been
responsible for only a small proportion of the overall exposure of a claimant to
asbestos dust, or his insurers, but it would be wrong to have regard to that fact
when considering the issues raised by these appeals. Parliament has willed it so.
The facts in Greif as found by the judge
59. Mrs Costello died of mesothelioma in January 2006 at the age of 74. She
had worked for Greif or their predecessors at their factory at Ellesmere Port,
Cheshire, between 1966 and 1984. Greif exposed those working at that factory to
Page 26
asbestos dust in breach of duty. The greatest exposure was on the factory floor, but
to a much lesser extent asbestos dust permeated to other parts of the factory. Mrs
Costello’s exposure was in those other parts as she moved around the factory.
60. This occupational exposure was very light. The judge, His Honour Judge
Main QC, heard expert evidence which quantified this exposure and compared it to
the environmental exposure that would be experienced by everyone. While he held
that he could “only use the broadest sorts of estimates” as to Mrs Costello’s
asbestos exposure he none the less based some very specific findings on this expert
evidence. He held that her exposure to asbestos over her working life at Greif’s
factory increased the risk to which environmental exposure subjected her from 24
cases per million to 28.39 cases per million – an increase of risk of 18%.
61. It was on the basis of this finding that the judge held that the claimant’s
case on causation had not been made out. His starting point was that the special
rule in Fairchild had no application where there was only one tortfeasor and where
the competition as to causation was between an innocent and a tortious source of
dust. In that situation he adopted an approach to causation which had been
adopted, by agreement between the parties, in an earlier case on similar facts in the
Cardiff County Court decided by HH Judge Hickinbottom: Jones v Metal Box Ltd
(unreported) 11 January 2007:
“53. (ii) It was common ground that, in order to succeed with the
claim, the claimant must show that as a result of her exposure to
asbestos dust at work as I have described, Mrs Jones’ risk of
mesothelioma at least doubled from that which it would have been
without that exposure. That in my judgment is a correct analysis of
the position with regard to medical causation: because unless the
claimant can show that the risk was doubled, then it is more likely
than not that the mesothelioma had an idiopathic rather than an
occupational cause…”
Thus Judge Hickinbottom applied the “doubles the risk” test.
62. Applying that test Judge Main held:
“On the facts of this case, the claimant could only succeed if she
were able to prove that all Mrs Costello’s exposure to asbestos was
within the Oil Sites premises, cumulatively, over her 18 years
employment exceeded her environmental risks. Here environmental
risks are the same as those ‘idiopathic’ risks referred to by Judge
Page 27
Hickinbottom. This in my judgment regrettably, she failed to do.
Whilst Mrs Costello’s risk of contracting mesothelioma increased by
18% the bottom line is that it was caused by her environmental
exposure to asbestos. Her claim against the defendants accordingly
must be dismissed.”
63. In the Court of Appeal Smith LJ gave the leading judgment. In discussing
the legal principles applicable she first referred to McGhee and Fairchild. She then
considered the “doubles the risk” test in relation to cases of diseases other than
mesothelioma. She reached the following conclusion of general principle:
“20. The theory that causation could be proved on the balance of
probabilities by reference to a doubling of the risk of injury was first
applied by Mackay J in the oral contraceptive litigation XYZ v
Schering Health Care Ltd (2002) 70 BMLR 88. As a preliminary
issue, the parties agreed that the judge should examine the
epidemiological evidence relating to the risk of deep vein thrombosis
arising from two different types of oral contraceptive. The claimant
group could succeed only if the epidemiology showed that the risk of
harm arising from the type of contraceptive they had been taking
(which it was assumed they had not been warned about and would
not have taken if warned) was at least twice that arising from the
type which they had formerly been taking (which it was assumed
they had been warned about and which risk they had accepted). The
logic behind this was that, if the risk from potential cause A is x%
and the risk from the other potential cause B is 2.1x%, it is more
likely than not that the condition which has eventuated has been
caused by B.
21. Since the oral contraceptive case, this method of proving
causation has been applied in cases of lung cancer where the
claimant has been tortiously exposed to asbestos and non-tortiously
exposed to cigarette smoke, both of which are potent causes of the
condition. Expert evidence is received as to the relative risks created
by the two forms of exposure and, if, on the individual facts of the
case, the risk from the asbestos exposure is more than double the risk
from smoking, the claimant succeeds.
22. The only case of which I am aware in which this approach has
been applied or approved in the Court of Appeal is Novartis Grimsby
Ltd v Cookson [2007] EWCA Civ 1261. That was a case of bladder
cancer, in which the claimant had been tortiously exposed to
carcinogens in the course of his employment in a dye works. He had
also been a regular smoker. Both were potential causes of bladder
cancer. At trial, the defendant’s case was that the tortious exposure at
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work had been minimal. The recorder held that it was not minimal
and applied the Bonnington case [1956] AC 613; he held that the tort
had made a material contribution to the disease. On appeal, the
appellant employer argued, correctly, that that was wrong as the tort
could not be said to have made a contribution to the disease, only to
the risk of the disease developing. The claimant argued that the case
ought to come within the Fairchild exception so that all that was
necessary was to prove a material increase in risk. The appellant
employer contended that the Fairchild case [2003] 1 AC 32 should
not be extended to cover such a case. In the event, the Court of
Appeal observed that there was expert evidence, which the recorder
had accepted, to the effect that the tortious exposure had more than
doubled the risk arising from smoking. The court held that that was
sufficient for the claim to succeed.
23. In my view, it must now be taken that, saving the expression of a
different view by the Supreme Court, in a case of multiple potential
causes, a claimant can demonstrate causation by showing that the
tortious exposure has at least doubled the risk arising from the nontortious cause or causes.”
64. Smith LJ went on to consider whether the “doubles the risk” test could be
applied in relation to mesothelioma. She held that it could not. She did so on the
basis that by enacting section 3(1)(d) of the Compensation Act 2006 Parliament
had laid down a rule that causation in a mesothelioma case could be established by
proof of a material increase in risk: para 34. This precluded a defendant from
averring, in a case of mesothelioma, that the claimant had to satisfy the “doubles
the risk” test. She held, at para 27, that the judge should have applied the test of
material increase of risk, ie the Fairchild/Barker rule, and in consequence the
appeal should be allowed:
“it is not now possible for this court to consider whether, at common
law, the Fairchild exception should be limited in application to cases
in which it is quite impossible for a claimant to prove causation by
reference to a more than twofold increase in risk. That is because
Parliament has intervened by enacting section 3 of the Compensation
Act 2006 so that the common law simpliciter no longer governs
claims for damages in mesothelioma cases.”
65. Had Smith LJ held that the “doubles the risk” test could be applied to
mesothelioma, she would not have allowed the decision of the judge to stand. She
held that the “doubles the risk” test had been advanced without adequate notice, so
that Sienkiewicz had been wrong footed and denied a fair chance to deal with the
expert evidence. The case would have to be remitted for a new trial.
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66. Scott Baker LJ and Lord Clarke agreed with the judgment of Smith LJ.
Lord Clarke held that the Fairchild test had to be applied by reason both of
common law and the construction of section 3 of the 2006 Act.
Submissions
67. I can summarise the arguments advanced by Mr Stuart-Smith on behalf of
Greif as follows, adopting a different order to that adopted in his printed case:
i) The Court of Appeal erred in holding that section 3 of the 2006 Act
mandated the application of the Fairchild/Barker rule of causation in
mesothelioma cases.
ii) The Fairchild/Barker rule does not apply in this case because this is
a “single exposure” case.
iii) It is possible in this case to adopt a conventional approach to
causation by applying the “doubles the risk” test. This approach
demonstrates that Mrs Costello contracted mesothelioma as a result
of environmental exposure and not as a result of the slight additional
exposure to which she was subjected by Greif.
iv) The claim also fails because the exposure to which Greif subjected
Mrs Costello was not material. Occupational exposure is not material
unless it more than doubles the amount of environmental exposure to
which a claimant is subject. In the case of Mrs Costello the exposure
for which Greif was responsible was insignificant. The findings of
exposure made by the trial judge could not be supported by the
evidence and there was no justification for a fresh trial.
68. Mr Melton QC for Mrs Costello’s estate challenged all these submissions.
He submitted that the Fairchild test was applicable and attacked the application of
the “doubles the risk” test. He further submitted that the asbestos dust to which
Mrs Costello was subjected materially increased the risk that she would contract
mesothelioma and that, applying the Fairchild test and section 3 of the 2006 Act,
the Court of Appeal had properly held the claim to be made out in full.
Discussion
69. I propose to discuss the problems raised by this appeal under the following
five headings:
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i) The effect of section 3 of the Compensation Act 2006.
ii) Epidemiology and the nature of the “doubles the risk” test.
iii) Can the “doubles the risk” test be applied in multiple cause cases
involving diseases other than mesothelioma?
iv) Can the “doubles the risk” test be applied to mesothelioma cases.
v) What constitutes a material increase in risk?
vi) The result in this case.
The effect of section 3 of the Compensation Act 2006
70. The Court of Appeal treated section 3(1) as enacting that, in cases of
mesothelioma, causation can be proved by demonstrating that the defendant
wrongfully “materially increased the risk” of a victim contracting mesothelioma.
This was a misreading of the subsection. Section 3(1) does not state that the
responsible person will be liable in tort if he has materially increased the risk of a
victim of mesothelioma. It states that the section applies where the responsible
person is liable in tort for materially increasing that risk. Whether and in what
circumstances liability in tort attaches to one who has materially increased the risk
of a victim contracting mesothelioma remains a question of common law. That law
is presently contained in Fairchild and Barker. Those cases developed the
common law by equating “materially increasing the risk” with “contributing to the
cause” in specified and limited circumstances, which include ignorance of how
causation in fact occurs. The common law is capable of further development.
Thus section 3 does not preclude the common law from identifying exceptions to
the “material increase of risk” test, nor from holding, as more is learned about
mesothelioma, that the material increase of risk test no longer applies. The
Fairchild/Barker rule was adopted in order to cater for the ignorance that existed
at the time of those decisions about the way in which mesothelioma is caused.
Section 3 does not preclude the courts from reverting to the conventional approach
of balance of probabilities in mesothelioma cases should advances in medical
science in relation to this disease make such a step appropriate.
71. Greif contend that the Court should identify an exception to the
Fairchild/Barker rule where there has been only one occupational exposure to risk
and that, in those circumstances, the Court can and should apply the “doubles the
risk” test. Section 3 poses no bar to that contention; it must be considered on its
merits.
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Epidemiology and the nature of the “doubles the risk” test
72. The “doubles the risk” test is one that applies epidemiological data to
determining causation on balance of probabilities in circumstances where medical
science does not permit determination with certainty of how and when an injury
was caused. The reasoning goes as follows. If statistical evidence indicates that the
intervention of a wrongdoer more than doubled the risk that the victim would
suffer the injury, then it follows that it is more likely than not that the wrongdoer
caused the injury. I propose first to consider the authorities to which Smith LJ
referred to see the extent to which they support the general proposition that she
stated at para 23 of her judgment.
73. Smith LJ founded the general proposition in para 23 of her judgment (see
para 63 above) on one decision of Mackay J, one decision of the Court of Appeal
and on unspecified cases of exposure both to asbestos and to cigarette smoke.
When these are examined it becomes apparent that they exemplify the application
of the “doubles the risk” test in three quite different circumstances. I propose to
look at these before considering the nature of the epidemiological principle applied
in each of them.
74. XYZ is a lengthy and complex judgment devoted exclusively to a
preliminary issue on the effect of epidemiological evidence. The issue was whether
a second generation of oral contraceptives more than doubled the risk of causing
deep vein thrombosis (DVT) that was created by the first generation of oral
contraceptives. It was common ground that, if the claimants in this group litigation
could not establish this, their claims under the Consumer Protection Act 1987 were
doomed to failure. I do not believe that Smith LJ has correctly identified the
relevance of this issue. It was not whether the DVT suffered by the claimants had
been caused by the second generation of oral contraceptives which they had taken.
It was whether the second generation of contraceptives created a significantly
greater risk than the first. The experts appear to have been in agreement that the
“doubles the risk” test was the proper one to apply in order to resolve this issue.
Thus I do not believe that that decision affords any direct assistance to the question
of whether the “doubles the risk” test is an appropriate test for determining
causation in a case of multiple potential causes. It does, however, contain a
detailed and illuminating discussion of epidemiology and I shall revert to it when
considering that topic.
75. Shortell v BICAL Construction Ltd (Liverpool District Registry, 16 May
2008), another decision of Mackay J, was a claim in relation to a death caused by
lung cancer where there were two possible causes of the cancer. One was
occupational exposure to asbestos and the other was cigarette smoke. The
defendant was responsible for the former but not for the latter. Applying the
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Bonnington test of causation, the issue was whether the asbestos to which the
victim had been exposed had made a material contribution to the cause of the
victim’s lung cancer. The expert evidence, given by both medical and
epidemiological experts, but based in the case of each, I suspect, on
epidemiological data, was that asbestos and cigarette smoke not merely combined
cumulatively to cause lung cancer, but that they had a synergistic effect in doing
so. This evidence was enough, as I see it, to satisfy the Bonnington test of
causation, as the victim had been exposed both to significant quantities of asbestos
fibres and to significant cigarette smoke.
76. In these circumstances, I am puzzled by the following passages in the
judgment:
“49.The causation of lung cancer as opposed to mesothelioma is
dependent on an aggregate dose either of asbestos fibre or smoke. Mr
Feeny for the defendants rightly in my view concedes that if the
claimant proves on a balance of probabilities that the risk factor
created by his client’s breach of duty more than doubled the
deceased’s relative risk of contracting lung cancer then the
claimant’s case is proved, and the only remaining issue is
contributory negligence. For the reasons I have advanced above I am
satisfied on the balance of probabilities that once the estimate of 99
fibre/ml – years is accepted as I have accepted it the relative risk is
on any view more than doubled.
51. Where, as here, it is the case that the claimant has proved
causation against this defendant by showing a more than doubled
relative risk it is not relevant as between the claimant and the
defendant to argue that another agent (tortious or otherwise) may
also have contributed to the occurrence of the disease.”
Epidemiological evidence indicated that, had the victim not been a smoker, his
exposure to asbestos would have more than doubled the risk that he would get lung
cancer. I do not, however, see that it was essential for the claimant to prove this.
For this reason I question whether Smith LJ’s endorsement of the “doubles the
risk” test is correct in cases where asbestos and tobacco smoke have combined to
cause lung cancer.
77. Novartis Grimsby Ltd v Cookson [2007] EWCA Civ 1261, which was the
third case to which Smith LJ referred, was an appeal in which she gave the only
reasoned judgment. The claimant sought damages against his employers for
causing him bladder cancer. It is known that bladder cancer is caused by exposure
Page 33
to amines and the claimant had been so exposed from two sources. One was his
employment, which wrongfully exposed him to amines used in the manufacture of
dyes. The other was smoking, for cigarette smoke contains amines. There was
expert evidence, which the recorder accepted, that the occupational exposure had
more than doubled the risk caused by smoking. There was an issue as to whether
Bonnington applied or whether the claimant had to prove that “but for” the
occupational exposure he would not have suffered the cancer. Smith LJ did not
find it necessary to resolve this issue, for at para 74 she held that the “but for” test
was satisfied:
“In terms of risk, if occupational exposure more than doubles the risk
due to smoking, it must, as a matter of logic, be probable that the
disease was caused by the former.”
78. On analysis, it is only this last proposition that supports Smith LJ’s general
statement that a claimant can prove causation where there are a number of
potential causes of a disease or injury by showing that the tortious exposure had at
least doubled the risk arising from the non-tortious cause or causes. I agree with
her that, as a matter of logic, if a defendant is responsible for a tortious exposure
that has more than doubled the risk of the victim’s disease, it follows on the
balance of probability that he has caused the disease, but these are statistical
probabilities and the issue in this case is whether a statistical approach to
determining causation should be applied in place of the Fairchild/Barker test.
79. I have derived assistance in relation to the next section of this judgment
from the judgment of Mackay J in XYZ. He there set out a careful and detailed
introduction into the discipline of epidemiology and I shall gratefully borrow some
of the clear language that he used.
80. Epidemiology is the study of the occurrence and distribution of events (such
as disease) over human populations. It seeks to determine whether statistical
associations between these events and supposed determinants can be demonstrated.
Whether those associations if proved demonstrate an underlying biological causal
relationship is a further and different question from the question of statistical
association on which the epidemiology is initially engaged.
81. Epidemiology may be used in an attempt to establish different matters in
relation to a disease. It may help to establish what agents are capable of causing a
disease, for instance that both cigarette smoke and asbestos dust are capable of
causing lung cancer, it may help to establish which agent or which source of an
agent, was the cause, or it may help to establish whether or not one agent
combined with another in causing the disease.
Page 34
82. Epidemiological data can be obtained by comparing the relevant experience
(eg contraction of a disease) of a group or cohort that is subject to exposure to a
particular agent with the experience of a group or cohort that is not. Where an
agent is known to be capable of causing a disease, the comparison enables the
epidemiologist to calculate the relevant risk (RR) that flows from the particular
exposure. An RR of 1 indicates that there is no association between the particular
exposure and the risk. An RR of 2 indicates that the particular exposure doubled
the chance that the victim would contract the disease. Statistically the likelihood
that the victim would have contracted the disease without the particular exposure is
then equal to the likelihood that the victim would not have contracted the disease
but for that exposure. Where the RR exceeds 2 the statistical likelihood is that the
particular exposure was the cause of the disease. The greater the RR the greater the
statistical likelihood that the particular exposure caused the disease.
83. An RR of just over 2 is a tenuous basis for concluding that the statistical
probable cause of a disease was also the probable biological cause, or cause in fact.
The greater the RR the greater the likelihood that the statistical cause was also the
biological cause. One reason why an RR of just over 2 is a tenuous basis for
determining the biological cause is that the balance of that probability is a very
fine one. Another is that the epidemiological data may not be reliable. One reason
for this may be that the relevant survey or surveys have been insufficiently
extensive to produce data that is truly representative. Epidemiologists
conventionally seek to indicate the reliance that can be placed on an RR by
determining 95% confidence limits or intervals (C1) around it.
84. The approach that I have been describing focuses on one specific causal
agent or a number of specific causal agents. There may well, however, be other
causal factors that operate in conjunction with the agent exposure to which is the
particular object of investigation, eg the age or genetic susceptibility of the victim.
The identification of one probable cause of a disease does not preclude the
possibility that there are other contributory causes.
85. Mr Stuart-Smith in his printed case helpfully referred us to a number of
foreign authorities which demonstrate that the weight to be attached to
epidemiological evidence can vary significantly according to judicial policy. In
America the test of causation in toxic tort cases varies from state to state. The most
helpful case in the present context is Merrell Dow Pharmaceuticals Inc v Havner
(1997) 953 SW 2d 706, a decision of the Supreme Court of Texas, for this gives
detailed consideration to the “doubles the risk” test. The claim was one of a large
number brought against the manufacturer of the prescription drug Bendectin. The
parents of a child born with a limb reduction birth defect alleged that the cause of
this was Bendectin, taken by the mother when she was pregnant. The parents
sought to establish causation by epidemiological evidence which they contended
demonstrated that taking this drug more than doubled the risk of such birth defects.
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86. Giving the judgment of the court Phillips CJ remarked, at p 716, that the
“doubling of the risk” issue in toxic tort cases had provided “fertile ground for the
scholarly plow”. He proceeded to refer to much of this, summarising the position
as follows, at p 717:
“Some commentators have been particularly critical of attempts by
the courts to meld the more than 50% probability requirement with
the relative risks found in epidemiological studies in determining if
the studies were admissible or were some evidence that would
support an award for the claimant. But there is disagreement on how
epidemiological studies should be used. Some commentators contend
that the more than 50% probability requirement is too stringent,
while others argue that epidemiological studies have no relation to
the legal requirement of ‘more likely than not’.”
87. The Chief Justice went on to hold that, although there was not a precise fit
between science and legal burdens of proof, properly designed and executed
epidemiological studies could form part of evidence supporting causation in a
toxic tort case and that there was a rational basis for relating the requirement that
there be more than a “doubling of the risk” to the more likely than not burden of
proof.
88. At p 718 the Chief Justice commented:
“But the law must balance the need to compensate those who have
been injured by the wrongful actions of another with the concept
deeply imbedded in our jurisprudence that a defendant cannot be
found liable for an injury unless the preponderance of the evidence
supports cause in fact. The use of scientifically reliable
epidemiological studies and the requirement of more than a doubling
of the risk strikes a balance between the needs of our legal system
and the limits of science.
We do not hold, however, that a relative risk of more than 2.0 is a
litmus test or that a single epidemiological test is legally sufficient
evidence of causation. Other factors must be considered. As already
noted, epidemiological studies only show an association.”
He then emphasised the need for the design and execution of epidemiological
studies to be examined in order to identify possible bias.
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89. At pp 720-721 he made a comment that is particularly pertinent in the
context of this appeal:
“Finally, we are cognizant that science is constantly re-evaluating
conclusions and theories and that over time, not only scientific
knowledge but scientific methodology in a particular field may
evolve. We have strived to make our observations and holdings in
light of current, generally accepted scientific methodology.
However, courts should not foreclose the possibility that advances in
science may require re-evaluation of what is ‘good science’ in future
cases.”
Can the “doubles the risk” test be applied in multiple cause cases involving
diseases other than mesothelioma?
90. For reasons that I have already explained, I see no scope for the application
of the “doubles the risk” test in cases where two agents have operated
cumulatively and simultaneously in causing the onset of a disease. In such a case
the rule in Bonnington applies. Where the disease is indivisible, such as lung
cancer, a defendant who has tortiously contributed to the cause of the disease will
be liable in full. Where the disease is divisible, such as asbestosis, the tortfeasor
will be liable in respect of the share of the disease for which he is responsible.
91. Where the initiation of the disease is dose related, and there have been
consecutive exposures to an agent or agents that cause the disease, one innocent
and one tortious, the position will depend upon which exposure came first in time.
Where it was the tortious exposure, it is axiomatic that this will have contributed to
causing the disease, even if it is not the sole cause. Where the innocent exposure
came first, there may be an issue as to whether this was sufficient to trigger the
disease or whether the subsequent, tortious, exposure contributed to the cause. I
can see no reason in principle why the “doubles the risk” test should not be applied
in such circumstances, but the court must be astute to see that the epidemiological
evidence provides a really sound basis for determining the statistical probability of
the cause or causes of the disease.
92. McGhee may have been such a case. The facts were puzzling, for no other
workman had ever contracted dermatitis at the defendants’ brick kiln, so one
wonders what the basis was for finding that the lack of shower facilities was
potentially causative. Had there been epidemiological evidence it seems unlikely
that this would have demonstrated that the extra ten or fifteen minutes that, on the
evidence, the pursuer took to cycle home doubled his risk of contracting
dermatitis, or came anywhere near doing so.
Page 37
93. Where there are competing alternative, rather than cumulative, potential
causes of a disease or injury, such as in Hotson, I can see no reason in principle
why epidemiological evidence should not be used to show that one of the causes
was more than twice as likely as all the others put together to have caused the
disease or injury.
Can the “doubles the risk” test be applied in mesothelioma cases?
94. This question calls for consideration of the conundrum that I identified
when considering the decisions in Fairchild and Barker. In the course of argument
I put the conundrum to Mr Stuart-Smith. Why, if it was possible to equate
increasing exposure to increasing risk, could one not postulate that, on balance of
probabilities, where one employer had caused over 50% of a victim’s exposure,
that employer had caused the victim’s mesothelioma? Why could one not, by the
same token, postulate that where over 50% of the victim’s exposure was not
attributable to fault at all, on balance of probability, the victim’s mesothelioma had
not been caused tortiously? In short, why was there any need to apply the
Fairchild/Barker rule where epidemiological evidence enabled one to use statistics
to determine causation on balance of probability?
95. Mr Stuart-Smith replied that this was a question which puzzled him also.
He believed that the answer could be found in consideration given in earlier cases
to a hypothetical injury caused by either a blue or a red taxi-cab. This led to some
inconsequential discussion as to the colours of the cabs involved. The example in
question can be traced, via the speech of Lord Mackay in Hotson [1987] AC 750,
789 to the dissenting judgment of Brachtenbach J in Herskovits v Group Health
Cooperative of Puget Sound (1983) 664 P 2d 474, a decision of the Supreme Court
of Washington:
“Brachtenbach J dissented. He warned against the danger of using
statistics as a basis on which to prove proximate cause and indicated
that it was necessary at the minimum to produce evidence connecting
the statistics to the facts of the case. He gave an interesting
illustration of a town in which there were only two cab companies,
one with three blue cabs and the other with one yellow cab. If a
person was knocked down by a cab whose colour had not been
observed it would be wrong to suggest that there was a 75 per cent
chance that the victim was run down by a blue cab and that
accordingly it was more probable than not that the cab that ran him
down was blue and therefore that the company running the blue cabs
would be responsible for negligence in the running down. He pointed
out that before any inference that it was a blue cab would be
appropriate further facts would be required as, for example, that a
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blue cab had been seen in the immediate vicinity at the time of the
accident or that a blue cab had been found with a large dent in the
very part of the cab which had struck the victim.”
96. This example is an extreme example of the fact that statistical evidence may
be an inadequate basis upon which to found a finding of causation. Keeping to that
example, it was not possible to postulate that the risk of being knocked down by a
negligent driver of a taxi-cab was proportional to the number of taxi cabs in the
town. Much more significant would have been the care taken by the rival taxi
firms in employing competent drivers, and the past accident record of the firms in
question.
97. Thus the first answer to the conundrum may be that, in the case of
mesothelioma, epidemiological evidence alone has not been considered by the
courts to be an adequate basis for making findings of causation: that so long as
medical science is unable to demonstrate, as a matter of fact, the aetiology of
mesothelioma, data relating incidence to exposure is not a satisfactory basis for
making findings of causation.
98. Not only is the adequacy of epidemiological evidence relevant to the weight
to be attached to it. So is its reliability. A helpful description of the factors that can
limit the reliability of epidemiological evidence is to be found in an article by C E
Miller on “Causation in personal injury: legal or epidemiological common sense?”
in 26 Legal Studies No 4, December 2006, pp 544 – 569. Deducing causation in
relation to mesothelioma on the basis of epidemiological evidence requires a
comparison between the statistical relationship between exposure and the
incidence of the disease and the experience of the victim who has sustained the
disease. A number of factors make this exercise particularly problematic. The first
is the difficulty in collating sound epidemiological data. The second is the
difficulty of obtaining reliable evidence as to the relevant experience of the victim.
The third is uncertainty as to the adequacy of the epidemiological evidence that is
available as a guide to causation.
99. The epidemiological data that has been collated in relation to mesothelioma
relates largely to the exposure of victims to asbestos dust. It must be gathered from
the histories of those who, tragically, have succumbed to mesothelioma. Because
of the very long latency of the disease and the limited time between the first
experience of its symptoms and death, obtaining the necessary data is difficult.
Most of the data relates to victims who were subjected to substantial occupational
exposure to dust. This data has been extrapolated to cover victims who have had
very light exposure, but there is no certainty that this extrapolation is reliable.
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100. The same difficulty arises in relation to obtaining details of the relevant
experience of the particular victim. That difficulty is illustrated by the two appeals
before the Court.
101. The most significant inhibition on the use of epidemiological evidence to
determine causation in cases of mesothelioma is uncertainty as to the adequacy of
the data. The data is relied on as establishing that the risk of contracting
mesothelioma is proportional to exposure to asbestos dust. It used to be thought
that mesothelioma was probably triggered by a single asbestos fibre and that the
cause of the disease could be attributed exclusively to that one fibre. Were that the
case it would be reasonable to postulate that the risk of contracting the disease was
proportional to the exposure. In the words of Lord Hoffmann in Barker at para 26,
referring to the decision of Moses J at first instance:
“the more you are exposed, the more likely you are to get it, in the
same way as the more you spin the roulette wheel, the more is a
given number likely to come up.”
102. The single fibre theory has, however, been discredited. The amount of
exposure does not necessarily tell the whole story as to the likely cause of the
disease. There may well be a temporal element. The Peto Report also raised the
possibility (but no more) of synergistic interaction between early and later
exposures. Causation may involve a cumulative effect with later exposure
contributing to causation initiated by an earlier exposure. Applying the
conventional test of causation, the relevant question is, on balance of probability,
which exposures in an individual case may have contributed to causing the
disease? Epidemiology does not enable one to answer that question by considering
simply the relative extent of the relevant exposures.
103. The House of Lords was not, in Fairchild nor in Barker invited to consider
the possibility that it might be possible in an appropriate case to demonstrate by
epidemiological evidence that, on balance of probabilities, the mesothelioma had
been caused by exposure that was not wrongful, or alternatively that such evidence
might demonstrate that one particular employer had, on balance of probabilities,
caused the disease. Had it been I do not believe that the House would have been
persuaded that epidemiological evidence was sufficiently reliable to base findings
as to causation upon it. I believe that the cumulative effect of the various factors
that I have set out above justifies the adoption of the special rule of causation that
the House of Lords applied in Fairchild and Barker. The justification for that rule
may diminish or vanish as the aetiology of the disease is revealed by scientific
research. Nor does the rule wholly displace a conventional approach to causation.
Epidemiological data and medical science show that exposure once a cell has
Page 40
become malignant is not causative and thus exposure once that point is probably
passed, can be discounted as a potential contributor to the disease.
104. The possibility that mesothelioma may be caused as the result of the
cumulative effect of exposure to asbestos dust provides a justification, even if it
was not the reason, for restricting the Fairchild/Barker rule to cases where the
same agent, or an agent acting in the same causative way, has caused the disease,
for this possibility will not exist in respect of rival causes that do not act in the
same causative way.
105. I would add that even if one could postulate with confidence that the extent
of the contribution of a defendant to the victim’s exposure to asbestos precisely
reflected the likelihood that his breach of duty had caused the victim’s disease,
there would still be justification for the application of the Fairchild rule where all
the exposure was wrongful. Imagine four defendants each of whom had
contributed 25% to the victim’s exposure so that there was a 25% likelihood in the
case of each defendant that he had caused the disease. The considerations of
fairness that had moved the House in Fairchild would justify holding each of the
defendants liable, notwithstanding the impossibility of proving causation on
balance of probability.
106. Thus the conundrum is answered by saying that there are special features
about mesothelioma, and the gaps in our knowledge in relation to it, that render it
inappropriate to decide causation on epidemiological data as to exposure. So far as
concerns apportionment between tortfeasors jointly liable for causing
mesothelioma it is likely to be necessary to use epidemiological evidence faute de
mieux.
What constitutes a material increase in risk?
107. Liability for mesothelioma falls on anyone who has materially increased the
risk of the victim contracting the disease. What constitutes a material increase of
risk? The parties were, I think, agreed that the insertion of the word “material” is
intended to exclude an increase of risk that is so insignificant that the court will
properly disregard it on the de minimis principle. Mr Stuart-Smith submitted that
there should be a test of what is de minimis, or immaterial, which can be applied in
all cases. Exposure should be held immaterial if it did not at least double the
environmental exposure to which the victim was subject. It does not seem to me
that there is any justification for adopting the “doubles the risk” test as the bench
mark of what constitutes a material increase of risk. Indeed, if one were to accept
Mr Stuart-Smith’s argument that the “doubles the risk” test establishes causation,
his de minimis argument would amount to saying that no exposure is material for
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the purpose of the Fairchild/Barker test unless on balance of probability it was
causative of the mesothelioma. This cannot be right.
108. I doubt whether it is ever possible to define, in quantitative terms, what for
the purposes of the application of any principle of law, is de minimis. This must be
a question for the judge on the facts of the particular case. In the case of
mesothelioma, a stage must be reached at which, even allowing for the possibility
that exposure to asbestos can have a cumulative effect, a particular exposure is too
insignificant to be taken into account, having regard to the overall exposure that
has taken place. The question is whether that is the position in this case.
The result in this case.
109. Despite Judge Main’s heroic endeavours, the nature of the exercise on
which he embarked must raise doubts over his precise finding that Greif’s
wrongful exposure to asbestos dust increased the environmental exposure to which
Mrs Costello was subject by 18%. Having made that finding, Judge Main wrongly
applied the “doubles the risk” test rather than the Fairchild/Barker test. He did not
expressly consider whether the exposure to which Greif wrongly subjected Mrs
Costello was so insignificant that it could be disregarded as de minimis. None the
less, had he thought it de minimis, he might well have said so. He did describe the
very small quantities of fibres that might have been on furniture in Greif’s offices
as “of statistically insignificant effect and de minimis”: para 50.
110. I do not think that Judge Main would have dismissed the addition that
Greif’s wrongful exposure made to the risk that Mrs Costello would contract
mesothelioma as statistically insignificant or de minimis. If one assumes, as is
likely, that Mrs Costello’s disease was asbestos induced, it is plain that a very low
level of exposure sufficed to cause the disease. This accords with the expert
evidence that there is no known lower threshold of the exposure that is capable of
causing mesothelioma. No one could reasonably conclude that there was no
significant possibility that the incremental exposure to which Greif subjected Mrs
Costello was instrumental in causing her to contract the disease. I am in no doubt
that the wrongful exposure to which she was subjected materially increased her
risk of contracting mesothelioma.
111. The reality is that, in the current state of knowledge about the disease, the
only circumstances in which a court will be able to conclude that wrongful
exposure of a mesothelioma victim to asbestos dust did not materially increase the
victim’s risk of contracting the disease will be where that exposure was
insignificant compared to the exposure from other sources. I note that in Rolls
Royce Industrial Power (India) Ltd v Cox [2007] EWCA Civ 1189 counsel for the
Page 42
employer conceded that exposure to asbestos dust for a period of one week would
not be de minimis.
112. For these reasons I would dismiss the appeal in Greif.
ANNEX
A. In the Trigger litigation Rix LJ set out the following extract from the
judgment of Longmore LJ in Bolton Metropolitan Borough Council v Municipal
Mutual Insurance Ltd [2006 EWCA Civ 50, [2006] 1 WLR 1492:
“7 There are three forms of asbestos: brown (amosite), blue
(crocidolite) and white (chrysotile). Their fibres have different biopersistence: 20 years after exposure to fibres about half the inhaled
amosite fibres remain in the body, a smaller proportion of the
crocidolite fibres remains and, relatively, few chrysotile fibres
remain.
8 The human body is composed of cells of various types. Of the
fibres which reach the lungs many are engulfed by macrophages
(scavenger cells). The macrophages may then be expelled by the
mucosiliary process or may die within the lungs. All cells can and do
die for various reasons, but cells are in communication with each
other and the death of one can cause another to divide so, with some
exceptions such as men losing their hair with age, the number of
cells remains approximately the same throughout a person’s life.
When macrophages die in the lungs they release various chemicals,
some of which attract neutrophils, another type of cell, which can
engulf fibres. A different mechanism which destroys fibres in the
lungs is that they are dissolved in tissue fluids. Another mechanism,
by which the body protects itself, is that some fibres become coated
by proteinaceous material containing iron which, it is believed,
renders them less likely to produce fibrosis.
9 The division of cells in human tissue is important for
understanding how mesothelioma occurs. Each cell in the body
contains all the genetic information necessary for the construction
and functioning of the entire body. This information is contained in
the form of DNA, a molecule consisting of two intertwining strands.
The different structure and function of the various types of cell in the
Page 43
body occurs because in each cell only some of the genes contained in
the DNA are active and in different cells different genes are active.
The coded information in a DNA molecule is in the form of about
3,000,000,000 ‘base pairs’. Each pair consists of two collections of
atoms called nucleotides. There is one half of each pair in each of the
two intertwining strands. When cell division occurs the strands
unravel and two ‘daughter’ double helices are created. Normally the
daughters are identical with each other but sometimes they are not.
Dr Rudd uses the word ‘mutation’ for an imperfect copy. This word
‘mutation’ thus means a thing – a cell – and not a process, and is not a
synonym of ‘change’; for change Dr Rudd uses the term ‘generic
alteration’. I shall adopt this usage. The word ‘mutation’ does not
have any derogatory connotations. A mutation is different from, but
not necessarily worse than, the cell from which it is derived or
otherwise undesirable. The body contains what can be described as a
‘repair mechanism’ which sometimes corrects the discrepancy
between a daughter and its parent. This repair mechanism is vital to
normal health, and people whose repair system lacks some
components (a very rare condition) will die early, often of cancer.
Sometimes, however, a perfectly normal repair and correction
mechanism fails to correct a mutation. Such failure can lead to any
of three possibilities. First, the mutation may be unable to survive
and die. Secondly it may be better fitted for its purpose than the cell
from which it is derived, and this is the cause of evolution. As Dr
Moore-Gillon put it ‘Without the normal process of imperfect
copying, mankind (and indeed all other species) would not have
emerged’.
10 It is the third possibility with which this case is concerned. A
mutation which does not die, which is not repaired and which does
not perform its purpose better than the cell from which it was derived
may itself divide, and the ‘daughter’ cells or (to continue the parental
analogy) the grand-daughter or more distant descendants may in turn
die, be repaired or be mutations from the cell from which they are
derived. Eventually there may be a mutation which is malignant, i e a
cell which divides in an uncontrolled manner, as opposed to
maintaining the normal balance between cells dying and cells
dividing. It normally takes a ‘heredity’ of six or seven genetic
alterations before a malignant cell occurs. The body has ‘natural
killer’ cells which, as their name indicates, can target and destroy
mutations, possibly even after they have become malignant. A
tumour is a growth consisting of a number of cells dividing in that
uncontrolled manner. Mesothelioma is a tumour in the pleura…
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11 Asbestos fibres in the pleura increase the likelihood of genetic
mutation. It is now thought likely that, if there is a series of genetic
alterations which ends with a malignant cell in the pleura, fibres will
have acted in causing several of those genetic alterations, rather than
just one genetic alteration. However the final genetic alteration
which results in a malignant cell is not necessarily caused by fibres
directly. Fibres may also inhibit the activity of natural killer cells.
Pre-cancerous genetic alterations in cells do not give rise to any
symptoms or signs. They cannot be detected by any routine clinical
or radiological examination. It would be possible to detect them by
examining in a laboratory tissue taken from a part of the body
containing cells which have become genetically modified, but the
exercise would be pointless because pre-cancerous genetic
alterations do not necessarily or even usually lead to mesothelioma.
12 It is furthermore important to note that there may be a long time
lapse not only between exposure and the first formation of a
malignant cell but that there may be a similarly lengthy lapse of time
between first malignancy and the onset of noticeable symptoms such
as breathlessness.”
B. Rix LJ then summarised the findings of Burton J in the Trigger litigation,
which brought the findings of Longmore LJ up to date:
“50. The judge heard evidence from five internationally recognised
experts in the field: Dr Rudd and Dr Moore-Gillon, who have
between them given evidence in most if not all of the cases involving
mesothelioma in recent years including Fairchild and Bolton itself;
Professor Geddes, on whose pioneering work the first two experts
have based their own theories (see his crucial 1979 paper concerning
the rate of tumour growth, published in volume 73 of the British
Journal of Diseases of the Chest, The Natural History of Lung
Cancer: a Review based on Rates of Tumour Growth (the ‘Geddes
article’)); and Professor Phillips of the Institute of Cancer Research
and Professor Heintz of the Vermont Cancer Centre. The last two are
biochemists, the first three are respiratory consultants. The judge
observed that the evidence of the biochemistry experts is a new
feature of such litigation.
51. On the basis of this expert evidence, the judge remarked on two
matters which were common ground between the parties. One is that
it is the exposure to quantities of fibres which is causative of
mesothelioma, and the risk increases with the dosage. This was
Page 45
recognised already in Fairchild (see Lord Bingham at para 7; and
Lord Rodger at para 122, where the latter observed: ‘the greater the
number of asbestos fibres taken into the body, the greater are the
chances that one of them will trigger a malignant transformation’).
The second matter is that once the mesothelioma tumour is present
and assured of growth (ie has passed the stage where a malignant
mutation may die off), further asbestos exposure and indeed further
asbestos fibres in the body can make no difference and are not
causative.
52. Burton J also described ‘the unknowability and indescribability
of much of the pathogenesis of mesothelioma’ as being common
ground (at para 30). Subject to that caution, the judge made the
following findings about the disease. He described asbestos fibre as a
‘complete carcinogen’, ie no other agent or co-agent is required to
cause the ultimate malignancy (at para 130). Unlike a normal cancer
of spherical or similar shape which sooner or later can be seen on a
scan or x-ray, the mesothelioma tumour grows along the surface of
the lungs rather like a fungus and is thus practically undetectable,
and only becomes diagnosable when the symptoms of impaired
breathing bring it to the patient’s and his doctor’s attention. As the
details of actions 1-3 illustrate, that is only shortly before death. The
average time between manifestation/diagnosis and death is some
fourteen months.
53. The judge described the normal process of cell mutations in
healthy bodies and lungs. Even in a person who has not been
exposed to asbestos as part of his occupation, the lungs will typically
contain millions of asbestos fibres, albeit not the hundreds of
millions to be found in the occupationally exposed and with far less
proportionately of the more dangerous blue and brown asbestos
varieties. He said:
‘108…The mesothelial cells, like all cells in the body,
are constantly dividing: Dr Rudd told us that there are
10 trillion cells in the body and 50 billion are
replicated every day. Cell division, or mitosis, by
which the cell divides, duplicates its chromosomes and
passes on a complete set to each of its “daughters”, is
the norm; but there can be mutations – again Dr Rudd
told us that incorrect copying can take place in one in a
million cell divisions and thus possibly 5,000 times per
day in the human body, or every 17 seconds. The
body’s repair mechanisms are quick to correct and
Page 46
abort the mutations, but even if there are mutations
there are four possible consequences. The incorrect
copy may be unable to survive, and die; the mutation
can make no difference; the mutation can positively
improve the cell – hence evolution; or the mutated cell
can survive and can itself divide, passing on the
genetic alterations, eventually after many generations
and with further mutations creating a malignant cell.’
54. What then makes the difference between a normal and a diseased
process? The judge continued:
‘109. There will or may be thousands of mutations,
only one of which may have any deleterious effect on
successive mitosis. But, the experts gave evidence that
there are six or seven genetic alterations which are
required, not necessarily occurring in the same or any
particular order, which, when they are all in place, can
lead to a malignant cell. The characteristics of a
malignant cell are (i) self sufficiency of growth signals
(ii) insensitivity to growth-inhibitory signals (iii)
evasion of programmed cell death (apoptosis) (iv)
limitless replicative potential (v) the ability to invade
tissues and to metastasise ie to transfer to other parts of
the body (vi) the availability of its own blood supply –
obtained by a process which is called angiogenesis…
111. Once a cell has acquired what Dr Rudd calls a
‘full house’ of the necessary 6/7 mutations, and has
evaded all the bodily defences (described by Dr Rudd
as ‘full house plus’), then it can be described as a
malignant cell, and can and does begin a period of
uncontrolled growth by multiplication.
Notwithstanding what Dr Rudd has called evasion of
the bodily defences, Professors Phillips and Heintz [the
biochemists] conclude that many full house cells with
malignant potential may fail to grow into tumours. It
appears to be common ground, at any rate so far as the
biochemists are concerned, that such cell or cells at this
stage are still at risk from natural killer cells, although
they apparently develop a method of switching off the
signals which summon the natural killer cells or put
them on notice. There is also, despite the characteristic
of limitless replication, the possibility or probability, of
periods of dormancy. Professor Phillips points out that
the norm of 40 years from exposure to diagnosability
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suggests either that the mutation period lasts a long
time or that there are periods of tumour dormancy (or
both).’
55. The judge then described the growth of a malignant cell towards
the status of a mesothelioma tumour, premised on the figures to be
derived from the Geddes article concerning the more normal type of
spherical tumour. Professor Geddes found that the average rate of
doubling of cells was 102 days (albeit that was a speculative average,
which could vary between 45 and 130 days). It is only at a tumour
size of 106
cells (1 million cells) that it becomes unlikely for the
bodily defences, still until then available, to be able to neutralise it.
Angiogenesis then occurs at somewhere between 106
and 109
(1
billion cells). Symptoms of breathlessness will begin to be
experienced when the tumour is between 109
and 1012 (1 trillion
cells). In the biochemists’ view, angiogenesis occurred about 5 years
or so before death.”
C. The Peto and Rake study led the authors to the following conclusions:
“1. Mesothelioma risk is determined largely by asbestos exposure
before age 30, and ranges from a lifetime risk of 1 in 17 for ten or
more years of carpentry before age 30 to less than 1 in 1,000 in
apparently unexposed men and women. Our results suggest that the
predicted total of 90,000 mesotheliomas in Britain between 1970 and
2050 will include approximately 15,000 carpenters.
2. The risk of lung cancer caused by asbestos is likely to be of the
same order as the mesothelioma risk. This would imply that more
than 1 in 10 of British carpenters born in the 1940s with more than
10 years of employment in carpentry before age 30 will die of a
cancer caused by asbestos.
3. Asbestos exposure was widespread, with 65% of male and 23% of
female controls having worked in occupations that were classified as
medium or higher risk.
4. Britain was the largest importer of amosite (brown asbestos), and
there is strong although indirect evidence that this was a major cause
of the uniquely high mesothelioma rate. The US imported far less
amosite than Britain but used similar amounts of chrysotile (white
asbestos) and more crocidolite (blue asbestos), and US mesothelioma
Page 48
death-rates in middle age are now 3 to 5 times less than British rates.
British carpenters frequently worked with asbestos insulation board
containing amosite.
5. We found no evidence of increased risk associated with nonindustrial workplaces or those that were classified as ‘low risk’,
including motor mechanics and workers handling gaskets and mats
that may have contained asbestos.
6. The only potential non-occupational exposure associated with
increased risk was living with an exposed worker.
7. The increasing trend in female rates in Britain and a comparison
between British and US female rates both suggest that a substantial
proportion of mesotheliomas with no known occupational or
domestic exposure were probably caused by environmental asbestos
exposure. The sources of this presumably included construction,
building maintenance and industrial activities but may also include
release of asbestos from buildings due to normal occupation and
weathering.”
LORD RODGER
113. Defendants whose breaches of duty expose someone to asbestos and so
materially increase the risk that he will develop mesothelioma are liable jointly and
severally for the damage which he suffers if he does in fact develop mesothelioma.
The fundamental question in these two appeals is whether this special rule – the
so-called “Fairchild exception”, as it applies to mesothelioma – applies in cases
where only one defendant is proved to have exposed the victim to asbestos, but she
was also at risk of developing the disease from low-level exposure to asbestos in
the general atmosphere (“environmental exposure”). I would hold that the special
rule does apply in such cases.
Karen Sienkiewicz v Greif (UK) Ltd
114. In these proceedings the claimant, Mrs Karen Sienkiewicz, is the daughter,
and administratrix of the estate of, the late Mrs Enid Costello who died of
mesothelioma on 21 January 2006.
Page 49
115. From 1966 until 1984 Mrs Costello worked for the defendants’
predecessors in title at their factory premises in Ellesmere Port where they
manufactured steel drums. The process involved the release of asbestos dust into
the factory atmosphere. Although Mrs Costello worked mostly in an office, she
spent time in areas of the factory which were, from time to time, contaminated
with asbestos.
116. The trial judge held that Mrs Costello’s exposure to asbestos on the
defendants’ premises was “very light” and that it would have been through the
inhalation of the general factory atmosphere, as she moved about. The judge also
held that this exposure was in breach of the relevant legal duties owed by the
defendants to Mrs Costello.
117. It was common ground that, like anyone else, Mrs Costello would have
been subject to environmental exposure to low levels of asbestos in the atmosphere
in the areas where she lived.
118. The trial judge found that the defendants’ exposure of Mrs Costello to
asbestos over her working life at their premises “increased her background risk (of
contracting mesothelioma) from 24 cases per million to 28.39 cases per million, an
increase of risk of 18%.” Putting the point slightly more precisely, the
environmental risk of contracting mesothelioma was 24 cases per million;
exposure of the level of the occupational exposure in Mrs Costello’s case would
increase the risk of contracting mesothelioma to 28.39 cases per million – an
increase of 18%.
119. The trial judge concluded that the claimant had failed to establish that any
exposure by the defendants had caused Mrs Costello’s mesothelioma because
“once there is only one occupational cause for the mesothelioma the claimant has
to prove that it is the likely cause.” On this basis he held that the special rule of
law laid down by the House of Lords in Fairchild v Glenhaven Funeral Services
Ltd [2003] 1 AC 32 did not apply and that the claimant could therefore not succeed
on the basis that, on the balance of probability, Mrs Costello’s exposure to
asbestos in the course of her employment with the defendants had materially
increased the risk that she would contract mesothelioma. She could only succeed
by proving, on the balance of probability, that the defendants’ breach of duty had
caused Mrs Costello’s mesothelioma.
120. The Court of Appeal (Lord Clarke of Stone-cum-Ebony, Scott Baker and
Smith LJJ) allowed the claimant’s appeal: Sienkiewicz v Greif (UK) Ltd [2009]
EWCA 1159; [2010] QB 370. They held that the decision of the House of Lords in
Fairchild applied. The defendants’ breach of duty had materially increased the risk
Page 50
of Mrs Costello developing mesothelioma. So they were liable. The defendants
appeal against that decision.
121. Although the Court of Appeal ultimately held that the rule in Fairchild
applied to mesothelioma cases of this kind because of section 3 of the
Compensation Act 2006 (“the 2006 Act”), in the course of her judgment, [2010]
QB 370, 379, at para 23, Smith LJ made a very general statement about the
approach which courts should adopt to issues of causation:
“In my view, it must now be taken that, saving the expression of a
different view by the Supreme Court, in a case of multiple potential
causes, a claimant can demonstrate causation by showing that the
tortious exposure has at least doubled the risk arising from the nontortious cause or causes.”
An important issue in the present appeals is whether this guidance is sound.
Willmore v Knowsley Metropolitan Borough Council
122. In these proceedings the claimant is Mr Barré Willmore. He is the husband,
and administrator of the estate, of the late Mrs Dianne Willmore who died of
mesothelioma on 15 October 2009 at the age of 49. Prior to her death, Mrs
Willmore had raised proceedings for damages for her illness against Knowsley
Metropolitan Borough Council (“the Council”).
123. After her condition was diagnosed, Mrs Willmore made a number of
different allegations as to her possible exposure to asbestos. Initially she alleged
that she had been exposed to asbestos dust in the course of her employment with
the Army & Navy Stores in Liverpool between 1979 and 1981. But when she
raised her proceedings against the Council in February 2008 she alleged that she
had been exposed to asbestos when some prefabricated houses near her childhood
home in Huyton were demolished. She also alleged that she had been exposed to
asbestos while a pupil at her primary school run by the Council.
124. On 14 February 2008, however, Mrs Willmore read an article in the
Liverpool Echo referring to a report prepared by the Council which identified the
presence of asbestos in a number of secondary schools, including Bowring
Comprehensive, where she had been a pupil. On 27 November 2008 Mrs Willmore
amended the particulars of claim to allege, in essence, that when she first attended
Bowring Comprehensive, the construction of the school had not been completed
and she and other pupils had been exposed to asbestos as a result of workmen
Page 51
using materials containing asbestos. She also alleged that she had been exposed to
asbestos as a result of other disturbance of asbestos materials at the school. She
subsequently abandoned all her allegations of exposure to asbestos except those
relating to Bowring Comprehensive.
125. Following a trial in July 2009, Nicol J found that, while a pupil at Bowring
Comprehensive, Mrs Willmore had been exposed to the type of asbestos known as
amosite in three separate ways: (1) as a result of work involving the removal,
handling and disturbance of ceiling tiles in a corridor along which pupils,
including Mrs Willmore, passed; (2) as a result of pupils’ misbehaviour, which
caused ceiling tiles containing asbestos to be damaged or broken; (3) as a result of
asbestos ceiling tiles, including broken tiles, being stored in a girls’ lavatory which
had been used by Mrs Willmore on many occasions. The judge held that each of
these exposures to asbestos fibres had materially increased the risk of Mrs
Willmore contracting mesothelioma later in life. In so concluding, he found that
none of these exposures was de minimis. He awarded Mrs Willmore the agreed
gross sum of £240,000 as damages.
126. The Council appealed to the Court of Appeal. The Court of Appeal held,
[2009] EWCA Civ 1211, that the judge had been wrong to hold that she had been
exposed to asbestos as a result of pupils’ misbehaviour. But they confirmed that
the judge had been entitled to find that Mrs Willmore had suffered significant
exposure to asbestos from the other two sources. On that basis the Court upheld his
judgment and his award of damages. The Council now appeal to this Court. Since
the lower courts applied the Fairchild exception, obviously the same point as to its
application in this type of case arises. But the Council also challenge the judge’s
findings in fact.
The Defendants’ Legal Argument
127. As already indicated, the feature of both the cases under appeal to which the
defendants attach importance is that the proceedings are directed against only one
defendant. In this respect they are different from the leading authorities, Fairchild
v Glenhaven Funeral Services Ltd [2003] 1 AC 32 and Barker v Corus UK Ltd
[2006] 2 AC 572, in both of which the claimants alleged that the victims had been
exposed to asbestos as a result of a breach of duty by more than one employer. In
Barker, however, one of the three material exposures had occurred when Mr
Barker was working as a self-employed plasterer.
128. On behalf of the defendants in both of the appeals, Mr Stuart-Smith QC
characterised the present cases as “single exposure” cases: the claimants alleged
only one possible tortious source for the exposure. In both cases the exposure
Page 52
could be regarded as slight. In addition, the victims had been exposed to asbestos
in the general atmosphere in the areas where they lived. Counsel renewed the
argument that in such cases the special rule in Fairchild did not apply and that, in
order to establish liability, the claimant required to prove, on the balance of
probability, that the victim’s mesothelioma is to be attributed to her exposure to
asbestos as a result of the defendant’s breach of duty. The claimant could do this
by leading epidemiological evidence to show that the exposure by the defendant
had doubled the risk of the victim developing mesothelioma. This was essentially
the argument which the trial judge had accepted in Sienkiewicz: the claimant failed
because the defendants’ breach of duty had merely increased the risk of her
developing mesothelioma by 18% – far short of doubling the environmental risk.
Section 3 of the 2006 Act
129. In the Court of Appeal in Sienkiewicz [2010] QB 370, 379, para 26, Smith
LJ saw considerable force in the view that in Fairchild and Barker the House of
Lords had not been considering a single exposure case and that, if they had done
so, they would not have included such a case within the scope of the rule. But she
held that such speculation was now pointless since Parliament had intervened by
enacting section 3 of the 2006 Act, which had the effect that the common law
simpliciter no longer governed claims for damages in mesothelioma cases. In this
regard Smith LJ observed, [2010] QB 370, 381-382, at paras 34 and 35:
“34. However, in my view, Parliament used clear words which
provide that, in all mesothelioma cases, a claimant can take
advantage of section 3(2) provided that he or she can satisfy the four
conditions in section 3(1) and the fourth condition can, in my
judgment, be satisfied by proof of causation by reference to a
material increase in risk.
35. I conclude therefore that, in a mesothelioma case, it is not open
to a defendant to put the claimant to proof of causation by reference
to a twofold increase in risk. The judge was therefore wrong to
require the claimant in this case to attempt to cross that hurdle. If he
had applied the correct test on causation, namely whether or not the
tortious exposure had materially increased the risk, the answer was
plainly yes. In my view, the claimant should have succeeded and the
appeal must be allowed.”
Scott Baker LJ agreed with Smith LJ, as did Lord Clarke of Stone-cum-Ebony.
Lord Clarke considered, [2010] QB 370, 387, at para 57, that it was plain from the
Page 53
terms of section 3 and from the analysis of the common law that the respondent
was liable for the mesothelioma which caused Mrs Costello’s death.
130. Subsection (1) of section 3 of the 2006 Act describes the circumstances in
which the section is to apply in actions of damages for mesothelioma. According
to subsection (1)(d), it applies where “the responsible person is liable in tort, by
virtue of the exposure mentioned in paragraph (a) in connection with damage
caused to the victim by the disease (whether by reason of having materially
increased a risk or for any other reason).” Smith LJ appears to have considered
that, by referring to the defendant being held liable in tort “by reason of having
materially increased a risk”, Parliament had precluded any argument that, in
particular circumstances, a defendant could not be held liable on that basis. I
would not read the provision in that way.
131. Section 3 was not concerned with prescribing the basis for defendants being
held responsible for claimants’ mesothelioma. Rather, its purpose was to reverse
the decision of the House of Lords in Barker v Corus UK Ltd [2006] 2 AC 572.
The House had held that, where more than one defendant had materially increased
the risk that an employee would contract mesothelioma, liability was to be
attributed, not jointly and severally, but according to each defendant’s degree of
contribution to the risk. In section 3 Parliament laid down that, on the contrary,
where a defendant was held liable in a mesothelioma case, he was to be liable for
the whole of the damage caused to the victim and, if anyone else was held
responsible, they were to be liable jointly and severally. The reference to the
defendant having been held liable “by reason of having materially increased a risk”
is simply designed to show that the statutory rule applies in cases where the
defendant is held liable (as in Barker) on the basis of materially increasing the risk
to the claimant. But the concluding words, “or for any other reason”, show that
Parliament envisages that a defendant might be held liable on some other basis. In
that eventuality also he is to be liable for the whole of the damage and, if anyone
else is held responsible, they are to be liable jointly and severally.
132. It follows that section 3 of the 2006 Act does not shut out the appellants’
argument that in a single exposure case a defendant should not be held liable
unless the claimant proves on the balance of probability that his breach of duty
caused the victim’s mesothelioma. That argument and the more particular
argument, that the claimant must show that the defendant more than doubled the
risk of the victim developing mesothelioma, have therefore to be addressed on
their merits.
Page 54
The Rock of Uncertainty
133. The discussion and decision in Fairchild proceeded on the basis described
by Lord Bingham, [2003] 1 AC 32, 43, at para 7: “There is no way of identifying,
even on a balance of probabilities, the source of the fibre or fibres which initiated
the genetic process which culminated in the malignant tumour.” This was what he
described as the “rock of uncertainty”: [2003] 1 AC 32, 43G-H. On behalf of the
appellants, Mr Stuart-Smith accepted that this remains the position in cases where
a victim has been exposed to asbestos in the course of his employment with a
number of employers. The same would presumably apply if the victim had been
exposed to asbestos, say, when visiting a number of cinemas run by different
companies. But he submitted that, where the claimant alleges that only one
defendant wrongfully exposed her to asbestos and environmental exposure is also
a possible source of the asbestos which affected her, the claimant must prove on
the balance of probability that her disease was caused by the defendant rather than
by environmental exposure.
134. In Fairchild, as can be seen from Lord Bingham’s speech, at p 40, para 2, it
was common ground that “any cause of [the claimant’s] mesothelioma other than
the inhalation of asbestos dust at work can be effectively discounted” (emphasis
added). At the time, some commentators indeed found this surprising, since
exposure can occur in a variety of ways. Most obviously, perhaps, a factory may
pollute the surrounding area and lead to the residents inhaling asbestos fibres in the
atmosphere. But fibres are actually widespread in the atmosphere throughout most
of the country. One European study suggested that one person in seven shows lung
damage of a kind caused by exposure to asbestos. See the examples in Jane
Stapleton, “Lords a’leaping evidentiary gaps”, (2002) 10 Torts Law Journal 276,
277-279. But, for some reason, only certain people develop mesothelioma as a
result of being exposed to asbestos. The issue in the present appeals arises because
both parties accept that Mrs Costello and Mrs Willmore, who did develop
mesothelioma, might have developed it as a result of being exposed to asbestos in
the general atmosphere.
135. At first sight it is somewhat surprising that the defendants should submit
that in these cases the claimant must prove, on the balance of probability, that the
defendant’s breach of duty caused her illness, since Fairchild proceeded on the
basis that there is no way of identifying, on the balance of probability, the source
of the fibre or fibres which initiated the genetic process that culminated in the
victim’s malignant tumour. Medical science has not advanced significantly in this
respect in the intervening eight years. So counsel’s argument is – and must be –
that, in a case where the only possible source of the fibre or fibres which caused
the disease is either environmental exposure to asbestos or exposure by the
defendant, a claimant could always have proved, on the balance of probability, that
the defendant was the source of the relevant fibre or fibres by leading appropriate
Page 55
epidemiological evidence to show that the exposure by the defendant more than
doubled the background risk of the victim developing mesothelioma. So the
Fairchild exception would never have applied.
136. Take Sienkiewicz as an example. The defendants argue that the claim fails
since, on the basis of the expert evidence, the judge found that the exposure due to
their breach of duty increased Mrs Costello’s risk of developing mesothelioma by
only 18%. By contrast, it is said, if the expert evidence had shown that their
exposure had doubled the background risk, Mrs Costello would have proved that,
on the balance of probability, her mesothelioma had been caused by the
defendants’ breach of duty rather than by any environmental exposure. In that
event the claim would have succeeded. There is no rock of uncertainty and so no
room for the Fairchild exception. By applying Fairchild, the Court of Appeal had
erred in law and the appeal should therefore be allowed.
Unpacking the Defendants’ Legal Argument
137. The defendants’ argument appears simple, but it would actually involve a
major change in the law.
138. Usually, in English or Scots law, a court awards a claimant or pursuer
damages for his injuries only if the judge is satisfied, on the balance of probability,
that the wrongful act of the defendant or defender actually caused, or materially
contributed to, his injury. Unless he proves this, his claim will fail.
139. In the case of a disease like mesothelioma the claimant will be able to prove
on the balance of probability that he is suffering from mesothelioma and that he
has suffered loss as a result. He may also be able to prove, on the balance of
probability, that a defendant or a number of defendants negligently exposed him to
asbestos in the course of his employment with them, or while – as in Mrs
Willmore’s case – she was a pupil in a school run by the Council. What, however,
the claimant will be quite unable to prove, on the balance of probability, in the
present state of medical knowledge, is that he developed mesothelioma as a result
of inhaling any particular fibre or fibres and that, therefore, a particular defendant
was responsible for exposing him to the fibre or fibres that caused his illness.
Moreover, medical experts are no more able to tell whether the fibre or fibres
which triggered the claimant’s mesothelioma came from the general atmosphere
than they can tell whether they came from exposure during the claimant’s work
with one or other of a number of employers.
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140. Faced with the problem that, in the present state of medical science, a
claimant can never prove his case to the standard that the law usually requires, a
legal system may react in a variety of ways. It may simply adhere to its usual
stance and say that, since the claimant has not proved on the balance of probability
that the defendant actually caused his disease, the claim must fail. That was, in
effect, what the Court of Appeal decided in Fairchild v Glenhaven Funeral
Services Ltd [2002] 1 WLR 1052. Alternatively, if that approach seems to be
unduly harsh on victims, a system may hold that, if the claimant proves on the
balance of probability that the defendant’s breach of duty has exposed him to
asbestos, an evidential burden falls on the defendant to show that this exposure did
not play any part in the claimant’s illness. Menne v Celotex Corp 861 F 2d 1453
(10 Cir 1988) is a case in point. Another possibility would be that a system would
choose to hold a defendant liable because his breach of duty doubled the risk that
his employee would develop mesothelioma. The decision of the Supreme Court of
Texas in Merrell Dow Pharmaceuticals Inc v Havner (1997) 953 SW 2d 706 is an
example of that approach being carefully applied in relation to proof that a
mother’s consumption of a drug caused a birth defect in her baby. As I point out at
para 154 below, the court was conscious that it was deliberately applying a special
rule to deal with the particular evidential difficulties facing plaintiffs in that kind
of case. Or else a system may adopt a (different) rule to the effect that, if the
claimant proves, on the balance of probability, that the defendant materially
increased the risk that he would develop mesothelioma, then the defendant is to be
held to have contributed materially to the development of the claimant’s illness.
That is what the House of Lords appeared to do in Fairchild. In Barker v Corus
UK Ltd [2006] 2 AC 572, however, the approach in Fairchild was refined: it was
now said that a defendant was liable simply on the basis that his breach of duty had
materially increased the risk that his employee would contract mesothelioma and
the employee had done so.
141. The response of English law to the problem posed by the rock of
uncertainty in mesothelioma cases is therefore to be found in the combination of
the common law, as laid down in Fairchild and Barker, and section 3 of the 2006
Act. Defendants whose breaches of duty materially increase the risk that the victim
will develop mesothelioma are liable jointly and severally for the damage which
the victim suffers if he does in fact develop mesothelioma. This is the current
version of the Fairchild exception, as it applies in cases of mesothelioma.
142. Of course, the Fairchild exception was created only because of the present
state of medical knowledge. If the day ever dawns when medical science can
identify which fibre or fibres led to the malignant mutation and the source from
which that fibre or those fibres came, then the problem which gave rise to the
exception will have ceased to exist. At that point, by leading the appropriate
medical evidence, claimants will be able to prove, on the balance of probability,
that a particular defendant or particular defendants were responsible. So the
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Fairchild exception will no longer be needed. But, unless and until that time
comes, the rock of uncertainty which prompted the creation of the Fairchild
exception will remain.
Proof of a Fact and Proof of a Probability
143. Although a claimant cannot prove what happened, in any given case his
illness has a determinate cause. In other words, his mesothelioma was actually
caused by a particular fibre or fibres and so a particular defendant either did or did
not materially contribute to his contraction of the disease. Whether a defendant did
so is a matter of fact, but one which, in the present state of medical science, we can
never know.
144. In Hotson v East Berkshire Area Health Authority [1987] AC 750 the
plaintiff fell from a tree and sustained an acute traumatic fracture of the left
femoral epiphysis. He was taken to hospital, but his injury was not correctly
diagnosed or treated for five days. In the event, he suffered avascular necrosis of
the epiphysis, involving disability of the hip joint and the virtual certainty that he
would later develop osteoarthritis. The health authority admitted negligence. The
trial judge, Simon Brown J, found that, even if the hospital had diagnosed the
injury and treated the plaintiff promptly, there was a 75% chance that the necrosis
would still have developed. He held that the plaintiff was entitled to damages for
the loss of the 25% chance that he would have made a full recovery if treated
promptly: [1985] 1 WLR 1036. The Court of Appeal upheld the trial judge: [1987]
AC 750. The House of Lords allowed the health authority’s appeal.
145. The House of Lords emphasised that what had happened to the plaintiff by
the time he reached hospital was a matter of fact – albeit one as to which there was
no direct evidence and as to which the medical experts who gave evidence were
divided. As a matter of fact, by the time he reached hospital, the plaintiff either did
or did not have sufficient intact blood vessels to keep the affected epiphysis alive.
In the words of Lord Mackay of Clashfern, [1987] AC 750, 785A-B, on that
matter, having regard to all the evidence, including the conflicting medical
evidence, the trial judge took the view “that it was more probable than not that
insufficient vessels had been left intact by the fall to maintain an adequate blood
supply to the epiphysis …”. Lord Mackay went on to say, at p 785C-E:
“It is not, in my opinion, correct to say that on arrival at the hospital
he had a 25 per cent chance of recovery. If insufficient blood vessels
were left intact by the fall he had no prospect of avoiding complete
avascular necrosis whereas if sufficient blood vessels were left intact
on the judge’s findings no further damage to the blood supply would
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have resulted if he had been given immediate treatment, and he
would not have suffered the avascular necrosis.”
146. In Hotson therefore not only was the plaintiff’s condition by the time he
reached hospital a matter of fact, but it was one which, the House held, the trial
judge had been able to determine, on the balance of probability: insufficient
vessels were left intact to maintain an adequate blood supply to maintain the
epiphysis. Here, by contrast, although as a matter of fact, for instance, the
defendants’ exposure of Mrs Costello to asbestos dust either did or did not
materially contribute to her contraction of the disease, in the present state of
medical science we can never know – and the claimant can never prove – whether
it did or did not.
147. Lord Hoffmann made the same point in Gregg v Scott [2005] 2 AC 176,
196, at para 79, when he said that, for the law
“Everything has a determinate cause, even if we do not know what it
is. The blood-starved hip joint in Hotson’s case, the blindness in
Wilsher’s case, the mesothelioma in Fairchild’s case; each had its
cause and it was for the plaintiff to prove that it was an act or
omission for which the defendant was responsible. The narrow terms
of the exception made to this principle in Fairchild’s case only
serves to emphasise the strength of the rule. The fact that proof is
rendered difficult or impossible because no examination was made at
the time, as in Hotson’s case, or because medical science cannot
provide the answer, as in Wilsher’s case, makes no difference. There
is no inherent uncertainty about what caused something to happen in
the past or about whether something which happened in the past will
cause something to happen in the future. Everything is determined
by causality. What we lack is knowledge and the law deals with lack
of knowledge by the concept of the burden of proof.”
148. It appears that in the House of Lords in Hotson there was some argument
about the use of statistical evidence, but most members of the appellate committee
did not find it necessary to deal with it. Lord Mackay did address the issue,
however – while making it clear that his comments were obiter. At the hearing of
the present appeals counsel made some reference to Lord Mackay’s comments and
Lord Phillips has referred to them in his judgment. It may therefore be worthwhile
to look a little more closely at what Lord Mackay said in order to see whether it
has any application in the present case.
Page 59
149. Lord Mackay put forward a hypothetical example loosely based on McGhee
v National Coal Board [1973] 1 WLR 1. He supposed a case in which an employer
had negligently failed to provide washing facilities at the end of their shift for men
who had been exposed to brick dust in the course of their work. One of the men
developed dermatitis and sued his employer. He led epidemiological evidence
which showed that of 100 men working in the same conditions 30 would develop
dermatitis even though they had showered after their shift. But the evidence also
indicated that, if the men did not shower, 70 would develop dermatitis. Lord
Mackay observed, [1987] AC 750, 786D-E:
“Assuming nothing more were known about the matter than that, the
decision of this House [in the McGhee case] may be taken as holding
that in the circumstances of that case it was reasonable to infer that
there was a relationship between contraction of dermatitis in these
conditions and the absence of washing facilities and therefore it was
reasonable to hold that absence of washing facilities was likely to
have made a material contribution to the causation of the dermatitis.”
150. Two comments are appropriate. First, the decision of the House of Lords in
McGhee actually goes much further than holding that, in such circumstances, it is
reasonable to infer that the absence of washing facilities was likely to have made a
material contribution to the causation of the dermatitis. As Lord Mackay himself
pointed out, in McGhee there were no statistics. The House had to deal with the
appeal on the basis of the evidence of Dr Hannay, a dermatologist led by the
pursuer, which the Lord Ordinary had accepted. Dr Hannay, who was not crossexamined on the point, said that the provision of showers would have “materially”
reduced the risk of the pursuer contracting dermatitis: 1973 SC (HL) 37, 42. So the
lack of showers “materially” increased the risk of the pursuer contracting
dermatitis. In these circumstances, “from a broad and practical viewpoint,” Lord
Reid could see “no substantial difference between saying that what the defender
did materially increased the risk of injury to the pursuer and saying that what the
defender did made a material contribution to his injury”: McGhee v National Coal
Board [1973] 1 WLR 1, 5B-C. From his previous reference, at p 4D-F, to
Bonnington Castings Ltd v Wardlaw [1956] AC 613 it is evident that Lord Reid
was thinking of any increase in the risk that could not be regarded as de minimis.
There would, for example, have been a material (20%) increase in the risk in a
case like McGhee, if 30 out of the population of 100 workmen would have been
expected to develop dermatitis even after showering, but 36 would have been
expected to develop it if no showers were provided. On that basis the House would
have held the defenders liable.
151. Secondly, as Lord Phillips points out, Lord Mackay must be supposed to
have chosen the figures in his hypothetical example because, among the population
of 100 workmen exposed to brick dust, more than twice as many (70) would be
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expected to develop dermatitis if no showers were provided, as would be expected
to develop it even if showers were provided (30). In terms of the defendants’
argument in the present appeals, failure to provide showers would more than
double the risk. In that situation, assuming that nothing more were known, Lord
Mackay thought that the House might be taken as holding that it was reasonable to
infer that there was a relationship between contraction of dermatitis in these
conditions and the absence of washing facilities and therefore it was reasonable to
hold that absence of washing facilities was likely to have made a material
contribution to the causation of the claimant’s dermatitis.
152. Lord Mackay’s introductory words (“assuming nothing more were known”)
show that he was conscious that, if the House did indeed reason in that way, it
would be reasoning, from statistics about the situation in a population of 100
workmen in the same conditions, to the case of the individual claimant. Obviously,
care has to be taken in doing so. For example, if the claimant had some underlying
condition which made him particularly sensitive to brick dust, that would affect
any reliance that could be placed on the statistics in his case.
153. More fundamentally, however, it is necessary to see what the
epidemiological evidence would actually show in Lord Mackay’s hypothetical
case. Suppose the claimant, who had not been able to shower, developed
dermatitis. As a matter of fact, he either developed the dermatitis because of the
lack of a shower or he developed it simply because of his exposure to the dust. In
other words, either he was one of 30 who would have developed dermatitis
anyway, or he was one of the additional 40 who, the epidemiological evidence
suggested, would have developed it only because there were no showers. Ex
hypothesi, however, general medical science is incapable of saying into which
category the claimant falls. And epidemiological science is equally incapable of
determining that particular question – indeed it is no part of its function to do so.
154. In that situation a court could simply say that the claimant’s case failed
since he had not proved that he was among the 40 who would have developed
dermatitis only because there were no showers, rather than among the 30 who
would have developed it even if they had showered. Alternatively, a court might
say that it was more likely that the claimant’s dermatitis was caused by the lack of
showers. And, in fact, various courts have adopted an approach based on doubling
the risk as their way of dealing with the problems of proof in toxic tort cases. As
already mentioned at para 140 above, an example is the decision of the Supreme
Court of Texas in Merrell Dow Pharmaceuticals Inc v Havner (1997) 953 SW 2d
706 which Lord Phillips discusses at paras 85-89. It should be noticed, however,
that the starting-point for the court’s discussion was that “epidemiological studies
cannot establish the actual cause of an individual’s injury or condition.” The court
explained the basis of its approach in this way:
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“In the absence of direct, scientifically reliable proof of causation,
claimants may attempt to demonstrate that exposure to the substance
at issue increases the risk of their particular injury. The finder of fact
is asked to infer that because the risk is demonstrably greater in the
general population due to exposure to the substance, the claimant’s
injury was more likely than not caused by that substance. Such a
theory concedes that science cannot tell us what caused a particular
plaintiff’s injury. It is based on a policy determination that when the
incidence of a disease or injury is sufficiently elevated due to
exposure to a substance, someone who was exposed to that substance
and exhibits the disease or injury can raise a fact question on
causation.”
The court acknowledged that it was adopting a particular policy on what counted
as raising a question on causation in such circumstances. On the basis of McGhee
Lord Mackay envisaged that in an appropriate case the House of Lords would take
a somewhat similar approach.
155. Lord Mackay first suggests that in his hypothetical case the House could be
taken as holding that, on the basis of the statistics, it would be reasonable to infer
that there was a relationship between contraction of dermatitis in these conditions
and the absence of washing facilities. Assuming that the epidemiological evidence
is reliable, that is plainly so. He goes on to suggest that, on the basis of that
inference, it might be reasonable to hold that the absence of washing facilities was
likely to have made a material contribution to the causation of the dermatitis – by
which he means the claimant’s dermatitis. This is the critical step.
156. It is important to recognize that in such a case the claimant would not have
proved, on the balance of probability, that his exposure to the brick dust by the
defendant actually caused his dermatitis. Indeed the starting point of the entire
hypothetical example is that, in the present state of medical knowledge, the
claimant could not prove this. Assuming that the epidemiological study is reliable,
the statistics in Lord Mackay’s example would simply indicate that, if you took
100 workmen who developed dermatitis after working in the same conditions, you
would expect to find that 30 developed it after having showered and 70 developed
it when they had not been able to shower. So, by leading the epidemiological
evidence, the only “fact” that the claimant can prove and offers to prove, on the
balance of probability, is that in most cases the dermatitis would have been related
to the lack of showers. So, if the judge accepts the evidence, it may legitimately
satisfy him, on the balance of probability, not that the claimant’s dermatitis was
caused by the lack of showers, but that, in the absence of any evidence that the
claimant is atypical, it is more probable than not that his dermatitis was caused by
the lack of showers. In short, the chances are that it was. Whether, in any particular
case, the claimant’s dermatitis was actually caused by the lack of showers is a
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matter of fact – and one that remains unknown, if the only available evidence is
statistical. See Steve Gold, “Causation in Toxic Torts: Burdens of Proof, Standards
of Persuasion, and Statistical Evidence” (1986) 96 Yale LJ 376, 382-384.
157. Where the claimant led only statistical evidence, a court could simply say
that his case failed. Alternatively, as Lord Mackay envisaged, the court might have
held, exceptionally, that, where no other proof was possible, the defendant should
be held liable on the basis of Lord Mackay’s rule.
158. Of course, it is possible to conceive of a legal system which chose, as a
matter of policy, to make defendants liable for all the damage which a court was
satisfied, on the balance of probability, they had probably caused. But only the
legislature could alter English or Scots law so as to introduce a general rule to that
effect, which would change the very nature of the system and completely alter its
balance, in favour of claimants and against defendants and their insurers. In
Hotson Lord Mackay was not suggesting that English law operated, or should
operate, generally on that basis. On the contrary, he had just been at pains, along
with the other members of the appellate committee, to emphasise that in civil
proceedings for damages the role of the judge is to decide, on the balance of
probability, what actually happened. He introduced his discussion of the
hypothetical case by saying, [1987] AC 750, 786A-B, that he considered that it
would be unwise, however, “to lay it down as a rule that a plaintiff could never
succeed by proving loss of a chance in a medical negligence case.” He then
referred to McGhee. So he seems to have envisaged that the court might adopt
such an approach in an exceptional case like McGhee where, because of the state
of medical knowledge, the claimant could not prove his case on the usual
approach.
159. There is now no room, however, for Lord Mackay’s rule in cases of that
kind in English or Scots law since, in Fairchild, the House dealt with the problem
of proof which they present by adopting a different and – for claimants – much
less stringent rule. With Lord Mackay’s rule, the claimant would succeed if he
showed, on the balance of probability, that it was more likely than not that the
defendant’s breach of duty had materially contributed to the causation of his
dermatitis; under the rule in Fairchild, the claimant succeeds if he shows, on the
balance of probability, that the defendant’s breach of duty materially increased the
risk that he would contract dermatitis. Indeed, the rule in Fairchild is more
generous to claimants precisely because it is modelled on the rule which the House
had adopted in McGhee and which was itself more generous to pursuers than the
rule described by Lord Mackay. Put shortly, if the House had applied Lord
Mackay’s rule, the claimants in Fairchild would unquestionably have failed since
there was no evidence, whether epidemiological or of any other kind, to show that,
on the balance of probability, it was more probable than not that the breach of duty
of any of the individual defendants had materially contributed to the causation of
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the victims’ disease. All that the claimants could show was that, on the balance of
probability, each of the defendants had materially increased the risk that the
victims would develop mesothelioma. For the policy reasons which it gave, the
House of Lords held that this was enough.
Single Exposure Mesothelioma Cases
160. Similarly, in my view, there is now no room for introducing the doubling of
the risk approach in single exposure mesothelioma cases. As already explained, in
these cases, because of the state of medical knowledge, it is impossible to prove
whether the victim’s mesothelioma was actually caused by the defendant’s breach
of duty or by asbestos fibres in the general atmosphere. The claimant comes up
against the same rock of uncertainty. In that respect single exposure cases are no
different from multiple defendant cases and the same approach should be applied.
The point is covered by what Lord Hoffmann said in Barker v Corus UK Ltd
[2006] 2 AC 572, 584H-585B, at para 17, in a short passage with which all the
members of the appellate committee agreed:
“The purpose of the Fairchild exception is to provide a cause of
action against a defendant who has materially increased the risk that
the claimant will suffer damage and may have caused that damage,
but cannot be proved to have done so because it is impossible to
show, on a balance of probability, that some other exposure to the
same risk may not have caused it instead. For this purpose, it should
be irrelevant whether the other exposure was tortious or non-tortious,
by natural causes or human agency or by the claimant himself. These
distinctions may be relevant to whether and to whom responsibility
can also be attributed, but from the point of view of satisfying the
requirement of a sufficient causal link between the defendant’s
conduct and the claimant’s injury, they should not matter.”
The position accordingly is that in single exposure cases the Fairchild exception
applies and a claimant succeeds if he proves, on the balance of probability, that the
defendant’s breach of duty materially increased the risk that he would develop
mesothelioma.
161. Since that is the rule which applies in cases where the state of medical
knowledge makes it impossible for a claimant to prove whether a defendant’s
breach of duty actually caused his disease, there is no reason why a claimant needs
to prove anything more than that the defendant’s breach of duty materially
increased the risk that he would develop the disease. So in such cases the doubling
of the risk approach is irrelevant. And there is no room for Mr Stuart-Smith’s fall-
Page 64
back suggestion that, in single exposure cases, a material increase in risk should be
equated with doubling the risk. That would be utterly inconsistent with the
established law that, for these purposes, a risk is material if it is more than de
minimis. See the discussion of the hypothetical use of statistics in McGhee at para
150 above.
162. It also follows that there is no room in such cases for applying the approach
laid down by Smith LJ in the Court of Appeal in the passage quoted at para 121
above. The purported guidance to courts in that passage should not be followed.
163. Finally, nothing which I have said is intended to discourage the use of
epidemiological evidence or to depreciate its value in cases where a claimant has
to prove his case on the balance of probabilities. Far from it. Obviously, for
example, epidemiology is likely to lie behind much of the evidence on which a
court determines whether an exposure has materially increased the risk of the
claimant developing a disease. Epidemiological evidence may also be relevant
when deciding whether it would have been reasonable for a defendant to take
precautions to avoid the risk of the claimant suffering a particular injury – say, the
side-effect of a drug. And, of course – it must be emphasised once more –
epidemiological and statistical evidence may form an important element in proof
of causation. I have simply emphasised the point made by Phipson on
Evidence,17th ed (2010), para 34-27, that, unless a special rule applies, “Where
there is epidemiological evidence of association, the court should not proceed to
find a causal relationship without further, non-statistical evidence.” In other words,
since, by its very nature, the statistical evidence does not deal with the individual
case, something more will be required before the court will be able to reach a
conclusion, on the balance of probability, as to what happened in that case. For
example, where there is a strong epidemiological association between a drug and
some condition which could have been caused in some other way, that evidence
along with evidence that the claimant developed the condition immediately after
taking the drug may well be enough to allow the judge to conclude, on the balance
of probability, that it was the drug that caused the claimant’s condition.
164. Of course, in any actual dispute, the epidemiological evidence may be
contested. The judge will then have to decide which expert view he accepts and
how reliable the evidence is – whether, for example, the study has been properly
constructed and, in particular, what the confidence intervals are. In that respect
epidemiological evidence is no different from other evidence.
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Disposal
165. Since the Fairchild exception applies in single exposure cases, the
claimants in the present appeals were entitled to succeed if they proved that the
defendants’ breach of duty materially increased the risk that Mrs Costello and Mrs
Willmore would develop mesothelioma. There was therefore no error of law on the
part of the Court of Appeal. The defendants’ appeal in Sienkiewicz must
accordingly be dismissed.
166. So far as the law is concerned, the same applies to Willmore. In that case
the Council also appealed on the facts. The Court of Appeal reviewed the evidence
and the judge’s reasoning. Having rejected his finding on one point, they accepted
that he had been entitled to find that she had been exposed to asbestos in two other
ways and that those exposures had been material. It is important that judges should
bear in mind that the Fairchild exception itself represents what the House of Lords
considered to be the proper balance between the interests of claimants and
defendants in these cases. Especially having regard to the harrowing nature of the
illness, judges, both at first instance and on appeal, must resist any temptation to
give the claimant’s case an additional boost by taking a lax approach to the proof
of the essential elements. That could only result in the balance struck by the
Fairchild exception being distorted. Mr Feeny made a number of plausible
criticisms of the findings of Nicol J and of the approach of the Court of Appeal and
suggested that they had been unduly favourable to Mrs Willmore. Some of the
inferences which Nicol J drew in Mrs Willmore’s favour from the evidence
relating to her exposure at Bowring Comprehensive can properly be regarded as
very generous. With considerable hesitation, however, I have concluded that the
criticisms would not justify this Court in taking the exceptional step of disturbing
the concurrent findings of fact of the courts below. I would accordingly dismiss the
Council’s appeal on the facts. In the result, the appeal in Willmore must also be
dismissed.
LADY HALE
167. I pity the practitioners as well as the academics who have to make sense of
our judgments in difficult cases. But these cases are hard rather than difficult. We
are here concerned with one case of relatively light but long term exposure and one
case of very slight and short term exposure, both set against a lifetime of
environmental and other possible exposures about which nothing much is known.
As Lord Brown implies, Fairchild kicked open the hornets’ nest. The House of
Lords were confronted with several employers, each of which had wrongly
exposed their employees to asbestos, but none of which exposure could be shown
to have caused the disease. I find it hard to believe that their Lordships there
Page 66
foresaw the logical consequence of abandoning the “but for” test: that an employer
or occupier whose wrongful exposure might or might not have led to the disease
would be liable in full for the consequences even if it was more likely than not that
some other cause was to blame (let alone that it was not more likely than not that
he was to blame). But, as Lord Rodger has explained, that is the logical
consequence and there is nothing we can do about it without reversing Fairchild.
Even if we thought it right to do this, Parliament would soon reverse us, and it is
easy to understand why. Asbestos has long been known to be a dangerous (as well
as a useful) substance, employers and occupiers turned a blind eye to those dangers
long after they knew or should have known about them, and mesothelioma is a
dreadful disease.
168. In Barker, Mr Stuart-Smith tried very hard to persuade the House of Lords
that the Fairchild exception applied only where all the exposure was in breach of
duty. He failed in that, although he succeeded in persuading the majority that the
price to be paid for abandoning conventional rules of causation was aliquot
liability. Parliament swiftly disagreed. The Compensation Act 2006 restored the
principle that any tortfeasor is liable in full for an indivisible injury. But that leaves
us with the result that a defendant who may very well not have caused the
claimant’s disease – indeed probably did not do so – is fully responsible for its
consequences. I do not see any answer to that. It is the inevitable result of Barker,
made even more severe through the intervention of Parliament, but inevitable none
the less.
169. That means that in cases where the Fairchild exception applies, there is no
room for the “more than doubles the risk” approach to causation: it is not
necessary in order to establish causation and it is not an appropriate test of what is
a more than de minimis increase in risk. So we do not need to go into the relevance
of statistical probabilities to the finding of causation for the purpose of deciding
these cases. Nor, in the event, did the Court of Appeal need to do so. The reason
why Lord Phillips and Lord Rodger have discussed the subject at such length is the
obiter observation of Smith LJ, at para 23 of her judgment in Sienkiewicz, that “in
a case of multiple potential causes, a claimant can demonstrate causation by
showing that the tortious exposure has at least doubled the risk arising from the
non-tortious cause or causes.” Anything we say on the subject, therefore, is also
obiter.
170. However, I do agree with Lord Rodger that doubling the risk is not an
appropriate test of causation in cases to which the Fairchild exception does not
apply. Risk is a forward looking concept – what are the chances that I will get a
particular disease in the future? Causation usually looks backwards – what is the
probable cause of the disease which I now have? Epidemiology studies the
incidence and prevalence of particular diseases and the associations between both
of these and particular variables in the diseased population. From these it is
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possible to predict that a particular percentage of the population, for example of
women aged between 60 and 70, will contract a particular disease, for example,
breast cancer. It is also possible to say that certain variables, such as life-style or
age of first child-bearing, are associated with a greater chance of developing the
disease. So a doctor will sensibly advise her patient to behave in a way which will
reduce the risks. But if the disease materialises, the existence of a statistically
significant association between factor X and disease Y does not prove that in the
individual case it is more likely than not that factor X caused disease Y.
171. The same applies to less sophisticated calculations. The fact that there are
twice as many blue as yellow taxis about on the roads may double the risk that, if I
am run over by a taxi, it will be by a blue rather than a yellow one. It may make it
easier to predict that, if I am run over by a taxi, it will be by a blue rather than a
yellow one. But when I am actually run over it does not prove that it was a blue
taxi rather than a yellow taxi which was responsible. Likewise, if I actually
develop breast cancer, the fact that there is a statistically significant relationship
between, say, age at first child-bearing and developing the disease does not mean
that that is what caused me to do so.
172. But as a fact finder, how can one ignore these statistical associations? Factfinding judges are told that they must judge a conflict of oral evidence against “the
overall probabilities” coupled with the objective facts and contemporaneous
documentation: see, for example, Robert Goff LJ in Armagas Ltd v Mundogas SA
(The “Ocean Frost”) [1985] 1 Lloyd’s Rep 1, 57. Millions of pounds may depend
upon their decision. Yet judges do not define what they mean by “the overall
probabilities” other than their own particular hunches about human behaviour.
Surely statistical associations are at least as valuable as hunches about human
behaviour, especially when the judges are so unrepresentative of the population
that their hunches may well be unreliable? Why should what a (always middleaged and usually middle class and male) judge thinks probable in any given
situation be thought more helpful than well-researched statistical associations in
deciding where the overall probabilities lie? As it seems to me, both have a place.
Finding facts is a difficult and under-studied exercise. But I would guess that it is
not conducted on wholly scientific lines. Most judges will put everything into the
mix before deciding which account is more likely than not. As long as they
correctly direct themselves that statistical probabilities do not prove a case, any
more than their own views about the overall probabilities will do so, their findings
will be safe.
173. So in my view it would be wrong for judges to change their fact-finding
behaviour because of anything said in this case. On the issues of law, the Fairchild
exception has to apply to these single tortious exposure cases, no matter how
unjust it may seem to the defendants. Even if I were convinced of the merits of the
“more than doubling the risk” approach to causation in other contexts, which I am
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not, it does not apply in these cases. That is enough to dispose of the appeal in the
case of the late Mrs Costello. In the case of Mrs Willmore, the judge’s findings of
fact were truly heroic, and I would endorse what Lord Rodger says about this, but I
do not think that it is open to us to disturb them. I would dismiss both appeals.
LORD BROWN
174. Mesothelioma claims are in a category all their own, so special indeed that
Parliament in 2006 chose to legislate specifically for them: section 3 of the
Compensation Act 2006. Whilst entertaining no doubt that the position now
reached in respect of such claims is precisely as Lord Phillips and Lord Rodger
have explained and that these appeals must accordingly fail, I think it only right to
indicate just how unsatisfactory I for my part regard this position to be and how
quixotic the path by which it has been arrived at.
175. The present position, exemplified by the facts of these very appeals, can be
simply stated as follows: any person who negligently or in breach of duty exposes
another more than minimally to the inhalation of asbestos fibres will be liable to
make full compensation if that other develops mesothelioma more than five years
later (five years being now thought to be the minimum period between the
development of the first malignant cell and the diagnosis of the disease – see Lord
Phillips’ judgment at para 19(v)). That statement of the position holds true
irrespective of whether the victim was exposed by others to even longer and more
intensive inhalation (and indeed inhalation of more noxious fibres), whether
negligently or not, and irrespective too of any environmental or other exposure
(again, however intensive). It requires qualification only if and to the extent that
the victim negligently exposed himself to the inhalation of asbestos fibres (when
there may be a finding of contributory fault).
176. One need hardly stress how radically different such an approach to
compensation represents from that followed in all other cases of physical injury.
All other cases require that the claimant satisfies the “but for” test of causation.
True, in the case of cumulative injuries, the law holds a negligent employer liable
even if his negligence is responsible for part only of the victim’s condition
(provided only that it made a material, ie more than de minimis, contribution to the
development of the condition). I have difficulty, however, in seeing this as a true
exception to the “but for” test: although the claimant in Bonnington Castings Ltd v
Wardlaw [1956] AC 613, the case which first established the principle, recovered
full damages for his condition (pneumoconiosis from the inhalation of silica), that
appears to have been because the defendants took no point on apportionment; in a
series of subsequent such cases damages have been apportioned, however broadly
– for example, as between negligent and non-negligent exposure respectively in
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dust inhalation cases, in noise cases and in cases of vibration white finger, and, in
respiratory disease cases, between the damage caused by the inhalation of fumes or
other noxious agents on the one hand and the claimant’s habit of cigarette smoking
on the other.
177. It therefore seems to me that there is just one single authority that needs to
be noticed before one turns to the three stage process by which the present
approach to compensation in mesothelioma cases came to be dictated, namely, of
course, McGhee v National Coal Board [1973] 1 WLR 1. McGhee is undoubtedly
a problematic case. The House of Lords was later in Wilsher v Essex Area Health
Authority [1988] AC 1074 to regard it as not having laid down any principle of law
at all; rather it was described by Lord Bridge of Harwich, at p 1090, as merely “a
robust and pragmatic approach to the undisputed primary facts of the case” – on
the basis that, as in Bonnington Castings, the negligent prolongation of the
claimant’s contact with (in McGhee) brick dust had materially contributed to his
development (in McGhee) of dermatitis.
178. Rightly or wrongly, however (and whether rightly or wrongly now matters
nothing), the House of Lords in Fairchild v Glenhaven Funeral Services Ltd
[2003] 1 AC 32 found altogether greater force in McGhee. As was pointed out, for
example by Lord Nicholls, it had really not been open to the House in McGhee to
infer from the established facts that the employer’s negligence had caused or
materially contributed to the onset of his condition. In short, the House in
Fairchild regarded McGhee as authority for the application to certain cases of a
less stringent test than the usual “but for” test for establishing the necessary causal
connection between the employer’s negligence and the claimant’s condition. That
said, however, the judgments in Fairchild provided no support whatever for a
general principle of compensation in mesothelioma cases remotely as wide as I
have described the present position to be today. Quite the contrary. The
circumstances in which the more relaxed approach to causation said to have been
adopted in McGhee were held to apply to mesothelioma cases were narrowly
circumscribed. One should note particularly Lord Bingham’s six relevant factors
(conveniently set out at para 39 of Lord Phillips’ judgment), all of which had to be
present before the special rule of causation was to apply. Note too the agreement
between the parties in Fairchild that “any cause of [the claimant’s] mesothelioma
other than the inhalation of asbestos dust at work can be effectively discounted”
(Lord Bingham’s speech at para 2). Consider also the rationale identified by Lord
Bingham as justifying this special rule: the “strong policy argument in favour of
compensating those who have suffered grave harm, at the expense of their
employers who owed them a duty to protect them against that very harm and failed
to do so, when the harm can only have been caused by breach of that duty and
when science does not permit the victim accurately to attribute, as between several
employers, the precise responsibility for the harm he has suffered” (Lord Bingham
at para 33). Lord Bingham was there positing a situation where, for example, a
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mesothelioma victim had worked for three successive employers each, say, for
fifteen years, all of whom had negligently exposed him to the inhalation of
asbestos fibres. Faced with the “rock of uncertainty” – Lord Bingham’s graphic
characterisation of science’s inability to establish on a balance of probabilities
which particular source(s) of asbestos fibre exposure had caused mesothelioma to
develop – one can readily see how the House came unanimously to endorse this
new principle.
179. I am not, of course, suggesting that their Lordships in Fairchild were intent
on confining the application of this new principle quite so narrowly as that. Lord
Rodger, for example, expressly recognised (at para 170 of his speech) that “it can
also apply where, as in McGhee, the other possible source of the injury is a similar,
but lawful, act or omission of the same defendant”. But he immediately then
“reserve[d] [his] opinion as to whether the principle applies where the other
possible source of injury is a similar but lawful act or omission of someone else or
a natural occurrence”. The point I make is that it is hardly to be thought that had
the House, on the occasion of the Fairchild hearing, been considering not the facts
of those three appeals but instead the facts of the present appeals the claimants
would have succeeded and the law have developed as it has.
180. Before parting from Fairchild it is, I think, worth noting that, just as in
Bonnington Castings half a century before, the respondent defendants in Fairchild
similarly took no point on apportionment: their stance now as then was one of all
or nothing – doubtless in the hope (and perhaps even the expectation) of defeating
the claims in their entirety.
181. Coming then to stage two of the three stage process, by which the present
position with regard to mesothelioma cases came to be established, Barker v Corus
UK Ltd [2006] 2 AC 572, one finds the House having to face up to some of the
problems it had left open with Fairchild and, as it seems to me, beginning to have
second thoughts both as to the juristic basis for this special rule of causation which
Fairchild held to apply in certain toxic tort cases and as to where the abandonment
of the “but for” principle was taking the law. In the result, the Fairchild approach
was (as Lord Rodger now puts it at para 140 of his judgment) “refined”; Lord
Hoffmann explained that Fairchild had recognised a new tort, that of negligently
increasing the risk of personal injury (although, of course, the injury had to
eventuate before any tort was committed), and logically it followed that any liable
defendant should be liable only for his aliquot share of the victim’s loss, not for its
entirety. The damage was no longer to be treated as the indivisible mesothelioma
but rather as the readily divisible creation of the risk of developing mesothelioma.
Damages, therefore, were to be apportioned according to the contribution made by
any particular defendant to the overall risk. On that basis, of course, the special
rule whereby the “but for” test of causation is relaxed applies equally whether or
not other exposures are partly tortious and partly non-tortious, or indeed wholly
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non-tortious, and whether they result from natural causes or indeed, from the
employee’s own negligence.
182. It is to my mind quite clear that the preparedness of the majority of the
court in Barker to extend the reach of the Fairchild principle this far was
specifically dependent upon there being aliquot liability only. Lord Rodger alone
thought that liability under the Fairchild exception to the “but for” rule should be
for full compensation (“in solidum”). But he made clear that had that been the
view of the majority, then in a case where the victim had himself been solely
responsible for a material exposure – especially where, as in one of the three
appeals before the court in Barker, the victim had himself been at fault – he would
have applied the normal “but for” rule for proof of causation.
183. The third and final stage of the process by which the law with regard to
compensation in mesothelioma cases came to reach its present position was, of
course, Parliament’s enactment of section 3 of the Compensation Act 2006. I have
no doubt that Lord Rodger is right (at paras 131 and 132 of his judgment) in saying
that the sole effect of section 3 is to reverse the House’s decision in Barker on the
issue of quantum; in no way does it pre-empt or dictate the proper approach of the
common law to questions of causation and liability. On the other hand it would be
a remarkable thing for this Court now in effect to reverse the decision in Fairchild
and revert, in mesothelioma cases as in all others, to the normal, “but for”, rule of
causation – the principle, vindicated periodically down the years in cases of
indivisible no less than of cumulative injury (Gregg v Scott [2005] 2 AC 176 being
the latest such decision in point), that to establish liability the claimant must show
that but for the defendant’s negligence he would probably not have suffered his
injury (or at least not have suffered it to the full extent that he has).
184. In my judgment it could only be by reversing Fairchild and allowing no
exception whatever to the normal rule of causation that this Court could now avoid
what Lord Phillips (at para 58 of his judgment) rightly describes as the “draconian
consequences” of coupling section 3 to the Fairchild/Barker principle: the liability
in full even of someone “responsible for only a small proportion of the overall
exposure of a claimant to asbestos dust”. There is in my opinion simply no logical
stopping place between the case of successive negligent employers dealt with in
Fairchild itself (apparently circumscribed though that decision was) and the
extreme (“draconian”) position now arrived at, well exemplified as it seems to me
by the facts of these very appeals. If, because of the “rock of uncertainty”, the law
is to compensate by reference to negligence which merely increases the risk of
such injury as then develops, why should not that relaxation of the normal rule of
causation apply equally when, as here, there is but one negligent employer (or
negligent occupier) as when there are several? As Barker recognised, there can be
no rational basis for confining the special rule within narrow bounds, whatever
may have been contemplated by the House in Fairchild.
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185. In short, the die was inexorably cast in Fairchild – although, as already
suggested, it is doubtful if that was then recognised and it is noteworthy too that,
even when in Barker it came to be recognised, it was then thought palatable only
assuming that compensation was going to be assessed on an aliquot basis.
Parliament, however, then chose – although, of course, only in mesothelioma cases
– to go the whole hog.
186. The result must surely be this. As I began by saying, mesothelioma cases
are in a category all their own. Whether, however, this special treatment is justified
may be doubted. True, as Lord Phillips observes at the outset of his judgment,
mesothelioma is indeed a hideous disease. (And it is perhaps also the case, as Lord
Phillips suggests at para 104, that mesothelioma, after all, may result from the
cumulative effect of exposures to asbestos dust.) The unfortunate fact is, however,
that the courts are faced with comparable rocks of uncertainty in a wide variety of
other situations too and that to circumvent these rocks on a routine basis – let alone
if to do so would open the way, as here, to compensation on a full liability basis –
would turn our law upside down and dramatically increase the scope for what
hitherto have been rejected as purely speculative compensation claims. Although,
therefore, mesothelioma claims must now be considered from the defendant’s
standpoint a lost cause, there is to my mind a lesson to be learned from losing it:
the law tampers with the “but for” test of causation at its peril.
187. There is a rough justice about the law of personal injury liability as a whole.
To compensate a claimant in full for a lost finger because there was a 60:40 chance
that he would have worn protective gloves had they been made available to him
may be regarded as rough justice for defendants. But it is balanced by the denial of
compensation to a claimant who cannot establish that he would probably have
worn the gloves – or whose finger the judge concludes was probably already
doomed because of frostbite. Save only for mesothelioma cases, claimants should
henceforth expect little flexibility from the courts in their approach to causation.
Since Fairchild and Barker there has been much academic focus on a supposedly
critical distinction between so-called “single agent” and “multiple agent” cases, the
suggestion being that the former more readily lend themselves to special rules of
causation than the latter. For my part I have difficulty even in recognising the
distinction between these categories, at any rate in some cases. But I have greater
difficulty still in accepting that the courts should now, whether on this or any other
basis, be thinking of creating any further special rules regarding the principles
governing compensation for personal injury. The same logic which requires that
the claims of these respondents succeed to my mind requires also that the courts
should in future be wary indeed before adding yet further anomalies in an area of
law which benefits perhaps above all from clarity, consistency and certainty in its
application.
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LORD MANCE
188. Cases of mesothelioma are subject to the special rule of causation
established in Fairchild v Glenhaven Funeral Services Ltd [2002] UKHL 22;
[2003] 1 AC 32 and developed in Barker v Corus UK Ltd [2006] UKHL 20;
[2006] 2 AC 572, but significantly amended by the Compensation Act 2006. I
agree that this special rule is applicable to both the appeals before this court,
although in each (a) only one person (an employer in one case, a school in the
other) is shown to have exposed the victim of mesothelioma to asbestos, the only
other such exposure being the general low-level atmospheric exposure incurred by
members of the public at large, and (b) the exposure by that person did no more
than increase the sufferer’s general low-level atmospheric exposure to asbestos
“materially” (or, more specifically, in the case of Mrs Costello represented by Mrs
Sienkiewicz, by some 18%). The submission that causation can be shown by
proving a doubling of the ambient risk, or can be negatived by disproving this, is
inconsistent with, or would make a radical and uncertain inroad into, the special
rule.
189. I reach this conclusion in agreement with the reasoning on this aspect of
Lord Phillips, Lord Rodger, Lady Hale and Lord Dyson, on the basis that our
understanding of the aetiology of mesothelioma remains as incomplete and
inadequate as ever. I also concur with the further remarks of Lady Hale in her first
paragraph and of Lord Brown in his judgment about the impossibility of going
back on Fairchild, as well as on the lesson of caution that the history may teach in
relation to future invitations to depart from conventional principles of causation. I
too would therefore dismiss the appeal in Mrs Costello’s case.
190. An interesting debate has, somewhat unexpectedly, developed about the
significance or value of epidemiological or statistical evidence relating to a
population or group in the context of decision-making in particular cases. I share a
reluctance to place too much weight on such evidence. This is not because
statistics are lies, or because truth can be stranger than fiction. It is because the law
is concerned with the rights or wrongs of an individual situation, and should not
treat people and even companies as statistics. Despite the intense sympathy which
can arise in particular cases like the present, an attribution of liability based
substantially on statistical evidence, that, viewing the relevant population or group
as a whole, it is more likely than not that the particular defendant was negligent or
causatively responsible, appears to me most undesirable.
191. That epidemiological evidence used with proper caution, can be admissible
and relevant in conjunction with specific evidence related to the individual
circumstances and parties is, however, common ground and clearly right. What
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significance a court may attach to it must depend on the nature of the
epidemiological evidence, and of the particular factual issues before the court.
192. Whether and if so when epidemiological evidence can by itself prove a case
is a question best considered not in the abstract but in a particular case, when and
if that question arises. If it can, then, I would hope and expect that this would only
occur in the rarest of cases.
193. In other cases, there will be continuing good sense in the House of Lords’
reminder to fact-finders in Rhesa Shipping Co SA v Edmunds (the “Popi M”)
[1985] 1 WLR 948 that it is not their duty to reach conclusions of fact, one way or
the other, in every case. There are cases where, as a matter of justice and policy, a
court should say that the evidence adduced (whatever its type) is too weak to prove
anything to an appropriate standard, so that the claim should fail.
194. The American material which we have seen, particularly Smith v Rapid
Transit Inc (1945) 58 NE 754, Merrell Dow Pharmaceuticals Inc v Havner (1997)
953 SW 2d 706 and “Causation in Toxic Torts: Burdens of Proof, Standards of
Persuasion, and Statistical Evidence” by Steve Gold (1986) 96 Yale LJ 376,
demonstrates, with innumerable further references, the detailed and extensive
thought which has been given across the Atlantic to the significance and use of
epidemiological or statistical evidence. In that light and without hearing fuller
argument, as well as because it raises fact-specific issues and is unnecessary for
the resolution of these appeals, I think it inappropriate to say more about the use of
epidemiological evidence.
195. On the material before us, I would myself see Willmore v Knowsley
Metropolitan Borough Council as a case where there was no sufficient proof that
the defendant exposed the claimant to asbestos. The judge found exposure on a
slender and speculative basis which Lady Hale describes as heroic. But, the
concurrent findings below on two of the three bases of exposure found by the
judge are entitled to some weight, and on that basis I do not dissent from the
general view that the appeal on fact in Willmore should also be dismissed.
LORD KERR
196. What has been called “the Fairchild exception” was described in a variety
of ways in Barker v Corus UK Ltd [2006] 2 AC 572 but common to all the various
formulations is the proposition that where employers through breach of duty
expose their employee to asbestos and thereby materially increase the risk to the
employee of developing mesothelioma, they will be jointly and severally liable if
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he or she develops that condition. This involved a modification of the previously
applicable legal rules in relation to the causation element in employers’ liability
claims. That alteration was thought necessary in order to cater for the particular
difficulties that asbestos related disease presents.
197. Implicit in the modification of the normal rule is the acceptance that an
employer thus found liable may, in truth and in fact, not have been responsible for
the damage at all. This is the price that it was deemed necessary to pay in order to
hold the balance of justice between the parties. Because of the limitations of
medical and scientific knowledge, it was recognised that it would be unjust to
enforce a rigorous requirement of proof that a particular employment had actually
caused or contributed to the damage.
198. A potent factor in this equation was that the insidious nature of asbestos and
the calamitous consequences that exposure to it can cause, allied to the current lack
of scientific knowledge about the aetiology of mesothelioma, warrant a different
approach to the conventional burden of proof. To insist on its stringent application
would set what would in many instances prove an impossible practical difficulty in
the way of a claimant. These considerations – viz the constraints that arise from the
unavailability of scientific proof and the dreadful illnesses that can result from
asbestos exposure – are just as relevant in the approach to so-called “single
exposure” cases as they are in cases of multiple employment exposure cases.
199. The use of the expression “single exposure” may be misleading in this
context. In Fairchild v Glenhaven Funeral Services Ltd [2003] 1 AC 32 the
defendants had argued that the claims should be dismissed because there were
various exposures each of which could have caused the mesothelioma and each of
which might not have done so. In the present cases the appellants’ argument
resolves to essentially the same proposition. They suggest that there were two
possible sources of exposure in each case – in Mrs Costello’s case exposure while
employed by the defendant and environmental exposure and in Mrs Willmore’s
case exposure while at school and environmental exposure. It is argued that each
of these exposures might have caused the mesothelioma but each of them might
not have done so. In effect, therefore, the appellants submit that there is more than
one possible source for the mesothelioma that both women suffered. The
difference in these cases is not that they involved a single exposure but that each
had a tortious and a non-tortious source of exposure. But the same difficulties as to
proof as arose in Fairchild and Barker afflict the present cases. And it was those
difficulties that prompted the modification of the causation rules.
200. It might be suggested that it is easier to accept that several employers, none
of whom could be positively identified as having caused or contributed to the
condition, should have to participate in the compensation package, on the basis
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that one of them (at least) had actually caused the mesothelioma and because each
of the employers had, in any event, been prepared to have their employee run the
risk of contracting the disease. But that is not the basis on which the adjustment to
the requirements of proof was made. That adjustment was made precisely because,
as a matter of policy, it was considered that it would be unfair to impose on a
claimant a requirement of proof which in most cases, because of the limitations of
scientific knowledge, was quite incapable of fulfilment. In so far as such
considerations might be considered relevant, however, the fact remains that both
defendants in the present appeals were prepared to countenance a material increase
in the risk to Mrs Costello and Mrs Willmore. The circumstance that the other
possible source of mesothelioma in these cases was non-tortious should make no
difference.
201. Nor did it in Barker. In that case it was expressly accepted by Lord
Hoffmann, Lord Scott of Foscote and Lord Rodger of Earlsferry that the Fairchild
exception did apply to a “non-tortious source of risk”. At para 17 Lord Hoffmann
said:
“The purpose of the Fairchild exception is to provide a cause of
action against a defendant who has materially increased the risk that
the claimant will suffer damage and may have caused that damage,
but cannot be proved to have done so because it is impossible to
show, on a balance of probability, that some other exposure to the
same risk may not have caused it instead. For this purpose, it should
be irrelevant whether the other exposure was tortious or non-tortious,
by natural causes or human agency or by the claimant himself. These
distinctions may be relevant to whether and to whom responsibility
can also be attributed, but from the point of view of satisfying the
requirement of a sufficient causal link between the defendant’s
conduct and the claimant’s injury, they should not matter.”
202. Lord Scott stated that he was in “complete agreement” not only with Lord
Hoffmann’s conclusions but also with his reasons for reaching them (para 50) and
at para 97 Lord Rodger said:
“Starting from ‘the McGhee extension’, counsel considered whether
Fairchild would apply where one or more of the sources of exposure
to asbestos dust had been lawful but unconnected with any
wrongdoer. For instance, the victim had been employed for a period
before the dangers of exposure to asbestos dust should have been
known in the industry and there had been no fault on the part of the
employer. Having reserved my opinion on the point in Fairchild, I
would now hold that the rule should apply in that situation.”
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203. For the reasons given by Lord Phillips and Lord Rodger in the present
appeals, therefore, I agree that there is no basis on which the Fairchild exception
should not be applied in these cases and, on that account, that the appeals should
be dismissed. The policy reason for introducing the modified rule in that case
applies with equal force here and it would be anomalous and arbitrary to require
these respondents to establish that it was twice as likely that the indicted exposure
was the cause of the mesothelioma, while not imposing such a requirement on a
claimant in a multiple employer exposure case. In all relevant respects the
appellants are in an exactly similar position to a defendant in such a case. In both
instances none of the defendants can be proved to have caused the mesothelioma
but all have materially increased the risk by wrongfully exposing Mrs Costello and
Mrs Willmore to asbestos.
204. In these circumstances the interesting debate that has been had between
Lord Phillips and Lord Rodger as to the use to which epidemiological evidence
might be put is, at this stage certainly, academic. But I wish to say that I share the
misgivings that have been expressed about the capacity of this type of evidence to
prove that mesothelioma is more likely to have been caused by a particular
exposure, even if advances in medical and scientific knowledge erode the “rock of
uncertainty”.
205. Epidemiology is the branch of medical science which normally deals with
the incidence and prevalence of disease in large populations and with the detection
of the sources and causes of disease. It involves the collection of data, usually over
significant periods. Unless these coincide with periods of relevant exposure or
replicate conditions of exposure experienced by individual claimants, the use of
such data to seek to establish any specific proposition in an individual case
requires to be treated with great caution, in my opinion. It is an essential and
minimum requirement, as Brachtenbach J said in Herskovits v Group Health
Cooperative of Puget Sound (1983) 664 P 2d 474, that there be evidence
connecting avowedly relevant statistical information produced by the
epidemiological studies to the facts of the case. In my view, no such connection
was made in the present appeals. The “epidemiological evidence” which was
adduced consisted of a series of assumptions and speculations rather than actual
data which could be related to the experience of those who developed
mesothelioma. What the testimony amounted to was the promotion of a theory
rather than the establishment of facts and it did not constitute evidence on which
reliable conclusions could be reached.
206. There is a real danger that so-called “epidemiological evidence” will carry a
false air of authority. It is necessary to guard against treating a theory based on
assumptions as a workable benchmark against which an estimate of the increase in
risk could be measured. Whether and in what circumstances epidemiological
evidence can assist in the determination of whether a particular case of
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mesothelioma is likely to have been caused by a particular exposure will have to
be decided according to the particular circumstances of an individual case. In my
view, the epidemiological material adduced in evidence in the present case could
not have assisted in the determination of that issue.
LORD DYSON
207. The central question that arises in these appeals is whether the so-called
Fairchild exception applies in a “single exposure” case, that is to say a case where
a victim has been exposed to asbestos by a single defendant in breach of duty and
has also been exposed to asbestos in the general atmosphere. In Fairchild itself,
the victims had been exposed to asbestos by a number of defendants in breach of
their duty of care. The limitations of medical knowledge prevented them from
being able to prove on the balance of probability which exposure had caused their
mesothelioma. In order to avoid injustice, the House of Lords held that proof on
the balance of probability that each defendant’s wrongdoing had materially
increased the risk of contracting the disease was sufficient to satisfy the causal
requirements for liability. For understandable reasons, the Court of Appeal had
applied a conventional approach and had dismissed the claims because the
claimants had been unable to prove on the balance of probability that their
wrongful exposure to asbestos by any particular defendant had caused their
disease. Each defendant was able to say that the offending asbestos might have
been the result of exposure caused during the claimants’ employment by a
different defendant. Thus it was that the claims were rejected by the Court of
Appeal on what Lord Bingham called “this rock of uncertainty”.
208. The Fairchild exception was created to circumvent the rock of uncertainty.
It is implicit in the reasoning in Fairchild (repeated in Barker) that, if the rock of
uncertainty were to disappear in the light of increased medical knowledge, then the
rationale for the Fairchild exception would disappear and claimants would be
required to prove their cases on the balance of probability in the usual way. It is
common ground that medical knowledge about the aetiology of mesothelioma has
not materially advanced since Fairchild. Mr Stuart-Smith QC accepts that, if this
were a multiple exposure case, the claimants would not be required to prove on the
balance of probability (whether by the doubling of the risk test or otherwise) that
their mesothelioma had been caused by wrongful exposure to asbestos. All that
they would have to prove was that the defendant or defendants had materially
contributed to the risk of mesothelioma.
209. There has been no previous decision on a single exposure case. In Barker,
the House of Lords held that the Fairchild exception applied even where not all the
exposures to asbestos which could have caused the claimant employee’s
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mesothelioma involved breaches of duty by his employers (in that case, the
employee was also exposed to asbestos during a period when he was selfemployed). At para 17, Lord Hoffmann said that the purpose of the Fairchild
exception was:
“to provide a cause of action against a defendant who has materially
increased the risk that the claimant will suffer damage and may have
caused that damage, but cannot be proved to have done so because it
is impossible to show, on a balance of probability, that some other
exposure to the same risk may not have caused it instead. For this
purpose, it should be irrelevant whether the other exposure was
tortious or non-tortious, by natural causes or human agency or by the
claimant himself. These distinctions may be relevant to whether and
to whom responsibility can also be attributed, but from the point of
view of satisfying the requirement of a sufficient causal link between
the defendant’s conduct and the claimant’s injury, they should not
matter.”
210. Lord Scott expressed the same view at para 59. But Barker was not a single
exposure case.
211. So why should the Fairchild exception not be applied in a single exposure
case? Mr Stuart-Smith advances a number of reasons. He submits that there is no
suggestion in any previous case that exposure to asbestos in the general
atmosphere should be taken into account as a relevant exposure for the purposes of
the Fairchild exception. The breathing of ambient air, which should merely be
regarded as part of the ordinary vicissitudes of life, is not under the control of any
single person or group of persons and should not be treated in the same way as
exposures to a carcinogen controlled and caused by an identifiable individual.
212. In my view, these are not good reasons for disapplying the Fairchild
exception in a single exposure case. In view of the present state of medical
knowledge, a single exposure claim would founder on the same rock of uncertainty
as a multiple exposure claim. The exception was devised as a matter of policy to
overcome the injustice that claimants would suffer if they were prevented by the
rock of uncertainty from establishing causation in mesothelioma cases. This policy
justification for the exception is articulated in a number of the speeches in both
Fairchild and Barker: see, for example, per Lord Bingham at para 33 and Lord
Nicholls at paras 41 and 42 in Fairchild. There is no reason in policy or principle
why the exception should not apply to a single exposure claim just as it does to a
multiple exposure claim. It is true that none of the previous decisions involves a
single exposure claim. But that is not a good reason for refusing to apply the
Fairchild exception if there is no material difference between single and multiple
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exposure claims. It is also true that the breathing of ambient air is a vicissitude of
life. But that is not a good reason for distinguishing Fairchild either. On the
present state of medical knowledge, the rock of uncertainty is as much of a
problem for victims of single exposure as for victims of multiple exposure.
213. It is implicit in Fairchild and Barker that, if it were possible for a victim of
mesothelioma to establish causation on the balance of probability in the
conventional way, then the rationale for the Fairchild exception would disappear.
Mr Stuart-Smith submits that causation can be established in the conventional way
in a single exposure case (but, he accepts, not yet in a multiple exposure case). He
says that a claimant can prove causation on a balance of probability by proving
that the tortious exposure has at least doubled the risk arising from the non-tortious
cause. This was the approach adopted by Judge Main in Sienkiewicz and adopted
as a correct statement of the law by Smith LJ at para 23 of her judgment. In fact,
Smith LJ seems to have considered that it was a legitimate approach even in multiexposure cases, since she referred to a doubling of the risk arising from “the nontortious cause or causes” (emphasis added).
214. Lord Phillips and Lord Rodger are in agreement that there is no scope in
single exposure mesothelioma cases for the application of a doubling of the risk
test based entirely on epidemiological evidence. But their reasoning differs to
some extent. Lord Phillips considers that it is not possible to prove causation on
the basis of epidemiological evidence alone because first it is not sufficiently
reliable (paras 97 to 101), and secondly there continue to be gaps in our
understanding of the aetiology of mesothelioma (paras 102 to 105). If these
shortcomings in our understanding were made good, then it is implicit in the first
reason that, if epidemiological data were to become sufficiently reliable, victims of
mesothelioma would be able (and therefore required) to prove causation on the
balance of probability on the basis of epidemiological evidence alone.
215. Lord Rodger agrees with Lord Phillips’s second reason. But his objection to
proof on the basis of epidemiological evidence alone is not based on the
unreliability of epidemiological data. It is more fundamental than that.
216. Lord Rodger draws a distinction between claimant A, who proves on the
balance of probability that a defendant probably injured him, and claimant B, who
proves on the balance of probability that a defendant actually injured him. He says
that, as a matter of law, claimant B will succeed but claimant A will fail. A
claimant who seeks to prove his case on the balance of probability in reliance
entirely on statistical evidence will inevitably fail, since he is able to do no more
than prove on the balance of probability that the defendant probably injured him.
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217. I am grateful to Lord Rodger for drawing attention to the article by Steve
Gold, “Causation in Toxic Torts: Burdens of Proof, Standards of Persuasion, and
Statistical Evidence” (1986) 96 Yale LJ 376. The article distinguishes between
“fact probability” and “belief probability”. The former is a more than 50%
statistical probability of an event having occurred. An illustration of this is the
75% probability that the victim was run down by a blue cab in the example given
by Brachtenbach J in Herskovits v Group Health Cooperative of Puget Sound
(1983) 664 P 2d 474 (see para 95 of Lord Phillips’s judgment). The latter is a more
than 50% belief in the decision-maker that a knowable fact has been established.
Mr Gold points out that, particularly in toxic tort cases, US courts have often
“collapsed” the distinction between fact probability and belief probability and
simply asked the question whether the fact that the claimant seeks to prove has
been established as “more likely than not”.
218. In my view, this is an important distinction and it is of particular relevance
in relation to causation in toxic torts. It is often the basic impossibility of proving
individual causation which distinguishes toxic tort cases from ordinary personal
injury cases. As Mr Gold points out, epidemiology is based on the study of
populations, not individuals. It seeks to establish associations between alleged
causes and effects. With proper scientific interpretation, these correlations lend
great weight to an inference of causation. However, in an individual case,
epidemiology alone cannot conclusively prove causation. At best, it can establish
only a certain probability that a randomly selected case of disease was one that
would not have occurred absent exposure.
219. Ultimately, questions of burden and standard of proof are policy matters for
any system of law. It is trite law that our system requires a civil claim to be proved
by a claimant on the balance of probability. It is a matter of policy choice whether
and, if so, in what circumstances the courts are willing to find causation proved on
the balance of probability on the basis of epidemiological evidence alone. In the
United States, some courts have been willing to find causation established on the
balance of probability on the basis of epidemiological evidence alone. They have
been criticised by Mr Gold for collapsing the distinction to which I have referred.
220. As I have said, the House of Lords produced in the Fairchild exception a
particular policy response to the causation problems created by the lack of
scientific knowledge about the aetiology of mesothelioma. This response has been
confirmed by the 2006 Act. In these circumstances, I agree with Lord Phillips and
Lord Rodger that there is no room for the application of a different test which
would require a claimant to prove (whether on the basis of doubling of the risk or
otherwise) that on the balance of probability the defendant caused or materially
contributed to the mesothelioma.
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221. It follows that I do not find it necessary to decide whether there are any
circumstances in which, as a matter of English law, causation can be proved on the
basis of epidemiological evidence alone. I am unaware of any English authority in
which the question whether causation can be proved in a straightforward personal
injury case on the basis of epidemiological evidence alone has been the subject of
decision. Toxic torts, such as mesothelioma, give rise to particular causation
problems. That is why special rules sometimes have been devised so as to avoid
injustice. Such problems are not inherent in straightforward personal injury cases
where it must be rare for a claimant to rely exclusively on epidemiological
evidence to prove his or her claim. The claimant will almost always also be able to
point to some specific evidence relating to the particular circumstances of the case.
I note that in Smith v Rapid Transit Inc (1945) 317 Mass 469, 58 NE 2d 754 it was
held on the facts of that case that statistical likelihood alone was insufficient to
support a finding that the bus that injured the plaintiff was the defendant’s.
222. But ultimately, as I have said, it is not necessary for the resolution of the
present appeal to decide whether epidemiological evidence alone suffices, since
Lord Phillips and Lord Rodger are agreed that there has been no material change in
the understanding of the aetiology of mesothelioma and there is no basis for
distinguishing single exposure cases from multiple exposure cases. It seems to me,
however, that there is no a priori reason why, if the epidemiological evidence is
cogent enough, it should not be sufficient to enable a claimant to prove his case
without more. Our civil law does not deal in scientific or logical certainties. The
statistical evidence may be so compelling that, to use the terminology of Steve
Gold, the court may be able to infer belief probability from fact probability. To
permit the drawing of such an inference is not to collapse the distinction between
fact probability and belief probability. It merely recognises that, in a particular
case, the fact probability may be so strong that the court is satisfied as to belief
probability. Whether an inference of belief probability should be drawn in any
given case is not a matter of logic. The law does not demand absolute certainty in
this context or indeed in any context. Judges are frequently called upon to decide
difficult and finely balanced questions on the balance of probability and sometimes
say that they have reached their conclusions after much anxious consideration of
the facts. It is true that, once the facts have been determined, they are treated as
having been established and, subject to any appeal, they cannot be challenged. But
the judge may even acknowledge in his judgment that he cannot be certain that the
facts are as he found them to be. He cannot exclude another possibility. But he is
satisfied on the balance of probability as to the facts and that is all that the law
requires.
223. I would in any event endorse what Lord Phillips has said about the limits of
epidemiological evidence at paras 97 to 101 and also what he has said about what
constitutes a “material increase in risk” at paras 107 and 108. I also agree with
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what Lord Rodger has said at paras 130 to 132 about the observations by Smith LJ
about the effect of section 3 of the 2006 Act.
224. For these reasons, I would dismiss these appeals.
