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You are here: BAILII >> Databases >> England and Wales Court of Appeal (Civil Division) Decisions >> Heneghan v Manchester Dry Docks Ltd & Ors [2016] EWCA Civ 86 (15 February 2016) URL: https://www.bailii.org/ew/cases/EWCA/Civ/2016/86.html Cite as: [2016] WLR(D) 87, [2016] ICR 671, [2016] EWCA Civ 86, [2016] 1 WLR 2036 |
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ON APPEAL FROM THE HIGH COURT OF JUSTICE
QUEEN'S BENCH DIVISION
MR JUSTICE JAY
HQ12X03121
Strand, London, WC2A 2LL |
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B e f o r e :
LORD JUSTICE TOMLINSON
and
LORD JUSTICE SALES
____________________
CARL HENEGHAN (SON AND EXECUTOR OF JAMES LEO HENEGHAN, DECEASED) |
Appellant |
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| - and - |
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MANCHESTER DRY DOCKS LIMITED00722056 LIMITED CARILLION CONSTRUCTION (CONTRACTS) LIMITED R. BLACKETT CHARLTON LIMITED S.C. CHEADLE HULME LIMITED KELLOGG BROWN & ROOT LIMITED |
Respondents |
____________________
David Platt QC and Peter Houghton (instructed by BLM LLP) for the Respondents
Hearing dates : 18 & 19/01/2016
____________________
VERSION
OF JUDGMENT
Crown Copyright ©
Master of the Rolls:
Heneghan)
who died of lung cancer; where (ii) it is common ground that the cancer was caused by his exposure to asbestos fibres; (iii) he was exposed to the asbestos inter alia whilst he was employed successively by each of the six defendants; (iv) biological evidence cannot establish which (if any) of the exposures triggered the cell changes in his body which led to his contracting the disease; but (
v)
epidemiological or statistical evidence can establish by how much the exposure attributable to each defendant increased the risk that he would contract the disease. The question is: how should the law deal with the issue of causation as between the claimant and each defendant in these circumstances? Jay J applied the so-called Fairchild exception (Fairchild
v
Glenhaven Funeral Services Ltd [2002] UKHL 22, [2003] 1 AC 32) and awarded damages against each defendant in proportion to the increase in risk for which it was responsible. The claimant appeals with the permission of the judge and says that the judge should have held that each defendant had materially contributed to the cancer and was liable for damages in full. The defendants say that the judge reached the right conclusion for the right reasons.
Heneghan
was born on 8 March 1938. During the course of his working life, he was exposed to respirable asbestos fibres and dust. He was diagnosed as suffering from lung cancer in early 2012 and died from the disease on 3 January 2013.
Heneghan's
exposure to asbestos over the course of his working life can be quantified as 133 fibres/ml years; (ii) the total exposure for which the six defendants were responsible was 46.9 fibres/ml years (i.e. 35.2% of the whole exposure); (iii) the doses or exposures for which the defendants were responsible range from 2.5% to 10.1%; (iv) cumulative exposure of 25 fibres/ml years is sufficient to enable an inference properly to be drawn that lung cancer in any individual case is attributable to asbestos, provided that there is a minimum ten year interval from first exposure to onset of the cancer; (
v)
the 25 fibres/ml year criterion remains appropriate for exposure to mixed fibre types with a preponderance of amphiboles: if exposure involved equal quantities of amphiboles and chrysotile, then cumulative exposure of 40 fibres/ml year is probably necessary to double the risk of lung cancer; and (
vi)
since the deceased's exposure included 114 fibres/ml years of amphibole, the relevant threshold is likely to be below the threshold of 40 fibres/ml years, and the parties have been content to proceed on the agreed basis of a more than five-fold increase in the risk of lung cancer attributable to Mr
Heneghan's
cumulative exposure to asbestos over the whole of his employments.
Some medical common ground
"15. On 12 November 2013 the medical experts produced a Joint Statement to the Court, points 2, 3 and 5 of which are relevant for present purposes:
'2. His risk of lung cancer was increased by smoking and by asbestos exposure.
3. On the balance of probabilities he would not have developed the lung cancer if he had not been exposed to asbestos.
…
5. The risk that lung cancer will develop increases with the amount smoked and with the dose of asbestos received. If a lung cancer does develop, then the duration and severity of symptoms and the eventual outcome are not affected by the amounts of smoking or asbestos exposure which led to that increase in risk.'
16. The medical experts are also agreed about the multiple mechanisms involved in the carcinogenesis of asbestos-related lung cancer. This involves a consideration of the microbiological processes occurring in cells, in particular cellular DNA, of the inhibitive effect asbestos has on programmed cell death, and of the reduction in the effectiveness of the body's natural defences against cancer caused by the presence of asbestos fibres in lung tissue. The precise detail does not matter for present purposes; it is sufficient to record that the experts are in general agreement that anything between four and seven stages in cellular mutation is required before the emergence of a cancer cell which may potentially progress to become a clinically apparent carcinoma of the lung.''
The two stages of the causation question
victim
would suffer the injury, it follows that it is more likely than not that the tortfeasor caused the injury. Some doubt has been expressed as to the
validity
of the doubling the risk test, at any rate for mesothelioma cases: see, for example, per Lord Phillips in Sienkiewicz
v
Greif UK Ltd [2011] UKSC 10, [2011] 2 AC 229 at paras 94 to 106. But there can be no doubt as to the
validity
of applying it to answer the first question. The deceased's lifetime risk of developing lung cancer had he not smoked and not been exposed to asbestos fibres was of the order of 0.5%. As I have said, the parties proceeded on the agreed basis that the cumulative effect of the deceased's exposure to asbestos over the whole of his employments resulted in a more than fivefold increase in the risk of his contracting the disease. I leave out of account the complication of the extent to which, having regard to the multiplicative effect of the smoking, the risk attributable to the exposure to asbestos was even greater. On any
view,
the exposure to asbestos more than doubled the risk of the deceased contracting the disease. That is why it was common ground that it was established in this case that the cancer was caused by that exposure.
Heneghan
would develop lung cancer. None of the defendants exposed him to an amount of asbestos close to 25 fibres/ml years (see para 3 above). Only one employer, W Blackwell (who had not been sued), was responsible for exposure in excess of 25 fibres/ml years (56% of the total exposure).
The Fairchild exception
v
National Coal Board [1973] 1 WLR 1.
v
Corus UK Ltd [2006] UKHL 20, [2006] 2 AC 572. In that case, the deceased who died of mesothelioma had been exposed to asbestos during three periods of his working life: while working for a company which had become insolvent; while working for the defendant; and while he was self-employed. It was held that the defendant was liable only in proportion to his own contribution to the exposure to the asbestos and therefore to the risk that the deceased would contract mesothelioma. It was irrelevant whether the other exposure was tortious, non-tortious, by natural causes or caused by the employee himself.
Summary of the judgment of Jay J
"Whether material contribution may be inferred in relation to any of the Defendants raises difficult questions. At one stage during the course of the trial, I was inclined to think that Dr Moore-Gillon [the defendants' expert] – in refusing to accept that such an inference may be drawn – was applying a higher standard of proof than the probabilistic standard that the common law recognises, and on that account I considered that I could properly embrace Dr Rudd's thesis into its furthest reaches. Upon further reflection, and mindful that no other court has been so bold as to infer material contribution to the damage in a lung cancer or similar case where there has been no doubling of the risk, I have concluded that even if Dr Moore-Gillon did err in that respect, he was right to baulk at drawing such an inference. Although the causation of lung cancer is dose-related, it does not follow from the proposition that because 2.5% of the dose may be attributed to the Fourth Defendant, that Defendant has materially contributed to the carcinoma. Asbestos burden cannot be equated with the silica dust which causes pneumoconiosis. The greater the accumulation of such dust in the lungs; the greater the damage that is being caused to the lung tissue of an individual patient with that disease. The dust is directly contributing to the disease process. The greater the exposure to asbestos fibres, on the other hand, the greater the risk that lung cancer may result. Although I would agree that 2.5% represents millions of asbestos fibres with the potential to cause a fatal disease process, whether these fibres actually did so remains an open question. Recourse to epidemiology or statistics does not resolve that agnosticism, nor does recourse to the microbiology. Indeed, an accurate application of the epidemiological and statistical data leads to the conclusion that, in relation to the causative potency of the Fourth Defendant's involvement, it cannot be said on the balance of probabilities that this exposure contributed to the deceased's lung cancer. It increased the risk of that cancer occurring, but the quantum of that increase was by avery
considerable margin below 51%."
"it is simply a question of doing the basic arithmetic and reaching the conclusion that the contributions of each of the defendants, whetherviewed
individually or collectively, amount to less than 51%. The relative risk is less than 2 and/or the chances are less than 51%".
Heneghan's
overall exposure in the case of W Blackwell should be regarded as sufficient to prove "this hypothetical claim on the balance of probabilities". This was a matter of "basic arithmetic". This observation was obiter: it was formed no part of the judge's essential reasoning. Both parties criticise this paragraph of the judgment (for different reasons). It is not necessary to decide whether these criticisms are well-founded.
"In my judgment, it makes no sense in this sort of case to say that each Defendant's exposures materially contributed to the disease process, invoking the second limb of Lord Reid's formulation in Bonnington Castings. Adopting Lord Reid's approach in McGhee, the evidence does not establish that every asbestos fibre, or exposure, was or must have been implicated in the disease process. The aetiology of lung cancer is different from silicosis or pneumoconiosis. In those cases, which depend on the gradual accumulation of lung dust, the disease process is continuous and the concept of material contribution has an intelligible role. In lung cancer cases, there is no analogue to the gradual accumulation in the lungs of asbestos or cigarette smoke. The risk of the disease eventuating is proportionate to the quantum of exposure, but that is a statistical judgment, not an assessment which may be linked to the physical presence of deposits of dust in the lung."
The appellant's case
v)
the fibres from each source were likely to have played a part in the carcinogenic process; and (
vi)
each defendant, therefore, materially contributed to the contraction of the disease.
Discussion
vi).
v
Wardlaw [1956] AC 613. The disease in that case was pneumoconiosis which is a divisible disease (i.e. one whose severity increases with increased exposure to the agency). Thirdly, where causation cannot be proved in either of these ways, for example because the disease is indivisible, causation may be established if it is proved that the defendant materially increased the risk of the
victim
contracting the disease: the Fairchild exception. Mesothelioma is an indivisible disease.
Heneghan
would contract lung cancer. It is that the exposure attributable to each defendant contributed to the disease itself. In short, he says that this is a Bonnington Castings case. In Bonnington Castings, a steel dresser was exposed in his employment to silica dust emanating from the pneumatic hammer at which he worked and also from swing grinders. The defendant employer was not liable for the dust emanating from the hammer, because no dust extraction plant was known or practicable. But the employer was liable for the dust which emanated from the swing grinders. Lord Reid said at page 621:
"The medical evidence was that pneumoconiosis is caused by a gradual accumulation in the lungs of minute particles of silica inhaled over a period of years. That means, I think, that the disease is caused by the whole of the noxious material inhaled and, if that material comes from two sources, it cannot be wholly attributed to material from one source or the other. I am
in agreement with much of the Lord President's opinion in this case, but I cannot agree that the question is: which was the most probable source of the respondent's disease, the dust from the pneumatic hammers or the dust from the swing grinders? It appears to me that the source of his disease was the dust from both sources, and the real question is whether the dust from the
swing grinders materially contributed to the disease." (emphasis added)
"It is proved not only that the swing grinders may well have contributed but that they did in fact contribute a quota of silica dust which was not negligible to the pursuer's lungs and therefore did help to produce the disease."
"Estimates of the relative risk for asbestos-associated lung cancer are based on different-sized populations. Because of the high incidence of lung cancer in the general population, it is not possible to prove in precise deterministic terms that asbestos is the causative factor for an individual patient, even when asbestosis is present. However, attribution of causation requires reasonable medical certainty on a probability basis that the agent (asbestos) has caused or contributed materially to the disease. The likelihood that asbestos exposure has made a substantial contribution increases when the exposure increases. Cumulative exposure, on a probability basis, should thus be considered the main criterion for the attribution of a substantial contribution by asbestos to lung cancer risk. For example, relative risk is roughly doubled for cohorts exposed to asbestos fibers at a cumulative exposure of 25 fiber-years or with an equivalent occupational history, at which level asbestosis may or may not be present or detectable. Heavy exposure, in the absence of radiologically diagnosed asbestosis, is sufficient to increase the risk of lung cancer. Cumulative exposures below 25 fiber-years are also associated with an increased risk of lung cancer, but to a lesser extent."
via
blood or lymphatic systems so that "seeding" takes place elsewhere and new foci of cancer can develop. He explains that for a cell to begin to behave with these characteristics, it is necessary for it to have acquired a series of mutations. The number is not known with certainty and probably
varies
from cancer to cancer. Even when a cell in a bronchus does acquire the necessary set of mutations, this does not mean that a clinically significant cancer is inevitable. This is because of the defences afforded by the body's immune system.
very
clearly during his re-examination:
"Where we have a process which is essentially random, a series of accidents, a stochastic process, it is never going to be appropriate to have a deterministic model of causation. You are never going to say this employer contributed to this fibre which had that effect on that cell."
view,
the judge was right to find support for his conclusion in the decision of the High Court of Australia in Amaca Pty Ltd
v
Ellis [2010] HCA 5. The deceased died from lung cancer. During his working life, he had been exposed to respirable asbestos fibres with two employers. He also smoked cigarettes. It is pertinent to note that the Fairchild exception has not been recognised by Australian law. The case proceeded on the basis that no medical evidence could say why the deceased had developed lung cancer. The central question was whether it had nevertheless been proved that it was more probable than not that the exposure to asbestos attributable to either defendant had been a cause of the lung cancer. The plaintiff relied on epidemiological evidence as the basis for an inference that the lung cancer had been caused by the fibres attributable to both defendants. All the witnesses agreed that the risk of contracting cancer from smoking was many times greater than the risk from inhalation of asbestos.
"This description of the issue of causation in Bonnington Castings shows how different it is from the issue of causation in this case. The issue in Bonnington Castings was whether one source of an injurious substance contributed to a gradual accumulation of dust that resulted in disease. The issue here is whether one substance that can cause injury did cause injury. Or, to adopt and adapt what Starke J said in Adelaide Stevedoring Co Ltdv
Forst, was Mr Cotton's cancer "intimately connected with and contributed to" by his exposure to asbestos? Questions of material contribution arise only if a connection between Mr Cotton's inhaling asbestos and his developing cancer was established. Knowing that inhaling asbestos can cause cancer does not entail that in this case it probably did. For the reasons given earlier, that inference was not to be drawn in this case. Questions of what is a material contribution do not arise. "
v
Secretary of State for Energy and Climate Change [2012] EWHC 2936 (QB). This case is referred to as Phurnacite because it concerned eight claimants who had all worked at the Abercwmboi Phurnacite Works in South Wales which produced a smokeless fuel with the trade name "Phurnacite". They claimed damages for a range of conditions including lung cancer and bladder cancer. They alleged that their conditions had been caused by their exposure to two carcinogens which are present in coal tar pitch. The three lead claimants with claims for lung cancer were exposed to carcinogens both from their occupational exposure at the Phurnacite Plant and as a result of their smoking. In addition, each of them would have been subject to other factors such as environmental exposure to carcinogens. The judge said (para 8.50) that all these factors were likely to have played some part in the carcinogenic processes going on in the claimants' bodies, processes which were, by their nature, random.
victim
develops lung cancer after exposure to two sources of asbestos, both exposures will on the balance of probabilities have contributed materially to the carcinogenic process which resulted in the development of the cancer. Every exposure to a carcinogen will play a part in the carcinogenic process going on in an individual's body. Dr Rudd accepted that, in any individual case, it was not possible to say what had "caused" the ultimate step that had resulted in the formation of the malignant cell leading to the cancer. At para 8.21, the judge recorded that Dr Rudd had said that, if he had been asked the same questions now as he had been asked during the Fairchild case, he would have said that it was probable that the asbestos fibres from each source had contributed to the carcinogenic process. This would mean that there was no need for the Fairchild exception at all: in a claim arising from mesothelioma, the claimant should succeed 100% on the basis of the material contribution to damage principle.
view
as Dr Moore-Gillon in the present case: he accepted that both exposures would have contributed to the risk of a lung cancer developing. But he did not consider that it was possible to determine whether one, both or neither of the exposures had actually been involved in the causal sequence of the formation of an individual cancer.
very
different situation from Bonnington Castings, where the additional dust exposure caused by the defendant's breach of duty did have a cumulative effect by adding to the total dust exposure. It was also different from Bailey
v
Ministry of Defence [2009] 1 WLR 1052 where there was clear medical evidence that the defendant's negligence had added to the claimant's weakness which had in turn resulted in her cardiac arrest and consequent brain damage.
view,
he is right not to do so. I find Swift J's analysis compelling and I agree with the reasons she gave for holding that the Bonnington Castings principle could not be invoked. For present purposes, what matters is that it is based on her acceptance of agreed medical evidence as to the aetiology of lung cancer which was not materially different from the agreed medical evidence in the present case. Mr Allan seeks to distinguish Phurnacite. As I understand it, he relies on the fact that in Phurnacite it was not established whether the carcinogens resulted from smoking, occupational exposure or both. On the other hand, in the present case it has been established that the carcinogens were caused by exposure to asbestos fibres. But that does not affect the
validity
of Swift J's reasoning for not applying the Bonnington Castings test for the purposes of the present case. In my
view,
the judge was right to adopt the reasoning in Phurnacite. In short, Bonnington Castings cannot be pressed into service to bridge the gap left by the evidence.
v
National Coal Board. A workman contracted dermatitis. The issue was whether this was attributable to (i) his work in the dusty brick kilns where he worked without adequate washing facilities (for which his employer was responsible) or (ii) the effect of his cycling home caked with sweat and dust (for which his employer was not responsible). The pursuer relied on Bonnington Castings and argued that the first source of noxious dust (lack of adequate washing facilities) had made a material contribution to his injury. At p 4F, Lord Reid said:
"In the present case the evidence does not show – perhaps no one knows – just how dermatitis of this type begins. It suggests to me that there are two possible ways. It may be that an accumulation of minor abrasions of the horny layer of the skin is a necessary precondition for the onset of the
disease. Or it may be that the disease starts at one particular abrasion and
then spreads, so that multiplication of abrasions merely increases the
number of places where the disease can start and in that way increases the
risk of its occurrence.
I am inclined to think that the evidence points to the formerview.
But
in a field where so little appears to be known with certainty I could not say that that is proved. If it were then this case would be indistinguishable
from Wardlaw's case. But I think that in cases like this we must take a
broaderview
of causation. 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. Plainly
that must be because what happens while the man remains unwashed can
have a causative effect, though just how the cause operates is uncertain.
I cannot accept theview
expressed in the Inner House that once the man
left the brick kiln he left behind the causes which made him liable to
develop dermatitis. That seems to me quite inconsistent with a proper
interpretation of the medical evidence. Nor can I accept the distinction
drawn by the Lord Ordinary between materially increasing the risk that the disease will occur and making a material contribution to its occurrence.
There may be some logical ground for such a distinction where our
knowledge of all the material factors is complete. But it has often been
said that the legal concept of causation is not based on logic or philosophy. It is based on the practical way in which the ordinary man's mind works in the everyday affairs of life. From a broad and practicalviewpoint
I can 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.
I would therefore allow this appeal."
view
of causation". This broader
view
of causation was adopted as a matter of policy in order to arrive at a just solution. Mr Allan's invocation of the Bonnington Castings test ignores the fact that there is a fundamental difference between making a material contribution to an injury and materially increasing the risk of an injury. If the two were the same, Fairchild would not have been seen to be the ground-breaking decision that it was, and the decision in Barker would have been difficult to understand. Fairchild could hardly have been described by Lord Hoffmann at para 1 in Barker as "an exceptional and less demanding test for the necessary causal link between the defendant's conduct and the damage" than requiring proof that the defendant did cause the damage in fact. Moreover, it is clear that the House of Lords in Fairchild did not proceed on the basis of the fiction that a defendant who had created a material risk of mesothelioma was deemed to have caused or materially contributed to the contraction of the disease itself: see per Lord Hoffmann at paras 31 to 33 in Barker. As Lord Hoffmann said at para 34, if the basis of liability is the wrongful creation of a risk or chance of causing damage, "the damage which the defendant should be regarded as having caused is the creation of such risk or chance". It seems to me that these statements are fatal to Mr Allan's submission that the creation of a material risk of injury is to be equiparated with making a material contribution to the injury. At para 40, Lord Hoffmann said that the Fairchild exception was created because the alternative of leaving the claimant with no remedy was thought to be unfair. If Mr Allan is right, it is difficult to see why the claimant in Fairchild did not succeed on the Bonnington Castings test.
view
of causation in this case. He says that such a
view
requires the application of the Bonnington Castings test. I do not agree. That test is to be applied where the court is satisfied on scientific evidence that the exposure for which the defendant is responsible has in fact contributed to the injury. This is readily demonstrated in the case of divisible injuries (such as silicosis and pneumoconiosis) whose severity is proportionate to the amount of exposure to the causative agent.
view
in the Supreme Court decision in International Energy Group Ltd
v
Zurich Insurance Plc UK [2015] UKSC 33, [2015] 2 WLR 1471. Thus, Lords Neuberger and Reed said at para 191 that the Fairchild exception is "applicable to any disease which has the unusual features of mesothelioma". The possibility of its application in cases concerning other injuries or diseases was also expressly contemplated by Lord Hodge (para 109) and Lord Sumption (para 127).
Conclusion
Heneghan's contracting of lung cancer. All of the defendants did, however, materially contribute to the risk that he would contract lung cancer. The judge was, therefore, right to apply the Fairchild exception.
Lord Justice Tomlinson:
Lord Justice Sales: