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England and Wales Court of Appeal (Civil Division) Decisions |
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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: http://www.bailii.org/ew/cases/EWCA/Civ/2016/86.html Cite as: [2016] ICR 671, [2016] 1 WLR 2036, [2016] EWCA Civ 86, [2016] WLR(D) 87 |
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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 LIMITED 00722056 LIMITED CARILLION CONSTRUCTION (CONTRACTS) LIMITED R. BLACKETT CHARLTON LIMITED S.C. CHEADLE HULME LIMITED KELLOGG BROWN & ROOT LIMITED |
Respondents |
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David Platt QC and Peter Houghton (instructed by BLM LLP) for the Respondents
Hearing dates : 18 & 19/01/2016
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Crown Copyright ©
Master of the Rolls:
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
The Fairchild exception
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 a very 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, whether viewed individually or collectively, amount to less than 51%. The relative risk is less than 2 and/or the chances are less than 51%".
"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
Discussion
"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."
"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."
"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 Ltd v 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. "
"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 former view. 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
broader view 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 the view 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 practical viewpoint 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."
Conclusion
Lord Justice Tomlinson:
Lord Justice Sales: