Indivisible Injury and the Material Contribution Test

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1. In Michael Holmes v Poeton Holdings Ltd [2023] EWCA Civ 1377 the Court of Appeal, in something of a tour d’horizon of the relevant authorities, revisited the “material contribution” test in the context of an indivisible disease or injury – that is an injury or a disease that, once contracted, its severity will not be influenced by the total amount of agent that caused it.  In contrast, the severity of a divisible disease or injury is affected by the total amount of agent that has caused it.  In reversing the first instance decision, the Court of Appeal held that the material contribution test did apply to cases of indivisible injury or disease and found that it could not be proved that the defendant’s breach of duty had materially contributed to the claimant developing Parkinson’s disease.  The lead judgment was given by Stuart-Smith LJ.


2. Mr Holmes (“MH”) worked for the appellant, Poeton Holdings (“PH”), for nearly 40 years before ill health forced him to retire in 2020.  In 2014 he had been diagnosed with Parkinson’s disease, an indivisible disease.  MH pursued PH for damages because he claimed it acted in breach of its common law and statutory duty in the period from 1982 to 1997 by exposing him to unsafe levels of Trichloroethylene [“TCE”] in the course of his employment.  His Honour Judge Harrison, sitting in the County Court at Cardiff, found that both breach of duty and causation had been established.  Accordingly, PH was liable for all the consequences of MH contracting Parkinson’s disease (referred to in the judgment as a claim for 100% damages).

3. PH mounted an appeal on the issue of causation.  Broadly, it was submitted that the Judge had adopted the wrong legal test for establishing causation in an indivisible case and that the Judge failed to consider whether MH would have developed Parkinson’s disease in any event, so that the exposure to TCE made no difference.  Further, that the evidence available to the Judge showed no more than that TCE may have caused an elevation of the risk of contracting Parkinson’s disease; that it did not demonstrate that exposure to TCE was capable of causing Parkinson’s disease or that MH’s exposure had caused his contraction of the disease.

4. TCE, a carcinogen was heavily used by PH, consuming 7-8 tonnes per year.  It was known to be particularly harmful, even before it was known to be a carcinogen.  Indeed, as early as 1973, the Factories Inspectorate issued guidance for its usage.  By 1976, and again in 1984, the Health & Safety Executive issued daily exposure limits, which persist to this day.  The Judge accepted that exposure to TCE can act upon the dopaminergic neurons – damage to the same being an accepted cause of Parkinson’s disease, albeit the precise aetiology and pathogenesis of the condition is only partially understood and remains the subject of ongoing research.  The Judge at first instance had accepted MH’s evidence as to the levels of his exposure during his time as a general worker and as a foreman.  It was not asserted by MH that he had been exposed to unsafe levels of TCH after his promotion to management after 1997.

“Material contribution” and the “but for”test of causation

Divisible and indivisible cases

5. Divisible diseases, once initiated, have the characteristic that their severity will be influenced by the total amount of the agent that has caused the disease.  Whereas once an indivisible disease is contracted, its severity will not be influenced by the total amount of agent that caused it.  The classic distinction in asbestos-related diseases is between asbestosis and mesothelioma. Mesothelioma is an indivisible disease because, although the risk of developing a mesothelioma increases in proportion to the quantity of asbestos dust and fibres inhaled, the condition once caused is not aggravated by further exposure and the severity of the condition, if it occurs, is not thought to be affected by variations in the victim’s overall exposure. Asbestosis is a divisible disease because all of the victim’s exposure to asbestos will contribute to the severity of his eventual disease.  Holtby v Brigham & Cowan [2000] 3 All ER 421 established that, in a case of a divisible disease such as asbestosis, the burden rests upon the Claimant to prove that the defendant who has been sued was responsible for the whole or a quantifiable part of his disability.

6. The case of Wilsher v Essex AHA [1988] A.C. 1074 was described by Stuart-Smith LJ as being of fundamental importance.  In that case, the claimant was a premature baby who, due to the defendant’s negligence, was given an excessive amount of oxygen – this was a well-known cause of retrolental fibroplasia (“RLF”).  Whilst it was held that the excessive oxygen could have caused the RLF, and the Judge held that it increased the risk of the same, there were four other possible causes of the RLF, which meant that the defendant’s negligence was only of a number of possible causes of the RLF.  In the House of Lords it was emphasised that ‘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, e.g. 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 was wholly different from McGhee v National Coal Board [1973] 1 W.L.R. 1 where there was only one candidate that could have caused the insult (brick dust).  Whereas in Wilsher, a failure to take preventative measures against one out of five possible causes was held to not be evidence as to which of those five caused the injury.  The House of Lords thereby rejected any suggestion that there could be a reversal of the burden of proof, or any modified approach to causation, despite the fact that the Judge’s findings on the defendant’s negligence was not disturbed: ‘there was nothing to show that the risk which the defendant’s staff had created – that the plaintiff would develop [RLF] because of an unduly high level of oxygen – had eventuated.’

“Material contribution” since Bonnington

7. In Bonnington Castings Ltd v Wardlaw [1956] AC 613 two separate causes were identified, both of which could have caused the claimant to contract pneumoconiosis (a divisible disease).  For one (silica dust from pneumatic hammers) there was no breach of duty.  For the other (silica dust from swing grinders) there was.  The issue was whether the tortious breach had caused the disease.  If so, the defendant would be liable, and vice versa.  It was not sufficient for a claimant merely to show that there had been a breach of duty.  Rather, the employee had to ‘…in all cases prove his case by the ordinary standard of proof in civil actions: he must make it appear at least that on a balance of probabilities the breach of duty caused or materially contributed to his injury.’  Lord Reid went on to hold that it was established that the dust from the swing grinders had made a “substantial contribution”.

8. Although pneumoconiosis is a divisible disease, the Bonnington principle was expressed in terms that were appropriate to indivisible diseases, rather than to divisible ones.[1]  Therefore PH, in its appeal, could draw no comfort from the fact that Bonnington was a case on a divisible disease.  Bonnington itself provided little guidance on what is sufficient to constitute a “material contribution”.  Lord Reid said that it is a question of degree and that a contribution which comes within the exception de minimis non curat lex is not material.  Otherwise, it is material; and the tortious contribution from the swing grinders was “not negligible” and therefore sufficed.  The claimant received 100% of his damages in Bonnington.

9. The details and arguments in Nicholas v Atlas Steel Foundry and Engineering Co Ltd [1957] 1 WLR 613 closely followed those in Bonnington.  Viscount Simonds (who had been a party to the decision in Bonnington) held that the question was ‘…whether in addition to these particles he was, owing to the fault of the respondents, bound to inhale a number of other particles which made a material contribution to his illness. In determining whether a material contribution was made, I must apply the test recently laid down in this House in Bonnington Castings Ltd. v. Wardlaw and say that a contribution is material unless the maxim “de minimis” can be applied to it.’  The defendant was held to be liable.  However, Stuart-Smith LJ felt that the judgment in Nicholas was as ambiguous about the nature of pneumoconiosis as it was in Bonnington, and he did not consider that the fact that the disease in Nicholson was pneumoconiosis led to the conclusion that the statement of principle articulated in Bonnington, and applied in Nicholson, is directed (let alone solely directed) to cases of divisible injury or disease.  McGhee, he said, provided substantial support that the Bonnington principle applies to cases of indivisible disease or injury.  ‘To my mind it seems clear that the Bonnington principle of “material contribution” should apply to indivisible diseases; divisible diseases are approached differently.’

10. In Bailey v MOD [2009] 1 WLR 1052 (CA) the defendant submitted that unless the claimant could establish that, but for the defendant’s negligence, the claimant’s injury would not have happened, she could not succeed. That proposition was rejected.  Rather, it was held that ‘In a case where medical science cannot establish the probability that “but for” an act of negligence the injury would not have happened but can establish that the contribution of the negligent cause was more than negligible, the “but for” test is modified, and the claimant will succeed.’  Stuart-Smith LJ noted the sustained criticism that the reasoning in Bailey has been subject to.  However, he held that ‘we are bound in the light of Bailey to find that the Bonnington “material contribution” principle applies to cases of indivisible injury and that, where the principle applies, the claimant does not have to show that the injury would not have happened but for the tortious exposure for which the defendant is responsible.’

11. After a review of all the relevant authorities (most of which have been referred to above) PH’s submission that the Bonnington principle was only applicable to cases of divisible injury was rejected.

Levels of Exposure

12. It was observed that HHJ Harrison did not make specific findings about the duration of the exposure or the levels of the exposure. And that the likelihood of the TCS exposure having contributed to a mechanism involving the destruction of dopaminergic neurons must be affected by both the frequency and the levels of exposure.  It was also observed that the Judge did not seek to identify the extent to which any exposure was not tortious (the exposure which fell within safe limits) and what the incremental quantity and effect of the tortious exposures may have been.  Despite the Judge’s very generalised findings, the Court of Appeal did not feel that there was any justification to reverse his conclusion that MH was regularly exposed to levels of exposure significantly in excess of the short-term limit value and for a significant number of days a year in excess of the long-term value.  This was because ‘the extreme generality of the conclusion provides little or no real insight into the extent to which Mr Holmes was tortiously exposed to TCE. This is not necessarily a criticism of the judge, because, at least to some extent, this lack of specificity may have been because of deficiencies and lack of precision in the evidence, but it is a significant feature when one comes to consider issues of causation.’

Generic Causation

13. It was highlighted that proof of causation for the purposes of legal liability is different from “scientific proof”, as causation has to be decided on the basis of current knowledge.  It was common ground that the causation of Parkinson’s disease is poorly understood.  The question was whether exposure to TCE can cause (or materially contribute to the causing of) Parkinson’s disease.  The mechanism of interest being the destruction of the patient’s dopaminergic neurons.

14. The Judge had been correct to observe that multifactorial factors might involve multiple genetic factors only, and that MH would have been exposed to many environmental factors.  There was no doubt that TCE is neurotoxic. There was also no doubt that it operates in different ways and with different results.  The expert evidence set out all of the possible effects of exposure to TCE, of which there were many, and which were very unpleasant.  However, the list of effects did not provide a justification for assuming that, because TCE is neuro-toxic, it is capable of affecting the dopaminergic neurons at the dose levels to which MH was exposed.

15. The evidence upon which the Judge relied, to support the hypothesis that exposure to TCE could cause (or materially contribute to the causing of) Parkinson’s disease, was found to be weak.  The joint statement of the epidemiological experts provided that ‘In our view, the epidemiological evidence for……and for TCE and [Parkinson’s disease] all [fall] far short of that required to deduce causal associations.’

16. A central part of the Judge’s reasoning was that TCE is neurotoxic and had been shown to damage dopaminergic cells in animals, whilst citing two papers on the matter, which he accepted had to be approached with care.  The Court of Appeal held that, in the light of these studies the Judge had been entitled to conclude that a plausible neurological pathway had been established; and Professor Schapira [PH’s neurological expert] was correct to concede that a causative link between TCE and PD could not be disproved so that, in that sense, it was possible that TCE was a cause of the condition. But the evidence had significant limitations: ‘In my judgment, the propositions and evidence on which he relied did no more than to establish that TCE was a risk factor for Parkinson’s disease and that there is a plausible mechanism based on the rodent studies for a finding that TCE may cause or materially contribute to the development of Parkinson’s disease. Although TCE has long been identified as a compound of interest, the evidence to prove generic causation is lacking whether one is applying the legal or a scientific standard of proof. To my mind the critical gap, given the absence of epidemiological evidence supporting a causative link, is the present inability to extrapolate from the rodent studies to the impact of TCE exposure in humans, not least because of the great disparity in relative exposure levels.’

17. For these reasons, it was held that the evidence before the Judge did not justify a finding of generic causation (i.e. that exposure to TCE was capable of causing Parkinson’s disease).

Individual Causation

18. If correct about generic causation, it followed that individual causation (i.e. that exposure to TCE had caused MH to develop Parkinson’s disease) could not be proved.  MH could not ‘prove that the tortious exposure to TCE caused or materially contributed to his developing Parkinson’s disease unless, possibly, there were features of his case that are not reflected in the generic evidence that compel a finding of causation, such as a relevant and repeated response to challenge and rechallenge by exposure to TCE.  Such features are absent in this case.’

19. Other difficulties facing MH included the fact that he would have been exposed to many environmental factors.  Nothing was known about any of the other environmental factors in his case and whether, or to what extent, such other environmental factors increased the risk of his developing Parkinson’s disease.  Further, it has to be proved that it was the tortious exposure, rather than the innocent exposure, that played a relevant causative role: ‘Proof of tortious exposure does not prove that the tortious exposure has caused or materially contributed to damage.’[2]  Additionally, despite it being accepted that our knowledge of genetic factors affecting the development of Parkinson’s disease is incomplete, several genetic risk factors had been identified, but MH had not been tested.

20. Commenting once again on the extreme generality of the Judge’s findings, it was pointed out that ‘no evidence was identified by the judge (and no evidence has been drawn to our attention) to substantiate a causative link between the tortious exposure and damage to Mr Holmes’ dopaminergic neurons.  The difficulty this creates comes into sharp focus when one returns to the question: have Poeton’s breaches of duty caused or materially contributed to the development of Mr Holmes’ disease?’  MH’s neurological expert opined that damaged dopaminergic cells could set in train a cascade of degeneration of nerve cells resulting when a critical point is reached (70%) in the development of the condition.  Using that number as a simplified guide, Stuart-Smith LJ ruled that it was simply not possible to say whether the tortious exposure to TCE had damaged or destroyed 35% of MH’s dopaminergic cells, whether it had damaged or destroyed 1%, whether it had damaged or destroyed 0%, or some number in between.  There was an ‘absence of sufficient evidence that Poeton’s tortious exposure of Mr Holmes to TCE has caused or materially contributed to his infinitely regrettable disease.’

21. The Judge had therefore reached the wrong conclusion in this case.  The appeal was allowed on the basis that, although it had been established that exposure to TCE is a risk factor for the development of Parkinson’s disease, the Judge’s finding that tortious exposure to TCE caused or materially contributed to MH’s disease was not sustainable on the evidence and he was wrong.

[1] See Bonnington at 621-626

[2] See Wilsher

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