Causation in personal injury after (and before) Sienkiewiczlest_

Transcription

1 Legal Studies, Vol. 32 No. 3, September 2012, pp DOI: /j X x Causation in personal injury after (and before) Sienkiewiczlest_ Chris Miller* Leverhulme Emeritus Research Fellow Three forms of material contribution are discussed within the context of the traditional but for test of causation. The NESS test (Necessary Element in at least one Sufficient Set) is shown to offer a more appropriate approach when causal over-determination is present as in, for instance, Fairchild and other cases involving multiple sources of asbestos. The particular problems posed by the recent Sienkiewicz case are then examined. It is argued that removing the incoherence in the common law of causation in personal injury will require the judiciary to overcome its antipathy to statistical evidence. INTRODUCTION The aim of this paper is to review the current status of the English (and Scots) law of causation in the light of the recent ruling of the Supreme Court in Sienkiewicz v Greif (UK). 1 This was the Supreme Court s first foray into the labyrinth that causation has now become. However, it must be recalled that most of the seven members could claim some involvement, whether in the House of Lords or the Court of Appeal, in two earlier key precedents, viz Fairchild v Glenhaven Funeral Services Ltd 2 and subsequently Barker v Corus (UK) plc. 3 (The now sadly late) Lord Rodger was the only judge who participated in the final determination of all three cases, so he was perhaps most familiar with the quixotic 4 path which has led to the current position. When discussing the state of the law of causation before Sienkiewicz, the current author has had the benefit of reading Professor Bailey s review 5 in this journal. The first half of the current paper serves as a response to Bailey; and it agrees with him that the English law on causation in negligence is beset with incoherence although the current author takes issue with Bailey over its source. The second part of this paper seeks to show that, while the ruling in Sienkiewicz revealed the scale of the incoherence, it offered little indication as to how it might be * c.e.miller@salford.ac.uk. The author is grateful to two referees for helpful criticisms of an earlier draft. The author acknowledges his debt to the Leverhulme Trust for the funding which has enabled him to continue his research. He is particularly grateful to Ken Oliphant and Colm McGrath for many convivial discussions about causation during his visit to the Institute for European Tort Law in Vienna in October [2011] UKSC Fairchild v Glenhaven Funeral Services Ltd; Fox v Spousal (Midlands) Ltd; Matthews v Associated Portland Cement Manufacturers (1978) Ltd and others [2002] UKHL Barker v Corus (UK) plc (formerly Saint Gobain Pipelines plc); Murray v British Shipbuilders (Hydrodynamics) Ltd; Patterson v Smiths Dock Ltd and others [2006] UKHL Lord Brown, above n 1, para SH Bailey Causation in negligence: what is a material contribution? (2010) 30 LS Published by Blackwell Publishing, 9600 Garsington Road, Oxford OX4 2DQ, UK and 350 Main Street, Malden, MA 02148, USA

2 Causation in personal injury after (and before) Sienkiewicz 397 removed. The Supreme Court unanimously affirmed the ruling of Lady Justice Smith 6 in the Court of Appeal and dismissed Greif (UK) s (and a conjoined) 7 appeal but, since all seven justices believed that they were tightly constrained by the House of Lords ruling in Barker, their comments were mostly obiter. However, these comments ventured into an area the forensic role of epidemiological (or other forms of statistical) evidence which has given rise to deep disagreements between academic analysts. When a suspicion of the role of statistical evidence 8 leads to a denial of its admissibility in court, this creates a formidable obstacle to claimants who can offer only the findings of epidemiological studies when maintaining that their health has been harmed by, for example, a defective drug. For that reason, Lord Rodger s call for a less dogmatic approach demands attention. Such an approach, and a more open and realistic awareness of the full implications of granting liability for negligent increases in risk, might hold the key to lessening the incoherence. 1. THREE TYPES OF MATERIAL CONTRIBUTION In his review of causation in the English common law of negligence Professor Bailey asks: [w]hat is a material contribution? And he concludes that [i]t would make the law more coherent if the term material contribution were confined to situations that satisfy the but for test in the normal way. 9 A subsidiary aim of this paper is to show that, quite contrary to Bailey, resort to material contribution (or to some cognate phrase) has been necessitated, at least from 1956, by situations in which the but for test fails to identify the negligent act or omission which can be said to be the cause of foreseeable and materialised harm. To understand why the but for test sometimes fails, we need to engage with the problem of causal over-determination, the legal significance of which was first examined by Honoré and Hart 10 and subsequently by R Wright, 11 whose NESS test will be discussed below. And while it is agreed with Bailey that this area of law lacks coherence, this paper will argue that the incoherence does not reside in any mis-application of the but for test but rather in the consequences of recent attempts to restrict the scope of liability for negligent acts (or omissions) which materially increase the risk of an injury which subsequently eventuates. 12 (a) Type 1: simple acts or omissions, necessary for the eventuation of an injury Shakespeare leaves us in no doubt that it was Macbeth who murdered Duncan. It is equally clear that Lady Macbeth was an accessory: not only did she incite her husband 6. [2009] EWCA Civ Willmore v Knowsley Metropolitan Borough Council [2011] UKSC This suspicion usually pleads in aid that most hoary of old chestnuts, the paradox of the Blue Bus Company and Sienkiewicz was no exception, see text, below n Above n 5, at HLA Hart and A Honoré Causation in the Law (Oxford: Clarendon, 1985). 11. RW Wright Causation in tort law (1985) 73 CLR For an introduction to the NESS test, which takes issue with some of its critics as well as, occasionally, Wright himself, see C Miller NESS for beginners in R Goldberg (ed) Perspectives on Causation (Oxford: Hart Publishing, 2011). 12. This paper makes no reference to liability for pure risk, that is, near misses which, by good fortune, do not result in injury. Although advocated by some academics, this proposal represents a digression in an area which is already difficult enough.

3 398 Legal Studies, Vol. 32 No. 3 to do the wicked deed, she also ensured that the victim and his attendants had drunk enough wine to prevent them waking. If but for Macbeth s action Duncan would not have died (that night in Inverness Castle) then the same must be said of the actions of Lady Macbeth. Those of a philosophical bent might describe her intervention as a necessary element in a set of events and conditions which was sufficient to bring about Duncan s death. Alternatively we might describe her role as a material contribution to the crime. But this phrase fails to convey the sense in which her actions made possible (alternatively, were necessary pre-conditions for) the act which we more readily think of as the cause, namely, Macbeth thrusting a dagger into Duncan s heart. Shakespeare gives us other, equally relevant examples of what we shall label Type 1 contributions in Julius Caesar. Imagine that Caesar needs to lose eight units of blood before he dies and that each of the eight conspirators inflicts a wound which results in the loss of just one unit. So, in this instance, we can say, for each of the eight, but for his action, Caesar would not have died. Alternatively, the action of each conspirator is a necessary element in the causal sequence which proved sufficient for Caesar s death. (b) Type 2: multiple sufficient sets If, in the above account of Caesar s demise, we choose to say that each conspirator materially contributed to the death, we would not be using the phrase in the sense that it was used in Bonnington Castings v Wardlaw. 13 Here identical dust emitted from two different sources, one tortious the other not, was routinely inhaled by the pursuer when working in this dusty atmosphere; and his health was impaired. But since it was not possible to claim that but for the tortious dust Wardlaw would not have suffered his respiratory dysfunction the evidence strongly hinted that he would have suffered harm from the non-tortious dust alone he could not succeed by what Professor Bailey labels the normal way. 14 Although the non-tortious source produced the greater proportion of the dust, the tortious source contributed an amount which exceeded de minimis and was therefore a material contributing cause of [Wardlaw s] illness 15 and liability with full damages was imposed on the respondent employer. It is easy to grasp that Bonnington s dust is cumulative or additive in effecting harm as was Caesar s blood loss. So why would but for apply in Julius Caesar but not in Bonnington? Because Caesar s death required eight units of blood to be lost and that required each and every one of the eight conspirators to inflict a wound which shed one unit of blood. The eight-unit threshold meant that each wound was necessary and therefore each conspirator s action could pass the but for test. If however the threshold was only four units, then we might say that four of the conspirators were redundant. But since we can t identify the four who were necessary and the four who were not, it is tempting to say that all eight made a material contribution to the assassination. The problem with Bonnington is that any discussion of a threshold is far from explicit. Lord Keith argued that had it not been for the cumulative effect the pursuer would not have developed pneumoconiosis when he did and might not have 13. [1956] 1 All ER Above n 5, at Per Lord Keith, above n 13, at 627.

4 Causation in personal injury after (and before) Sienkiewicz 399 developed it at all. 16 This suggests that he believed it needed the tortious dust to cross some threshold and thus cause (or, at least, advance the onset of) the respiratory disorder. But none of the other members of the House spoke in these terms and if the ratio of Bonnington does reside in this passage, then there was no need to use the phrase material contribution because the tortious dust would have been a but for cause in the normal way. In view of the role which the ruling in Bonnington has played over the past 50 years in personal injury law, interpreting it now as a Type 1 contribution in disguise is not helpful even if that was the way it was seen by the House in But for is a test of necessity not sufficiency; it cannot be applied where there is more than one plausible causal pathway each of which is alone sufficient to give rise to the injury. In other words, but for breaks down in the face of causal overdetermination and Bonnington can be interpreted as a simple example. 17 The NESS approach can address this problem because it recognises that there may be more than one set of necessary elements which are sufficient to give rise to a harmful effect. The classic example is that of the house burnt down when lightning strikes one corner while an arsonist sets light to another here we have two independent causes, either of which can bring about the destruction of the house but neither can pass the but for test. It is not difficult to invent an example with a larger number of different sufficient sets. Again suppose that Caesar s death would result if only four units of blood were to be lost. Brutus may not be a member of the set of four comprising, for example, Metellus, Cinna, Trebonius and Casca but he is a member of (and a necessary element in) 35 of the 70 different combinations (sufficient sets); and the same can be said of each conspirator. 18 Regardless of the intentions of the House when determining Bonnington, the key to the judgment is that it covers various combinations of dust concentrations; it is not dependent on a knowledge of the magnitude, or even the existence, of a threshold in the relationship which links dust concentration with respiratory dysfunction. The lasting effect of the judgment is that this type of uncertainty in the scientific evidence does not pose an insuperable barrier to recovery for otherwise deserving claimants. Lawyers sometimes refer to the type of injury suffered by Wardlaw as divisible but this paper will instead use the term cumulative because it better describes the way in which the various agents of harm combine to make their respective contributions. And this cumulative, Bonnington-like contribution to injury will be labelled Type 2. The designation, material contribution Type 1, will be reserved for contributions which, like Macbeth s act and his wife s role in Duncan s murder, are necessary elements in the single set of events and conditions which is sufficient to account for the materialised harm. Any event which makes a Type 1 contribution will pass the but for test in the normal way. 16. Ibid, at Most of the criticism of NESS tends to be focused on its treatment of a more complex form of over-determination, viz pre-emption; see for instance R Fumerton and K Kress Causation and the law: preemption, lawful sufficiency and causal sufficiency (2001) 64 Law & Contemporary Problems 83 and also D Fischer Causation in fact in omission cases [1992] Utah L Rev For a demonstration of the ability of NESS to counter criticisms of its treatment of pre-emption without inventing what R Wright calls causal priority, see C Miller, above n A reviewer of an earlier draft has suggested that a better illustration of Bonnington over-determination would consist of one conspirator severing a major artery while another simply opens a small vein. I gratefully accept that suggestion.

5 400 Legal Studies, Vol. 32 No. 3 (c) Type 3: material increase in a risk which then eventuates in injury To illustrate the third, and perhaps the most important, form of material contribution, we need to revisit Caesar s assassination. But instead of death arising from cumulative blood loss, we must now imagine that just one of the eight dagger thrusts penetrates the heart or a major artery, whereupon death is inevitable if not quite instantaneous. All eight would-be assassins seek to find this fatal spot but only one succeeds and we cannot tell who that was. We believe that seven were guilty of attempted murder since it was only by chance that they did not make the fatal thrust. It is not straining ordinary language to say that all eight materially increased the risk of the fatal injury, which did indeed eventuate. And that is the way that English common law currently describes what we shall label Type 3 contribution. It is one which the House of Lords was obliged to articulate in the multiple asbestos employer appeals in Fairchild 19 and subsequently in Barker, 20 where they were required to refine their approach in some very significant ways. Before we can discuss these, it is necessary to distinguish clearly between Type 2 and Type 3 contributions. In Type 2 each contribution increases the amount of exposure to some harmful agent to the point, possibly, of exceeding a threshold above which a particular pathology occurs. In Type 3, the amount of harm is fixed; what we are concerned with is whether or not that harm actually occurs; each contribution adds to the probability that it will occur and occur it unquestionably does. In both Types 2 and 3, we cannot pick on any one particular contribution and say but for that contribution, the harm would not have arisen. (d) McGhee v National Coal Board Before being upstaged by Fairchild, McGhee v National Coal Board 21 was arguably the most important Type 3 case in British law. But with the hindsight of the enormous attention this case has attracted, McGhee can now be seen as an unlikely candidate for the weighty role it played. Before explaining this point, it is necessary to describe the evidential uncertainty, which was to trigger so much judicial creativity. The pursuer was employed in the defendant s brickworks removing bricks from a kiln. This work exposed him to a certain amount of dust but the breach of duty lay in the defendant s failure to make available showers, which would have enabled him to remove the dust immediately after coming off shift. In the event, James McGhee had to cycle home with the dust still caked to his skin before he could wash. He suffered dermatitis. The key questions on which the rival experts (consultant dermatologists) could not agree were: was the non-tortious (early) exposure alone sufficient to give rise to dermatitis; or did the onset of the condition require in addition the tortious (late) exposure consequent upon the absence of showers in the workplace? In the leading speech in the House of Lords, Lord Reid believed that there were two possible ways by which this form of dermatitis was initiated. One consisted of a an accumulation of minor abrasions of the horny layer of the skin ; 22 and in the other, 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 19. Aboven Aboven [1973] 1 WLR Ibid, at 4.

6 Causation in personal injury after (and before) Sienkiewicz 401 increases the risk of the disease. 23 And although he believed that the evidence pointed towards the former (accumulation) explanation, this was far from proven, and so he turned to the point of agreement between the experts, namely, that the additional (later) exposure incurred in cycling home with the dust still adhering added materially to the risk that this disease might develop. 24 Material contribution Deterministic But for satisfied Defining cases Type 1 Yes Yes Macbeth Type 2 Yes No (unless necessary to exceed threshold) Bonnington Type 3 No No McGhee; Fairchild Had Lord Reid followed his original inclination and accepted the accumulation explanation then, as he noted, the case would have been indistinguishable from [Bonnington]. 25 It is not difficult to show that McGhee and Bonnington can be distinguished and that Bonnington is a special case of the more general McGhee. The effect of Bonnington s dusts is deterministic, that is, increased exposure to dust increases the degree of respiratory dysfunction not the probability of its arising. (Since the occurrence of some dysfunction is taken as certain, its probability = 1; the equivalent probability in McGhee is unknown.) 26 Another of the differences is that, in Bonnington, the exposures were concurrent, while in McGhee, they were consecutive. So, if the etiology were one where dermatitis would result once some threshold in the cumulative exposure was exceeded, McGhee could claim that the negligence was a but for cause of his injury only by arguing that that threshold was not crossed in the earlier (non-tortious) period of exposure. But this was not claimed in court and, in the event, Lord Reid was attracted to the pursuer s risk argument and finally opined that he saw no substantial difference between a material increase in risk and a material contribution to injury. 27 So, despite being unwilling to assume a cumulative mechanism (whereby the tortious and non-tortious exposures combine so as to exceed a threshold beyond which dermatitis arises) Lord Reid invokes the ruling in Bonnington by equating material increase in risk with material contribution. But the word risk is nowhere used in Bonnington and this case therefore seems an unlikely authority for a ruling (in McGhee) which is inherently probabilistic. But that is what Lord Reid s preferred explanation increasing the number of places where the disease may start entails. (Each abrasion is equivalent to a premium bond: 28 the more bonds (abrasions) I collect and the longer I hold them, the 23. Ibid. 24. Ibid. 25. Ibid. 26. If McGhee creates a genus of material contribution, Bonnington turns out to be a rather primitive species. In fact, the occupational deafness case of Thompson v Smiths Shiprepairers (North Shields), below n 42, is a more interesting exemplar because, although deterministic, its bare skeleton closely mirrors McGhee s: a period of non-tortious exposure to an occupational agent (noise in this instance) of injury is followed by exposure to a tortious source of the same agent, which would have been less harmful had control measures not been negligently absent. 27. Above n 21, at Why a premium bond rather than a lottery ticket? Because a premium bond retains its capacity to win a prize from one draw to the next. An asbestos fibre once absorbed into the

7 402 Legal Studies, Vol. 32 No. 3 greater my chance of winning the prize (incurring the injury). The period of tortious exposure extends the time for any abrasion to initiate dermatitis: the longer a cache of premium bonds remains eligible, the more draws they take part in, and the greater the chance that one will eventually be drawn as a prize-winner.) Each of the eight conspirators sought to inflict the wound which, by itself, would result in Caesar s death, but we are unable to identify a but for cause, namely, the one who succeeded. However, we can accept that each one increased the risk that this outcome would eventuate. So what our various Type 3 cases have in common is, once again, over-determination. In the absence of further evidence, a but for cause of the eventuated injury cannot be identified among the rival candidates, each of which is sufficient to cause the injury. And it is the uncertainty created by that absence which encourages the language of risk and each of our candidates can be said to increase the risk which eventuates in injury. In the mesothelioma cases, the asbestos fibre plays a role which, although analogous to the dust abrasion in McGhee, makes the probabilistic character of the causal explanation more easily grasped. The single fibre theory invites us to compare each fibre to a premium bond and thus the more bonds we buy (the more fibres we inhale) the greater our chance of winning (initiating the process which culminates in mesothelioma). And this remains true even if, as is likely, the process requires more than one fibre or if asbestos is implicated at more than one stage in the process by which a cell in the pleura (or peritoneum) becomes malignant. Despite its curious provenance the Fairchild exception, 29 as it is now known, is now part of the English common law of negligence civil liability may attach to negligent acts or omissions which materially increase the risk of an injury. Before discussing how may becomes does, it is necessary to note that, whenever the courts have granted a claimant the benefit of the exception, but for has been suspended. To reiterate: that is because but for cannot be used where there are two or more sets of events and conditions, each of which is sufficient to offer a credible causal explanation. 2. THE FAIRCHILD EXCEPTION Are the characteristics which we have identified in McGhee such as to establish this ruling as a general principle of liability for negligently increasing a risk which eventuates in injury? Those members of the House who decided Fairchild and then Barker were adamant that it should not be. The reasons why the Fairchild exception must remain no more than an exception, which arises only in very carefully delineated circumstances, have been discussed at length in the literature. 30 The speech 31 of Lord Bingham in Fairchild is the primary source, followed by those of Lord Hoffman in that case and then in Barker. 32 Lord Bingham identified six characteristics, present in body similarly retains, over time, its mysterious role in the mutations that culminate in mesothelioma. 29. Per Lord Hoffman in Barker, above n 3, para 13, where he claimed that in determining McGhee, the House had treated it as an application avant la lettre of the Fairchild exception. Given its greater generality as well as its seniority, McGhee arguably has a better claim to be eponymous. 30. Perhaps the most insightful commentary is to be found in J Stapleton Lords a leaping evidentiary gaps (2002) 10 Torts LJ Above n 2, paras Lord Hoffmann s speech in Barker is discussed below, see text at n 62.

8 Fairchild, which must be present in any case where the claimant wishes to invoke the exception and establish causation without passing the but for test: (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. 33 Of these six conditions, the two most important for the discussion of Sienciewicz in section 4 below are: (6) that current medical science does not enable us to identify the cause of (or, more precisely in Fairchild, the particular employer whose negligently controlled asbestos was implicated in) the claimant s mesothelioma; and (5) that any cause other than asbestos absorbed at work can be dismissed. It was scientific uncertainty which had been central to the ruling in McGhee and, when removing McGhee from the limbo in which it had effectively lain since the House of Lords decision in Wilsher v Essex Area Health Authority, 34 Lord Bingham added a further condition: that any increase in risk must involve only a single agent. 35 In discussions of the various personal injury cases which cannot enjoy the benefit of the Fairchild exception, Wilsher 36 has become the definitive example. In this medical negligence case, the claimant s blindness could have resulted from the eventuation of the risk posed by any one of five different agents: four of these were natural hazards attendant upon premature births, the fifth was a negligently executed medical procedure. It was impossible to tell which of these five were instantiated on this occasion. The evidential uncertainty appears to be comparable with that which obtained in McGhee but the House of Lords has affirmed, most recently in Barker, that the dissimilarities between the five agents of risk meant that the Wilsher decision should be seen as correct, even though the negligence could be said to have increased the risk of the eventuated injury. (There is one, perhaps obvious, conclusion which must be drawn from Wilsher: agents of risk cannot be treated as identical, or even substantially similar, simply because they share a capacity to bring about the same form of harm the agents must be substantially similar in themselves and not just in their outcomes.) The single agent condition was manifestly satisfied when McGhee developed dermatitis after his employer negligently failed to supply washing facilities: the non-tortious dust on his skin was the same agent (of the risk of dermatitis) as that which remained when the means of washing it off promptly was denied. (A moment s thought will reveal that the single agent criterion is automatically satisfied by a negligent omission such as that of the National Coal Board here.) In Fairchild, 33. Above n 2, para [1988] 1 All ER Above n 2, para Above n 34. Causation in personal injury after (and before) Sienkiewicz 403

9 404 Legal Studies, Vol. 32 No. 3 exposure to asbestos was believed to be the sole agent of the risk of mesothelioma and occupational exposure, resulting from negligent control by various employers, was assumed to be the sole source of that risk. When re-visiting the single agent criterion in Barker, Lord Hoffmann first dismisses the doubt he had voiced in Fairchild and then states the mechanism by which it caused the damage, whatever it was, must have been the same. 37 He then gives, as an example of an injury which falls outside the Fairchild exception: a lung cancer which could have been caused either by smoking or by asbestos. 38 This example was considered by the Court of Appeal in Novartis Grimsby Ltd v John Cookson. 39 Here, it was agreed that the claimant s bladder cancer could have been due to certain amines (and other carcinogens to which he was exposed when employed in the manufacture of dyestuffs) or to his smoking habit. It was decided that because the amines in question are also found (along with numerous other carcinogens) in tobacco smoke, a common mechanism was at work and hence this case could fall within the ambit of the Fairchild exception. In the event, this claimant did not need to rely on the exception: he won his case on orthodox grounds once it was accepted that the tortious exposure accounted for 70 per cent of the risk of incurring this particular form of cancer. In view of the extent of the consideration this issue was to receive in Sienkiewicz, it is worth noting the unequivocal language which Lady Justice Smith uses when applying the doubles the risk rule: In my view, if [appellant s counsel] is right and the correct test for causation in a case such as this is the but for test and nothing less will do, that test is plainly satisfied on the facts as found. The natural inference to draw from the finding of fact that the occupational exposure was 70 per cent of the total is that, if it had not been for the occupational exposure, the respondent would not have developed bladder cancer. In terms of risk, if occupational exposure more than doubles the risk due to smoking, it must, as a matter of logic [sic], be probable that the disease was caused by the former. 40 In section 4(b) below, an analysis of the doubles the risk rule questions the suggestion that logic is involved. But before we can justify that point within a wider review of the status of Type 3 material contribution in the aftermath of Sienkiewicz, it is useful to conduct an equivalent critique of Type 2 where, as we shall argue, coherence is less than total. 37. Above n 3, para 24, his position, on the single agent criterion, now seems indistinguishable from that which Lord Rodger formulated in Fairchild, viz a substantially similar criterion or one in which risk is increased if not by exactly the same agency [...] at least by an agency that operated in substantially the same way ; above n 2, para He may well be correct in assuming that the mechanisms by which asbestos and tobacco smoke lead to lung cancer are dissimilar but they could have a multiplicative or synergistic effect, as Lord Phillips suggested in Sienkiewicz, above n 1, para 75. This example of synergy was judicially considered in Amaca Pty Ltd v Ellis [2009] HCA Trans [2007] EWCA Civ Ibid, para 74. It is not clear whether a 30% reduction of damages was applied in Novartis, as perhaps it should have been following Barker and, as a cancer other than mesothelioma, falling outside the remit of the Compensation Act 2006.

10 Causation in personal injury after (and before) Sienkiewicz DISSIMILAR AGENTS OF CUMULATIVE INJURY Bonnington was a deterministic case; hence there was no need to invoke the concept of risk or any other probabilistic term. And there was no need to lay any weight on the fact that there was only one agent of the harm: the tortious and non-tortious dusts were concurrent, indistinguishable and cumulative in producing what lawyers like to term a divisible injury. It is this indistinguishability which underpins the assumption of a cumulative effect and, if present, a threshold. This indistinguishability was also present in other (Type 2) deterministic cases which have relied on Bonnington: the cumulative effect of asbestos exposure in causing asbestosis; 41 a similarly cumulative effect of (occupational) noise in giving rise to deafness 42 and of the role of hand-held tools in vibratory white finger. 43 In these cases, the courts have developed the use of proportionate damages to reflect the relative contributions of different employers and of non-tortious exposures (retreating from the traditional all or nothing as applied, without challenge, in Bonnington). These cases may have revised the calculation of damages but they have not changed our understanding of the role of Type 2 material consideration in establishing causation. But certain limitations in that understanding are exposed by Bailey v Ministry of Defence. 44 Following surgery at the first defendant s hospital to remove a gall stone, Miss Bailey became extremely weak, developed pancreatitis and was subsequently sent to an intensive care unit. When her condition stabilised, she was transferred to the renal ward of a hospital managed by the second defendants. When given a drink, she vomited and was unable to clear her throat. The aspirated vomit caused a cardiac arrest which in turn led to severe brain damage. In the subsequent negligence action against the first and second defendants, the judge at first instance found that the cardiac arrest had been caused by the claimant s weakness which was deemed to have had two cumulative causes: the negligent lack of care by the first defendant and the claimant s pancreatitis (which had not resulted from the first defendant s negligence). He dismissed the claim against the second defendant but found the first defendant liable: their negligent lack of care had contributed materially to the claimant s overall weakness and this was sufficient to establish causation. In the Court of Appeal, Lord Justice Waller s reasoning is not always transparent but his conclusion: [t]he instant case involved cumulative causes acting so as to create a weakness and thus the judge in my view applied the right test, and was entitled to reach the conclusion he did, 45 endorses the first instance application of Bonnington. But there remains a question: does a case like Bailey require something more than a simple reliance on Bonnington? Lack of care and pancreatitis are very different entities; if they are assumed to have a cumulative effect on overall debility (which was deemed a necessary condition of the claimant s inability to safely expel the aspirated vomit) then a further assumption is required here. Lack of care and pancreatitis must operate in essentially the same way when adding to the body s weakness; and their respective contributions must, at least in theory, be measurable on a common scale. But where the cumulants of injury 41. Holtby v Brigham & Cowan (Hull) Ltd [2000] 3 All ER Thompson v Smiths Shiprepairers (North Shields) [1984] 1 QB Allen v British Rail Engineering Ltd [2001] EWCA Civ Bailey v Ministry of Defence [2008] EWCA Civ Ibid, para 47.

11 406 Legal Studies, Vol. 32 No. 3 are identical (as in Bonnington, Holtby 46 and Thompson 47 ) the existence of a common scale is taken for granted and then it is only the possibility that one of the sources is sufficient by itself to be causal which prevents an orthodox application of but for. But if the cumulants are different, does that make a difference in law? Is it enough to argue that, if they appear to be cumulative, they must operate in the same way and that it is reasonable to imagine one contributing, say, five units and the other seven thus exceeding the threshold of 11? Or is it necessary to adduce evidence which explains this similarity of operation? The phrase operate in the same way is the deterministic equivalent of similar capacity to bring about the same outcome which, as argued above, cannot be invoked by Wilsher-like claimants seeking to avail themselves of the Fairchild exception. But whether the scientific evidence is framed in terms of different components of an eventuated risk or in terms of cumulants towards an exceeded threshold can have considerable implications for an action in negligence. And in a case like Bailey, it is far from clear, to the layperson at least, that a pathological condition, which cannot be described more precisely than weakness, can be consigned with any confidence to either category. This must be even truer in regard to the many factors which conspire to cause harm to mental health. In the context of occupational stress, Lady Justice Hale (as she then was) commented:...if it is established that the constellation of symptoms suffered by the claimant stems from a number of different extrinsic causes then in our view a sensible attempt should be made to apportion liability accordingly. There is no reason to distinguish these conditions from the chronological development of industrial diseases or disabilities...nor is there anything in [Bonnington or McGhee] requiring a different approach. 48 Thus from a purely juridical perspective, uncertain causation in negligence cases involving psychiatric harm may be discussed in the same terms as the physical injury cases discussed hitherto: either a sum of cumulants or a sum of probabilities (Type 2 or Type 3). It could be that, should it ever appear, a comprehensive theory of the human mind will require combinations of both or, indeed, a complex variety of genetic and environmental factors combined in ways which science has yet to understand. A theory of the mind one which could reliably predict that a given individual will, on witnessing a tragedy or being subject to excessive stress, behave in ways which we currently label neurotic seems a very long way off. Meanwhile, opting for a Bonnington-like contribution assumes, at very least, a common scale on which the different extrinsic causes can be seen to have a cumulative effect. On the other hand, an approach which involves adding probabilities avoids the problem of the elusive common metric; but different extrinsic causes will, if they are probabilistic, fall foul of the single agent requirement. To rephrase our earlier statement of the obvious: different [probabilistic] causes cannot leap the single agent hurdle simply by pointing to their common ability to instantiate the same outcome. If Bailey or a comparable case were ever to be heard by the Supreme Court, it would have to decide whether dissimilar agents are covered by the rule in Bonnington. 46. Above n Above n Hatton v Sutherland [2002] 2 All ER 1, at 20.

12 Causation in personal injury after (and before) Sienkiewicz 407 If it were held that they are, this would make it harder to justify their continued exclusion in indeterministic (Type 3 increased risk) cases. If they are not, then Bonnington, which we argued above is already a special case, would be explicitly restricted to injuries attributable to multiple sources (at least one being tortious) of the same deterministic agent of harm. Many readers of this paper might recoil from the theological character of its exegesis of the differences between a Bonnington-like and a McGhee-like contribution. They might well point instead to judicial good sense in suspending but for when it leads to paradox and injustice for otherwise deserving claimants (such as Mr Fairchild). They might therefore look with approbation on the pragmatic approach adopted by Mr Justice Turner in the British Coal Respiratory Disease Litigation (BCRDL). 49 After dismissing much of the testimony of the defendant s expert witnesses as unreliable, he was able to state his findings on causation in language which is immediately comprehensible to any layperson, for example: [i]t is probable, but not certain, that there is a common causal pathway to both cigarette and mine dust induced emphysema which usually gives rise to breathlessness. 50 He then awarded damages which were apportioned according to the relative durations of the tortious and non-tortious exposures and to the smoking habit of each of the eight claimants in this test case. It might seem pedantic therefore to suggest that another of his conclusions [i]n the individual smoker it is not possible to attribute the cause of breathlessness either to the one insult or the other, this is so whether or not there is a common pathway 51 suggests that his apportionment went beyond what is expressly approved by common law. But anyone with a knowledge of recent developments in the law of causation cannot help but view BCRDL through the lens of Fairchild. The facts (1) that tobacco smoke and silica dust are dissimilar entities and (2) that smoking is not under the control 52 of the (defendant) employer cannot be easily dismissed. In BCRDL, the contributions were taken as cumulative but it is not obvious that the ruling in Bonnington is broad enough to embrace the particular circumstances of the coal-miners test case (or those of Bailey). Where the evidence is unable to identify the type of the material contribution (that is, whether the putative causal factors combine in a deterministic or probabilistic manner) a prudent scientist errs on the side of caution and assumes complexity rather than simplicity. And complexity (or rather, a higher level of generality) points, as we have argued above, to McGhee as the default ruling to apply whenever but for is found wanting Re British Coal Respiratory Disease Litigation QBD 23/01/98 unreported. 50. Ibid, para Ibid. 52. See below n One of the many merits of Lord Reid s risk increased formulation of the rule in McGhee (see text at n 27) is that it is applicable whether the uncertainty, which gives rise to that increase, is epistemic, that is, derives from our incomplete understanding of the processes causing dermatitis, or whether that uncertainty is objective, that is, it derives from an inherent randomness in the processes themselves; for a further discussion of the different approaches to probability, see DH Mellor The Matter of Chance (Cambridge: Cambridge University Press, 1971). A protracted philosophical debate on the differences might have obviated Lord Reid s pragmatic solution.

13 408 Legal Studies, Vol. 32 No SIENKIEWICZ V GREIF (UK) (a) The rock of uncertainty Novartis 54 was a case where the defendant s negligence was assessed as having a 70 per cent chance of having been the cause of the claimant s bladder cancer and, although he might well have qualified for the Fairchild exception, he did not need to plead it: his suit succeeded on orthodox grounds, namely, a particular interpretation of the balance of probabilities. Sienkiewicz 55 is different, primarily because the balance of probabilities here is claimed by the defendant. The respondent was the administrator of the estate of her mother (Enid Costello) who had died of mesothelioma. Mrs Costello: had worked for Greif or their predecessors at their factory at Ellesmere Port, Cheshire, between 1966 and Greif exposed those working at that factory to 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. 56 Evidence based on scientific modelling of both the occupational and environmental (that is, from the background concentration of asbestos prevailing in Ellesmere Port) exposure suggested that: lifetime environmental exposure created a risk of mesothelioma of 24 cases per million [and] cumulative occupational exposure...gaverise to a risk of 4.39 cases per million. 57 And since the occupational risk represents only 18 per cent ( ) of the background, the claimant cannot succeed on the orthodox grounds, interpreted here as requiring the negligently increased risk to exceed 50 per cent. But the orthodox approach is suspended when the Fairchild exception applies. In the Court of Appeal, Lady Justice Smith 58 argued that a material increase in risk constituted, after Fairchild, proof of causation in mesothelioma cases and this (common law) notion of proof satisfied s 3(1)(d) of the Compensation Act and therefore the defendant was liable in solidum. Lord Clark added that he could see no reason why it should make any difference that it might have been possible for the claimant to show that [the non-tortious, environmental] exposure doubled the risk. 60 The primary question facing the Supreme Court was: does the Fairchild exception apply when there is only one tortious source of asbestos? If, because of a single exposure limitation or for some other reason, the Fairchild exception did not apply, 54. Above n Above n 1, at para Ibid. 57. Above n 6, para 9. I have referred to these numerical estimates as derived from modelling rather than epidemiological studies. This view is supported by Lord Mance in the Supreme Court who wrote, rather disparagingly: [t]he 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, above n 1, para Above n 6, para Compensation Act 2006 (ch 29),s3ofwhich restored, to mesothelioma victims, the joint and several liability which Fairchild had imposed but which, in Barker, had been replaced by damages factored by the estimate of each defendant s contribution to the increased risk. 60. Above n 6, para 55.

14 then it would be necessary to consider the appellant s second contention that their tortious exposure had not doubled the risk (above background) and that, therefore, causation had not been established. Since all seven judges were satisfied that the exception did apply, any of the comments on doubles the risk (which, for reasons which should become clear from Appendix A, will henceforth be labelled the RR > 2.0 rule ) were strictly obiter. But their importance for the current status of the common law of causation cannot be understated. The question can a victim of a single tortious source of risk enjoy the benefit of the Fairchild exception? invites the glib response of whose formulation? Consider first Lord Bingham s (in Fairchild) whose six conditions were quoted in section 2 above. If the first condition Cwasemployed at different times and for differing periods by both A and B istakenliterally, the exception clearly cannot apply to a single employer. And the fifth any cause of C s mesothelioma other than the inhalation of asbestos dust at work can be effectively discounted is no less fatal to a claim which recognises a risk posed by non-occupational exposure to asbestos. Lord Hoffmann s original formulation seems less restrictive: [f]irst, we are dealing with a duty specifically intended to protect employees against being unnecessarily exposed to the risk of (among other things) a particular disease. Second, the duty is one intended to create a civil right to compensation for injury relevantly connected with its breach. Third, it is established that the greater the exposure to asbestos, the greater the risk of contracting that disease. Fourth, except in the case in which there has been only one significant exposure to asbestos, medical science cannot prove whose asbestos is more likely than not to have produced the cell mutation which caused the disease. Fifth, the employee has contracted the disease against which he should have been protected. 61 When Barker obliged Lord Hoffmann to return to the subject, he now had to consider whether the recognition of a mesothelioma victim s non-tortious exposure to asbestos made a difference. From the following passage of his speech: [t]he 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. 62 it is clear that a distinction between a tortious and a non-tortious exposure is now irrelevant when the other conditions for the Fairchild exception are satisfied. The importance of this passage cannot be understated: the President and three other judges of the Supreme Court chose to quote it when determining Sienkiewicz. For Lord Rodger, whether or not there is more than one tortfeasor, it was still 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 61. Above n 2, para Above n 3, para 17. Causation in personal injury after (and before) Sienkiewicz 409

15 410 Legal Studies, Vol. 32 No. 3 up against the same rock of uncertainty. 63 So, this curious metaphor of a rock of [scientific] uncertainty has now been used to justify the extension of the Fairchild exception to a single tortfeasor v environmental exposure case. But it must be remembered that this uncertainty was one of Lord Bingham s conditions when the exception was first formulated to overcome the particularly thorny problem raised by multiple tortfeasors. So, the question arises: at what point does a reduction in evidential uncertainty mean that the Fairchild exception can no longer be invoked? 64 And since it is a defendant who stands to gain from a non-application of the exception, this can be re-phrased: at what point might the court accept a defendant s evidence that he can show that his negligent source of exposure was not the cause of the claimant s injury? 65 Arguably, this point is reached when the defendant s account is accepted on the traditional standard of the balance of probabilities (BOP). The fact that the etiology of mesothelioma is so inherently uncertain does not mean that the credibility of any evidence about this particular form of cancer is to be judged against some standard other than BOP. Credibility and uncertainty must be distinguished. If the accused insists that she has absolutely no recollection of where she was on the night of the murder, this is a statement of high uncertainty; the jury s degree of belief in this statement is quite independent and may lie anywhere within the range 0 to 100 per cent, that is, from total rejection to total acceptance. The Fairchild exception is not confined to mesothelioma. So reflecting more generally, we can see that if the exception is indeed founded upon the rock of uncertainty, then any claimant wishing to avail herself of it must be prepared to demonstrate that advances in scientific understanding have not left it so eroded as to remove its rock-like status. That is what her opponent has every incentive to establish and, if successful, the exception would not apply and the claimant would then need to establish causation on orthodox grounds. 66 And in this regard, counsel for Greif (UK) might have thought he had succeeded in sufficiently eroding the rock when their (18 per cent) estimate of the increased risk of the mesothelioma (from which the claimant died) stemming from their negligent control over asbestos was accepted at first instance. An increased risk of 18 per cent is equivalent to a relative risk of only 1.22, so why did Greif (UK) not succeed in their appeal? 63. Above n 1, para This is the question posed by S Steel in his comment on Sienkiewicz in the Court of Appeal, Uncertainty over causal uncertainty: Karen Sienkiewicz (Administratrix of the Estate of Enid Costello Deceased) v Greif (UK) Ltd 73 (2010) MLR This is not to assume, or to argue for, a reversal of the burden of proof. It simply recognises that, since the claimant s burden is considerably eased when the exception applies, the defendant has every reason to question its application. 66. Imagine that, in the future, the science of dermatology is so advanced that the cause of the type of dermatitis suffered by James McGhee can be determined with a reliability comparable to that of DNA testing today. At what point between then and now (or rather, 1972) can a rock of uncertainty be said no longer to exist in regard to dermatitis and occupational exposure to brick dust? It would be the point at which the fact-finder accepts on BOP the claimant s (defendant s) causal account of the injury which holds that the delay in washing was (was not) a necessary element. By relying on BOP, the demise of the exception is signalled by a familiar legal criterion rather than a scientific one.

16 Causation in personal injury after (and before) Sienkiewicz 411 (b) The RR > 2.0 rule The pros and cons of the RR > 2.0 rule are discussed in Appendix A. That discussion is informed by the voluminous literature, predominantly US in origin, related to numerous civil actions in which evidence from epidemiological studies was central. Appendix A argues that the RR > 2.0 rule represents lawyers too simplistic attempts to infer, from the epidemiological evidence, whether or not causation has been established on BOP. It further argues that such attempts have so many shortcomings that this rule should never be seen as binding in a tort action. But how exactly did the Supreme Court view the role of RR > 2.0 in cases where the Fairchild exception does not apply? Only Lord Phillips is prepared to declare that he can see no reason in principle why [RR > 2.0] should not be applied in such circumstances. 67 But his delineation of such circumstances is hard to understand. In contrast, Lord Rodger was unequivocal in his rejection of the approach laid down by Smith LJ in the Court of Appeal which endorsed doubles the risk. 68 Lady Hale agreed that [RR > 2.0] is not an appropriate test of causation in cases in which the Fairchild exception does not apply. 69 No similarly explicit statements, for or against, are to be found within the other four speeches. All seven display varying degrees of suspicion of epidemiological or statistical evidence as evidence per se, especially when unaccompanied by additional evidence which shows a specific causal link between the defendant s breach and the eventuation of the claimant s injury. Lord Rodger made some telling observations. In particular, he argues that:... inanyactual 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. 70 And that respect refers to the need for the evidence to be found credible by the judge (or jury). The fact that epidemiological evidence usually offers a numerical estimate of increased risk makes no difference: that evidence, as a whole, is rejected or accepted by reference to the balance of probabilities criterion; and whether 2.0 > RR > 2.0, the fact-finder is never bound by that statistic. The independence of the estimate of relative risk (RR) and the estimate of the credibility (0 > p > 1) which the fact-finder ascribes to that estimate (or, more strictly, the overall evidence from which it emerges) is the point which Gold stressed, 25 years ago, in an article 71 which three members of the Supreme Court chose to cite with approval in Sienciewicz. Quite apart from dismissing RR > 2.0 as a binding interpretation of BOP, there is the separate issue of the admissibility of epidemiological evidence in establishing individual, as distinct from general, causation. Again Lord Rodger gets to the nub of 67. Above n 1, para Ibid, para 162. It is not entirely clear whether or not Smith LJ was confining her comment to cases in which the exception applied. But Lord Phillips, ibid, para 121, believed that she had made a very general statement about the approach which courts should adopt to issues of causation and Lord Rodger referenced this paragraph when stating his opposition. 69. Ibid, para Ibid, para S Gold Causation in toxic torts: burdens of proof, standards of persuasion, and statistical evidence (1986) 96 Yale LJ 376.

17 412 Legal Studies, Vol. 32 No. 3 the issue by showing that a claimant who wishes to rely upon an epidemiological study would need to show that she was not atypical 72 of, for instance, the cases in a case-control study which was viewed, in the epidemiology community, as having shown a causal link between a given injury and a certain exposure. By way of an example: if the cases consisted of British Asian women who developed breast cancer in their fifties and who earlier took drug D during pregnancy, if she can demonstrate that she falls within all these (four) categories, then she is not atypical and this might be seen as sufficient for her to establish specific causation given that the study shows D to be causal generally. In addition Lord Rodger suggests that a claimant who develops the condition immediately after taking the drug 73 is in a stronger position. But, again, temporal proximity would be just one point in the causal account which, as in any civil proceedings, forms part of the claimant s overall evidence whose credibility is to be gauged against BOP by the fact-finder at first instance. When considering the merits of any epidemiological study which claimed to have identified a causal mechanism, a court might seek advice on the extent to which the study satisfied the Bradford Hill 74 (or some similar) criteria. These nine criteria are used to justify the inductive leap which cannot be avoided when accepting that a statistical association (or relative risk) is indicative of an underlying causal mechanism. A strong association is simply the first of the nine; temporality requiring the exposure to precede its effect is another. The Bradford Hill criteria do not offer a proof of causation: they simply provide a structure to guide a decision maker, for example, a government minister who faces calls to ban a drug because of its alleged side-effects. If cited in civil proceedings, these criteria would form part of the overall epidemiological evidence which, as Lord Rodger has observed, is no different from other evidence. 75 But in Sienkiewicz, they were not cited. 76 Since the circumstances of the case were held to qualify for the Fairchild exception, the claimant was not required to make the inductive leap towards specific causation: it was sufficient to demonstrate a material increase in a risk which had eventuated in mesothelioma. In that respect, all seven judges found the evidence sufficiently probative. And since s3ofthecompensation Act 2006 applied, no question of apportionment arose and, notwithstanding the 18 per cent figure, Greif (UK) was required to pay full (rather than proportionate) damages for the claimant s injury. (c) Hotson revisited In order to weigh the full implications of what was the Supreme Court s first venture into the labyrinth that causation has become, a useful starting point is Lord Brown s astonishing aside 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 72. Above n 1, para Ibid, para A Bradford Hill The environment and disease: association or causation? (1965) 58 Proc R Soc Med Above n 1, para In any event, they would be of little help in this case where the risk estimates came, not so much from an epidemiological study published in a peer-reviewed journal, but from ad hoc calculations; see the comments of Lord Mance, above n 56.

18 Causation in personal injury after (and before) Sienkiewicz 413 the law have developed as it has. 77 But if Sienkiewicz had come to court before the Fairchild exception had been proposed, was it bound to have failed? If the doubles the risk rule had been applied, the answer must be yes. But what if the ruling in McGhee (not then viewed as an application of the exception avant la lettre ) had been invoked, would this have increased the claimant s chances? It is a single agent, omission case and one involving an increase in risk (and a material increase since 18 per cent can hardly be dismissed as de minimis). And Sienkiewicz might well have succeeded on these grounds had it arisen in the 16 years after McGhee but before the House of Lords determined Hotson v East Berkshire Area Health Authority. 78 The presence of numerical estimates of the negligent/non-negligent contributions to overall risk of the (eventuated) injury mean that Sienkiewicz and Hotson are conceptually very close. On the two occasions when the House of Lords commented on the ruling in Hotson, they declared it to be sound. 79 So regardless of the doubts of some academic analysts over this notoriously difficult decision, 80 Hotson would appear to have to be distinguished before Sienkiewicz could succeed. And if the 25 per cent estimate of negligently increased risk was deemed insufficient in Hotson, the same would very probably have been said of the 18 per cent in Sienkiewicz. In Hotson, Lord Mackay hypothesised an epidemiological study by which to illustrate a successful loss of chance claim for damages for McGhee-like dermatitis. For Lord Phillips, this illustration proved cryptic, but it was also irrelevant because the numbers which Lord Mackay invented amounted to RR > 2.0 and therefore the doubles the risk rule was not challenged. Thus we can infer little about the status of a claim based upon epidemiological evidence which gives an estimate of 1.0 < RR < 2.0 but where the evidential circumstances are otherwise comparable with those of McGhee. There is no rule of law or history that obliges key precedents to emerge in a sequence which is most pleasing to legal theorists. But this speculation over the likely fate of Sienkiewicz had it arisen in the pre-fairchild era is not entirely idle. In Hotson, the two sources of risk were similar but not identical, as they (asbestos) were in Sienkiewicz; but an important factor common to these two cases was that the non-tortious source of risk was not under the control 81 of the respective defendant. 77. Above n 1, para [1987] AC Per Lord Rodger in Barker, above n 3, para 64 and in Gregg v Scott [2005] 2 AC 176 passim. However, Lord Rodger in Sienkiewicz observes that there is [following Fairchild] no room, however, for Lord Mackay s rule in cases of that kind in English or Scots law. Above n 1, para See J Stapleton The gist of negligence [1988] LQR 389; C Miller Liability for negligently increased risk: the repercussions of Barker v Corus UK (plc) (2009) 8 Law, Probability and Risk I have borrowed the term control from Stapleton, above n 30. She sees it as one of six characteristics shared by McGhee and Fairchild. Initially, and when referring to Lord Bingham s fifth condition (see text, above n 32), she describes the shared factor as all relevant exposures to risk occurred in the victims workplace, above n 30, at 285. When later explaining why Wilsher lay outside the exception, she writes that it was because not all sources of risk were under the control of the defendant, ibid, at 287. This latter construction must surely be preferable if the Fairchild exception is not to be confined to occupational injury. It is possible to argue that, in Barker, the condition of all sources of risk under the control of the defendants was not necessarily infringed: Mr Barker, when self-employed, was equivalent to any of the other (defendant) employers in that this exposure (now non-negligent but not environmental) was no less under his control.

19 414 Legal Studies, Vol. 32 No. 3 (The defendant in McGhee exercised control over both the tortious and non-tortious sources of risk and therefore defendant-control could become a condition of the Fairchild exception.) If that is accepted, then Sienkiewicz, regardless of any dispute over scientific uncertainty, fell outside the remit of the exception. The key issue is not whether there is only one tortious exposure but whether the competing, background exposure is under the control of the defendant. (Any speculation on the exception applying in Novartis should also recognise that the background source of risk, viz the claimant s smoking habit, was clearly outside the defendant s control.) (d) Epidemiological evidence: the claimant s dilemma Sienkiewicz has confirmed that, where the Fairchild exception applies, it is this material increase in (eventuated) risk that constitutes the harm for which, outside mesothelioma cases, damages will be made proportional to that risk. But epidemiological evidence will usually be expressed in terms of an increased risk over background; and a claimant who wishes to rely on the exception would be well advised to use such evidence only to establish the risk increase (viz RR > 1.0). The more robust she claims her evidence to be, the greater the chance that it might fail the test of uncertainty. But if and when she is denied the benefit of the exception, she has every incentive to stress just how reliable and probative her evidence is. She will find herself in this far less privileged, orthodox position if she fails the uncertainty test, the similar agent rule or, in theory, the defendant-control rule. Mesothelioma cases now constitute a special category within the exception, so instead imagine litigation involving a child neurologically damaged by a vaccine. The natural risk of this condition is 82 per cent and the tortious risk, under the control of the vaccine manufacturer, is 18 per cent. These figures are accepted at first instance and 18 per cent damages are awarded. But this scenario assumes that the background and vaccine-related risks are substantially similar in terms of their etiology. Should this similarity test be failed, the claimant now faces the orthodox burden of establishing causation in negligence. Lord Rodger called for epidemiological evidence to be treated no differently from any other form of evidence. But since the Supreme Court was far from unequivocal in opposing the RR > 2.0 interpretation of the balance of probabilities, it is hard to imagine the lower courts being willing to depart from the received wisdom and to concede causation for a negligently increased risk which fails to exceed the background. But recall that whether the claimant receives 18 per cent or 0 per cent damages might hang upon some recondite, physiological question about the precise way, say, the measles virus is implicated in some neurological disorder and about the capacity of the measles vaccine to bring about the same condition. 82 However, Sienkiewicz does little to encourage our hapless claimant to use epidemiology to further her objective. And quite apart from the Fairchild exception, Sienkiewicz raises many questions about the forensic role of epidemiological studies generally. Lord Phillips is exercised by what he sees as an inherent lack of adequacy 83 in epidemiological data. In contrast, Lord Dyson recognises that, for many toxic torts, epidemiological evidence is all that a claimant can call upon, yet he 82. This point is developed in more detail in a discussion of XYZ v Schering Health Care Ltd [2002] EWHC 1420 (QB) in C Miller Causation in personal injury: legal or epidemiological common sense? (2006) 26 LS Above n 1, para 98.

20 Causation in personal injury after (and before) Sienkiewicz 415 still believes that in straightforward personal injury cases where it must be rare for a claimant to rely exclusively on epidemiological evidence to prove...her claim... [she] will almost always also be able to point to some specific evidence relating to the particular circumstances of the case. 84 One might respond that straightforward cases tend to be settled out of court. Reference was made to the, less than straightforward, American case 85 in which the Blue Bus paradox originated. Here, the jury were told not to infer that it was one of (defendant) B s buses that caused a particular accident, simply because company B owned most of the buses (>50 per cent) that passed the accident location. But this case is over 65 years old and the bench in Sienkiewicz made no reference to more recent and lively debates in the literature concerning the probative value of inferences about individuals which are drawn from statistics relating to groups. 86 (e) A conventional determination of Fairchild? In view of the Supreme Court s concern at the current state of the law of personal injury, it would be ironic if the present situation could have been avoided. Professor Beever 87 has come up with a way of determining Fairchild (still in the claimants favour) which does not rely explicitly on McGhee or any other risk added precedent. Nor does it require resort to any policy considerations. In effect it is an attempt to finesse the key evidential uncertainty, namely, the identity of the employer whose asbestos was implicated in the development of the claimant s mesothelioma. In the absence of any other information, the indifference principle 88 would suggest that any one source of asbestos was as likely as not to have been involved (that is to say, each negligent employer carries a probability of involvement P(A) = 1/2). The present author is not convinced by Beever s subsequent analysis but it is not difficult to come up with a simple, orthodox (balance of probabilities) approach which could have determined Fairchild, as Beever claims. It is necessary to assume that at least one fibre is necessary and that the probability of any one source (A, B, C, D,...)being the origin of an effective fibre is exactly 1/2 (that is, each source was as likely to have supplied a hit as a miss ). If it is known that mesothelioma has eventuated, then at least one fibre must have been involved; it is then straightforward 89 to show that, for any number of sources, the ex post probability of the involvement of any one source is always greater than 1/2. And if we then apply the p > 50 per cent, or the doubles the risk, interpretation of BOP, then all the sources (A, B, C, D,...)must be held liable. 84. Ibid, para Smith v Rapid Transit, Inc 317 Mass 469; 58 N.E.2d 754 (1945). 86. See for example, P Tillers If wishes were horses: discursive comments on attempts to prevent individuals from being unfairly burdened by their reference classes (2005) 4 Law, Probability and Risk 33 at A Beever Rediscovering the Law of Negligence (Oxford: Hart Publishing, 2007) p If there are n mutually exclusive possibilities and we have no further information about them, then we should assign an equal probability (1/n) to each of them. 89. If there are m sources each with a probability of 1/2 of being a hit and 1/2 being a miss, there are 2 m combinations of which any one source (A) will feature as a hit in 2 m-1. We know ex post the diagnosis of the tumour that the total miss possibility did not arise; hence the probability of A having been involved is: m m P( A) = 1 2 /( 2 1) > 1/ 2 for all m 1.