BLM Emerging Risks Team - Report on Definition, Causation and Epidemiology

Transcription

1 BLM Emerging Risks Team - Report on Definition, Causation and Epidemiology 23 September 2014 Nick Pargeter Partner, BLM London T E [email protected] Malcolm Keen Solicitor, BLM London T E [email protected] 1

2 Contents Page 1 Introduction 3 2 Definition of emerging risk 3 3 Causation 4 4 Tests for causation 5 5 The place of epidemiology, the but for test and doubling of risk 8 6 The Fairchild exception 13 7 Fairchild and cancers other than mesothelioma 14 8 Sienkiewicz 15 9 Analysis of causation in cancer claims Carcinogenic agents Reviewing epidemiological studies Conclusion 29 2

3 1. Introduction In this paper we examine the key elements in emerging risks: definition, causation and epidemiology. Definition in this section we consider the essentials of analysing emerging risks including identification, assessment of the risks, and uncertainties. Causation in this section we consider medical/scientific causation and legal causation. We analyse the principles of causation and how and where different tests will apply. We also consider the place of epidemiology, the categorisation of carcinogenic agents and a short guide on interpreting the key elements in epidemiological studies. 2. Definition An emerging risk can be defined as: (i) a risk from a newly identified hazard to which exposure may occur or: (ii) a risk from an unexpected new or increased exposure and/or susceptibility to a known hazard. 1 The HSE has defined a hazard as something such as an object, a property of a substance, a phenomenon or an activity - that can cause adverse effects. 2 Seaton et al observed that the introduction of all new technologies can have unexpected consequences both beneficial and harmful. 3 Uncertainty Emerging risks are inherently uncertain. And by its nature an emerging risk is difficult to quantify (since, for example, there is little or no claims history). Uncertainty for a particular emerging risk broadly has three main elements: (i) Adverse health effects Can the agent potentially cause illness/injury? What are the adverse health effects likely to be? Are they severe or minor, long lasting or transient? Is there an exposure threshold before illness/injury follows? Will every person exposed suffer harm or just some? Such uncertainty requires awareness and analysis of medical, scientific and epidemiological research. (ii) Numbers of people potentially exposed; potential claims numbers and value What is the past, current and predicted future use of the agent? Who has been/will be exposed? What is the extent of exposure? What are the likely sources and numbers of potential claims? To 1 Definition and description of emerging risks within the EFSA s mandate, European Food Safety Authority, Scientific Committee & Advisory Unit, EFSA/SC/415 Final, 10 July A. Seaton et al, Nanoparticles, human health hazard and regulation, J. R. Soc. Interface (2010) 7, S119-S129 3

4 whom will claims be targeted employers, suppliers, manufacturers? What is the likely value of claims? Again medical, scientific and epidemiological research is important. Are potential claims being fuelled by the media? (iii) Legal developments What is the regulatory regime? What official guidance is available and what knowledge will potential defendants be deemed to possess? Is exposure at certain levels safe or should a precautionary approach be adopted? What does case-law in the U.K. and in other jurisdictions show? What is the likely test for proof of causation? Does the medical, scientific and epidemiological evidence show a causal relationship between exposure and harm? Are claims likely to be successful? This is likely to be the least uncertain of the three elements. Strategy Emerging risks are characterised not only by uncertainty but also by constant development. Advances in science and technology can create new risks; increased knowledge can help assess these risks but can also lead to identification of new risks associated with known hazards; changes to the law and official guidance can impact on potential liability. There may also be policy trigger issues. So the key elements in approaching emerging risks are: Identification Analysis Assessment, quantification & risk reduction strategies. One concept which arguably straddles all three main elements is causation. Causation is perhaps best analysed within the framework of legal developments. 3. Causation Introduction Causation in emerging risks has two elements: (i) medical/scientific causation and (ii) legal causation. These two stages amount to proving that the agent in question caused the condition, and then attributing legal responsibility. At common law and under the Consumer Protection Act 1987 (CPA), causation is one of the elements which must be proved before there can be liability. Section 2(1) CPA explains the general principle underlying the Act: where damage is caused by a defect in a product, the producer is liable for that damage. Assuming that the insured s product is found to be defective, the insured will be liable for damage caused by the defect. Damage is defined by section 5(1): Subject to the following provisions of this section, in this Part damage means death or personal injury or any loss of or damage to any property (including land). So damage includes personal injury. Section 45(1) defines terms in the Act. It states: personal injury includes any disease and any other impairment of a person's physical or 4

5 mental condition; 4. Tests for causation Background The rules concerning causation of disease have developed in large part as a result of industrial disease cases. The principles are relevant to product liability, employers liability and public liability. Dame Janet set out the traditional test to prove causation for an injury: The basic rule of causation in tort is the but for rule which requires that the claimant must show that, but for the defendant's breach of duty, he would probably not have suffered the injury complained of. 4 In Sienkiewicz v. Grief (UK) Ltd [2011] UKSC, Lord Phillips explained: This broad test of balance of probabilities means that in some cases a defendant will be held liable for damage which he did not, in fact, cause. Equally there will be cases where the defendant escapes liability, notwithstanding that he has caused the damage, because the claimant is unable to discharge the burden of proving causation. Developments in the but for test If we consider the but-for test as the paradigm way of deciding causation, there are three primary developments/changes to the test relevant in to emerging risks. They have sometimes been characterised as entirely new tests, and sometimes as modifications of or developments in the existing test. They are: (i) Material contribution test (ii) The place of epidemiology in the but for test doubling of risk (iii) A test currently restricted to the asbestos-related cancer mesothelioma known as the Fairchild exception Material contribution test As Dame Janet said, the leading case in which the but for rule was first modified in English law was Bonnington Castings Ltd v Wardlaw [1956] AC 613. The claimant developed pneumoconiosis as a result of inhaling silica dust part of which was tortious, and part of which was non-tortious. The employers alleged that he would have developed the condition from the non-tortious exposure alone so should not recover. The House of Lords held that the claimant could recover, and in full; the negligent exposure had made a material contribution to his condition. The contribution was material if it was more than minimal (de minimis). So the claimant succeeded in full although he had not satisfied the but for test. 4 J. Smith, Causation the search for principle, JPIL 2009, 2,

6 In Bonnington, there was no attempt to persuade the court that the claimant should recover for only that part of his injury which could be attributed to the employer's negligence. The injury was treated as indivisible. Today, such an injury would be treated as divisible and the experts would provide the information necessary for apportionment - the defendant s liability for damages would be in proportion to the extent of the injury caused by its breach (such as in a noise-induced hearing loss claim for example). But Bonnington showed how the but for test could develop, and how a claimant can recover damages where the defendant s tort contributes (more than minimally) to the claimant s condition. An arguably unusual feature in respect of the material contribution test is the significance of whether percentage contributions of the tortious agents can be determined. If the condition is poorly understood and medical science is unable to quantify the contributions of the various causes, but can say that the contribution of the negligent factor was more than minimal, the defendant will be liable in full. The finding of liability is thus based not on the probability of the defendant s fault causing the injury but on how well understood a particular condition is by medical science. A similar anomaly would also occur in relation to the apportionment of damages. Where medical science can divide responsibility between the causes in a divisible injury, damages can be similarly apportioned. Where no such assessment is possible (an indivisible injury), the defendant, whose tortious exposure makes a more than material contribution to the condition, will be liable for the entire loss. The difference again appears to be the state of medical science rather than the degree of fault. It is of course important to distinguish between contribution to the cause (ie. to the disease itself) and contribution to the risk of the disease occurring. We discuss this in relation to Lord Phillips views on causation of lung cancer below. In principle, if the injury is divisible (where there is a dose-related correlation between exposure and the extent of the disease - such as deafness or vibration white finger) damages can be apportioned. If the injury is indivisible damages cannot be apportioned and the claimant recovers in full (subject to contributory negligence). If the defendant s negligence materially contributed to the injury (ie. it was more than minimal), the claimant is entitled to damages in full. This view is supported by Bailey and Dickins. In Bailey v. MOD [2008] EWCA 883, proof of causation was considered in a clinical negligence case. The claimant suffered brain damage after she inhaled vomit and suffered cardiac arrest because she was too weak (because of pancreatitis) to protect her airway. The claimant accepted that the pancreatitis was the major cause but argued that the defendant s negligent treatment had made more than a minimal contribution to her weakness had she been properly treated, she would probably not have become as ill as she did, she would have recovered sooner and would not have been so weak that she inhaled her vomit, leading to cardiac arrest and brain damage. At first instance, the judge held that the defendant s negligence in treating the claimant made a material contribution to the injury and the claimant succeeded in full. The Court of Appeal considered whether the judge, in finding liability, was entitled to depart from the but for test and whether it was enough for the claimant to establish that, on a balance of probabilities, a lack of care made a material contribution (something more than negligible) to the 6

7 claimant s weakness. The Court of Appeal upheld the trial judge s decision. Waller LJ concluded that in a cumulative cause case such as Bonnington, the but for test is modified and noted that in Fairchild the House of Lords introduced an exception to the but for test. He also considered that a distinction could not be made between medical negligence cases and others. He summarized the position in cumulative cause cases where medical science cannot establish the probability that but for the defendant s 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 should be modified and the claimant should succeed. In Dickins v. O 2 Plc [2008] EWCA, the Court of Appeal considered, amongst other things, causation and apportionment in a work-related stress claim. The claimant, a regulatory finance manager, suffered a psychiatric injury and, in finding for the claimant, the trial judge held that the defendant employer s negligence made a material contribution to the claimant s injury. However, the defendant s fault was not the only cause of the claimant s injury. In addition to tortious factors, non-tortious factors were also relevant - she had a psychologically vulnerable personality and problems in her home life. The trial judge apportioned damages half each between the defendant and the non-tortious factors. The Court of Appeal considered that the correct test for causation in a psychiatric injury case was the one propounded by Hale LJ (as she then was) in Hatton v. Sutherland [2002] EWCA Civ 76 [2002]. The employee does not have to show that the breach of duty caused all the ill-health it is enough to show that the breach made a material contribution. The defendant was liable because its breach satisfied this test. There were other non-tortious factors but the defendant s fault materially contributed to the claimant s injury. Apportionment was not in issue between the parties (both accepted the judge s apportionment of damages as 50% due to the defendant s negligence). However, Smith LJ looked at whether apportionment of damages was appropriate in a psychiatric injury case such as this one. The Hatton guidance indicates that an attempt at apportionment should be made in psychiatric injury cases with more than one cause. Smith and Sedley LJJ were critical of this approach. Smith LJ found little difference between Dickins and Bailey. As in Bailey, the defendant s breach had made a material contribution to the injury but it was not possible to say that, without the breach, the claimant would have suffered the injury. Smith LJ considered (obiter) that the injury here was indivisible and doubted whether apportionment was appropriate in the case of a psychiatric injury with multiple causes: where the defendant s breach has made a material contribution to the injury (ie. it was more than de minimis) but it is not scientifically possible to exactly quantify that contribution, and the injury is indivisible, damages should not be apportioned (though there may be a reduction in some heads of damage for future risks of non-tortious loss). Smith and Sedley LJJ considered that a psychiatric injury with more than one cause was indivisible and damages should not be apportioned. Once a claimant has shown that the defendant s negligence has materially contributed to the injury, the defendant will be liable for all the damages. However, this part of the judgment is obiter (as is the Hatton guidance in relation to apportionment). 7

8 Material contribution test and cancer The key issue in respect of application of the material contribution test to cancer is whether it can be said that the tortious and non-tortious agents acted together (ie. both contributed to the cancer) or whether it can only be said that the two agents each contributed to the risk. We examine this question below. In Sienkiewicz, Lord Phillips explained that: Where disease is caused by the cumulative effect of the inhalation of dust, part of which is attributable to breach of duty on the part of the defendant and part of which involves no breach of duty, the defendant will be liable on the ground that his breach of duty has made a material contribution to the disease Bonnington Castings Ltd v Wardlaw [1956] AC 613. He continued: That disease [pneumoconiosis] is divisible. The severity of the disease depends upon the quantity of silica inhaled. The defendant did not, however, argue that, if held liable, this should only be to the extent that the dust for which it was responsible had contributed to the plaintiff s symptoms. It was held liable for 100% of the disease. There have, however, been a series of cases at first instance and in the Court of Appeal in which it has been recognised that where there has been a number of exposures of a claimant to bodily insults that have cumulatively caused a divisible disease, responsibility should be apportioned so that an individual defendant is liable for no more than his share of the disease. 5. The place of epidemiology, the but for test and doubling of risk As well as the material contribution test, in recent years epidemiology has been used to assist the courts in deciding causation. The doubling of risk test is an alternative method of proving causation in which the claimant succeeds if he can show by means of expert epidemiological evidence that his tortious exposure doubled the risk which he would otherwise have had (ie. from non-tortious causes) of developing the condition for which he seeks damages. In XYZ v. Schering Health Care Ltd. [2002] EWHC 1420 (QB), a group litigation in which the claimants alleged they had suffered cardio-vascular injuries as a result of taking certain oral contraceptives, epidemiology was pivotal. Mackay J noted that: Epidemiology is the study of the occurrence and distribution of events (such as disease) over human populations. It seeks to determine whether statistical associations between these events and supposed determinants can be demonstrated. Whether those associations if proved demonstrate an underlying biological causal relationship is a further and different question from the question of statistical association on which epidemiology is initially engaged. Mackay J considered that: If factor X increases the risk of condition Y by more than 2 when compared with factor Z it can then be said, of a group of say 100 with both exposure to factor X and the condition, that as a matter of 8

9 probability more than 50 would not have suffered Y without being exposed to X. If medical science cannot identify the members of the group who would and who would not have suffered Y, it can nevertheless be said of each member that she was more likely than not to have avoided Y had she not been exposed to X. Mackay J found that the most likely figure to represent the relative risk was around 1.7. So the claimants failed. (A relative risk of 2 or more shows a doubling of the non-tortious risk already present.) In McTear v. Imperial Tobacco Ltd [2005] CSOH 69, the claimant argued that her husband s death from lung cancer had been caused by smoking cigarettes (John Player s) manufactured by the defendant between 1964 and 1992, and that and throughout the period during which the deceased smoked them the defendant was negligent in selling cigarettes, or in any event in selling them without appropriate warnings. In deciding in the defendant s favour, Lord Nimmo Smith stated: The [claimant] relies on epidemiology to prove general causation. I have not been sufficiently instructed by the expert evidence relating to this discipline to be able to form my own judgment as to whether or not this averment is proved. Lord Nimmo Smith added: In any event, the [claimant] has failed to prove individual causation. Epidemiology cannot be used to establish causation in any individual case, and the use of statistics applicable to the general population to determine the likelihood of causation in an individual is fallacious. Given that there are possible causes of lung cancer other than cigarette smoking, and given that lung cancer can occur in a non-smoker, it is not possible to determine in any individual case whether but for an individual's cigarette smoking he probably would not have contracted lung cancer. In Novartis Grimsby Ltd v. John Cookson [2007] EWCA Civ 1261, the claimant alleged that his bladder cancer had been caused by exposure to carcinogenic aromatic amines whilst employed by the defendant at its dyestuffs manufacturing plant between 1964 and The claimant had smoked 10 or 20 cigarettes a day until giving up in 1980 and it is known that smoking can also be a cause of bladder cancer. It was accepted by both sides that this source of exposure and occupational exposure would have had at least an additive, if not multiplicative effect. The parties disagreed, however, on the relative potency of the effect of smoking and occupational exposure. At first instance the judge found that the defendant had exposed the claimant to significant amounts of carcinogenic substances, such exposure was in breach of its duty to the claimant and that exposure to such substances had probably made a material contribution to the development of the claimant s bladder cancer. Consequently, the defendant was liable to compensate the claimant for the development of his illness. However, the Court of Appeal (Dame Janet Smith Smith LJ then) had a different view. The claimant had smoked 10 or 20 cigarettes a day until giving up in 1980 and it is known that smoking can also be a cause of bladder cancer. Smith LJ concluded that the Recorder was entitled to prefer the evidence of the claimant s expert who considered that occupational exposure had made a contribution of 70-75% of the total risk with 9

10 smoking making a 25-30% contribution. In other words, occupational exposure had more than doubled the risk due to smoking. Novartis illustrates the primacy of the but for test. Smith LJ accepted the claimant s submission that, in line with the conventional test, causation was established if the defendant s breach of duty caused or materially contributed to the disease. Once the Recorder had accepted that occupational exposure was the major contributing cause the case was virtually over. At first instance, the Recorder had said he could not distinguish between the situation here and that in Bonnington. The defendant in Novartis submitted that this approach was incorrect and that the Recorder had applied the wrong test. The defendant argued that Bonnington had only been applied where the disease had been caused gradually by the cumulative effect of exposure to, for example, dust, noise or vibration; in such a case the negligent exposure would have contributed to the disease. However, such cases, where only part of the exposure was caused by the defendant s breach and which were formerly determined in accordance with Bonnington, would now, following Thompson v. Smiths Shiprepairers [1984] 1 All ER 881, be subject to apportionment of damages. The claimant would no longer recover all the damages - the court would apportion damages to reflect the extent of damage caused by the defendant s breach. The defendant s view was that bladder cancer was not divisible in this way. The claimant s disease had been triggered by the cumulative effect of amines from smoking and from his work. Each exposure gave rise to a risk of bladder cancer (and the combination increased the overall risk) but neither exposure made the disease more severe. Each exposure only contributed to the risk that bladder cancer would develop but did not contribute to the disease. Once developed, the seriousness of the disease was independent of the extent of exposure. The defendant s view was that, by approaching the issue as he had done, the Recorder had permitted the claimant to prove causation by showing only that the occupational exposure had made a material contribution to the risk that he would develop the disease. The correct approach should have been the but for test whether, if it were not for the occupational exposure in breach of duty, the claimant would probably not have developed bladder cancer. The defendant submitted that this question could not have been answered in the claimant s favour. Smith LJ in the Court of Appeal concluded that had the claimant s occupational exposure to amines contributed to the risk of developing bladder cancer to a lesser extent than his smoking then these issues would have to be resolved but, since the Recorder accepted the claimant s expert s evidence that occupational exposure accounted for 70-75% of the total, they did not need to be considered. It was not necessary for the Recorder to go into Bonnington. The occupational exposure had more than doubled the risk due to smoking. If the defendant s submission that the but for test for causation applied here was correct, that test was plainly satisfied; since occupational exposure accounted for 70% of the total, it may be inferred that but for the occupational exposure (ie. had there been no occupational exposure), the claimant would not have developed bladder cancer. In other words, if occupational exposure more than doubled the risk due to smoking, it is probable that the former caused the disease. 10

11 In Shortell v. BICAL Construction Ltd, unreported, High Court, 16 May 2008, the deceased, born in February 1932, had worked as a jointer fixing together sections of electricity cables in power stations where he alleged he was exposed to asbestos dust in the course of his employment. He died from lung cancer in July The deceased had also been a smoker. There was no radiological evidence that he suffered from asbestosis but he did have signs of bilateral pleural plaques and pleural thickening. The judge accepted that the claimant s total asbestos dose was 99 fibres/ml years. The claimant s medical expert s evidence was effectively agreed by the parties. He proposed that: (a) Asbestos and tobacco smoke are established risk factors for the development of lung cancer; (b) The risk (in both cases) increases in proportion to the dose (of asbestos received/tobacco smoked); (c) The two factors have a multiplicative interaction. When both present, the overall risk is greater than the sum of the two; (d) Following mainstream medical opinion, the risk of lung cancer from asbestos is not confined to those with asbestosis (the precursor theory is that asbestosis must be present); (e) According to the 1997 Helsinki criteria, a cumulative exposure of 25 fibre/ml years is sufficient to attribute a causal role to asbestos in the development of lung cancer. But controversy exists as to whether a higher figure is required where exposure is to chrysotile; (f) A cumulative exposure of 25 fibre/ml years approximately doubles the risk of lung cancer; (g) An exposure of 99 fibre/ml years would, on its own, increase the risk of lung cancer by a factor of five. The claimant s medical expert also stated that if the deceased had smoked till age 49, the risk of developing lung cancer would have been about 5%. He also said that the Helsinki criteria presuppose a mixture of fibre types; if the deceased had been exposed to fibre types in the proportion 50:50, chrysotile: amphibole, a figure of 40fibre/ml years would result in a doubling of the risk. The claimant s medical expert also considered the multiplicative effect of asbestos and smoking and referred to the work of Doll and Peto in The claimant s medical expert estimated the deceased s risk factor from asbestos at five fold, acting synergistically on a 5% risk of lung cancer from smoking. This gave a risk from both hazards of 25%. Thus, the synergistic effect of asbestos increased the total risk of lung cancer from 5% to 25% - an increase of 20%. The claimant s medical expert considered that asbestos therefore accounted for 20% out of 25% or 80% of the deceased s total risk. If the deceased had smoked for a longer period up to 1987 his smoking would have conferred a risk factor of 8% for the development of lung cancer. This would have been increased five-fold by the effect of asbestos. His overall risk would thus have gone from 8% to 40%. Of the total risk, asbestos would have accounted for 32% out of 40% - again 80% of the total risk of developing lung cancer. The claimant s medical expert considered that the deceased s asbestos burden, on its own, satisfied the but-for test for causation. The claimant s and the defendant s medical experts 11

12 agreed that, in combination with his risk from smoking, the smoking attributable risk is likely to have been more than doubled by the asbestos attributable risk. Consequently, it could be said that it was both the experts view that the deceased would not have developed lung cancer had he not been exposed to asbestos. Asbestos exposure contributed 80% of the risk of contracting lung cancer. So the claimant succeeded in showing that more than doubled relative risk. In respect of contributory negligence for smoking, damages were reduced by 15%. In Amaca Pty Ltd & others v. Ellis [2010] HCA 5, the deceased died of lung cancer. He had been exposed to asbestos whilst working for two employers. He had also smoked - between 15 and 20 cigarettes a day for 26 years prior to diagnosis. Smoking and asbestos exposure both increase the risk of lung cancer. The question for the High Court of Australia (Australia s highest court) was legal causation: could it be shown that it was more probable than not that asbestos exposure was a cause of the deceased s lung cancer? Breach of duty was not in issue. Risks of smoking and asbestos Expert epidemiological evidence at trial indicated that the probability of the deceased s lung cancer being caused by smoking alone was at least 67%. And one expert put this probability at 92%. The experts agreed that the risk from smoking was many times greater than the risk from asbestos. The High Court examined three of the claimant s propositions in detail: (i) Smoking and asbestos must work together. The evidence did not support the proposition that, if a person has smoked and has been exposed to asbestos, and has developed lung cancer, the two must have worked together. (ii) The only two explanations for the deceased developing cancer which needed to be considered were (a) that smoking was the sole cause or (b) that the combined effect of smoking and asbestos was the cause. The High Court considered that the field of debate could not be confined in this way. (iii) Combined exposure to tobacco smoke and asbestos is more dangerous than exposure to one or the other. Therefore, it was more probable than not that the deceased s cancer was caused by exposure to both. Exposure to asbestos made a material contribution to the deceased s cancer. The critical question was whether exposure to asbestos was a cause of the deceased s cancer. The expert epidemiological evidence put the probability that the deceased s cancer was caused by exposure to asbestos (whether alone or in combination with smoking) at 23% at the most (one expert put the probability at 1%). The High Court considered that the epidemiological studies showed that: (a) it was more probable than not that smoking was a cause of the deceased s lung cancer; and 12

13 (b) the risks and probabilities associated with asbestos, whether alone or in conjunction with smoking, are low and not sufficient to infer that it was more probable than not that that exposure to asbestos was a cause of the deceased s condition. In the High Court s view: It was not shown to be more probable than not that asbestos was a cause of (a necessary condition for) his [the deceased s] cancer. It was not shown that exposure to asbestos made a material contribution to his cancer. Material contribution was not shown because a connection between [the deceased s] inhaling asbestos and his developing cancer was not demonstrated. The claimant relied on Lord Reid s statement in Bonnington that: What is a material contribution must be a question of degree. A contribution which comes within the exception de minimis non curat lex is not material, but I think that any contribution which does not fall within that exception must be material. The High Court distinguished Bonnington. In Bonnington, the issue was whether one source of silica dust contributed to a gradual accumulation of this dust resulting in pneumoconiosis. But here, the issue was whether a substance (asbestos) which can cause injury, did cause injury. In other words, was the deceased s lung cancer intimately connected with and contributed to by his exposure to asbestos? The issue of material contribution could only arise if a connection between the deceased s asbestos exposure and his lung cancer could first be established. Knowing that asbestos can cause cancer did not mean that it probably did. The issue of material contribution was thus not relevant. The High Court considered that no scientific or medical examination could say, with certainty, what caused the deceased s lung cancer (or lung cancer in any other case). The courts must ask whether it is more probable than not that X was a cause of Y. Saying only that asbestos may have been a cause of the deceased s cancer was not sufficient. Observing that a small percentage of cases of cancer were probably caused by exposure to asbestos does not identify whether an individual is on of that group. The claimant thus failed to establish causation and the defendant s appeals were successful. 6. The Fairchild exception The House of Lords arguably created an exception currently only applicable in mesothelioma claims. Expansion of this method of proving causation beyond mesothelioma to other forms of cancer could have dramatic consequences. However, as discussed below, the Fairchild exception is likely to remain confined to mesothelioma for the foreseeable. As Lord Phillips explained in Sienkiewicz, a special rule of causation applicable in mesothelioma cases was created by Fairchild v. Glenhaven Funeral Services Ltd [2002] UKHL 22: Lord Phillips explained: 13

14 Unusual features of the disease led the House of Lords to create a special rule governing the attribution of causation to those responsible for exposing victims to asbestos dust. This was advanced for the first time in Fairchild v Glenhaven Funeral Services Ltd [2002] UKHL 22; [2003] 1 AC 32 and developed in Barker v Corus UK Ltd [2006] UKHL 20; [2006] 2 AC 572. Parliament then intervened by section 3 of the Compensation Act 2006 further to vary this rule. Lord Phillips stated: The rule in its current form can be stated as follows: when a victim contracts mesothelioma each person who has, in breach of duty, been responsible for exposing the victim to a significant quantity of asbestos dust and thus creating a material increase in risk of the victim contracting the disease will be held to be jointly and severally liable for causing the disease. Causation is satisfied not on the basis that the defendant s tort has caused the claimant s condition, not because it has materially contributed to the claimant s condition but that it has contributed to the risk of the condition arising. The Fairchild exception (which followed the House of Lords decision in McGhee v. National Coal Board [1973] 1 WLR 1) was devised, as Lord Phillips put it, because of ignorance about the biological cause of the disease. It was accepted in Fairchild and Barker that this rendered it impossible for a claimant to prove causation according to the conventional but for test and this caused injustice to claimants. The claimants in Fairchild were exposed to asbestos by more than one employer. Where there are two or more exposures, science could not say in which employment exposure to the fibres which caused the disease took place. As Lord Rodger explained: The discussion and decision in Fairchild proceeded on the basis described by Lord Bingham, : There is no way of identifying, even on a balance of probabilities, the source of the fibre or fibres which initiated the genetic process which culminated in the malignant tumour. This was what he described as the rock of uncertainty The operation of the Fairchild exception has arguably been re-interpreted by the Supreme Court in the EL Trigger Litigation and by the Court of Appeal in IEG v. Zurich (discussed later). 7. Can the Fairchild exception apply to cancers other than mesothelioma? In Fairchild, Lord Bingham said: It would be unrealistic to suppose that the principle here affirmed will not over time be the subject of incremental and analogical development. Cases seeking to develop the principle must be decided when and as they arise. In Clough v. First Choice Holidays and Flights Ltd. [2006] EWCA Civ 15, a case concerning a catastrophic injury at a holiday complex abroad, the Court of Appeal considered application of the Fairchild exception. In Clough, the President of the Queen s Bench Division indicated that it was not enough for a claimant to show that the defendant created an increased risk of injury. Fairchild did not apply. But the claimant did not have to go so far as to show that the defendant s 14

15 negligence was the only cause of his injury: it was enough to show that the defendant s negligence made a material contribution to the injury. In Novartis, Smith LJ said obiter that: It seems to me that it is highly arguable that the mesothelioma exception [ie. the Fairchild exception] should apply to bladder cancer and that it would be sufficient if a claimant were to prove that the occupational exposure had made a material contribution to the risk of him developing the disease. Given that Smith LJ had found that occupational exposure had more than doubled the risk due to smoking it was not necessary to consider this further. But which of three tests should apply to cancer claims? 8. Sienkiewicz In Sienkiewicz, the Supreme Court examined all three tests. In Sienkiewicz (concerning two cases where the claimants developed mesothelioma after exposure to very low levels of asbestos), the Supreme Court held that the Fairchild exception governing proof of causation applies where there is only one tortious exposure. In Sienkiewicz, the deceased had been exposed to asbestos whilst working in an office at factory premises. Her exposure occurred as she moved around the factory. The claimant in Willmore alleged that the deceased s mesothelioma had been caused by negligent exposure to asbestos whilst a pupil at the defendant s school. The Supreme Court held that the Fairchild exception applies where there is only one defendant just as it applies where there are two or more defendants. The claimant will succeed if he proves that the defendant s breach of duty materially increased the risk of the claimant developing mesothelioma. The doubling of risk test does not apply in mesothelioma cases. But the justices also made obiter comments about causation in lung cancer claims (including the material contribution test), and the place of epidemiology/doubling of risk. Sienkiewicz causation in lung cancer Lord Phillips stated that the material contribution test can apply to asbestos-related lung cancer claims. He said at para. 90 (quoted in full below) that: Where the disease is indivisible, such as lung cancer, a defendant who has tortiously contributed to the cause of the disease will be liable in full. It is arguable that Lord Phillips view cannot be right. At para. 75 Lord Phillips said: Shortell v BICAL Construction Ltd, was a claim in relation to a death caused by lung cancer where there were two possible causes of the cancer. One was occupational exposure to asbestos and the other was cigarette smoke. The defendant was responsible for the former but not for the latter. Applying the Bonnington test of causation, the issue was whether the asbestos to which the victim had been exposed had made a material contribution to the cause of the victim s lung cancer. The expert evidence, given by both medical and epidemiological experts, but based in the case of each, I suspect, on epidemiological data, was that asbestos and cigarette smoke not merely combined 15

16 cumulatively to cause lung cancer, but that they had a synergistic effect in doing so. This evidence was enough, as I see it, to satisfy the Bonnington test of causation, as the victim had been exposed both to significant quantities of asbestos fibres and to significant cigarette smoke. This arguably cannot be correct for two reasons: (i) Shortell was not decided on the material contribution test it was decided on the basis of doubling risk; and (ii) the cause of lung cancer. Mackay J considered the risks of smoking and asbestos he did not say that they must have acted together to cause the disease. ie. the analysis was about risk, not contribution to the disease. The cancer could have been caused by smoking alone. This is clear from Mackay s judgment. At para 49 he said: Mr Feeny for the defendants rightly in my view concedes that if the claimant proves on a balance of probabilities that the risk factor created by his client s breach of duty more than doubled the deceased s relative risk of contracting lung cancer then the claimant s case is proved,.... For the reasons I have advanced above I am satisfied on the balance of probabilities that once the estimate of 99 fibre/ml years is accepted as I have accepted it the relative risk is on any view more than doubled. At para 51 Mackay J states: Where, as here, it is the case that the claimant has proved causation against this defendant by showing a more than doubled relative risk it is not relevant as between the claimant and the defendant to argue that another agent (tortious or otherwise) may also have contributed to the occurrence of the disease. At paragraphs 90 and 91 of Sienkiewicz Lord Phillips said: Can the doubles the risk test be applied in multiple cause cases involving diseases other than mesothelioma? 90. For reasons that I have already explained, I see no scope for the application of the doubles the risk test in cases where two agents have operated cumulatively and simultaneously in causing the onset of a disease. In such a case the rule in Bonnington applies. Where the disease is indivisible, such as lung cancer, a defendant who has tortiously contributed to the cause of the disease will be liable in full. Where the disease is divisible, such as asbestosis, the tortfeasor will be liable in respect of the share of the disease for which he is responsible. 91. Where the initiation of the disease is dose related, and there have been consecutive exposures to an agent or agents that cause the disease, one innocent and one tortious, the position will depend upon which exposure came first in time. Where it was the tortious exposure, it is axiomatic that this will have contributed to causing the disease, even if it is not the sole cause. Where the innocent exposure came first, there may be an issue as to whether this was sufficient to trigger the disease or whether the subsequent, tortious, exposure contributed to the cause. I can see no reason in principle why the doubles the risk test should not be applied in such circumstances, but the court must be astute to see that the epidemiological evidence provides a really sound basis for determining the statistical probability of the cause or causes of the disease. 16

17 These two paragraphs arguably contain a number of errors. In particular, Lord Phillips view ignores the causation of lung cancer (discussed below). As evidenced by Lord Phillips comments at para. 75, he appears to be characterising risks with causes. We discuss Lord Phillips mistake in relation to the Phurnacite Litigation below. Sienkiewicz - Doubling of risk and the place of epidemiology Whilst affirming that the Fairchild exception applies in mesothelioma cases, the Supreme Court in Sienkiewicz also gave somewhat mixed messages in respect of relying on statistical evidence to prove causation in claims relating to other conditions. Notwithstanding Lord Phillips views at paras. 90 and 91, it is arguable that no clear majority view can be elucidated (and this part of the judgment is obiter). Smith LJ considered the place of epidemiology following Sienkiewicz in Ministry of Defence v. Wood [2011] EWCA Civ 792. In Wood, the claimant sought damages for a neurological condition akin to Parkinson s disease. He alleged the condition had been caused by exposure to organic solvents (dichloromethane and trichloroethylene) whilst working as a painter and finisher in the RAF between 1987 and The defendant admitted breach of duty but argued that: (i) There was no satisfactory scientific evidence that the organic solvents could cause permanent neurological damage (though they could cause temporary harm and even death). (ii) The claimant had not suffered permanent damage his symptoms were psychological. The claimant served in the RAF from 1975 but Crown immunity applied before Smith LJ considered that S (one of the claimant s medical experts) was arguing that even where there is no supportive epidemiology, there are other means by which causation could be established. S relied on the Bradford-Hill criteria - nine criteria to help determine causation (A. Bradford-Hill, The Environment and Disease: Association or Causation? Proceedings of the Royal Society of Medicine, 58 (1965) 295). Smith LJ considered that it was implicit from the criteria that it is not always necessary to have proof by epidemiological study before concluding that a particular agent has caused a certain effect. The Court of Appeal concluded that: (i) There was clear evidence of a very high level of exposure (in particular between 1989 and 1992/93) sometimes several times greater than the permitted exposure. (ii) There was some scientific evidence of an association between heavy solvent exposure and neurological damage. Taken together, studies demonstrated that there was probably a link between heavy and prolonged solvent exposure and neurological damage - enough to satisfy a judge on the balance of probabilities. It was not now established in the scientific sense that there is a causal connection between heavy solvent exposure and neurological damage. However, on the claimant s evidence (unrebutted by the defendant) in legal terms a probable connection has been made out If this connection was accepted, it was a short step to conclude that this claimant s condition was caused by solvent exposure. The defendant was liable. In Wood, some elements are likely to be confined to the case itself. The judge at first instance was heavily critical of one of the defendant s experts in neurology and disregarded his evidence. The Court of Appeal found that the judge was entitled to form this adverse view. Wood does suggest 17

18 some principles of general application though. For example, Wood suggests that epidemiology is not definitive in proving causation. Wood and Sienkiewicz both suggest this but in different ways. In Wood the claimant s expert thought it unlikely that there were would ever be an epidemiological study which would demonstrate a clear association between solvent exposure and chronic neurological damage. In Sienkiewicz, the balance of the Supreme Court Justices views suggests that where epidemiological evidence (often expressed as evidence of the tortious factor doubling the risk of the non-tortious factor) is present, on its own, it is not enough to prove causation. As Lord Rodger said (para. 163): since, by its very nature, the statistical evidence does not deal with the individual case, something more will be required before the court will be able to reach a conclusion, on the balance of probability, as to what happened in that case. For example, where there is a strong epidemiological association between a drug and some condition which could have been caused in some other way, that evidence along with evidence that the claimant developed the condition immediately after taking the drug may well be enough to allow the judge to conclude, on the balance of probability, that it was the drug that caused the claimant s condition. Wood and Sienkiewicz arguably show a more holistic approach to causation, recognising the difference between epidemiology alone, and an analysis of all available evidence. As Lord Mance put it in Sienkiewicz (para. 190): I share a reluctance to place too much weight on such [epidemiological] evidence. This is not because statistics are lies, or because truth can be stranger than fiction. It is because the law is concerned with the rights or wrongs of an individual situation, and should not treat people and even companies as statistics. It can also be noted that Smith LJ considered that it is implicit from the Bradford-Hill criteria that it is not always necessary to have scientific proof by epidemiological study before one can reach a sensible conclusion that a particular agent has caused a certain effect. Other forms of evidence are of probative value. The Bradford Hill criteria grew out of Sir Austin Bradford-Hill s work with Sir Richard Doll on smoking and lung cancer. Mackay stated in XYZ v. Schering Health Care Ltd, that the famous epidemiologist Sir Austin Bradford Hill in an address in 1965 considered the difficult question of when a statistically apparent association between A and B should be translated into the proposition that A causes B. He proposed nine criteria for consideration, which have been described as an attempt to systematise common sense, The criteria are: (i) The strength of the association. He cited the 9-10 fold difference between smokers and nonsmokers in terms of the risk of cancer and the fold increase for heavy smokers, as against the two fold increase for coronary thrombosis. (ii) Consistency derived from repeated observations by different persons in different places and at different times; (iii) Specificity. Is the association specific to the exposure in question? 18

19 (iv) Temporality; as it states in the criteria, which is the cart and which is the horse? For example, does a particular occupation promote infection or are the people who selct this kind of work more liable to contract the infection whatever the environment? (v) Biological gradient also known as a dose response relationship; is there a clear doseresponse curve? (vi) Plausibility; Is the suspected causation plausible? But what is biologically plausible depends on the knowledge of the day. (vii) Coherence is what is known of the relationship coherent with all other knowledge? (viii) Experimental evidence. (ix) Analogy from other fields. Lord Phillips in Sienkiewicz explored the limits of epidemiological evidence. He considered an example found in the dissenting judgment of Brachtenbach J in Herskovits v Group Health Cooperative of Puget Sound (1983) 664 P 2d 474, a decision of the Supreme Court of Washington. Herskovits was considered by Lord Mackay in Hotson v. East Berkshire Area Health Authority [1987] AC 750. Considering the dissenting judgment of Brachtenbach J, Lord Mackay said: He warned against the danger of using statistics as a basis on which to prove proximate cause and indicated that it was necessary at the minimum to produce evidence connecting the statistics to the facts of the case. He gave an interesting illustration of a town in which there were only two cab companies, one with three blue cabs and the other with one yellow cab. If a person was knocked down by a cab whose colour had not been observed it would be wrong to suggest that there was a 75 per cent. chance that the victim was run down by a blue cab and that accordingly it was more probable than not that the cab that ran him down was blue and therefore that the company running the blue cabs would be responsible for negligence in the running down. He pointed out that before any inference that it was a blue cab would be appropriate further facts would be required as, for example, that a blue cab had been seen in the immediate vicinity at the time of the accident or that a blue cab had been found with a large dent in the very part of the cab which had struck the victim. As Lord Rodger said: it must be emphasised once more epidemiological and statistical evidence may form an important element in proof of causation since, by its very nature, the statistical evidence does not deal with the individual case, something more will be required before the court will be able to reach a conclusion, on the balance of probability, as to what happened in that case. For example, where there is a strong epidemiological association between a drug and some condition which could have been caused in some other way, that evidence along with evidence that the claimant developed the condition immediately after taking the drug may well be enough to allow the judge to conclude, on the balance of probability, that it was the drug that caused the claimant s condition. 19

20 Expansion of the Fairchild exception Sienkiewicz suggests that the Fairchild exception is now confined to mesothelioma, with little chance of extension to other conditions. As Lord Brown said: As I began by saying, mesothelioma cases are in a category all their own. Lord Brown emphasised this point: Save only for mesothelioma cases, claimants should henceforth expect little flexibility from the courts in their approach to causation. Since Fairchild and Barker there has been much academic focus on a supposedly critical distinction between so-called single agent and multiple agent cases, the suggestion being that the former more readily lend themselves to special rules of causation than the latter. For my part I have difficulty even in recognising the distinction between these categories, at any rate in some cases. But I have greater difficulty still in accepting that the courts should now, whether on this or any other basis, be thinking of creating any further special rules regarding the principles governing compensation for personal injury. As we consider below, there are two stages to causation proving causation of the disease, and then attributing legal responsibility. 9. Analysis of causation in cancer claims the Phurnacite Litigation and IEG Mrs Justice Swift considered these issues in a very thorough judgment last October in Jones v. (1) Secretary of State for Energy and Climate Change and (2) Coal Products Ltd [2012] EWHC 2936 (QB) (the Phurnacite Litigation). About 250 claimants registered claims in the Phurnacite Workers Group Litigation. They sought damages for two groups of conditions: (a) chronic obstructive pulmonary disease and chronic bronchitis; and (b) cancer of the lung, bladder and skin. The claimants alleged these conditions were caused by exposure to dust and fumes containing carcinogenic substances in the course of their work at the Phurnacite plant. The plant, opened in 1942, manufactured a smokeless domestic fuel with the trade name Phurnacite. The plant closed in The trial dealt with eight lead claims. The claimants alleged common law negligence and breaches of various provisions of the Factories Acts 1937 and 1961, the Patent Fuel Manufacture (Health and Welfare) Special Regulations 1946, and the Control of Substances Hazardous to Health (COSHH) Regulations Swift J restated the principle that a claimant will only succeed in establishing liability in a personal injuries claim if he can prove on the balance of probabilities that the defendant s tort caused or materially contributed to the injury. The claimants argued that the court should decide causation on the basis that their occupational exposure had made a material contribution to their cancers as per Bonnington. The defendants advocated application of the doubling of risk test. 20

21 Material contribution Swift J considered Bonnington. Swift J noted that pneumoconiosis is a divisible disease - ie. doserelated its severity dependent on the quantity of dust inhaled, but that the defendant had not sought apportionment between tortious and non-tortious exposure. In later decisions involving divisible conditions, liability has been apportioned between different defendants, and between tortious and non-tortious exposure. Swift J also considered Bailey v. MOD [2008] EWCA 883, a clinical negligence case, in which Waller LJ summarised the position in cumulative cause cases and considered that in a case where medical science cannot establish the probability 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. Doubling of risk Swift J considered Shortell and noted that the defendant conceded that if the claimant could prove on the balance of probabilities that the risk created by its breach of duty had more than doubled the deceased s risk of contracting lung cancer, the claimant would succeed. The judge found that the claimant s asbestos exposure more than doubled the risk of lung cancer which would otherwise have existed so the claimant succeeded in establishing causation on the balance of probabilities. Swift J noted that in the Atomic Veterans case in the Court of Appeal [2010] EWCA Civ 1317, Smith LJ considered that the material contribution test (as in Bonnington and Bailey) only applies where the condition is divisible (an increased dose worsens it). Smith LJ considered cancer an indivisible condition so the material contribution test would not apply. Swift J also noted that in Sienkiewicz, Lord Phillips (para. 75, discussed above) considered that the judge in Shortell need not have relied on the doubling of risk test. Instead, Lord Phillips considered that asbestos and cigarette smoke not merely combined cumulatively to cause lung cancer, but that they had a synergistic effect in doing so. Lord Phillips considered that Shortell fell within the Bonnington principle of material contribution. In Sienkiewicz, Lord Phillips also said he could see no scope for application of the doubling of risk test in cases where two agents have operated cumulatively and simultaneously in causing the onset of a disease. In such a case, Bonnington would apply (paras. 90 and 91, discussed above). Where the disease is indivisible (as with lung cancer), Lord Phillips considered that a defendant who has tortiously contributed to the case of the disease will be liable in full. Where the disease is divisible the defendant will be liable in respect of the share of the disease for which he is responsible. Swift J s view Since lung cancer is an indivisible condition, it did not seem to Swift J that the views of the Court of Appeal in Atomic Veterans and Lord Phillips in Sienkiewicz could be reconciled. Swift J also considered that dicta of the Supreme Court in Sienkiewicz relating to the doubling of risk test, and 21

22 the use of epidemiological evidence other than in cases of mesothelioma must be regarded as obiter. Swift also considered that the injury in Bailey was brain damage which was indivisible. The defendant s negligence had made an unquantifiable contribution to the weakness that led to development of the brain damage. This view meant that the fact that an injury is indivisible does not necessarily preclude the Bonnington principle according with Lord Phillips view in Sienkiewicz. Causation of lung cancer The experts agreed that where an individual had inhaled certain carcinogenic agents as a result of both smoking and occupational exposure, there is likely to have been an interaction between the two exposures. The claimant s expert considered that in any individual case where a lung cancer has developed, both exposures will on the balance of probabilities have contributed materially to the carcinogenic process which resulted in the development of the cancer. The defendant s expert disagreed. He considered that both exposures would have contributed to the risk of a lung cancer developing. But it was not possible to determine whether one or both or neither of the exposures had actually been involved in the causal sequence of formation of an individual cancer. The defendant s expert considered that in the absence of evidence supporting the doubling of risk, any attempt to say that an occupational carcinogen had actually contributed to the chain of causal events that led to a particular cancer developing was a step too far. Submissions The claimants argued that they had established that in each of the lung cancer cases, the claimant s occupational exposure had made a material contribution to the development of the cancer. It was not necessary to show a doubling of the risk. The claimants submitted that the evidence suggested that it was probable that carcinogens resulting from both smoking and occupational exposure had contributed to development of the lung cancers. The defendants submitted that the doubling of risk test was appropriate here. The defendants noted that Lord Phillips had approved the doubling of risk test in circumstances where there are competing alternative causes. The defendants argued that the Bonnington principle was inappropriate here, and that it was impossible to say with confidence that the occupational exposure had made a material contribution to the cancer. The defendants also submitted that if the court were to accept the claimants submissions, in every case where a claimant could show tortious exposure to a carcinogen greater than de minimis, and had developed a cancer, he would be able to establish causation. Swift J s conclusion on causation of lung cancer Swift J noted that the three lead claimants with lung cancer claims were exposed to carcinogens both from their occupational exposure at the Phurnacite plant, and from smoking. Each would also have been subject to other factors such as environmental exposure. Swift J considered that it 22

23 was not possible to say in relation to any individual cancer which factor or factors caused or contributed to its development. In respect of a cancer suffered by a claimant, the occupational carcinogen might or might not have contributed. If it did contribute, it might have played a very minor or an extremely major role. Other factors such as smoking or environmental exposure might have been the sole cause of the cancer. Or they might have played no part. Or they might have played a more minor or a more major role than the occupational exposure. It was not accurate to describe occupational exposure to carcinogens as a one of a number of cumulative causes. It is a very different situation from Bonnington, where the additional exposure caused by the defendant s breach had a cumulative effect by adding to the claimant s total dust exposure. It did not seem to Swift J that in Shortell the asbestos and cigarette smoke could be properly said to have acted cumulatively to cause the claimant s lung cancer. The multiplicative effect referred not to the biological mechanism which caused the cancer but to the increased effect on risk resulting from exposure to a combination of the two carcinogens. Swift J considered that in Shortell asbestos and cigarette smoke had combined cumulatively to increase the risk of lung cancer (not to cause the lung cancer). Swift J considered that it could not be right to approach the cases of lung cancer (nor bladder cancer) by applying the Bonnington principle. Adopting the claimants arguments would also mean that in any case of cancer where a claimant could establish tortious exposure to a carcinogen that was material, he would succeed in proving causation and would be entitled to 100% damages. This result would not be fair to defendants. Swift J considered that the appropriate approach here was the doubling of risk test. The majority of members of the Supreme Court in Sienkiewicz accepted that the test can be used in appropriate circumstances although there was concern about over-reliance on epidemiological evidence alone. (Swift J concluded that out of the two lead claimants with lung cancer, two succeeded in showing that the risk of lung cancer was more than doubled by occupational exposure. The third did not.) But what would be the case if there was tortious exposure with more than one employer? We consider this below. Bladder cancer Swift J noted that the major known causes of bladder cancer are occupational exposure to carcinogenic chemicals and cigarette smoking. However, many bladder cancer cases have no identifiable cause. The first issue to be determined was whether there was epidemiological evidence to support the proposition that bladder cancer can be caused by exposure to substances of the kind which the relevant claimants encountered at the Phurnacite Plant. The claimants conceded that they could 23

24 not point to a specific study within the medical literature which established beyond doubt the link between bladder cancer and exposure to dust and/or fume of the type encountered at the Phurnacite Plant. However, they argued that there was evidence in the literature that made it very likely that such a link did exist. In particular, they relied on studies in the coal gasification and aluminium smelting industries. The defendants argued that the epidemiological evidence did not support the claimants case. In particular, they referred to the absence of evidence of an association between bladder cancer and work on the carbonisation process in the coke production industry. Conclusion on bladder cancer Swift J found that, although the epidemiology suggested that it was possible that the fumes emitted during the carbonisation process at the Phurnacite Plant may have contained sufficient quantities of one or more substances capable of giving rise to an increased risk of bladder cancer, the epidemiological evidence, taken on its own, fell short of establishing that fact on a balance of probabilities. Swift J did not accept that the substances to which the relevant claimants were exposed made a material contribution to the development of their bladder cancer. She considered that the claimants would be able to succeed only if they were able to establish that their exposure had doubled the risk of them developing cancer. Even if her view on the strength of the epidemiological evidence were different, on the available material Swift J was not able to quantify the increase in the risk of bladder cancer as a result of exposure to carcinogenic substances. Thus in relation to bladder cancer none of the claimants could establish causation. Significance of the Phurnacite Litigation Swift J s judgement is very significant for occupational cancer claims. The Phurnacite litigation clearly suggests that in occupational cancer cases the Bonnington principle will not apply. Where there are competing potential tortious and non-tortious causes, a claimant will not be able to prove causation merely by showing some greater than de minimis exposure to asbestos (or another carcinogenic agent to which he is exposed at work). Instead, the doubling of risk test applies. Swift J s analysis shows that because of the nature of the development of cancer, the appropriate method to assess a particular cancer s most likely cause is by assessing and comparing the risks arising from the competing potential causes. As two of the experts agreed in their joint statement: Because of the stochastic nature of carcinogenesis, the question of whether a particular human cancer has or has not been caused by (for example) occupational exposure can only be addressed in terms of likelihood; occupational exposure to a carcinogenic chemical will increase the likelihood of cancer occurring in an exposed individual, and if exposures are high enough will cause a discernable increase in the number of cancers occurring in an exposed population. Any scientific assessment of causation can only result in an expression, either quantitative or qualitative, of the likelihood that an occupational carcinogen has been the cause. 24

25 The above statements suggests two points: (i) causation in cancer must be assessed by risk; and thus (ii) epidemiological evidence or doubling the risk of the non-tortious factor - must be the basis for assessing causation. As Swift J put it: [The claimant s expert] has no means of assessing the likelihood that occupational exposure has in fact contributed to the lung cancer suffered by any individual claimant. He said that, when there has been substantial exposure to carcinogens, both occupational and from cigarette smoking, the odds against all the mutations necessary to produce a cancer having occurred entirely coincidentally without any contribution by those carcinogens would be very long indeed. However, it seems to me that the only way to assess what those odds really are - and whether, on a balance of probabilities, the occupational carcinogen has made a contribution in any individual case - is by reference to the risk factors revealed in the relevant epidemiological material. So following Swift J s reasoning, the appropriate approach will be the doubling of risk test which arguably reasserts the primacy of the traditional but for test but expressed in statistical terms. This is in keeping with the present flow of disease jurisprudence. The Phurnacite Litigation also emphasises the principle that a defendant ought only to compensate for damage it has actually caused. In addition, Swift J s judgment shows a realistic approach to current scientific knowledge about the causation of cancer. Swift J also noted the dangers of extending the Fairchild exception beyond mesothelioma claims. But her comments probably related to her judgment on medical rather than legal causation. But of course, in Phurnacite, there was only one employer s tortious exposure. Notwithstanding her noting the potential problems associated with using statistical and/or epidemiological evidence as the sole basis for a decision on causation identified in Sienkiewicz, Swift J s view suggests that the doubling the risk test and the use of epidemiological evidence remains appropriate. Swift J considered that the Supreme Court Justices views in Sienkiewicz relating to the doubling of risk test, and the use of statistical and epidemiological evidence other than in cases of mesothelioma are obiter. Swift J adroitly clarified Lord Phillips approach to Shortell. In Shortell the asbestos and cigarette smoke did not act cumulatively to cause the claimant s lung cancer. Instead they acted together to increase the risk of lung cancer. Swift J recognised that in an occupational cancer claim where the claimant has also smoked, the cancer may have resulted from smoking alone it is not the case that the potential causes must have acted cumulatively. Swift J distinguished between those conditions which can properly be characterised as divisible - ie. dose-related severity related to the level of exposure, and indivisible conditions such as lung cancer. However, the judgment was arguably less clear about the circumstances in which the material contribution test would apply. 25

26 Swift J considered Atomic Veterans in which Smith LJ in the Court of Appeal found that the material contribution test (as in Bonnington) only applies where the condition is divisible. However, Swift J did not cite Smith LJ s own contrary view in Dickins v. O 2 Plc [2008] EWCA Civ 1144, a stress claim. Smith LJ considered the psychiatric injury in Dickins indivisible, and doubted whether apportionment was applicable to a psychiatric injury with multiple causes. Smith LJ s obiter view was that, where the defendant s breach has made a material contribution to the injury (ie. it was more than de minimis) but it is not scientifically possible to exactly quantify that contribution, and the injury is indivisible, damages should not be apportioned. Swift J in the Phurnacite litigation also considered that the brain injury in Bailey was indivisible, but nevertheless considered that the fact that an injury is indivisible does not necessarily preclude the material contribution test. Future problems where there are multiple tortfeasors The application of the doubling of risk test in cancer cases could potentially lead to a scenario very similar to that encountered in Fairchild. Where there is only one defendant, application of the doubling of risk test can show whether or not the defendant s tort has doubled the risk from the non-tortious factor. But what if there are two or more defendants? It could be impossible to say that asbestos attributable to one particular tortfeasor alone doubled the risk (and so was causative). Two scenarios may be considered: (i) One defendant - where its exposure doubled the risk that defendant will be liable in full. (ii) More than one defendant where the combined exposure doubled the risk. In this scenario the tortious exposure has, according to the doubling of risk test caused the asbestos-related lung cancer. But what if this is the result only when the total tortious exposure is combined ie. as against each individual defendant, the risk is not doubled? How will the courts approach this scenario? The above scenario suggests a two-step process: (i) causation of the disease; and then (ii) legal responsibility/causation. This is conceptually similar to the two-stage process identified by Professor Stapleton 5 in her article considering Amaca v. Ellis (considered above). (Professor Stapleton identified two elements that the claimant must prove: an (a) agency point that asbestos had been causally involved in the cancerous process ; and (b) a defendant-involvement point that asbestos inhaled as a result of the individual defendant s breach was so involved. ) 5 J. Stapleton, Factual causation and asbestos cancers, LQR, 2010, 126,

27 In the scenario at (ii) above, the first stage (1) is proven on the basis of doubling the risk the claimant can successfully prove causation. But it is the second stage which is problematic. How will claimants try to bridge the gap between steps (1) and (2)? How can causation for an individual defendant in scenario (ii) be proved? All that can be shown is that each defendant individually contributed to the risk (and in combination doubled the risk). Given Swift J s analysis of the stochastic nature of the development of cancer, it cannot be shown that each individual defendant s exposure contributed to the disease. This suggests three main possible outcomes: (i) Claim fails Given Swift J s analysis of the development of cancer, the claimant cannot show that any single defendant s exposure doubled the risk so the claim fails. (ii) The Fairchild scenario If Swift J s view of the stochastic nature of cancer is correct, a claimant will only be able to satisfy stage (2) and prove causation if he is able to succeed on the basis of contribution to risk. How can this be done? The courts will be required to expand the ambit of the Fairchild exception beyond mesothelioma claims. It is arguable that the House of Lords decision in Barker v. Corus [2006] UKHL 20 would then apply so that damages would be apportioned according to contribution to the risk - each defendant would be liable for its own share. (We discuss later whether Barker is still good law). Would the courts be willing to increase Fairchild s reach? Recent Supreme Court jurisprudence suggests not. Legislative intervention may be required. It is arguable that given attitudes to smoking, asbestos-related lung cancer is less politically sensitive than mesothelioma. (iii) Material contribution The gap could also be bridged by applying the material contribution test to stage (2). Once stage (1) is satisfied could it then be said that each defendant s fault has made a material contribution not merely to the risk but to the condition itself? The question of divisibility would then arise. Would an individual defendant be liable for the whole of the damage? Or could stage (2) be characterised as divisible and damages would be apportioned? This approach avoids the need for the courts to extend the Fairchild exception. But unless there is a change in the understanding of how cancer is caused (ie. it is shown that both tortious and non-tortious exposures must operate together to cause the disease rather than the two agents merely combining to increase the risk, it is difficult to see how the material contribution test could apply. The Phurnacite Litigation thus affirms the doubling the risk test, and arguably shows the flaws in Lord Phillips view of lung cancer in Sienkiewicz. However, the judgment rests on scientific knowledge on the cause of cancer ie. that it is stochastic in nature. If this changes, the basis of Phurnacite will change, and the appropriateness of the doubling of risk test could become vulnerable. 27

28 A different causation test - material contribution to damage would apply if it could be shown that lung cancer was divisible and all asbestos contributed to the cancer. This would be contrary to Swift s analysis of the development of cancer, of course. However, Swift J s judgment affirms the integrity of the medical view that lung cancer is indivisible and that it can only be said that asbestos exposure increases the risk of lung cancer. As Swift J makes clear, how can it be said that asbestos always contributes to damage when lung cancer might have developed in any event from tobacco or environmental causes? However, Swift J discounted the view of Dr Rudd whose evidence was that every exposure to a carcinogen will play a part in the carcinogenic process going on in an individual s body. 10. Carcinogenic agents Since 1971 the International Agency for research on Cancer (IARC - a body of the World Health Organisation, which conducts research on the causes and mechanisms of human cancer) has categorised 970. The IARC categorise agents into one of 5 groups: Group 1 - agents are carcinogenic (this includes alcoholic drinks and asbestos) Group 2A - agent probably carcinogenic (where there is limited evidence of carcinogenicity in humans and sufficient evidence in experimental animals) (this includes; Group 2B - agent possibly carcinogenic to humans (where there is limited evidence of carcinogenicity in humans and less than sufficient evidence in experimental animals or vice versa); Group 3 - agent not classifiable (inadequate evidence in humans and inadequate evidence in experimental animals); Group 4 - agent probably not carcinogenic (evidence suggesting lack of carcinogenicity in humans and experimental animals). 11. Reviewing epidemiological studies The relative risk (RR) is the risk of a disease occurring relative to exposure a way of showing the likelihood of the disease (or any other event) event occurring in the exposed group compared to the non-exposed group. [ A relative risk (RR) of 1 suggests no increase in risk between exposed and non-exposed. A 50% increase in risk is represented as an RR of 1.5. It is the doubling of the relative risk which is key when the RR is 2 or more. An odds ratio (OR) is a method (often used in epidemiological studies) of comparing whether the probability of a certain outcome (such as incidence of a disease) is the same for the case group and the control group. The odds ratio shows how much more likely it is that a person in the case group will develop the outcome in question compared to a person in the control group. It is obtained by dividing the odds of the outcome occurring in the case group by the odds of it occurring in the control group. An odds ratio of 1 suggests that the outcome (the disease, here) is equally likely in both the case group and the control group. An odds ratio greater than one suggests that the outcome is more likely in the case group. 28

29 Confidence intervals are a way of expressing the statistical accuracy of an estimate. Confidence intervals describe the range within which a result for a whole population would occur for a specified proportion of times a survey or test was repeated among a sample of the population. If an estimate has a high error level, the corresponding confidence interval will be wide, and the less certainty we can have that the survey results describe the situation among the whole population. So a narrow confidence interval suggests greater reliability. 12. Conclusion overall The identification, analysis and assessment of emerging risks involves the interaction of science and law. It requires consideration of risks relating to adverse health effects, the potential incidence and extent of such effects, the applicable legal and regulatory environment, and whether and how causation will be proved. Risk reduction strategies are thus dependent on interdependent knowledge and analysis. It is therefore vital to keep up to date with scientific research, and developments in the law of causation (and breach of duty). Developing knowledge relating to constantly changing processes and products is also matched by developments in the law of causation. Past experience has shown that the law can change to address the effect of tortious agents when they become known to be harmful. The paradigm way of proving causation remains the but-for test. But this test has developed in three main ways: the material contribution test, the application of epidemiology to the but for test, and the contribution to the risk test, currently restricted to mesothelioma claims, and arguably likely to remain so. 29