Legal developments in asbestos claims

Transcription

1 Legal developments in asbestos claims Toby Scott Partner, BLM Stockton-on-Tees Birmingham Cardiff Leeds Liverpool London Manchester Southampton Stockton-on-Tees

2 Asbestos Working Party Report Why was it prepared? The answer is in the graph (Appendix A). For many years there had been a close correlation between claims, observed deaths and the HSE model. Modelled male mesothelioma deaths and claims Claims experience has deviated dramatically from previously close correlation to deaths and there was a concern that the overall trend line would need to be varied UK Mesothelioma 2003 to 2007 In claims deaths In claims (30% higher) deaths (18% higher) Even so claims appear to be increasing at almost twice the rate of deaths compared to prior experience. Possible explanations? a Each sufferer making claims to more insurance companies. This was discounted because an increasing number of insurers would lead to a falling trend in average cost per (insurance) claim whereas the trend is increasing in line with inflation. It was felt this was a contrast. The Data Protection Act prevents more detailed analysis. b Greater levels of insurance coverage. It was accepted that insured proportion of each claim has been increasing entirely Unsurprising as the years pass but too gradual to explain the discrepancy. c Reduction of delays This was considered and discounted d Increasing propensity to sue (P7) This appeared to be the most likely explanation. Other features 36% of all victims made an insurance claim in % of all victims made an insurance claim in 2007 Claimant to insurance claims figures have reduced from 1:2.4 to 1:2.1 in 4 from 2003 to 2007 NHS National Mesothelioma Framework In one specialist centre lifetime diagnosis increased from 50% to 95% over eight years Younger victims more likely to claim Legal developments in asbestos claims_tos_0909 1

3 Professor Peto and Others, March 2009 (Extract of Appendix B) UK mesothelioma death rate highest in world. 1 in 40 of all cancer in men aged less than 80 1 in 170 of all men born in 1940s will die of mesothelioma Risk of mesothelioma 1 in 1000 from environmental exposure Exposure to amosite in building industry underestimated much higher in UK compared to US continued until 1980s Britain was the largest importer of amosite Higher prediction of mesothelioma deaths? Future projection HSE projection will underestimate deaths Past deaths are not a reliable indicator of future death roles 10% increase in deaths production (20% more likely) Mesothelioma observed and predicted death (P12) See graph of observed and projected deaths (2004) (Appendix C). The revised bell curve is likely to show a higher annual death rate. We do not know if the peak will occur later. 2 Breach of duty Context Those coming to asbestos claims for the first time are often surprised that in a large proportion of claims employers or their insurers pay damages where the employer could not have known about the risks or taken precautions to eliminate risks to employees. Some history dates of knowledge The development of knowledge of the dangers of an asbestos related disease. Even in the early 20 th Century medical practitioners were beginning to report injury and death of patients from asbestosis. Reports of Doctor Merewether the Medical Inspector of Factories from 1930 was the first publication of significance and made a number of recommendations that led to the passing of the Asbestos Industry Regulations 1931 which I will be covering later. These regulations were directed towards the manufacturing industry whose workers were perceived to be at risk of asbestosis arising as a result of heavy exposure. In 1965 the Newhouse & Thompson paper highlighted the risks of much lower concentrations of asbestos exposure as found in industries outside of the asbestos manufacturing industry. This led to an asbestos scare of real resonance leading to the publication in October 1965 of a comprehensive article in the Sunday Times about these risks. Traditionally courts have allowed employers a period of time in which to react to developing knowledge of risk and to take precautions to eliminate such risks. Employers cannot expect the courts to allow that level of leniency in other cases and we have seen reported decisions of employers having a period of grace, if we can call it that, of one or two years. Rule of thumb: The asbestosis range You may be familiar with the concept of the asbestosis range from lung cancer cases. This range is the level of cumulative asbestos exposure in terms of the nature, extent and duration of exposure that is regarded as necessary to either cause or give rise to a risk of asbestosis arising. Based upon the history at common law this provides a potential rule of thumb. Legal developments in asbestos claims_tos_0909 2

4 Rule of thumb - Pre 1965 exposure within the range will be in breach - Post 1965 all significant exposures likely to be in breach How useful? The fact is, not without some modification, that when employers settle many cases every year involving exposure to asbestos before 1965 below the asbestosis range. They do this because of the impact of statutory duties. Also periods of intense exposure, if brief may be below the range but causative of exposure, and will be in breach because the exposures represented a foreseeable risk of harm (of asbestosis). Impact of statutory duties There are two key provisions that we need to remember: (i) (ii) (iii) The 1931 Asbestos Industry Regulations were enacted to protect employees engaged in the asbestos industry. These regulations are virtually uniformly alleged or pleaded against employers but the reality is that they only apply to employees in the industry engaged in asbestos manufacturing processes for over eight hours a week; The 1937 Factories Act imposes obligations to ventilate workplaces and to take steps to remove dust and fumes. The majority of statutory duties impose obligations to remove dust and fumes either likely to be injurious or to take precautions so far as practicable and do not therefore impose obligations in excess of common law obligations. Section 4 however and possibly section 47 do impose higher duties. In Ebbs v James Whitson [1952] (P16) the Court of Appeal concluded that it is immaterial as to whether an occupier knew or ought to have known that dust might be injurious to health and it is the Factories Acts which are generally and correctly regarded as creating this higher duty. A suggested rule of thumb I set out here a possible approach: Is it a factory? If yes, is exposure significant/in excess of de minimis If no: Pre-1965 (1968) is exposure above the asbestosis range? Abraham v G Ireson & Son (Properties) Limited and Others Essentially close focus needs to be made on the key issue of whether statutory duties imposing a higher obligation do in fact apply. If they do then all exposures in excess of de minimis are likely to be in breach. If they don t, however, and many of the decided cases concern cases without statutory duties then you should be exploring the possibility of a liability defence. Before 1965 such defences might arise with mild to moderate exposures and after 1965 such defences might arise where exposures are trifling or insignificant. (Note Abraham v G Ireson & Son (Properties) Limited and another Swift J 31/7/09 claimant employed by one employer between August 1956 to 1961/62 with exposure limited to use of asbestos string for caulking joints of pipes exposure described as very light and intermittent). Legal developments in asbestos claims_tos_0909 3

5 With another employer 1962/63 to 1965 low level of exposure whilst using asbestos scorch pads to protect surfaces such as skirting boards when soldering pipe joints with a blow lamp. This exposure described as modest and infrequent. The claimant argued that association between asbestos dust and risk of pulmonary injury was known from the 1950s and that there was no safe level. On review of literature however Swift J concluded that although literature and Factories Inspectors Reports concluded that asbestos dust was highly dangerous the message was delivered within the context of the known risk of asbestosis and exposure to significant quantities of dust. But this type of exposure was not foreseeable prior to the publication of the Newhouse & Thompson paper. Swift J rejected the claimant s assertion that the Building Regulations 1948 and the Construction (General Provisions) Regulations 1961 should be construed objectively and so statutory duties did not change the common law position. Post 1965 (1968) is exposure significant? We are concerned here with levels of exposure that are so low in terms of nature, extent and duration as to be insignificant the only basis upon which common law liability can be avoided after A breach of any relevant statutory duties (if causative) will lead to recovery or will it? Relative risk defence The claimant will need to establish a breach of statutory or common law duty and must also establish that the breach is causative. Breach of duty and causation in these claims is therefore inextricably linked. The claimant will need to establish that the breach is causative this is what is known by relative risk defence. Sienkewicz v Grief (25/11/08) This office worker in a contaminated building with exposures levels giving rise to an 18% increase in the background risk. Failed at first instance. The case now proceeds to the Court of Appeal. The deceased was employed by the defendant who were predecessors from 1966 until She was employed as an office worker who was, on occasions, required to visit other areas of the defendant s premises at Ellesmere Port. The trial judge accepted the medical evidence and the defendant s engineer as to likely fibre levels and concluded that, over 18 years, the claimant s total likely cumulative asbestos exposure was fibres/ml hours. To put this into context, this should be compared to a minimum limit for the asbestosis range of 25 fibres ml/years below which individuals are not at risk of developing asbestosis. The judge found as a fact that the deceased s working life for the defendant increased her background risk from 24 to cases per million, an increase in risk of 18%. That statistic requires some discussion. Firstly: (a) (b) (c) The judge declined the claimant s invitation to follow a Fairchild type formulation to causation on the basis that he did not need to distinguish between the causative potency of exposure with two tort feasors, but here one tort feasor seen against the presence of other environmental (or background) exposure. He accepted that, as Fairchild would not have an application, it was not open to him to simply consider whether there was a material increase in risk. Accepted the defendant s submission that the claimant had to prove that the occupational exposure was a more likely cause, on the balance of probabilities, of the mesothelioma than any background environmental exposure. Legal developments in asbestos claims_tos_0909 4

6 (d) On the basis of the statistics, the background risk (24 cases per million) is six times more likely as a potential cause than the occupational exposure (which increased the background risk by 4,000,000). As stated above, the case proceeds to the Court of Appeal and the clue to the claimant s approach lies in the concluding sections of the judgment and the discussion of the claimant s contentions that the Fairchild type formulation should be extended to assist claimants who can prove a material increase in risk. The relevance of this type of approach to, for example, lung cancer cases is obvious and so we will await the decision of the Court of Appeal with interest. 3 Evidential standards Challenges for claimants Dead or untraceable workmates. Ageing clients. No documentation Confused working environment here we mean occupiers, contractors and subcontractors all working in the same workplace. The condition may be the only real evidence of exposure In a significant minority of cases claimants will present with an asbestos related condition generally mesothelioma in circumstances where family and friends had not anticipated it and this causes the evidential challenges discussed above. The claimant is then left having to construct a case. We often reach a situation where the condition itself may be the only evidence of exposure and the only evidence of exposure with the defendant is second-hand through the testimony of family members giving evidence to the court as to what they were told by the deceased or by friends of the deceased. Construction of a case They will often, except in the most extreme cases, find just enough evidence to satisfy a court. Earlier failure to report exposure is not fatal for example in Maggs v Anstey (2007) EWHC515 (QB) when the claimant developed symptoms he was certain that he had never been exposed to asbestos but as time passed he was able to recall a single instance of exposure for one weekend in the late 1960s early 1970s. Some corroboration of this came from written diary entries made by Mr Maggs with little more than a reference to a delivery of copper at Avonmouth Docks. The claimant s recollection and the diary entries did at least corroborate that at some point in the late 1960s and early 1970s he had been involved in a delivery from Avonmouth Docks and it was not necessarily unreasonable for the court to infer that this delivery is the same as that in the diary entries but the court did however feel entitled to infer that the delivery occurred after Role of engineer Evidentially dubious cases have in the past been lost by claimants with trial judges expressing surprise that engineers were not engaged. Claimant's solicitors, often on the recommendation of Counsel, will generally seek to involve an engineer at the earlier stage in such cases. These engineers effectively provide the judicial polyfiller for the evidential cracks in a claimant s case giving evidence, for example, as to what conditions at work would have been like or what the claimant s work would have involved and what precautions would have or would not have been Legal developments in asbestos claims_tos_0909 5

7 taken. It is not of course the role of an engineer to provide lay witness evidence and such evidence can be criticised as being essentially speculative particularly where an engineer will have qualified many years after the alleged exposure and where the evidence is effectively given on the strength of the engineer s involvement in other cases. Trial judges do however find this sort of evidence helpful and are indulgent to claimants even in the face of protests from defendant s counsel. I will discuss this further in a minute but these types of case need to be considered very pro-actively even in the pre-litigation stages where often the damage can be done or risks averted. Indirect evidence and judicial inferences We saw in Maggs how a judge could make inferences in the absence of direct evidence as a means of finding an evidentially proven case. Brett v Reading University [CA 14/2/07] The use of judicial inferences was considered in Brett in which the deceased supervised a demolition of a library which contained asbestos. The trial judge rejected the claim on the basis that no evidence had been adduced that the relevant contractors had failed to carry out the work properly. The Court of Appeal upheld the decision at first instance. They concluded that there was no evidence of exposure to asbestos during the course of the work. Significantly they were of the view that if there had been no other exposure (and the deceased had been exposed in other employment) then the inference that there was exposure during this work would have been irresistible although the development of the mesothelioma could be explained by the other exposures. It seems to me that it is the issue of potential other exposures that provides the key to the judicial approach in these cases. Compare Cox v Rolls Royce [22/11/07] Mr Cox worked for the defendant for an unspecified period in 1966/67. Mrs Cox maintained that her late husband was exposed whilst working in power stations but Mr Cox had not provided a witness statement. The claimant s engineer described how employees who carried out work like Mr Cox would have been heavily exposed. The defendant s pointed to the fact that Mr Cox s application for industrial benefits identified four other periods of exposure with other employers. The judge found for the claimant and was upheld by the Court of Appeal. Conclusions sauce for the goose? (i) (ii) (iii) The defence of these types of claim is probably only where there is clear evidence of exposure in other non-pursued employment; where there is no alternative explanation for the exposure then it is difficult to see how a defendant can overcome a claimant, assisted by an engineer. In such cases the cogency of evidence in respect of the other employment must be looked at very carefully. Frankly what is sauce for the goose is probably not sauce for the gander. Defendants will have to give trial judges little opportunity to find that evidence of exposure with the defendant is no stronger or more likely than exposure with other employers and even then Cox shows that the evidence of an engineer can be used to provide the basis for a judicial inference; The use of consulting engineers in these cases is therefore essential. So what can be done before the case litigates? Here are some hints: (a) Do not be afraid to make a qualified admission along the lines that if the claimant establishes exposure to asbestos in excess of de minimis then it is agreed such Legal developments in asbestos claims_tos_0909 6

8 exposure occurred in breach. This may deter the claimant from instructing an engineer; (b) (c) Be aware that an admission of negligent exposure is an admission of exposure to causatively significant levels particularly in mesothelioma claims; If the claimant is adamant that he is going to instruct an engineer then there can be no harm in participating in a joint instruction provided: You are satisfied as to the even-handedness of the engineer; The engineer agrees to restrict his expert evidence to the evidence supplied to him in the immediate case; Legal developments in asbestos claims_tos_0909 7

9 Minimal symptom claims Minimal symptom claims pleural plaques and beyond (i) Asymptomatic and pre-clinical DPT and asbestosis claims Asymptomatic and pre-clinical claims are in all probability a response by claimant lawyers to the failure of the pleural plaques litigation. Claims previously presented as pleural plaques claims can with the impact of high resolution CT scanning in many cases be converted to asymptomatic or pre-clinical claims for diffuse pleural thickening and asbestosis. This means that whilst the condition is diagnosable radiologically it may not be detectable on the basis of clinical signs and symptoms alone or indeed on the basis of conventional radiology alone. To all intents and purposes the claimant may feel no worse than the individual with pleural plaques. (ii) The threshold of recoverability So what is the threshold? The law in the strict sense of the word seems fairly settled if not its application to asbestos related disease claims. Cartledge v Jopling remains authority for the proposition that physiological injury is actionable. In Owen v Esso Exploration & Production His Honour Judge Stephen Stewart distinguished Mr Owen s asymptomatic pleural thickening and asbestosis detectible only on CT scan but not on x-ray from the claimant s asymptomatic silicosis because in Cartledge there was evidence of scarring, diminished elasticity of the lungs and depravation of reserved capacity. The claimants had failed to prove evidence of any significant effect on elasticity or functioning of lung tissue. He found for the defendants but acknowledged that if the claimant had proved significant effect on lung capacity, reserves or elasticity he may have decided differently. Beddoes v Vinters Armstrong (2009) The claimants in Beddoes called extensive medical evidence. The key features of the decision can be summarised: Two of the claimants failed on the same basis as Mr Owen - they were unable to prove any significant effect on lung capacity or reserve and so we do at least now have one judge s interpretation of how Cartledge is to be applied to asymptomatic asbestos cases. This is of course a County Court case and it is too early to determine whether or not other challenges can be made. On the basis of Judge Walton s decision the issue of recoverability will be fact specific with fairly detailed medical evidence required in each case. Quantum layers of damage Judge Walton adopted bottom up approach to assessing damages in the cases of Mr Beddoes and Mr Cooksey. He started with the decision of Lady Justice Smith in her minority judgment in Rothwell to the effect that claimants with pleural plaques should receive 5,000 provisional damages. He then sought to impose on top of that a supplement to reflect the claimant s additional symptoms and anxiety (the latter only being recoverable because damage had been proven). He then sought to impose a further supplement based upon what is now the uncontentious approach of discounting any likely final award with a discount for risk and a discount for accelerated receipt. Analysis On a top down analysis, particularly when the risk based supplement is increased to include nursing care and financial losses these awards seem too high and out of Legal developments in asbestos claims_tos_0909 8

10 alignment with other respiratory claims. I believe the reason for this lies not with the basic approach but a misapplication in relation to the middle layer. Claimants with pleural plaques were traditionally compensated for the anxiety within the 5,000 provisional damages award. This was Lady Justice Smith s 5,000 figure. Judge Walton added an additional 4,000 to cover symptoms and anxiety thereby doubly compensating the claimant for anxiety because anxiety had been included within the original bottom layer award. Mr Beddoes received 4,000 for 1.6% disability. On this basis the supplement for symptoms would increase as follows: % Disability Amount 5000 provisionals plus 1.6 4, , , , , , , , , , British Coal Compensation Scheme Equivalent (61-70) You will see that I have inserted the British Coal Compensation Scheme equivalent next to the supplements. It should be remembered that the British Coal Scheme was a mediated court approved agreement widely regarded at the time as generous to claimants. The figures are of course simply the middle layer for disability and anxiety, and are out of kilter with other common law awards. Even if the anxiety component of the middle layer is removed the increment for symptoms seems too high. You will see the two do not bear comparison particularly when one considers that COPD is a progressive condition and that the figures quoted above include solely the symptom based component of the award awarded as an immediate award within a provisional damages regime. In conclusion whilst providing some answers the decision in Beddoes is unlikely to be seen by insurers as providing an appropriate level of compensation for the true nature of the condition and equally we cannot rule out the prospect of claimants in the future seeking to effectively partially restore the pleural plaques regime by CT scanning and arguing for recovery on the basis of Cartledge v Joplin on the basis of radiological diagnosis alone. Within your pack you will find a hard copy of this presentation together with some supporting materials. If after this there are any other materials that you would like us to source for you please do not hesitate to telephone or me. Appendices A Modelled male mesothelioma deaths B Peto and Others March 09 Discussion Extract C Graph Observed and Predicted Deaths D Abraham v G Ireson & Son (Properties) Limited & others (Swift J 31/7/09) E Brett v University of Reading (CA ) F Cox v Rolls Royce ( ) Legal developments in asbestos claims_tos_0909 9

11 Berrymans Lace Mawer LLP 2009 Disclaimer This document does not present a complete or comprehensive statement of the law, nor does it constitute legal advice. It is intended only to highlight issues that may be of interest to clients of Berrymans Lace Mawer. Specialist legal advice should always be sought in any particular case. Information is correct at the time of release. O:\EVENTS\SEMINARS 2009\OCCUPATIONAL DISEASE_MANCHESTER SEPT09\MATERIALS\PAPERS\FORMATTED\FOR \2. ASBESTOS_TOBY SCOTT.DOC Legal developments in asbestos claims_tos_

12 APPENDIX A Modelled male mesothelioma deaths. Legal developments in asbestos claims_tos_

13 APPENDIX B Peto and Others March 09 discussion extract. Legal developments in asbestos claims_tos_

14 Health and Safety Executive Occupational, domestic and environmental mesothelioma risks in Britain A case-control study Prepared by the Institute of Cancer Research and the London School of Hygiene and Tropical Medicine for the Health and Safety Executive 2009 RR696 Research Report

15 4. DISCUSSION 4.1 OCCUPATIONAL EXPOSURE Occupational PMRs for mesothelioma based on last full-time occupation as recorded on death certificates provide the only detailed data on mesothelioma risks in Britain(McElvenny et al., 2005). The risk depends mainly on asbestos exposure below age 30 however (tables and 3.2.4), and our study provides the first overview of the distribution of risk in the British population, the extraordinary risks suffered by men who did the most dangerous jobs when they were young, and the contribution of environmental exposure, particularly to the families of exposed workers. Recall bias was minimised by structured questions about specific exposures, and our main analyses were based on job title, which should be less liable to differential response by cases than reported asbestos exposure. The value of lifetime job histories is illustrated by the data in table on men who had worked for at least 5 years in low risk industrial occupations. Their OR fell from 4.1 (95%CI: ) to only 1.1 (95% CI: ) when those who had also done more hazardous work were excluded. Among motor mechanics, for example, only 2 of 18 cases compared with 23 of 54 controls had never worked in other more hazardous occupations. Ninety four percent (481/512) of male mesotheliomas and 65% (725/1112) of male controls had worked in a hazardous occupation, implying an attributable fraction of 85% (table 3.4.2). The predicted lifetime mesothelioma risk for British men born in the 1940s who did more than 10 years of relevant work before age 30 is 5.9% for carpenters, 2.0% for plumbers, electricians and painters, and 0.8% for other construction workers (table 3.2.6). The lifetime risk is 1.8% for all high risk non-construction occupations, but this is a broad category that includes dockyard workers, cabin staff on cruise liners and marine engineers. This is the largest published study of mesothelioma risk in relation to lifetime occupational history, but much larger numbers would be needed to provide reliable estimates for individual occupations. Men who had worked in carpentry accounted for 21% of all male mesotheliomas and 4% of controls (table 3.2.3: 49/1112 controls, 105/512 cases), and 33% (table 3.4.3: 10/30) of mesotheliomas in men born since 1950 who started work in 1970 or later. The predicted eventual total of 90,000 mesothelioma deaths in both sexes in Britain by 2050 (Hodgson et al., 2005) will thus include about 15,000 former carpenters. The excess lung cancer risk in heavily exposed workers is likely to be of the same order as the mesothelioma risk (Darnton et al., 2006), so more than one in ten of all British carpenters born in the 1940s may die of a cancer caused by asbestos. A substantial proportion of these deaths will be among those who installed AIB as fireproofing required under building regulations(hmso, 1965) and these will far exceed any possible benefit to the public. Stringent working practices must now be maintained to ensure that the lower but potentially substantial risk to those now removing these same materials will not outweigh the reduction in risk to occupants and maintenance workers from asbestos in buildings. The ORs within each occupational exposure category were lower but still substantially increased even in men who recalled no substantial asbestos exposure, suggesting that many were exposed indirectly or could not identify the asbestos materials they handled. Most people report their own and their parents occupations correctly many years later(berney & Blane, 1997), but recall of past asbestos exposure shows poor reproducibility at re-interview(holmes & Garshick, 1991). A recent study of plumbers showed that many do not recognise the friable asbestos materials that they still 43

16 sometimes encounter(bard & Burdett, 2006). The increased risk for medium risk industrial work reflects widespread and often unrecognised contact with asbestos in metal working, electrical trades and assembly line work. A large proportion of the British population worked in these sectors (24% of male and 20% of female controls). There were too few occupationally exposed female mesotheliomas to estimate risks reliably, but table suggests that workplace exposure caused about 22% (24.5/110) of all female cases. The occupational hazard in women was concentrated in medium risk industrial settings, particularly assembly line work. 4.2 LOW-RISK OCCUPATIONS The preliminary analyses in table confirmed the validity of the medium and low risk industrial job categories. The risk for those who had worked in the low risk industrial group was not elevated once those who had also worked in medium and higher risk jobs were excluded (OR 1.1 in men, 0.5 in women), and the only evidence of an occupational risk outside high or medium risk and construction job categories was the 7 men and 2 women who reported substantial personal or bystander asbestos exposure in other occupations (table 3.4.2: combined OR 3.8, 95%CI ). There was little or no evidence of increased risk in non-industrial workplaces such as schools or hospitals after excluding those who also worked in higher risk jobs (appendix table 3.2.2f). The raised OR for female kitchen workers (OR 23.7 based on 6 cases and 1 control; 95%CI ) seems likely to be a chance finding. These cases did not report asbestos exposure, and no risk was seen in male kitchen workers (no cases and 9 controls). 4.3 NON-OCCUPATIONAL EXPOSURE The only substantial risk factor in those with no direct occupational exposure was living with a high-risk worker before age 30, which approximately doubled the risk in both sexes (combined OR 1.9, 95%CI ). The excess risk, which was confined to those who lived with an exposed worker before age 30, corresponds to an increase in lifetime risk of about 1 per 1,000. The risk due to such domestic exposure has been recognised for many years(bourdes et al., 2000; Joubert et al., 1991; Magnani et al., 2001; Newhouse & Thompson, 1965; Vianna & Polan, 1978). There was no overall risk in men and women who reported living within a mile of a potential environmental hazard (asbestos factory or disposal site, shipyard or power plant) before age 30, although the risk was non-significantly increased in those who lived near one of these potential sources for 20 or more years (OR 3.3, 95% CI , based on 3 cases and 6 controls). We had no means of identifying sites that produced substantial local exposure. There was certainly some hazard to residents around a few factories in the past(magnani et al., 2001; Newhouse & Thompson, 1965), but no risk was seen around others(hammond et al., 1979a), and many apparently environmental cases are related to occupational exposures(arblaster et al., 1995). There was no significant difference between current smokers and lifelong non-smokers either in this apparently unexposed subgroup (OR 1.5, 95%CI ) or overall (OR 1.2, 95%CI 0.9, 1.6). 4.4 BACKGROUND INCIDENCE RATE The unattributed cases in each row of table are presumably due to ambient or unreported asbestos exposure or to other or natural causes. This unexplained lifetime risk is similar for nonindustrial (including retail, office, educational, health care and agricultural) and low-risk industrial work, and corresponds to a predicted lifetime risk of 0.08% in men. The analysis of attributable risk in table indicates that these background cases accounted for 69.6 (14%) of the 512 male and 68.0 (62%) of the 110 female mesothelioma cases. The same analysis restricted to subjects born in 44

17 also gave similar male and female estimates for the number of unattributed cases (31.9/274 in men and 36.7/51 in women). Table shows that the male:female ratio of interviewed cases born (5.4:1) was close to that of all British mesothelioma deaths in among those born (5.7:1). The annual number of unexplained mesotheliomas is thus similar in men and women, and corresponds to a lifetime risk of the order of 1 per 1,000 among Britons of both sexes born in the 1940s. This unexplained rate accounts for almost two-thirds of our female cases, so the threefold increase since 1970 in the overall British female death-rate below age 65 implies at least a doubling in this background female rate. Most of this increase has occurred in the last 10 years, so it seems likely to be due to an increase in ambient asbestos exposure that coincided with the widespread occupational exposures of the 1960s and 1970s rather than to an increase in diagnostic awareness. The inference that the majority of female cases in the UK are due to asbestos exposure is also suggested by the much lower rates seen in both sexes in the US than in the UK (Rake et al., in press 2009). These observations suggest that at most a third,of all mesotheliomas currently occurring in British women are genuinely spontaneous cases unrelated to asbestos exposure, far lower than the 62% that are unexplained in our study. This implies that of the order of 100 female cases per year, and a similar number in men, are caused either by environmental asbestos exposure, or by unsuspected occasional or ambient exposure in occupational settings that we have classified as low risk. Our use of broad job categories as a proxy for asbestos exposure implies averaging a spectrum of risks within each category, but the similarity of the overall background rate in men and women, and in low-risk industrial and non-industrial workers, suggests that few of these cases were due to unreported occupational exposure. 4.5 LATENCY, PERIOD OF EXPOSURE AND FUTURE TRENDS The upper part of table shows that high or medium risk exposure beginning after age 30 did not cause a statistically detectable increase in risk (OR 1.7, 95%CI ). Among men already exposed for 10 or more years before age 30, however, a further 10 or more years of exposure after age 30 increased the OR from 6.8 to 13.1 for all high-risk work. The estimated factor is 2.1 (95%CI ) in an analysis restricted to these two subgroups, suggesting that the mesothelioma risk caused by asbestos exposure before age 30 is approximately doubled by a similar exposure after age 30. These analyses are however confounded by the limited recruitment period, as age at diagnosis and year of birth are almost completely correlated. There was no effect of exposure beginning after age 30 in men born since 1940 (appendix table 3.2.4a: OR 1.1, 95%CI ), but the risk was almost statistically significant in those born in (appendix table 3.2.4b: OR 3.0, 95%CI ). However, men born in were 35 in , when asbestos use was decreasing and less than 30 years before diagnosis. Exposure at age 35 in those born in occurred in , when asbestos was widely used and up to 45 years before diagnosis. If this apparently synergistic interaction between early and later exposure is real, the conventional additive model proposed almost 30 years ago(peto, 1978) on which most risk assessments(hei, 1991) and recent predictions of future mesothelioma incidence(hodgson et al., 2005) were based should be modified. Under this additive model most cases are caused by exposure at younger ages, and the additional effect of later exposure is much less. Lifetime risk estimates are based on the prediction that 0.59% of men born around 1945 will die of mesothelioma, which was derived by fitting an additive model of asbestos carcinogenesis (Hodgson et al., 2005). The death-rate in men born around 1945 is higher up to age 55 than in any earlier or later birth cohort, but few had substantial asbestos exposure after age 35, and we still do not know how rapidly their mortality will 45

18 increase at older ages. The suggestion that many apparently unexposed cases are due to an increase in ambient asbestos exposure in the 1960s and 1970s is also relevant to future projections. If those born after 1980 are at much lower risk from ambient as well as domestic exposure than those born before 1960 the national rate below age 40 may fall substantially by 2020 in both sexes. The future burden of mesothelioma is thus still uncertain. 4.6 RISKS TO CARPENTERS IN THE UK AND ELSEWHERE The risk to carpenters is particularly high in Britain, and also in Australia (Yeung et al., 1999). Other mesothelioma case-control studies (Agudo et al., 2000; Iwatsubo et al., 1998; Muscat & Wynder, 1991; Rodelsperger et al., 2001; Teschke et al., 1997) have not highlighted carpenters as being at particularly high risk. A study in British Columbia(Teschke et al., 1997) found inflated odds ratios for plumbers (OR=8.3, 95%CI ), painters (OR=4.5, 95%CI=1.0, 23.7) and electricians (OR=3.0, 95%CI=0.8, 11.6) as well as sheet metal workers and shipyard workers, though numbers were small. A German study(rodelsperger et al., 2001) found significantly raised odds ratios for electricians (OR=3.0) and mechanicians, fitters and plumbers (OR=2.8) as well as metal production & process workers (OR=2.1) and stationary engine & heavy equipment operators (OR=3.4). A population-based case-control study has recently been conducted in France. Preliminary results report increased risks of mesothelioma in plumbers, pipe-fitters, sheet metal workers and boilermakers, but no mention is made of an increased risk in carpenters(goldberg et al., 2006). A large non-interview case-control study in California obtained limited information on main occupation for over 2,000 mesothelioma cases and pancreatic cancer controls. The highest risk was in shipyard and construction industries, and increased odds ratios were seen for plumbers (OR=4.9, 95%CI= ), electricians (OR=3.8, 95% CI=2.0, 7.1) and painters (OR=2.6, 95% CI= ) but not for carpenters (OR=1.2, 95% CI= )(Pan et al., 2005). Two large cohorts of carpenters belonging to unions in the United States followed their members for cancer incidence(dement et al., 2003) and mortality(robinson et al., 1996). Death certificates for over 27,000 members of the US Carpenter s Union who died in were analysed. The PMR for cancer of the pleura (ICD 163) was 301 (95%CI= ) based on 27 deaths. A further 94 mesothelioma cases were found after manual review of death certificates(robinson et al., 1996). In a cohort of over 13,000 currently employed union carpenters in New Jersey who were followed for cancer incidence between the SIR for cancer of other parts of the respiratory system (ICD ) was 420 (95%CI ) based on 15 cases(dement et al., 2003). 4.7 CONTRIBUTION OF AMOSITE TO UK MESOTHELIOMA INCIDENCE Only 4 male mesotheliomas (<1%) reported working for more than 5 years in asbestos product manufacturing, so we could not distinguish the effects of different types of asbestos in this study, but it seems likely that a major cause of the extraordinary risk to British carpenters was cutting amosite board with power tools, which was widespread in the UK construction industry through the 1970s and continued into the 1980s. By 1960 the UK was importing 38% of total world amosite production, and extensive use of amosite AIB continued through the 1970s. The UK imported 24,000 tons of amosite in 1960, almost 40% of total world production, and extensive use continued until the mid 1970s. Cutting amosite AIB with power tools typically produced dust levels exceeding 20 f/ml(mrc, 1997), ten-fold higher than the control limit of 2 f/ml in manufacturing. In the UK up to 80% of amosite was used in AIB, which was used extensively by carpenters and was installed in over 20% of the ceiling area of new public buildings from (MRC, 1997). The mesothelioma risk caused by amosite is two orders of magnitude greater than for chrysotile (white asbestos)(hodgson & Darnton, 2000), and 9 of 10 lung samples from carpenters who began work in 46

19 the 1960s and died of mesothelioma contained more than 1 amosite fibre per µg. Five contained some crocidolite (blue asbestos), but only one exceeded 1 f/µg(mcdonald et al., 2001b), and crocidolite was not used in Britain after A comparison of current mesothelioma death rates and imports to the US (Virta, 2006) and UK (MRC, 1997) of white, brown and blue (crocidolite) asbestos also suggests that the much higher mesothelioma death-rate in the UK was caused by its much greater use of amosite, which constituted 14% of all asbestos imports into the UK in 1960, compared with only 3% in the US(MRC, 1997; Selikoff et al., 1972). The mesothelioma death-rate in men aged is now more than three times higher in the UK than in the US (US: 0.26 per 100,000 in , based on 139 deaths; UK: 0.87 per 100,000 in , based on 66 deaths). These men were born between 1950 and 1959, and few would have had much asbestos exposure before The UK used slightly less chrysotile during the 1970s (2.4 kg per head in 1970, 1.7 in 1980) than the US (3.1 kg per head in 1970, 1.5 in 1980), and the UK had virtually ceased using crocidolite by 1970, while US crocidolite imports increased from 8,900 tonnes in 1970 to a peak of 16,900 tonnes (0.08 kg per head) in 1978 and remained above 5,000 tonnes per year until However, the UK imported far more amosite per head than the US in the 1970s. UK amosite imports were 21,600 tonnes (0.4 kg per head) in 1970 and did not decline until after 1976, while US amosite imports fell from 12,900 tonnes (0.07 kg per head) in 1970 to 1,400 tonnes in 1976 (Virta, 2006) (MRC, 1997). Australia s mesothelioma death-rates are similar to Britain s, and so were its patterns of amosite and crocidolite use (Leigh & Driscoll, 2003). The mesothelioma risk caused by crocidolite was recognised by 1960(Wagner et al., 1960), and most uses had already ceased when it was effectively banned in the UK following the introduction of the 0.2 f/ml control limit in 1969(MRC, 1997). Amosite is also considerably more dangerous than chrysotile, but this was not generally accepted for a further 20 years, and the UK control limit remained the same for amosite as for chrysotile until 1983(BOHS, 1973) when it was reduced from 2 to 1 f/ml for chrysotile and from 2 to 0.5 f/ml for amosite. The 2 f/ml control limit was observed in most asbestos factories during the 1970s, but substantial asbestos exposure was common in the much larger workforce in construction, and uncontrolled cutting of amosite board with power tools continued in the UK until the 1980s. Among men born since 1950 who started work in 1970 or later, few if any of whom are likely to have used crocidolite products, 33% (10/30) of mesothelioma cases had been carpenters. 4.8 SPECULATIONS ON THE CONTRIBUTION OF CHRYSOTILE Most of the asbestos used in Britain was chrysotile, but amphibole exposure was also common, and we could not identify men who worked with chrysotile and were not also exposed to amosite or crocidolite. An interaction between chrysotile and amphibole asbestos has previously been suggested(acheson & Gardner, 1979), and the effects of protracted exposure shown in table suggest that asbestos acts both early and late in mesothelioma induction. A late-stage promoting effect of asbestos is also suggested by its synergistic interaction with smoking in causing lung cancer(berry & Liddell, 2004)(Hammond et al., 1979b). The effect on mesothelioma risk of stopping asbestos exposure is much less marked than that of stopping smoking on lung cancer risk (Peto et al., 2000), perhaps because amphibole fibres persist in the lung for many decades after exposure has ceased, so even brief exposure produces a lifelong carcinogenic stimulus. Most chrysotile fibres disappear from the lung within a year, and a limited period of chrysotile exposure causes very few mesotheliomas in workers with no other exposure. These observations suggest that chrysotile exposure could increase the lifelong mesothelioma risk in those whose lungs contain 47

20 persistent amosite or crocidolite, just as it causes a much larger increase in the lung cancer risk in lifelong smokers than in non-smokers(hammond et al., 1979b). Most exposed men also inhaled amphibole fibres, which were found in the lungs of 91% of British mesothelioma patients born since 1943 and in 51% of control lungs(mcdonald et al., 2001a). It is widely believed that chrysotile causes few mesotheliomas(mcdonald et al., 2001b), but an interaction between persisting lung burdens of amosite or crocidolite and the much larger amounts of chrysotile that were inhaled by many British workers could increase its effect. 4.9 CURRENT ASBESTOS HAZARDS A large amount of asbestos remains in many buildings, and an important practical question is whether this is still a substantial hazard to construction workers involved in renovation and maintenance of older buildings. The lung burdens of our cases should clarify this. Interviewed mesothelioma cases are followed up, and where possible lung tissue is obtained from post-mortem samples for measurement of asbestos fibres by optical and transmission electron microscopy. We are also obtaining occupational histories and lung samples from resected lung cancer patients, and from younger men and women treated surgically for pneumothorax. The aim of these studies is to relate lung burden to mesothelioma risk, to determine the amount and type of asbestos in the lungs of young building workers, and hence to estimate their continuing risk. They will also provide direct evidence on the contribution of the expansion of amosite use after crocidolite had been effectively phased out to the 50,000 or more mesotheliomas expected in the UK over the next 40 years. 48