Is there an exposure to asbestos which does not “legally cause” mesothelioma? Evidence from: C Gilham et al. Occup Environ Med (2015);0:1–10. doi:10.1136/oemed-2015-103074 Gilham et al, compared asbestos fibre burdens from the lungs of mesothelioma and lung cancer cases and from these, developed risk equations. 79% of the fibres they observed were amosite; the subjects were all resident in the UK. Fibre burden and diagnosis were objective and precise; which means the main uncertainties were in unintentional bias and biological variability, about which not much more could be done except by sub categorisation by genetic and epigenetic profile (which would require a much bigger study). Using mathematical methods adapted from the design of optical telescopes and electronic circuits, we have extended the reported analysis to make an original estimate of de minimis. Compared with background, and for asbestos fibres which are longer than 5 micrometres, the smallest detectable increase in the

Science is not the decider of fact. For example, cancer is probably the result of an accumulation within a given cell, of seven or so genetic changes, but the courts decide that any given cancer does not have a cumulative cause. The scientific probability of it not being cumulative in nature is very small indeed but the legal fact (following the Phurnacite case) is that it is not. For example, among those who make a claim for whiplash if 65% are actually injured and the test is 80% accurate then the Bayesian odds of making a diagnosis is six to one. The inference is that 86% will be diagnosed! Yet if a random sample of the population is assessed (annual prevalence ~ 1%), the odds are worse than eleven to one (against) that anyone given a whiplash diagnosis actually has such an injury. Given these scientific ‘facts’, the court would be forgiven for deciding either there was no such thing as whiplash or in the alternate, that everyone who makes a claim must be injured and it

The report outlines how noise pollution can affect wellbeing and perhaps also health. Annoyance and heart disease are highlighted here. The report follows an EU Directive on noise pollution and aims to encourage harmonisation of responses across Europe. Evidence from: European Environment Agency ISBN 978-92-9213-140-1 Oct (2010) Good practice guide on noise exposure and potential health effects Risk of heart attack has been related to environmental noise exposure. 11#1 4

Smoking as a contributor to the cause of occupational lung cancer has been taken to court, but the situation is unclear. The detailed mechanisms now being worked on will allow greater certainty in the future, but not yet. In the alternate, inflammation could be used as a catch-all mechanism. Any cause or contributor to inflammation could be cited as a contributory cause. Cancer is indivisible, BUT, details of the mechanism could provide defences based on timing of exposure, and de minimis. Smoking causes cardiovascular disease. Occupational or product contributions to this would be possible. Indivisible and divisible outcomes are both possible. Likely claims involving smoking would be when fine dust exposure is alleged to be a cause of indivisible heart disease. More speculative would occupational causes of debilitating high blood pressure or angina; both of which are divisible. Evidence from: A report of the Surgeon General (2010) ISBN 978-0-16-084078-4 How Tobacco Smoke Causes Diseas

An association with two specific biocides is reported and given the size and design of the study, the effects could be real. A plausible cumulative mechanism is supported. However, some data also suggest a lack of support for a cumulative mechanism. Previous reports from the same study failed to find a specific risk from rotenone or paraquat. Evidence from: CM Tanner et al. Environmental Health Perspectives. (2011) doi: 10.1289/ehp.1002839 Statistically significant adjusted odds ratios for individual agents and when grouped by mechanism type, combined with a plausible mechanism suggest a causal role for the two pesticides. 11#1 2

Evidence from environmental health research could eventually lead to liability exposure, based on material contribution. Of more immediate concern is the support for setting an occupational exposure standard; which would include  nanoparticles. Evidence from: Committee on the Medical Effects of Air Pollutants (COMEAP) (2010) ISBN 978-0-85951-685-3 The Mortality Effects of Long-Term Exposure to Particulate Air Pollution in the United Kingdom PM2.5 exposure is diffuse in nature and as such a specific insured would be hard to identify. Even if they were identified, the likelihood is that the pollution is not sudden and accidental. However, given the developing theory of liability for diffuse effects (climate change, biodiversity) it is conceivable that liability for PM2.5 exposure could one day be an issue for heart disease and stroke. 11#1 1  

The research provides some evidence that long term exposure to loud noise at work is associated with increased risk of some forms of heart disease. Evidence from: W Q Gan et al. Occup Environ Med (2011) Vol.68 p 183-190 Exposure to occupational noise and cardiovascular disease in the United States: the National Health and Nutrition Examination Survey 1999-2004 No account was taken of shift work, physical workload, noise exposure from road traffic, fine particulate air pollution in the workplace and residence. This was a cross-sectional experiment; causation is unclear. 11#1 16

IIAC observe a small increase in risk of lung cancer and bladder cancer in occupational painters. In their own analysis of the data, IIAC find the relative risk was approximately 1.25 and 1.10 respectively, each with high precision and statistically significant. However there was no correction for smoking. Other, work, reported since the IIAC review suggests an argument for material contribution could be attempted. Evidence from: IIAC November 2010 IIAC Commissioned Reviews 2010: Cancer risk in Painters In none of the cancers considered here, was there a doubling of risk associated with working as a painter. It is unlikely there will be prescription for industrial injuries disablement benefit. For civil cases the problem then moves on to one of material contribution rather than an outright presumption of causation. 11#1 13

The study lends some support to the contention that low levels of exposure to crystalline silica can cause lung cancer. Lung cancer risk was increased at levels of exposure below those likely to cause silicosis. If accurate, the findings imply that the current WEL of 0.1 mg.m-3 would not prevent all cases of lung cancer. Risk was detectable only after 25 years of low level exposure. Silicosis status was not reported or corrected for. Evidence from: L Preller et al. Occup Environ Med. (2010) Vol.67 p 657-663 Occupational exposure to silica and lung cancer risk in the Netherlands The current WEL for crystalline silica is 0.1 mg.m-3; equivalent to 4.5 mg.m-3.years for a working lifetime of 45 years. In 1993 HSE estimated that > 90,000 UK workers were exposed to levels in excess of this. 11#1 12

The key additional uncertainty introduced by increasing the scope of liability for environmental change arises as a result of the potential for sudden transitions in ecosystems and the value of the services they provide. If transitions and their effects could be predicted with confidence then they may be insurable. In our view, the uncertainties are currently too large. Evidence from: andrew@reliabilityoxford.co.uk The real problems are: • Pace of change, not change itself. Complex systems can be driven to the point where they become unstable and fail. All systems can be driven to the point where supply of ecosystem services cannot meet demand. The annual cost of adaptation or failing to adapt may become too high if the pace of change is too high. • Reversibility of change. Complex systems will always self stabilise. The work required to move from a new state induced by the insured to a state regarded as the right state can be complex and disproportionate. 11#1 11

Environmental Regulation has developed very significantly over the past 30 years, principally with respect to pollution prevention and, protection of valuable sites and resources such as drinking water. But biodiversity is a more generalisable concept which helps in the understanding of the “Common Good” that nature provides. Protection of this could be achieved by a combination of regulation and liability for remediation. The scope of the latter is currently unpredictable, but would initially operate through regulation and nuisance. This could change if concepts such as material interest, proximity and foreseeability are changed to suit political ends. While there is uncertainty, there is a need for insurers to engage with politicians. Evidence from: andrew@reliabilityoxford.co.uk Investment in response to adverse events could be insured, e.g. remediation of contaminated land. If this route is favoured then the price of insurance will depend very strongly on the specified quality of a

MMWR Weekly 8th December 2006 “Gastrointestinal Injuries from Magnet Ingestion in Children — United States, 2003–2006” Three cases of injury after swallowing magnets included as part of children’s toys. Autopsy in one case showed that two groups of magnets had joined across two loops of intestine, restricting blood supply to the tissues leading to sepsis. Surgery in another case found a magnet to have perforated the end of the small intestine. The editor [working for Center for Disease Control (CDC)] recommends that caregivers should keep products with magnets out of environments where children aged <6 years are playing and be aware of the unique risks if ingested.

The research demonstrates a mechanism whereby a joint injury could in principle aggravate, accelerate or cause a chronic joint disorder. Even where the injury does not directly damage the joint cartilages the proposal is that bleeding into the joint has the potential to have an irreversible damaging effect on that cartilage. Evidence from: NWD Jansen et al. Arthritis and Rheumatism (2007) Vol.56#1 p 199 – 207 “Exposure of Human Cartilage Tissue to Low Concentrations of Blood for a Short Period of Time Leads to Prolonged Cartilage Damage” The above mechanism could perhaps provide a non-psychosocial explanation for chronic neck pain following for example, whiplash neck injury. Osteoarthritis could perhaps be accelerated by such an injury. However, it is surprising that initial injury severity is not predictive of outcome after one year; if the above mechanism is valid this is what would be expected. Further detail: 6#9-10 22

In a glass house experiment, GM plants increased the soil concentration of Bt proteins but this change in soil conditions had no measureable effect on nematode or soil bacteria populations. Evidence from: BS Griffiths et al. Plant Biotechnology Journal (2007) Vol.5 p 60 – 68 “Varietal effects of eight paired lines of transgenic Bt maize and near-isogenic non- Bt maize on soil microbial and nematode community structure” Further detail: 6#9-10 21

Acoustic neuroma (AN) incidence has increased very significantly in the past decade; this paper explores some of the possible risk factors. Evidence from: ML Schoemaker et al. Int. J. Cancer (2006) Vol. 120 p 103–110 “Medical history, cigarette smoking and risk of acoustic neuroma: An international case-control study” Epilepsy, smoking and parity should be assessed in any future research into causes of AN. Further detail: 6#9-10 20

The statistical links between allergies and specific cancers continue to be reinforced and this paper finds that risk of glioma is reduced in those with a history of allergy. The lack of variation of protection with cancer type leads us to the tentative view that there would be unlikely to be an effect [protective or aggravating] of occupationally acquired allergy in the absence of atopy. Evidence from: MJ Schoemaker et al. Int. J. Cancer (2006) Vol.119 p 2165–2172 “History of allergies and risk of glioma in adults” It is tempting to propose that allergies have the effect of increasing the ability of the immune system to recognise, and eliminate, brain tumours. Further detail: 6#9-10 18

A link between emf exposure and poor prognosis for those with leukaemia has been proposed. This research sought evidence of associations between exposure and the recognised causes of poor prognosis and found none. Evidence from: DE Foliart et al. Bioelectromagnetics (2007) Vol. 28 p 69 – 71 “Magnetic Field Exposure and Prognostic Factors in Childhood Leukaemia” Lack of identifiable mechanism for a less good prognosis doesn’t mean there is no causal link. Further detail: 6#9-10 17

The case examined whether or not there was a duty of care to protect employees from exposure to noise of less than 90 dB(A) intensity. It concluded that in general 90 dB(A) was an acceptable threshold from 1963 up until 1987 when the case for an 85 dB(A) action level was first consulted on in public. It also established a method for determining noise induced hearing loss when loss was small and rejected a duty of care based on the prevention of harm when that harm could not be identified in an individual case. Harm from exposures at 85 dB(A) was probably undetectable. Evidence from: Parkes v Meridian Ltd [2007] EWHC B1 (QB) 14th Feb 2007. in an area where the hearing loss to be expected can be regarded as marginal, or minimal, or so small as not to be identifiable in individuals but only in a statistical sense there could in my view be no liability at common law for breach of duty in exposing employees at such levels. Degree of risk remains a valid test of the standard applied to the d

Contrary to mainstream opinion there was no clear link between susceptibility to allergens [i.e. Atopy] and asthma rates. Instead it was found that prevalence of atopy was uniform regardless of asthma rates. Interpretations include the strong possibility that there is an [unidentified] environmental cause of atopy. Evidence from: R Ronchetti et al. Int Arch Allergy Immunol (2007) Vol.142 p 79–85 “The Prevalence of Atopy in Asthmatic Children Correlates Strictly with the Prevalence of Atopy among Nonasthmatic Children” Further detail: 6#9-10 11

Evidence from: IARC Press release No. 173. 1st Feb 2007 “IARC Study Demonstrates Exposure to Coworkers’ Tobacco Smoke Increases Lung Cancer Risk” A more detailed report of this work will be published in an academic journal in the near future. For now, the following quote is indicative of the anticipated findings. For the first time, a clear dose-response between exposure to co-workers’ smoke and lung cancer risk was demonstrated, which greatly strengthens the causal interpretation of the increased lung cancer findings. It is noteworthy that the dose-response analysis showed a twofold increased risk of lung cancer among highly exposed workers. Comment Some Claimants could be convincing as to the probability that their only significant exposure was at work.

The German risk assessment institute concludes that there is a statistically significant association between exposure to pesticides and development of Parkinson’s Disease. There is insufficient evidence to determine the mechanism of this association. Evidence from: BfR Expert Opinion No. 033/2006, 27 June 2006 “Pesticide exposure and Parkinson’s disease (PD): BfR sees association but no causal relationship” Further detail: 6#9-10 8

Evidence of a significantly increased risk of TB among smokers is presented. Risks associated with passive smoking are less clear. Evidence from: HH Lin et al. PLoS Med 4(1): e20. doi:10.1371/journal.pmed.0040020 “Tobacco Smoke, Indoor Air Pollution and Tuberculosis: A Systematic Review and Meta-Analysis” Several reports have suggested that exposure to tobacco smoke increases the risk of catching Tuberculosis (TB) or, at least remaining in a disease state. This review attempts to consolidate opinion and quantify the risk. Further detail: 6#9-10 3

The meta analysis seems to show that there is no synergistic effect between silicosis and smoking in the risk of lung cancer. Evidence from: ITS Yu et al. Int. J. Cancer (2006) Vol.120 p 133 – 139 “Exploring the joint effects of silicosis and smoking on lung cancer risks” The problem of joint effects has been extensively developed for asbestos and smoking. Further detail: 6#9-10 1

Evidence from: L Mellemkjaer et al. Epidemiology (2006) Vol.17 p 668–673 “Risks for Skin and Other Cancers Up to 25 Years after Burn Injuries” The rate of skin cancer in burn victims was significantly reduced by 30%. Further detail: 6#7-8 30