Two key starting points: In a well managed system, the decision-maker will know how close to the wind he is sailing. He will know how big  a chance change in wind speed needs to be to give him that extra reward, or risk toppling the ship. Appetite for risk plays an important part; the more chance you take, the bigger the potential reward, and the bigger the potential cost of emergency action. It follows that the successful decision-maker will have a keen interest in the projection of revenue and outgo. Regulators and shareholders would expect expert, transparent and auditable systems, and experienced judgements to be in place. For an overview of the expected approach and how there are particular problems with liability insurance see : Emerging risks management – overview For liability insurance business, the plan begins with identifying the right definition of emerging liability risk:  projected liability exposure will probably exceed its anticipated level by more than its accept

Some of our most talented minds and the vast computing resources at their disposal have been devoted to climate modelling. This has been a huge academic exercise producing an array of approximate solutions which now seem to converge on a view about anthropogenic effects. Man has had and will have a measurable effect on the climate. The basic science is accepted but it is still unclear whether or not some key elements of the model have been missed out or are poorly approximated. This continues to drive the academic endeavour. Does this matter? The simple question soon reveals that in their tremendous efforts to make good physics the basic question has not been answered: are any of the models fit for purpose? If not, will they ever be? Fit for purpose implies that someone needs to be making some kind of decisions based on these models. But who? Politicians, insurers, estates managers, businesses, charities among others. But in each region each stakeholder will have different action thres

BERNARD DIXON, ETC., ET AL. v. FORD MOTOR COMPANY REPORTED IN THE COURT OF SPECIAL APPEALS OF MARYLAND No. 536 September Term, 2011 Plaintiffs expert [Dr Welch] on causation asserted: “every exposure to asbestos is a substantial contributing cause and so brake exposure would be a substantial cause even if [the plaintiff] had other exposures.” On cross-examination, Dr. Welch further explained her opinion that every exposure to asbestos is a “substantial contributing cause” of mesothelioma. The judgment analyses this as follows: Where the question of causation is probabilistic: “substantiality” and “responsibility” necessarily imply some test of magnitude, viz., how much must exposure have increased one’s risk of harm in order to hold the responsible party liable? “substantiality” is essentially a burden of proof For reasons we need not explore in detail, it is not prudent to set a singular minimum “relative risk” value as a legal standard.  The judgment refers to the problem, namely, th

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 authors find little evidence of injury or productivity problems associated with employing older workers. Even if age by itself is not predictive of injury or productivity problems, vulnerabilities do in fact increase with age. It is debatable whether a higher standard of care should automatically be considered at age above 50, but failure to look for known, very common, vulnerabilities at any age could be regarded as negligent. Evidence from: HSE RR832 (2011) An update of the literature on age and employment According to the report, Age by itself is not a valid trigger for a higher standard of the duty of preventive care; breach of duty would be established by the normal standards. 11#1 18

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.

Food Standards Agency 10th November 2006 “Dunbia NI recalls meat products” Over thirty month cattle cannot enter the food chain without first passing a BSE test. When a 54 month old cow was wrongly identified it was mixed with tissues from other animals resulting in 21 products being potentially contaminated with BSE. The products were withdrawn to be disposed of as animal by products. The news report did not say whether or not there was evidence of BSE in any of products. On the 12th of December FSA reported that an untested cow of 30 months and 10 days age had entered the food chain without being tested. The meat was supplied to a farm shop. Comment These incidents could give rise to anxiety in spite of official assurances that the risk is very low. _______ Health Protection Agency 18th January 2007 “4th case of variant CJD infection associated with blood transfusion” Diagnosis occurred nine years after receiving a blood transfusion from someone who later deve

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 answer seems to rely on whether or not there is evidence that fast food is inherently defective and whether or not the Big Food companies know it. The assertion is that it is not inherently defective and guilty knowledge would only be determined if a case went as far as the Discovery procedure. Evidence from: LS Pinchuk. Law.Com 28th Feb 2007 “Are Fast Food Lawsuits Likely to Be the Next ‘Big Tobacco’?” There is, apparently, no evidence that fast food is inherently defective. Further detail: 6#9-10 19

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

Early theories about the toxicity of nanoparticles include dependency on surface area, particle size and surface activity. In this case, surface activity [a measure of the ionic state of the surface] was the key variable in relation to lung inflammation. Evidence from: DB Warheit et al. Toxicological Sciences (2007) Vol. 95(1) p 270 – 280 “Pulmonary Bioassay Studies with Nanoscale and Fine-Quartz Particles in Rats: Toxicity is Not Dependent upon Particle Size but on Surface Characteristics” Surface activity can be measured in a standard way, but guidance as to safe or unsafe levels is not available. Further detail: 6#9-10 15

The extensive and logically structured report examines what research is needed to support the risk regulation of nanotechnologies. Attention is restricted to poorly soluble, engineered particles that may be encountered during manufacture or as free particles in a product and which have the potential to persist once in the body. In our view, a significant absence from the plan is the understanding of the mode of action of the nano particles; i.e. those actions which make them commercially exploitable. Evidence from: BfR August 2006 “DRAFT: Nanotechnology: Health and Environmental Risks of Nanoparticles– Research strategy” The research needs identified are based entirely on classical toxicology and exposure assessment concepts e.g. surface area, bio persistence, surface reactivity, stereochemistry. There is no mention of risk assessment for the intended property or action of the nano engineered product. The rationale is based on passive properties. Further detail: 6#9-10 14