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

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

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

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

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

The finding that use of sunbeds could lead to increased risk of melanoma and squamous cell carcinoma cancer should come as no surprise. Evidence from: IARC Press Release No 171 29th November 2006 “Sunbed use in youth unequivocally associated with skin cancer” Further detail. 6#9-10 13

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

The report lists current and developing applications of non-food crops and other measures designed to reduce dependence on fossil fuels and to increase sustainability and to reduce environmental impact. It also lists current drivers and barriers to uptake. In our view, opinion as to drivers and barriers is essential when forming opinion of potential liability exposure should there be any potential for harm associated with the product. Evidence from: DEFRA/DTI Nov 2006 “A strategy for non-food crops and uses Two year progress report” Renewable fuels produce large quantities of waste biomass and ash. Small scale bio-fuels production may escape appropriate engineering and operation standards or inspection. Waste management facilities may be inadequate. Further detail: 6#9-10 7

The ELD introduces a common framework for the assessment of damage, standards and financing of remediation. Many of the provisions already operate in England, Wales and NI. New defences are proposed but, in our view, would have limited scope if the directive is transposed as described in this consultation. New liabilities for remediation following release of micro and macro organisms are identified. New options of complementary and compensatory remediation are likely to be introduced. The Government proposes to resist the use of a “permit” and “development risk” defences. The ELD creates the possibility of using these defences but each jurisdiction can define the scope that applies. The choice of scope could be challenged. In our view, insurance against the costs of remediation would not experience a step change as a result of this directive and the way the UK government intends to transpose it. Liabilities to third parties would probably be unaffected though there may be more scope fo

The Scientific Panel on Food Additives, Flavourings, Processing Aids and Materials in Contact with Food has reconsidered its view of the toxicity of bisphenol A (BPA). New research points to the prescription of a lower degree of protection. BPA has been associated with endocrine disruption. Evidence from: The EFSA Journal (2006) 428 “2,2-BIS(4-HYDROXYPHENYL)PROPANE (Bisphenol A)” Applying the standard safety margins, the tolerable daily intake (TDI) rate for humans has now been set at 50 microgrammes per kg body weight; the previous TDI was set at 10 microgrammes per kg body weight. This is 100 times lower than the no observable adverse effect level in rat experiments. Further detail: 6#9-10 5

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

Acid copper chromate (ACC) has been in use as a wood preservative in industrial/commercial settings in Europe and in the USA since 1920. USEPA has now taken steps to ensure it continues to be excluded from sale for domestic purposes. Their concern is that chromate (Hexavalent Chromium) is both carcinogenic, an irritant and an allergen and that there will be some uncontrolled exposure. Treated wood should be disposed of as if hazardous waste (not just burnt). Evidence from: US EPA 8th Jan 2007 “Acid Copper Chromate (ACC) Residential Uses Won’t be Registered” Metal based wood preservatives have been in use for decades and pressure treated woods contain several kg of metal per cubic metre. Further detail: 6#9-10 2

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

Evidence from: F Wang et al. Plant Biotechnology Journal (2006) Vol.4 p 667 – 676 “A large-scale field study of transgene flow from cultivated rice (Oryza sativa) to common wild rice (O. rufipogon) and barnyard grass (Echinochloa crusgalli)” Pollen mediated gene flow is known to vary with distance between source and receptor, with family closeness and with timing. In this study a large area of land was planted with GM and non-GM rice at various times to ensure some synchronisation of flowering. In this experiment the GM rice was herbicide tolerant. The maximum transgene flow was between 11% and 18% when source and receptor were within 1 metre. Probability of flow decreased rapidly with distance reaching 0.01% at 150 to 250 metres. Probability was related to wind speed; greater transport distances were detected in areas with higher wind speeds. Gene flow to barnyard grass, grown amongst the GM rice for 5 successive years, could not be detected. Comment The rates of gene flow