Database

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