Evidence from: R Kanwal et al. JOEM (2006) Vol.48#2 p 149 – 157 “Evaluation of Flavorings-Related Lung Disease Risk at Six Microwave Popcorn Plants” O A Taiwo et al. JOEM (2006) Vol.48#3 p 275 – 282 “Incidence of Asthma Among Aluminum Workers” WHO Fact Sheet No 299 March (2006) “Electromagnetic Fields and Public Health: Static electric and magnetic fields” HSL/2006/19 “Summary Report on Additional Work Carried Out on the Monitoring of Chrysotile Containing Textured Decorative Coatings” Health Protection Agency RCE-2 “Dose Criteria for the Designation of Radioactively Contaminated Land” Health Protection Agency “Tuberculosis Update” Further detail: 6#1 48BB

Evidence from: EW Skorpinski et al. J Allergy and Clin Immunol. (2006) February p 463 – 464 “Two cases of accidental epinephrine injection into a finger” H Aksoy et al. Journal of Applied Tox. (2006) Vol. 26 p 10 – 15 “Genotoxicity study in lymphocytes of offset printing workers” T Murayama et al. Am J Ind Med (2006) Vol.49 p 1 – 7 “Estimation of Future Mortality From Pleural Malignant Mesothelioma in Japan Based on an Age-Cohort Model” TP Brown et al. Env Health Persp (2006) Vol.114#2 p 156 – 164 “Pesticides and Parkinson’s Disease—Is There a Link?” SK Obendorf et al. Arch. Environ. Contam. Toxicol. (2006) Vol.50 p 31 – 44 “Distribution of Pesticide Residues Within Homes in Central New York State” L Hou et al. Epidemiology. (2006) Vol.17 p 302 – 307 “Pendimethalin Exposure and Cancer Incidence Among Pesticide Applicators” HSE RR408 “Genetic variation in susceptibility to chronic effects of organophosph

Evidence from: RD Irwin. J. Appl. Toxicol. (2006) Vol. 26 p 72–80 “A review of evidence leading to the prediction that 1,4-butanediol is not a carcinogen.” L A Mucci et al. Int J Cancer (2006) Vol. 118 p 169 to 173 “Prospective study of dietary acrylamide and risk of colorectal cancer among women” C Pelucchi et al. Int. J. Cancer (2006) Vol. 118 p 467 – 471 “Dietary acrylamide and human cancer” RD Goodwin et al. Psychosomatic Medicine (2006) Vol.68 p 94–98 “Major Depression and Allergy: Does Neuroticism Explain the Relationship?” D Brodie. Industrial Law Journal. (2006) Vol.35 p 87 – 92 “The Enterprise and the Borrowed Worker” Viasystems (Tyneside) Ltd v Thermal Transfer (Northern) Ltd [2005] IRLR 983 (CA) AM Ruder et al. Environ Health Perspect. (2006) Vol.114 p 18–23. “Mortality among Workers Exposed to Polychlorinated Biphenyls (PCBs) in an Electrical Capacitor Manufacturing Plant in Indiana: An Update” AL Oakla

A new measure of mental vulnerability has been tested for its ability to predict objective heart disease. It was a significant moderate predictor. Mental vulnerability would probably increase the rate of reports of distress at work, leading to an association between stress and heart disease. Evidence from: LF Eplov et al. J Psychsom Res (2006) Vol.60 p 169 – 176 “Mental vulnerability—a risk factor for ischemic heart disease” Claims defence would be greatly enhanced by there being any history related to mental vulnerability, provided the employer knew and acted accordingly. Most of the indicators of vulnerability are out with any influence the employer can reasonably exert without an explicit request from the employee. Further detail: 6#1 36

Bullying has many parallels with chronic stress; its victims report higher levels of depression, anxiety and health complaints and it is, on the whole, subjective. Causal direction is unknown; providing opportunities for legal defence. Social forces within a given workplace can act to decide that a given duty holder is a bully and that certain persons are bullied. Claims can be thus contagious. Evidence from: AM Hansen et al. Journal of Psychosomatic Research (2006) Vol. 60 p 63 -72 “Bullying at work, health outcomes, and physiological stress response” In this study of 437 employees 5% reported having been bullied during the past 6 months. Among these, there were statistically significant higher scores on measures of somatisation (perception of symptoms with no organic cause), depression, anxiety and mental ill health. Further detail: 6#1 34

The research could form the justification for specific guidance on cleaning work and musculoskeletal discomfort. Introduction of such guidance would probably stimulate claims making. Cleaners are often supplied by agencies. Evidence from: V. Woods et al. International Journal of Industrial Ergonomics (2006) Vol.36 p 61 – 72 “Musculoskeletal ill health amongst cleaners and recommendations for work organisational change” Further detail: 6#1 32

Ergonomic factors were found to be predictive of back pain, as was fear of pain. The results for pain of a type that could be related to injury were not presented. There were some doubts about the exposure variables, which were measured by self report. Evidence from: A Van Nieuwenhuyse et al. OEM (2006) Vol.63 p 45 – 52 “The role of physical workload and pain related fear in the development of low back pain in young workers: evidence from the BelCoBack Study; results after one year of follow up” Large changes in liability exposure are unlikely unless fear of injury is made more likely. Further detail: 6#1 31

The study finds inconsistent evidence that children with leukaemia may be harmed by exposure to emfs at home. Evidence from: DE Foliart et al. British J Cancer. (2006) Vol.94 p 161 – 164 “Magnetic field exposure and long-term survival among children with leukaemia” For deaths, there was an association between exposure ≥ 0.3 μT and outcome; hazard ratio = 4.53 (95% CI = 1.49 to 13.7). Many parents would expect their child to survive leukaemia. It would be quite understandable that they would seek an explanation if the child dies. High exposure to emfs might encourage a claim. Case load can be estimated; in the UK there would be a maximum of 1 or 2 cases a year. Judgement as to the number of these that would have no other causal explanation, were strongly predicted to recover, and could provide evidence of emf exposure, would help insurers to manage the risk. Further detail: 6#1 28

In our view, shift work will not feature as a significant cause of gout. Gout affects around 5% of men aged over 60. Evidence from: M Uetani et al. Occupational Medicine. (2006) Vol.56 p 83 – 88 “A longitudinal study of the influence of shift work on serum uric acid levels in workers at a telecommunications company” In our view, shift work was a very weak risk factor for high UA levels. Alternative potential causes for gout are quite common and gout is arguably a divisible disease. Further detail: 6#1 25

Evidence from: WHO (Europe) EUR/05/5058531(2006) “Highlights on health in the United Kingdom 2004” According to WHO (2003) estimates, a person born in the United Kingdom in 2002 can expect to live 78.2 years on average: 80.5 years if female and 75.8 if male. graph: 6#1 24

Smoking during pregnancy may increase the risk of asthma in female offspring at the age of fourteen. There was no evidence that environmental exposure increased the risk of asthma at that age for either male or female offspring. Evidence from: R Alati et al. Epidemiology (2006) Vol.17#2 p 138 – 144 “In Utero and Postnatal Maternal Smoking and Asthma in Adolescence” The analyses show that maternal smoking during childhood does not affect asthma status at adolescence but that smoking heavily during pregnancy significantly increases the risk to females at age 14. The research also investigated the effect of passive smoking, and found no evidence of risk. Asthma in children is diagnosed at very high rates. The likelihood of maternal smoking during pregnancy is also high. Judgement as to causation theory would help tobacco risk managers to respond proportionately. Further detail: 6#1 21

Evidence from: The EFSA Journal. (2006) Vol.339 p 1 – 25 “…bovine bones used as an animal feed additive or as fertiliser” Bone meal constitutes approximately 1% of cattle feed by weight. Some bone meal is derived from cattle. What is the risk of BSE transmission? In the worst case considered in this report: In a beef cattle population of ~ 25 million this might be expected to give rise to on average 225 infected cattle per year. None of the scenarios produced an estimate lower than one case per year.

Extraction methods appear to reduce the potency of disease-causing prions. The risk from gelatin are many times lower than those from the contaminated foods that were consumed at the peak of the BSE epidemic. Evidence from: The EFSA Journal (2006) Vol.312 p 1 – 29 “Quantitative assessment of the human and animal BSE risk posed by gelatine with respect to residual BSE risk” The report concludes that restrictions on the use of brain and vertebrae in the production of gelatine are not justified. Further detail: 6#1 18

Claims that aspartame is carcinogenic may have been premature. Evidence from: The EFSA Journal (2006) 356, 1-44 “…a new long-term carcinogenicity study on aspartame” Dietary exposure to aspartame rarely exceed 10 mg/kg bw even in heavy users. Cancer is indivisible, aspartame use in processed foods is very common, strong evidence of carcinogenicity could cause problems to food manufacturers and their insurers. Further detail: 6#1 17

The asbestos exposure history for the GB working population is unknown. In the model presented here, relative asbestos exposure in occupational groups is assumed to correlate in some way with mesothelioma rates in those groups. After correcting for age and smoking effects, the model finds that the asbestos-related lung cancer: mesothelioma ratio is 0.65: 1 for the GB working population as a whole. Evidence from: AJ Darnton et al. Ann Occ Hyg. (2006) Vol.50#1 p 29 – 38 “Estimating the Number of Asbestos-related Lung Cancer Deaths in Great Britain from 1980 to 2000” As a rough estimate, allowing for deaths which occurred after age 74 the authors propose 11,500 asbestos related lung cancers in all in that period, compared with 17,491 total mesothelioma cases. Asbestos was responsible for around 3% of all lung cancer deaths. Further detail: 6#1 10

European Environment Agency Report No7 (2006) “How much bio-energy can Europe produce without harming the environment?” The report explores the potential for purpose grown feedstock for power and heating and the potential for recycling biomass wastes. Some wastes, their storage, transport and uses could present environmental liabilities and risks to persons. The main exploitable biowaste streams are solid agricultural residues (e.g. straw), wet manures, wood processing residues, the biodegradable part of municipal solid waste and black liquor from the pulp and paper industry.

The European climate is expected to change slowly i.e. decades not years. Several risks have been identified and measures could be taken to reduce the associated liabilities. Evidence from: Environment Agency. March (2005) “The Climate is Changing: Time to Get Ready” The report lists several areas where liability exposure change would be expected by extrapolation from current experience, but slow changes to exposure are readily accommodated in experince ratings. Further detail: 6#1 8

Provided they were non-smokers, lung cancer cases with an environmental exposure leading to daily urinary excretion levels of more than 24 nmol of cadmium could argue that cadmium was the most likely explanation for the cancer. Cadmium exposure maps for the UK are publicly available. Evidence from: T Nawrot et al. Lancet Oncol. (2006) Vol.7 p 119 126 “Environmental exposure to cadmium and risk of cancer: a prospective population-based study” The paper also suggests a synergistic effect with smoking. Blood tests would identify those at significant risk, and would suggest causation in non-smokers. Further detail: 6#1 6

This report, based on a meta-analysis of 27 publications, suggests that silicosis is related to the risk of lung cancer even among non-smokers. Evidence from: Y Lacasse et al. Scand J Work Environ Health (2005) Vol.31(6) p 450 – 458 “Meta-analysis of silicosis and lung cancer” In general it has been found that the more severe the silicosis the higher the risk of lung cancer.   further detail: 6#1 2  

The results suggest that silicosis is a prerequisite for silica-related lung cancer. Risk of lung cancer did not vary with cumulative dust exposure if there was no silicosis. There was no correction for the effects of smoking. There was some evidence that silica dust/silicosis was not the only geological determinant of lung cancer risk. Evidence from: W Chen et al. Am. J. Ind. Med. (2006) Vol.49 p 67 – 76 “Exposures to Silica Mixed Dust and Cohort Mortality Study in Tin Mines: Exposure-Response Analysis and Risk Assessment of Lung Cancer” In those with silicosis the risk of lung cancer varied with exposure; a clear rise in risk was detected once exposure to total dust exceeded 70 mgm-3 years. Respirable crystalline silica comprised around 4% of total dust in each mine. Further detail: 6#1 1  

Early signs of action on liability for environmental damage – expanding on the Habitats Directive. Evidence from: MacAlister Elliott and Partners Ltd / Economics for the Environment Consultancy Ltd Study on the Valuation and Restoration of Biodiversity Damage for the Purpose of Environmental Liability. The report describes restoration as being either return to baseline or compensatory or a mixture of the two. Much depends on economic valuation techniques. The Radar report is available to subscribers: SK 1#6 9

Identification of risk factors is a sensible precursor to designing interventions and seeing if they work as expected. It would seem obvious then that if a supposed risk factor turns out not to be valid then it should not feature in intervention studies or duty of care standards. Evidence from:  M.Hakkanen et al. Occupational and Environmental Medicine (2001) Vol.58 #2 p.129. Results show that the most significant risk factor for absence with diagnosable arm, neck and shoulder disorders is age: Age 30-40 Risk Ratio = 2.9 (95% confidence interval 1.2 to 7.1). High physical load was protective. The Radar report is available to subscribers: SK 1#2 5 Evidence from: G.A.M.Ariens et al. Occupational and Environmental Medicine (2001) Vol.58 #3 p.200. Among those sitting, neck pain (but not a diagnosis) was more likely if the neck was flexed by 20 degrees for more than 70% of the time. The Radar report is available to subscribers: SK 1#2 6 Evidence from: RSI conference 2nd March 2001. RSI was

It may be valid to apply a premium weighting on drivers who have recovered from TBI. Evidence from: BE Masel et al. Archives of Physical Medicine and Rehabilitation. November (2001) Vol. 82 #11. p 1526. A study of daytime sleepiness among TBI cases after apparently full recovery. Case series n = 71, 38 months after injury. Measured objectively in a live-in sleep laboratory. 47% hypersomnolance rate did not show up on self-report. That is, the hypersomnolant were unaware of their tendency to sleep during daytime. Comment It is generally held that motorists who fall asleep at the wheel would be aware that there was a risk in advance. This work suggests that former TBI cases (after 38 months) were unaware of their risk of daytime sleeping.

This Radar report collates a number of relevant findings in response to the Stewart report. Topics addressed include: Planning-related liability. Causation. Exposure control guidelines – duty of care. Childhood leukaemia – incidence. Risks to fire fighters. The Radar report is available to subscribers: 1#11 2