This high powered study failed to find any significant association between occupational exposure to low frequency EMFs and acoustic neuroma. Evidence from: UM Forssen et al. Am J Ind Med (2006) Vol.49 p 112 – 118 “Occupational Magnetic Field Exposure and the Risk of Acoustic Neuroma” There were significant numbers of cases and controls in all exposure groupings. The precision of the risk estimates was therefore unusually high. There were no statistically significant associations between exposure and outcome. Further detail: 6#1 29

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

The effectiveness of cognitive behavioural therapy as a treatment for electrical hypersensitivity suggests the disease is triggered and maintained by interpretation of perceived exposure. Illnesses created and maintained by perception alone are complex for insurers. A duty-holder could attempt to make reasonable accommodations but in so doing give the impression of meaningful care and may even encourage the harmful perception. Evidence from: GJ Rubin et al. Psychother Psychosm. (2006) Vol.75 p 12 – 18 “A Systematic Review of Treatments for Electromagnetic Hypersensitivity” Further detail: 6#1 27

This brief paper provides powerful evidence against any link between mobile phone use and the development of acoustic neuroma. Evidence from: PD Nelson et al. Neurology (2006) Vol. 66 p 284. “Trends in acoustic neuroma and cellular phones: Is there a link?” graph: 6#1 26

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: AJ Donato et al. Am J Physiol Heart Circ Physiol (2006) H272 – H278 “Differential effects of aging on limb blood flow in humans” Limb blood flow should be proportionate to the demands made by limb tissues. Failure to meet demand would lead to reduced performance (e.g. muscle power, endurance etc.) and several researchers have linked reduced blood flow with the early onset of fatigue and diffuse pain; a prelude to RSI. Muscle mass tends to decrease with age. In this research, the ability of the circulation to cope with muscles working at 60% maximum work rate was compared between 21 and 71 year old people. There were no significant differences in forearm blood flow with age, after correction for muscle mass. Comment If (insufficient) blood flow is related to the development of diffuse forearm pain we would not expect a generalised effect of ageing. There are many other factors which could affect blood flow, including Body Mass Index, general health, medication

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

Quantum Dots contain known toxins. They are protected by surface coatings but could deliver very high doses of toxin to individual cells if those coatings fail. Evidence from: R Hardman. Env. Health. Perspect. (2006) Vol.114#2 p 165 – 172 “A Toxicologic Review of Quantum Dots: Toxicity Depends on Physicochemical and Environmental Factors” Specific toxicity testing would be needed for each QD and combination of surface treatments. Accessibility provides the only risk assessment guide for underwriting these materials. Further detail: 6#1 20

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

Evidence from: F Greenaway. Am. J. Physiol. Regul. Comp. Physiol. (2006) Vol.290 p R188 – R189 “Virus-induced obesity” Human adenovirus 36 (Ad 36) was first described in 1980. Since then obesity rates have more than doubled. Symptoms of respiratory illness caused by adenovirus infection range from the common cold syndrome to pneumonia, croup, and bronchitis. Ad 36 is transmitted by direct contact, faecal-oral transmission, and occasionally, waterborne transmission (e.g. swimming pools). Over the years, evidence from animal experiments show consistently that animals and humans infected with Ad 36 have higher numbers of fat cells. Humans with antibodies to Ad 36 also tend to be of heavier weight, even in discordant twins. Other adenoviruses have been tested but none of these have this effect on humans. Comment Increased numbers of fat cells is not sufficient in itself to create obesity, but it helps. Obesity does not always follow infection. Ad 36 is now in general circulatio

The study finds weak evidence of a moderate link between exposure to loud noise and risk of acoustic neuroma. Evidence from: CG Edwards et al. Am J Epidemiol (2006) Vol.163 p 327–333 “Exposure to Loud Noise and Risk of Acoustic Neuroma” Acoustic neuroma (AN) is a slow growing benign tumour of the sheath of the eighth cranial nerve (hearing and balance), in close proximity to the brain. Exposure to loud noise at work is still commonplace. AN is indivisible, but rare. Insurers could estimate the number of cases attributable to loud noise at work and could judge for themselves how good any claim is likely to be. Potentially problematic for claimants is that hearing surveillance could be the main reason that AN is associated with noise exposure: accelerated diagnosis. Further detail: 6#1 15

Potassium Octatitanate whiskers are bio persistent and cause significant lung inflammation. Evidence from: T Oyabu et al. J Occup Health (2006) Vol.48 p 44-48 “The Effect of Lung Burden on Biopersistence and Pulmonary Effects in Rats Exposed to Potassium Octatitanate Whiskers (POW) by Intratracheal Instillation.” Potassium Octatitanate whiskers (K2Ti8O17) (POW) are typically of 5 μm in length and are classified as refractory ceramic fibres (aka Fybex). They are used as an asbestos substitute. Further detail: 6#1 11

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

MCS patients did not have unusually heightened sense of smell but did have a stronger emotional response to unpleasant and pleasant smells. Combined with the results of other work it would seem that MCS cases have an unusually strong interpretation of perceived exposures. Evidence from: D Papo et al. J Psychosom Research. (2006) Vol. 60 p 199 – 209 “Chemosensory function and psychological profile in patients with multiple chemical sensitivity: Comparison with odor-sensitive and asymptomatic controls” further detail: 6#1 5

It would seem from this study that multiple chemical sensitivity diagnosis does not correlate with objective measurements of exposure. Perceived exposure may be the more important factor. Evidence from: S Bornschein et al. Psychosom Medicine (2006) Vol.68 p 104 – 109 “Psychiatric Morbidity and Toxic Burden in Patients With Environmental Illness: A Controlled Study” further detail: 6#1 4  

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  

It would seem from this research that 12-hour shifts are no more hazardous than 8-hour shifts. For the workers studied here it would seem that the 12-hour shift was preferred. Evidence from: MD Johnson et al. International Journal of Industrial Ergonomics (2001) Vol.27 p.303. Many industries and services have begun to introduce rotating 12-h schedules. There have been concerns that such schedules may influence the rate of occupational injuries, workers health, and factors that may contribute to stress. Established 8-hour shift patterns are already known to produce sleep disturbance. 412 employees were selected for the study, which was controlled and selected on the basis of accurate representation of work types and employment contracts. Response rates were over 80%. Results from before and after the change in shift pattern were compared. With respect to amount of sleep, the responses were significantly in favour of the 12-h schedule over the 8-h schedule. The study also indicated that

Tackling work-related stress: a managers’ guide to improving and maintaining employee health and well-being. The new guide provides seven broad categories of management that could influence a person’s sense of well being. These are: • culture, • demands, • control, • interpersonal relationships, • change, • role clarity, and • individual factors such as training/skills/previous episodes. Evidence from: HSG 218. Comments While it may be that stress itself is the adverse outcome HSE seeks to address, stress is not in fact an injury. In short, standards for prevention of stress may have only a tenuous link with prevention of injury and as such would arguably be of little relevance to liability assessment. The experience of stress cannot be objectively measured, nor can it be precisely related to injury outcomes. The Radar report identifies several opportunities for defence should these guidance notes be used in evidence in claims. The Radar report is available to subscribers: SK 1#6 6 HSE

Diagnosis of pain problems depends very much on whether there is or ever has been tissue damage. Diagnostic methods will depend on causation assumptions and in turn, knowledge about causation depends on diagnostic method. the potential for circularity is apparent. In this setting, researchers attempt to identify diagnosis and causation. Evidence from: M Bennet. Pain. May (2001) Vol.92 #1-2 p 147 The diagnostic method in which variables were combined was found to have a sensitivity of 83% and specificity 87% with a corresponding positive predictive value of 86% and a negative predictive value of 84%. The test would tend to be used as evidence of tissue damage in RSI and back pain cases. The Radar report is available to subscribers: SK 1#5 2 Evidence from: C Meng et al. Journal of Rheumatology. June (2001) Vol. 28 #6 p 1271. Blood flow may be a response to or a cause of muscle pain. Either way its variation with MSD risk factor exposure would be of interest. This proof-of-principle study

Causation of mental breakdown has been accepted in some circumstances. Researchers usually study lower degrees of distress, and assume that causation would translate to the more serious outcomes. Causal direction and correction for personality traits is usually unclear. Even so, this is the research used by policy makers to define duty of care standards and  performance targets. Evidence from: J deJonge et al. Journal of Occupational and Organisational Psychology. Mar (2001) Vol.74 #1 p.29. The most interesting result is that emotional exhaustion predicted high, perceived job-demand and not the reverse. Emotional exhaustion could be anticipated to play a role in the development of psychological ill health. But this study seems to show that perceived job demands were not causal. The Radar report is available to subscribers: SK 1#3 6 Evidence from: A Tsutsumi et al. Scandinavian Journal of Work, Environment and Health. Apr (2001) Vol.27 #2 p 146. The authors conclude that job strain and

Although simple in principle, there are many opportunities for uncertainty in the development and deployment of GMOs. Environmental liability will be connected with professional indemnity and D&O. Contractual liabilities based on failure to perform and contamination of product are foreseeable. Evidence from: Meza TJ, et al. Transgenic Res., (2001) Vol.10,  p 53-67. Modified plants, when grown in stressful conditions may behave in undexpected ways. “Failure to sfafety” would seem to be a good principle to adopt. The Radar report is available to subscribers: SK 1#2 13 Evidence from: PL Bhalla et al. Int. Arch. Allergy & Immunology. 124(2001) Vol.1-3, p51-4. Pollen sensitisation could be addressed if the allergenic property of pollen was engineered out. This research tested the removal of allergen and whether the pollen remained viable. The Radar report is available to subscribers: SK 1#4 5 Evidence from: Crawley MJ, et al. Nature,  (2001) Vol. 409 6821, p 682-3 Escape

Stress is frequently assumed to affect the functioning of the immune system. If so, stress could increase vulnerability to disease. Reduced resilience could be described as a material contribution to outcome, or as a risk factor. It could also be that reduced immune system capacity increases a sense of lack of well-being. Views may be pieced together from research. Evidence from: Cohen S, et al. Psychological Stress and Antibody Response to Immunisation: A Critical Review of the Human Literature. Psychosomatic medicine 63(2001), 7-18 Not having found any evidence that stress moderates responses to immunisation, the authors propose that the stress effect must be in real life exposures, but don’t provide any evidence of this. The Radar report is available to subscribers: SK 1#2 9 Evidence from: SK Agarwal et al. Clinical and Experimental Allergy. Jan (2001) Vol. 31 p.25. A study of teenagers under stress, and effects on asthma. The hypothesis is that stress induces dysregulation of

A causal link between stress and heart disease would prompt significant liability exposure. Heart disease is very common. Feelings of being hassled are very common, and may be caused by heart disease or high blood pressure. Unravelling this knot will draw on disparate and incomplete studies. Evidence from: T.Hallman et al. Journal of Cardiovascular Risk Feb (2001) Vol.8 #1 p.39. After suffering manifest coronary disease it was found that compared with controls, there was excess family strife, physical stress, burn-out, daily hassles. Some of these could be subject to modification at work. The Radar report is available to subscribers: SK 1#2 7 Evidence from: GW Evans et al. Journal of Applied Psychology. Oct (2000) Vol. 85 #5 p.779. 40 experienced female office workers were assigned at random to a well-controlled trial of office work with or without open office noise at 55 dBA. Epinephrine, nor epinephrine and cortisol were measured before and after the test period. Subjects were asked