Soils are inadequately characterised (chemistry, physics, biology and rheology) and the interactions between key variables are not understood. Whether or not changes in soil microorganisms would be deemed harmful is not predictable. Commercially relevant soil properties are routinely recorded and could affect land values. There is no mechanism which allows foreseeability of the effects of GM agriculture on land values. Evidence from: AK Lilley et al. Trends in Biotechnology (2006) Vol.24#1 p 10 – 14 “Life in earth: the impact of GM plants on soil ecology?” Studies of microbes in the soil cannot (yet) provide general commercially valuable information. Macroscopic variables, such as water retention, are recorded routinely but linking them and any changes in them with GM agriculture remains speculative. Some changes would be described as contamination, some as changes in biodiversity (both would be of interest to the regulator in charge of remediation). Further detail: 6
State of the art review of the effects of mould exposure. Evidence from: RK Bush et al. J Allergy Clin Immunol (2006) Vol. 117#2 p 326 – 333 “The medical effects of ‘mold’ exposure” In a jurisdiction where evidence of causation is required, there would be very few successful liability claims. Further information: 6#1 39
Evidence from: HSL and HSE “Psychosocial Working Conditions in Great Britain in 2005” The report examined changes in the levels of the six chosen stressors and related these to self-reported stress levels. There was a link between relationship quality and stress levels but no consistent trend. there was no relevance from role clarity and changes at work. The work would support argument based on a proposed lack of relevance of the stress management standards. This could count in favour of Defendants or Claimants, depending on the circumstances of the case. Further detail: 6#1 38
Report of a seminar on stress. HSE continue to support the stress management standards though accepted there were limitations. The way forward is -seemingly – to identify weaknesses in managers and demonstrate what a good manager looks like. The way to find this out is – seemingly- to ask his employees. In another presentation – in what were seemingly ideal management conditions, workers tended to overwork. Both presentations adopted a position that the only way to tackle stress was at an ever increasingly sophisticated organisational level. In our view, this opinion was more about power politics than about evidence. Further detail: 6#1 37
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
Organisational intervention studies to date have produced very disappointing results; the interventions have usually failed. Reasons for this are discussed and tested. Evidence from: R Randall et al. Eur J Work and Org Psych. (2005) Vol.14 p 23 – 41 “Evaluating organizational stress-management interventions using adapted study designs” Group intervention approaches to risk management may have some construct validity but have no effect in practice for individuals at risk. Insurers should be at risk only when individual stress risk management has been rather obviously negligent. Further detail: 6#1 35
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
Duty of care standards tend to be based on fatigue management rather than injury prevention. This study develops an elaborate method of risk assessment, but it is unclear whether or not it would meet a balance of probabilities test. Use of precautionary duty of care standards could lead to claims inflation: the pains don’t go away and breach of duty is commonplace. Evidence from: RA Werner et al. J Occup. Rehab. (2005) Vol.15#1 p 27 – 35 “Predictors of Upper Extremity Discomfort: A Longitudinal Study of Industrial and Clerical Workers” Claims frequency magnification is unlikely given that the wrong duty of care standards are already in place. Further detail: 6#1 33
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
Evidence from: Health Protection Agency RCE-1 Feb (2006) “Power Frequency Electromagnetic Fields, Melatonin and the Risk of Breast Cancer” An interaction between exposure to power frequency emfs and the production of the hormone melatonin has been the subject of 20+ years of research. Motivation for this research was provided by the possibility of a role of melatonin in the risk of breast cancer. The conclusion: In aggregate, the evidence to date does not support the hypothesis that exposure to power frequency emfs affects melatonin levels or the risk of breast cancer.
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: 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
The ILO report emphasises the presumed relative vulnerability of older workers. If correct, rating for EL or WC could justifiably include and age factor. Evidence from: ILO: Conditions of Work and Employment Series No.15 (2006) “Conditions of work and employment for older workers in industrialized countries: Understanding the issues” Further detail: 6#1 23
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
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