Is there an exposure to asbestos which does not “legally cause” mesothelioma? Evidence from: C Gilham et al. Occup Environ Med (2015);0:1–10. doi:10.1136/oemed-2015-103074 Gilham et al, compared asbestos fibre burdens from the lungs of mesothelioma and lung cancer cases and from these, developed risk equations. 79% of the fibres they observed were amosite; the subjects were all resident in the UK. Fibre burden and diagnosis were objective and precise; which means the main uncertainties were in unintentional bias and biological variability, about which not much more could be done except by sub categorisation by genetic and epigenetic profile (which would require a much bigger study). Using mathematical methods adapted from the design of optical telescopes and electronic circuits, we have extended the reported analysis to make an original estimate of de minimis. Compared with background, and for asbestos fibres which are longer than 5 micrometres, the smallest detectable increase in the

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

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 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

The study confirms that there is no risk-free exposure to Radon. It also finds no interaction between radon and smoking; the risks are simply additive. In our view, this means that compensation issues should remain separate; material contribution should not be an issue. Evidence from: S Darby et al. Scand J Work Env Health (2006) Vol.32 supp1 p 1-16. “Residential Radon and lung cancer – detailed results of a collaborative analysis of individual data on 7148 persons with lung cancer and 14,208 persons without lung cancer from 13 epidemiological studies in Europe.” For lifelong non-smokers, the risks of lung cancer at 100 Bq/m³ and 400 Bq/m³ were estimated to be 1.2 and 1.6 respectively, relative to no radon exposure. For those smoking 15 – 20 cigarettes per day the relative risk of lung cancer would be 25.8 at 0 radon exposure, 29.9 at 100 Bq/m³ and 42.3 at 400 Bq/m³. Further detail: 6#7-8 3

Evidence from: MC Turner et al. Int. J. Cancer. (2006) Vol.118 p 3124-3132 An overview of the association between allergy and cancer A Navas-Acien et al. Environ. Health. Persp. (2006) Vol.114 p 641 – 648. Arsenic Exposure and Type 2 Diabetes: A Systematic Review of the Experimental and Epidemiologic Evidence KZ House et al. PNAS (2006) Vol.103. p 12291 to 12295 Permanent carbon dioxide storage in deep-sea sediments A Schreier et al. J. Psychiatric. Res. (2006) Vol.40 p 283 -292 Clinical characteristics of Major Depressive Disorder (MDD) run in families – A community study of 933 mothers and their children MM Weissman et al. Am J Psychiatry. (2006) Vol. 163 p 1001 – 1008 Offspring of Depressed Parents: 20 Years Later J Szabo et al. Bioelectromag. (2006) Vol.27 p 451 – 457 Occupational 50 Hz Magnetic Field Exposure Measurements Among Female Sewing Machine Operators in Hungary Further detail: 6#5-6 55 BB

The study adds weight to the view that exposure to environmental tobacco smoke could be associated with an increased risk of early, spontaneous abortion. Evidence from: L George et al. Epidemiology (2006) Vol.17 p 500 – 505 “Environmental Tobacco Smoke and Risk of Spontaneous Abortion” Abortion is an indivisible outcome. The relative risk of spontaneous abortion was increased for women exposed to ETS; OR = 1.7 (95% CI = 1.2 to 2.4) and for women who smoked; OR = 2.1 (95% CI = 1.4 to 3.3). Further detail: 6#5-6 25

This reasonably high quality study found evidence that exposure to environmental tobacco smoke was associated with a small increase in risk of glucose intolerance [a pre-diagnostic indicator of diabetes] within a 15 year timescale. Evidence from: TK Houston et al. BMJ (2006) Vol. 332 p 1064 – 1069 “Active and passive smoking and development of glucose intolerance among young adults in a prospective cohort: CARDIA study” For risk assessment purposes it would be helpful to know how many people have no other predispising vulnerability to developing diabetes. Further detail: 6#5-6 24

The report clearly asserts that lung cancer, heart disease and sudden infant death syndrome are causally related to exposure to environmental tobacco smoke. Asthma is not caused by exposure but there is limited evidence that frequency and intensity can be increased by it. Evidence from: United States Department of Health and Human Services. June 2006 “The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General.” For heart disease and for lung cancer the independent additional risk from ETS exposure is of the order of 25%. Those who regard exposure to risk being equivalent to material contribution would probably regard this as compensable but, so far, legal precedent in the UK would tend to exclude this as a cause of action in its own right. Further detail: 6#5-6 23

HSC have implemented the requirement to set reduced levels of protection when work with asbestos is described as sporadic. Evidence from: HSC/06/55 July 2006. “A comparison of the risks from different materials containing asbestos” At the 9 May meeting, the Commission agreed that including in the Approved Code of Practice (ACoP) a peak exposure level of 0.6 fibres per cm³ in the air measured over a ten minute period would provide a useful determinant of when exposure might be considered to be sporadic and of low intensity. Exactly how this ties in with the Compensation Act 2006 remains to be seen. It is highly likely that claims will be made when known exposures are below the level described as sporadic. Would they be in breach or not? Further detail: 6#5-6 11  

In hamsters, co-exposure to crocidolite and one strain of SV40 virus had the effect of amplifying the risk of mesothelioma from asbestos. SV40 has not been conclusively shown to be a cause of mesothelioma in humans, and in our view, is unlikely to be. Evidence from: B Kroczynska et al. PNAS (2006) Vol.103#38 p 14128 – 14133 “Crocidolite asbestos and SV40 are cocarcinogens in human mesothelial cells and in causing mesothelioma in hamsters” The joint potency of virus and asbestos was higher in hamsters. Given joint and several liability for asbestos exposure it seems unlikely anyone would bring SV40 into play. Further detail: 6#5-6 10

The effect of the Barker judgement was reversed within a matter of weeks. This Bill provides that joint and several liability applies to these kinds of claims. Evidence from: Hansard: Amendments agreed 19th July 2006. “Compensation Bill” The absolute language used in this bill is intended to give rise to a guarantee of compensation for mesothelioma cases. However the language used is absurd and will give rise to uncertainties. Included is the possibility that exposure to asbestos the day before a diagnosis of mesothelioma is made, could be found responsible for the disease. There are other scenarios where the Act will give offence against natural justice. There is growing concern that contribution to risk should be measured in a more rational way. The real tests will come when an administrator or public body has a duty to minimise exposure to past liabilities. Further detail: 6#5-6 8  

The report highlights the unintentional but ubiquitous contamination of food by man made chemicals. Sources are diverse but high levels in some foods could be thought to predominate and therefore be the principle source of exposure. Foods with high levels are recorded here. Evidence from: World Wildlife Fund September 2006 “Chain of Contamination: The Food Link” The report lists chemicals and foods which contain them in large quantities. Further detail: 6#5-6 3

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

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

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

This review was created at the outset of the Radar project. The summary here covers diagnosis, causation, foreseeability, duty of care, prognosis, rehabilitation, mitigation, exposure variation. Evidence from: Andrew@reliabilityoxford.co.uk Early attempts to audit stress risk were conceptually flawed. The Radar report is available to subscribers: SK 1#1 3

This review was created at the outset of the Radar project. A summary of the findings for diagnosis, causation, foreseeability, duty of care, prognosis, rehabilitation. Evidence from: andrew@reliabilityoxford.co.uk The Radar report is available to subscribers: SK 1#1 1

This was an 8 year longitudinal study of those in pain. Pain is commonplace and usually meaningless but what if it was indicative of risk of cancer? Evidence from: GJ Macfarlane et al. BMJ. (2001) #7314 p 662. The report includes estimates of the prevalence of pain and the statistical association between pain and cancer outcomes. It would appear that the pain being described by people before they died had no direct link with the cancer that killed them. The Radar report is available to subscribers: 1#9 12

The concern is that if inflammation is a potent cause of lung cancer then any negligent cause of inflammation could be cited as a potential contributor to outcome. This research studied the effect on lung cancer risk of chronic inflammation arising from infection with a bacterium that causes mild pneumonia. Evidence from: H Koyi et al. APMIS. September (2001) Vol. 109, #9 p 572. Inflammation is such a common response to environmental exposures that the need for specific carcinogens to cause cancer would be greatly reduced. The Radar report is available to subscribers: 1#9 11

At the end of the study, High extraversion (women only) was predictive of new cases OR = 1.86 (95% CI = 1.16 to 2.96). Life woes and stress were not predictive. Evidence from: E Huovinen et al. Allergy. October (2001) Vol. 56 # 10 p 971. The potential to link occupational stress to incident allergy seems to be reduced by this finding. The Radar report is available to subscribers: 1#9 10

This academic paper reports a risk function linking death from coronary heart disease to age, diastolic blood pressure, cholesterol and smoking.  Evidence from: JJMcNeil et al. Journal of Cardiovascular Risk. Feb (2001) Vol.8 #1 p.31. When there are multiple possible causes, the contribution made by a negligent exposure may be estimated if the contribution from all other relevant exposures is known. Heart disease is a slowly developing condition leading to sudden deterioration. The Radar report is available to subscribers: 1#2 4