Short term effects of exposure are well-known and usually reversible. This study sought an association between cumulative exposure and signs of peripheral nerve symptoms (PNS). Evidence from: A Pilkington et al. Occupational and Environmental Medicine. November (2001) Vol.58 # 11 p 702. Short term effects were observed as expected. The Radar report is available to subscribers: 1#10 17

If shift work increased the intensity of heart disease risk factors by some non-volitional mechanism then there would be a good case for controlling shift work in a way which counteracts that mechanism. But first, is there a significant effect on risk factors? Evidence from: B Karlsson et al. Occupational and Environmental Medicine. November (2001) Vol.58 # 11 p 747. A study of known risk factors for heart disease and their association with shift work. 27,485 Swedish workers took part. Blood and build were analysed. Obesity was found to be more prevalent among all ages of women shift workers, but only two age groups of men. Increased triglycerides (>1.7 mmol/l) were found for two groups of shift working women but not men. Impaired glucose tolerance was found among 60-year old women shift workers. Comment The authors conclude that shift work presents an increased risk of heart disease. However, risk factors for disease are not indicators that disease will necessarily occur. Strengths

If BMI is a risk factor for asthma then it should also be a risk factor for atopy. But it isn’t, according to this study. The suggestion is that either atopy or asthma may be being misdiagnosed. Atopy is diagnosed by objective tests. Evidence from: E von Mutius et al. Thorax. November (2001) Vol.56 #11 p 835. Does body mass index (BMI) correlate with diagnosis of childhood asthma? 7505 children aged between 4 – 17 took part in the study. Extensive background details and medical exam for status. Physician diagnosis or treatment for asthma was used to identify asthmatics. Relative to lowest quartile, BMI, top quartile OR = 1.77 (95% CI = 1.44 to 2.19) BMI was not correlated with atopy. Comment Possible explanations include a high rate of false diagnosis (activity intolerance is used by many physicians as a clear sign of asthma or direct effect of being overweight on breathing or sensitisation of an inflammatory mechanisms?

The research report referenced here examines the feasibility of providing written instruction informing about signs and personalised care for each child with a known predisposition. It finds that such personalised programmes can be obtained and managed successfully. Evidence from: DA Moneret-Vautrin et al. Allergy. November (2001) Vol. 56 # 11 p 1071 Allergy prevention and response would seem to be reasonably practicable in schools. The Radar report is available to subscribers: 1#10 14

Asthma diagnosis rates in children increased very significantly in the past 20 years. The search for environmental cause has been intense. But how big could the environmental proportion of new cases be? Evidence from: G Koeppen-Schomerus et al. Archives of Diseases in Childhood. November (2001), Vol. 85 #5 p 398. In 1999 Genetics accounted for 70% of asthma diagnoses. It would be interesting and useful to know if the same proportion was still found now. If an environmental cause of asthma diagnosis inflation is found then the maximum proportion would be 30% of cases. The Radar report is available to subscribers: 1#10 13

If injury can be a cause of MS then why not a virus which causes nerve inflammation? The study sought associations between exposure to 21 different pathogens and risk of MS using discordant twin pairs. Evidence from: M Bergkvist et al. Acta Neurologica Scandinavica. November (2001) Vol.104 #5 p 262. The lack of any detectable effect from any of these pathogens suggests that if a pathogen is responsible it wasn’t one of these and, that neuro inflammation is not a prime cause either. The Radar report is available to subscribers: 1#10 12  

The International Agency for Research on Cancer (IARC) has published a monograph on low frequency emfs. They conclude that exposure is possibly carcinogenic to humans. The opinion arises from consistent evidence of detectable risk of leukaemia in children exposed to more then 0.4 micro Tesla time weighted average. Evidence from: IARC monographs series. In our view, this does not represent a date of knowledge on generic causation. A number of objections to the IARC conclusion are acknowledged by IARC and expert opinion more widely. The Radar report is available to subscribers: 1#10 11

There is some consensus that the risk of lung cancer posed by asbestos dust exposure is usually of the order RR = 5, that from smoking, RR= 10 and from the combination, RR = 50. This review paper suggests an alternative view, that the asbestos related risk is actually reduced by co-smoking. Evidence from: FD Liddell. Ann Occup Hyg. Jul (2001) Vol. 45(5) p 341-56. The author introduces the term: relative asbestos effect, to account for the competition between smoke and asbestos to be the first to actually cause the cancer. The Radar report is available to subscribers: 1#10 10

There was no association between lung asbestos burdens and survival times. Survival time did vary by cancer cell type. If known, cell type could assist with initial reserving. Evidence from: Neumann V, et al. Int Arch Occup Environ Health. (2001) Aug;74(6) p 383-95. Time between first known occupational exposure and diagnosis was 38 year on average. The Radar report is available to subscribers: 1#10 9

Preliminary work on distinguishing long from short prognosis following diagnosis with mesothelioma. Evidence from: Bongiovanni M, et al. Cancer. 2001 Sep 1;92(5) p 1245-50. A test which could distinguish cases into brackets such as up to 12 months and more than 24 months survical would assist with reserving. The Radar report is available to subscribers: 1#10 8

The report provides some evidence that fear of movement is a good predictor of continued disability with back pain. This remained true even after correction for actual impairment and disability. Evidence from: JM Fritz et al. Pain. October (2001) Vol.94 #1 p 7. There are standard questionnaires to assess fear of movement. Degree of pain, and volitional disability would probably work just as well. The Radar report is available to subscribers: 1#10 7

Pain in the neck or upper limbs and sensory symptoms were common in the non-manual workers overall (with 1 week period prevalences of 30% and 15%, respectively), and were associated with older age, smoking, headaches and tiredness or stress. Evidence from: KT Palmer et al. Occup. Med. Sep (2001) Vol.51(6) p 392. The report records that disabling symptoms were much less frequent, that keyboard work had no influence on neck or elbow pain, and moderate influence on shoulder and arm pain. Pain is not the same as injury. The Radar report is available to subscribers: 1#10 6

Nerve function is affected by carpal tunnel syndrome (CTS). This paper suggests that testing nerve function before CTS is diagnosable will identify some of those who are on the path to injury. This would allow intervention if the cause was subject to a duty of care. The test will not be added to surveillance requirements until it is fully characterised. Evidence from: RA Werner et al. Muscle and Nerve. September (2001) Vol.24 #11 p 1462. The Radar report is available to subscribers: 1#10 5

Neck pain is commonplace and usually trivial. This paper reports the most common risk factors in people who are asked to think about neck pain. Being involved in a car accident often leads to people being asked to think about neck pain. Evidence from: PR Croft et al. Pain. September (2001) Vol.93 #3 p 317. The data provides a baseline against which the rate of whiplash claims can be estimated, assuming that causation is not needed before a claim is made but that there is some disability. This should be an extreme upper limit. For example, if there were 1 million RTAs per year the maximum number of non-cause claims would be 100,000. The Radar report is available to subscribers: 1#10 4

Neck pain immediately after any violent event stimulates  of precautionary responses in medics. It is likely that these responses have a high rate of harmful effect on those not seriously injured, while preventing permanent disability in those who are. This research suggests a selection method. Evidence from: IG Stiell et al. Journal of the American Medical Association. October (2001) Vol. 286 # 15 p 1841. The Radar report is available to subscribers: 1#10 3

This study provides results which are directly useful in liability exposure estimates. Evidence from: Keith T Palmer et al. Occupational exposure to noise and hearing difficulties in Great Britain. Contract Research Report 361/2001 HSE The Radar report is available to subscribers: 1#10 2

Noise induced hearing loss is still an issue. This reform of duty of care standards will bring more people within the claimant population. Poor understanding in the courts risks providing compensation for trivial harm. Given that exposure measurement is also subject to considerable uncertainty, a Duty to ensure exposure (with hearing protection) is less than 85 dB(A) would seem to be in accord with the requirements of civil liability (for the 50 year old male manual worker). That is, exposure below this value would not be shown to have on the balance of probabilities, contributed to measured HTLs. Evidence from: andrew@reliabilityoxford.co.uk A full description of the noise Directive its strengths and weaknesses. The Radar report is available to subscribers: 1#10 1

BS8800 Occupational Health and Safety Management Standard This British Standard was first approved and published in 1996 and has since been converted into a commercial certification scheme, referred to as OHSAS 18001. On several occasions since 1996, there have been attempts to convert BS8800 into an international (ISO) standard for the purposes of certification (akin to ISO 9000 etc.). Support has come from several countries but the issue is confused by rival bids from ILO and other national standards organisations. It may be that imported certification schemes would be recognised as valid in the UK, thereby taking advantage of the UK’s inability to come up with its own scheme. Opposition to a certifiable standard has been fierce and mainly from industry. All British Standards have to be reviewed. The review period for BS8800 was 5 years. BRE and ABI were original participants in the creation of BS8800 and were therefore invited to attend a review meeting in September 2001. Participan

It could be argued that physiotherapy could play a role in recovery if it helps overcome obstacles (such as temporary pain relief) to return to normal activity. While there was no evidence in the review to support this, it would be presumed by most practitioners. Anecdotal support for this presumption is persistent and strong. Evidence from: RD Herbert et al. BMJ. October (2001) #7316 p 788. Recommendations for prevention and treatment of chronic MSK pain are: don’t get chronic get active; return to normal activity. Massage and manual therapy and other physical modalities are not proven or are variable. The Radar report is available to subscribers: 1#9 13

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

Outcome of interest = brain cancer. No increased risk was found for either lifetime exposure or the most recent 5 years of exposure. No Dose Response effect was found. Evidence from: T Sorahan et al. Occupational and Environmental Medicine. October (2001) Vol.58 # 10 p 626. The report includes data on the emfs exposure profile and electricity generation workers. The Radar report is available to subscribers: 1#9 8 Evidence from: DA Savitz. Occupational and Environmental Medicine. October (2001) Vol.58 # 10 p 617. The commentator seriously doubts the need for any more expenditure and effort on epidemiology in this area until some new biologically credible mechanism has been proposed. Even then, the new studies would need to quantitatively account for why previous studies had not established a significant risk. 1#9 9

A strong but uncertain association between solvent exposure and low sperm count was determined. Evidence from: N Cherry et al. Occupational and Environmental Medicine. October (2001) Vol.58 # 10 p 635. The Radar report is available to subscribers: 1#9 7