Although some asbestos-related diseases are essentially specific to occupation (eg mesothelioma, asbestosis) others, like lung cancer, are not. This has led to concerns that certain asbestos-related cancers may be under-diagnosed, especially in smokers seeking compensation. Verger and colleagues have reported on physicians’ attitudes to such cases and the potential barriers to compensation as evidenced by a cross-sectional survey of French general practitioners and pulmonologists.¹ Participants were presented with case vignettes differing only in relation to a worker’s smoking status and asked to assess whether they were work-related. Respiratory specialists were four times more likely than general practitioners to classify a case as occupational. Classification was also three times more likely for non-smokers than smokers and more likely among physicians with a high workload or a perception that assessing occupational attribution was a part of their job description. The paper highlights the difficulty of making reliable occupational attribution in such cases and the potential biases that can then arise.

The role of genetics in workers’ susceptibility to occupational exposures is an area of substantial and growing interest to researchers and policy makers alike. This month’s Journal contains a welcome Education review by Christiani and coworkers outlining the scope and the limitations of genetic screening and genetic research in occupational medicine.² The high prevalence of genetic variants in the general population has been an encouragement to undertake such activities and the authors see potential value in mechanistic research and studies that help to set safer occupational exposure limits for genetically vulnerable sub-groups. However, they argue against the value of routine wide-scale genetic screening in the workplace.

Cadmium is a ubiquitous environmental pollutant that accumulates and persists in the body, with several recognised adverse health effects. Recent interest has focused on the role of cadmium in hypertension and cardiovascular disease, there being some evidence that peripheral arterial disease is related to cadmium levels in blood and urine. In this issue, Schutte and coauthors report novel findings on the relation between 24-h urinary cadmium excretion and various markers of arterial structure and function involving the main arterial tree.³ They have found that increased cadmium body burden was associated with a lower aortic pulse wave velocity; a lower pulse pressure throughout the arterial system; and higher femoral distensibility. Cadmium levels were not, as previously reported, associated with decreased arterial function in peripheral leg arteries and the authors call for clarification through further prospective and mechanistic studies.

This month’s Journal also includes a report on trends in airborne particulates in the European rubber industry since the 1970s,⁴ a meta-analysis related to benzene exposure and non-Hodgkin lymphoma⁵ and a case–control study of beryllium and lung cancer that evaluates the influence of temporal confounders.⁶

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