Occupational Asthma Reference

Cullinan P, Occupational asthma, Occup Environ Med, 2008;65:151-151,

Keywords: commentary, exposure measurement

Known Authors

Paul Cullinan, Royal Brompton Hospital, London, UK Paul Cullinan

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There is a long and sometimes ignoble history of occupational diseases being normalised and/or wrongly attributed to factors outside the workplace. In 1919, for example, a local physician blamed the "black lung" of Appalachian coal miners on "housing conditions and hurtful forms of recreation".1 Sixteen years later the disease was still considered "an ordinary condition that need cause no worry".2 When occupational diseases are considered "natural", or are ascribed to characteristics of the worker or his domestic environment, then there is little incentive to improve working conditions.

The last decade or so has seen a paradigm shift in our understanding of occupational asthma. It is no longer considered a disease that solely reflects individual susceptibility; there is now a consistent body of evidence relating its incidence—at least at a population level—to the intensity of allergen exposure in the workplace. Thus, even if the details of exposure-response relations and their thresholds (if any) remain hazy, it has become an imperative to ensure control of such exposures. Success in doing so and in reducing disease incidence has been claimed for, among others, enzyme asthma in the detergent industry,3 latex asthma in healthcare workers4 and diisocyanate asthma in a variety of settings.5

Such published examples of primary preventive interventions share three characteristics: first, they are remarkably casual over even the most basic of epidemiological principles; second, they tend to describe multifaceted programmes and the role of exposure control rather than, say, employee education in reducing disease is unclear; and third, they employ at best crude and always ecological measures of allergen exposure. Heederik and van Rooy, expert in such matters, call for better measurement to improve the interpretation of such interventions and develop appropriate inferences from them. Even if they are not explicit in what they mean by "sound" exposure assessment, there must be few who would disagree with them.

More will find difficulties with their second call which concerns the management (the "tertiary prevention") of workers who have already developed occupational asthma. Current practice incorporates complete exposure avoidance which all too often implies a change of occupation and consequent hardship. In this issue Heederik and van Rooy argue for studies of exposure reduction (rather than complete avoidance) in case management essentially incorporating careful exposure assessment, presumably at a personal level (see page 10.1136/oem.2005.024711).6 Individual case management by continued but reduced allergen exposure is contentious not least because for many years experts in occupational asthma have been claiming that only the cessation of all further exposure can be effective in recovery. This "expert" argument is based on the hypersensitive immunology of occupational allergy, the observation that affected employees frequently have symptoms at extremely low levels of exposure and the claim that the prognosis of the disease is related adversely to the duration of symptomatic employment. It is also, perhaps, an argument of prudence. In fact the efficacy of complete exposure avoidance is far from certain and nor is it clear that further exposure of any degree after the onset of symptoms is detrimental to prognosis in all types of disease. Moreover there are some settings in which continued exposure is countenanced with the connivance if not the blessing of employers and their occupational health advisors; laboratory animal asthma is one such example, reflecting perhaps the capital value of labour in that sector.

It seems timely to open debate in this area but it would be naive to ignore the very real difficulties posed by any "well-designed intervention study" on workers with occupational asthma. Ironically the issues of exposure measurement may be the least of these problems. Any such study would need to be based within a workplace—more probably an occupational sector—with a sufficient and continuing experience of the disease, and would of course require the cooperation not only of employers but also of their insurers and lawyers. It is likely that there will be considerable resistance. Measuring exposure reduction implies detailed knowledge of exposures prior to any intervention—not easy to incorporate within a study design. Nor will it be straightforward to be sure that the reduction has been sufficient to prevent the persistence of disease and will continue to be so. Subjective reports of symptomatic resolution would need to be verified by objective and sustained evidence of reduced airway inflammation. Some of the newer non-invasive methods of assessment (sputum induction or measurement of exhaled NO) might be valuable additions to the serial assessment of peak flow of bronchial responsiveness.

Therefore the difficulties will be more than just ethical. Nonetheless I welcome the debate. If nothing more, it is time we learned properly how to enrich the currency with which we measure the effects of occupational asthma. Experts tend to worry about asthma; patients are at least as worried about their jobs.

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