title: Occupational asthma.
abstract: The workplace can be responsible for approximately one in 10 cases of adult-onset asthma. Two types of occupational asthma (OA) are distinguished by whether they arise after a latency period that is necessary for acquiring sensitization or as a result of acute exposure to irritant materials (irritant-induced asthma). The pathophysiology of OA with a latency period is similar to that of nonoccupational asthma, whereas the mechanism of irritant-induced asthma is still uncertain. HLA haplotypes and other genetic polymorphisms have been found to be associated with OA. According to various sources of data, the overall frequency of OA has remained stable in the last 10 years, although the frequency of causal agents vary. Registers of causal occupations and agents have been issued on Web sites (eg, www.asmanet.com ). Improved sampling methods have shown that the degree of exposure plays a key role in the onset of the disease, whereas prospective data collected in high-risk workplaces have also identified personal risk factors (eg, atopy, smoking, and rhinoconjunctivitis). A diagnosis of OA should no longer be based on a compatible history only but should be confirmed by means of objective testing. Once the diagnosis is confirmed, the worker should be removed from exposure, and satisfactory compensation programs should be offered, the most important being retraining programs with financial compensations because affected workers are generally young. The cost-effectiveness of prevention programs in high-risk workforces should be assessed.
authors.affiliation: Department of Respiratory Medicine, Sacré-Coeur Hospital, Montreal, Quebec, Canada.
authors.forename: J L
authors.initials: JL
authors.lastname: Malo
authors.forename: M
authors.initials: M
authors.lastname: Chan-Yeung
mesh_terms: D001249:Asthma / Q000453:epidemiology / Q000209:etiology* / Q000235:genetics / Q000276:immunology; D020022:Genetic Predisposition to Disease; D006801:Humans; D007603:Jurisprudence; D009784:Occupational Diseases / Q000453:epidemiology / Q000209:etiology* / Q000235:genetics / Q000276:immunology; D012307:Risk Factors