Substantial epidemiologic and clinical evidence indicates that agents inhaled at work can induce asthma. In industrialized countries, occupational factors have been implicated in 9 to 15% of all cases of adult asthma. Work-related asthma includes, immunologic occupational asthma (OA), characterized by a latency period before the onset of symptoms; nonimmunologic OA, which occurs after single or multiple exposures to high concentrations of irritant materials; work-aggravated asthma, which is preexisting or concurrent asthma exacerbated by workplace exposures; and variant syndromes. Assessment of the work environment has improved, making it possible to measure concentrations of several high- and low-molecular-weight agents in the workplace. The identification of host factors, polymorphisms, and candidate genes associated with OA is in progress and may improve our understanding of mechanisms involved in OA. A reliable diagnosis of OA should be confirmed by objective testing early after its onset. Removal of the worker from exposure to the causal agent and treatment with inhaled glucocorticoids lead to a better outcome. Finally, strategies for preventing OA should be implemented and their cost-effectiveness examined.
Occupational asthma / Ce, Mapp; P., Boschetto; P., Maestrelli; Fabbri, Leonardo. - In: AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE. - ISSN 1073-449X. - STAMPA. - 172:3(2005), pp. 280-305. [10.1164/rccm.200311-1575SO]
Occupational asthma
FABBRI, Leonardo
2005
Abstract
Substantial epidemiologic and clinical evidence indicates that agents inhaled at work can induce asthma. In industrialized countries, occupational factors have been implicated in 9 to 15% of all cases of adult asthma. Work-related asthma includes, immunologic occupational asthma (OA), characterized by a latency period before the onset of symptoms; nonimmunologic OA, which occurs after single or multiple exposures to high concentrations of irritant materials; work-aggravated asthma, which is preexisting or concurrent asthma exacerbated by workplace exposures; and variant syndromes. Assessment of the work environment has improved, making it possible to measure concentrations of several high- and low-molecular-weight agents in the workplace. The identification of host factors, polymorphisms, and candidate genes associated with OA is in progress and may improve our understanding of mechanisms involved in OA. A reliable diagnosis of OA should be confirmed by objective testing early after its onset. Removal of the worker from exposure to the causal agent and treatment with inhaled glucocorticoids lead to a better outcome. Finally, strategies for preventing OA should be implemented and their cost-effectiveness examined.
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