Abstract

Surveillance programs established around the world have determined that diisocyanate chemicals are the most common cause of occupational asthma. In the United States approximately 100, 000 workers are exposed to these chemical compounds in the workplace each year and 5-10% of these workers will develop occupational asthma. There are no known reliable risk factors or biomarkers which can be used to predict which exposed worker will develop diisocyanate-occupational asthma. Diisocyanate-occupational asthma workers manifest characteristic physiologic responses after specific bronchoprovocation which correlate with pathologic changes in their airways. However, the mechanism(s) for diisocyanate-occupational asthma remains unclear. Specific IgE antibody production to diisocyanates is found in only 10-30% of these workers. Bronchial biopsies and bronchoalveolar lavage have confirmed the presence of T-lymphocytes and eosinophils in the airways of these workers suggesting that T-cell mediated immune responses are more likely to play a central role in this disease. It is essential to diagnose diisocyanate-occupational asthma as early as possible in order to prevent or reduce the significant asthma morbidity associated with continuous long term exposure to these chemicals. Treatment of choice is removal of the worker from further exposure. Prospective studies evaluating larger populations of diisocyanate-exposed workers is essential for a better understanding of the pathogenesis and natural course of diisocyanate-occupational asthma.

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