Abstract

To review the clinical features and underlying mechanisms of occupational asthma in an attempt to glean insights into various other forms of asthma. Published literature, including consensus guidelines on diagnosis and management of occupational asthma. This article represents a synthesis of these data sources and the opinion of the author. Occupational asthma may be caused by a variety of mechanisms, including both IgE-dependent and non-IgE-dependent immunological processes. IgE-dependent mechanisms are responsible for reactions to all high-molecular-weight occupational antigens and to some but not all low-molecular-weight antigens. Factors in sensitization and onset include the general genetic predisposition to make IgE and the specific responsiveness of the individual to particular allergens. Once sensitized, the main factor that influences the onset of symptoms is the degree of exposure. In general, the higher the level of exposure, the more likely the sensitized person is to develop asthma. Occupational asthma can be induced by a variety of agents that appear to use different mechanisms to affect the airway. Studies of the remission of occupational asthma indicate that resolution is a slow process. However, the study of occupational asthma may eventually allow us to identify treatments that will accelerate remission or induce remission in other forms of asthma.

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