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Occupational asthma: Pathogenesis

Louis-Philippe Boulet, MD
Jean-Luc Malo, MD
David I Bernstein, MD
Section Editor
Peter J Barnes, DM, DSc, FRCP, FRS
Deputy Editor
Helen Hollingsworth, MD


The label "asthma in the workplace" encompasses several entities: (1) asthma exacerbated at work by various environmental conditions; (2) occupational asthma; and (3) variants (eg, eosinophilic bronchitis) [1]. Occupational asthma is a disease characterized by variable airflow limitation, airway hyperresponsiveness, and inflammation resulting from an inciting agent only found in the workplace [2].

The pathogenesis and pathology of occupational asthma will be reviewed here. Issues related to other aspects of occupational asthma are discussed separately. (See "Occupational asthma: Definitions, epidemiology, causes, and risk factors" and "Occupational asthma: Clinical features and diagnosis" and "Reactive airways dysfunction syndrome and irritant-induced asthma".)


Two main types of occupational asthma have been recognized [1,3]:

Immunologically mediated. This type includes IgE and nonIgE-mediated responses following chronic exposure to high or low molecular weight agents.

Nonimmunologic, irritant mediated. This type includes reactive airways dysfunction syndrome (RADS) caused by a single high level exposure to an irritant and also chronic lower level exposure. (See "Reactive airways dysfunction syndrome and irritant-induced asthma".)


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Literature review current through: Jan 2016. | This topic last updated: Dec 22, 2015.
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