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Occupational asthma: Pathogenesis

INTRODUCTION

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 [1].

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".)

TYPES

Three main types of occupational asthma have been recognized [1,2]:

  • Immunologically mediated with participation of specific IgE
  • Immunologically mediated without evidence of participation of IgE
  • Nonimmunologic, irritant mediated, also known as sensitizer induced. 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".)

Some occupational agents, such as diisocyanates, may induce asthma through more than one mechanism. As an example, asthma may develop in subjects after a diisocyanate spill by causing acute airway injury and reactive airways dysfunction syndrome (RADS), while in others, sensitization to diisocyanate develops with lower levels of exposure. (See "Reactive airways dysfunction syndrome and irritant-induced asthma".)

            

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Literature review current through: Apr 2013. | This topic last updated: May 11, 2012.
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