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Occupational asthma: Management, prognosis, and prevention

Catherine Lemière, MD
David I Bernstein, MD
Section Editor
Peter J Barnes, DM, DSc, FRCP, FRS
Deputy Editor
Helen Hollingsworth, MD


Occupational asthma (OA) is a form of work-related asthma that is characterized by variable airflow obstruction, airway hyperresponsiveness, and airway inflammation induced by exposures in the work environment rather than exposures encountered outside the workplace [1]. Work-exacerbated asthma (also known as work-aggravated asthma) is defined as preexisting or concurrent asthma that worsens in the workplace, but is not induced by it.

The agents that cause OA include both immunologic and nonimmunologic stimuli [2]. Immunologic OA is the classic form of OA in which the worker's immune system is sensitized to an occupational agent through IgE-mediated or other immune recognition. Similar to asthma in general, immunologic OA appears to be heterogeneous and includes several phenotypes [3]. The term nonimmunologic OA is used to refer to irritant-induced asthma that results from single or multiple exposures to irritant substances at a high level of intensity. Reactive airways dysfunction syndrome (RADS), is a form of irritant-induced asthma, acutely induced by accidental high level irritant exposures in the workplace (eg, sulfur dioxide, chlorine, smoke inhalation).

The diagnosis of immunologic OA is based on the occurrence of new adult-onset asthma or worsening of previously quiescent asthma following an initial occupational exposure to a causative agent, evidence of reversible airflow obstruction and/or airway hyperresponsiveness (based on pulmonary function testing), and demonstration of respiratory sensitization to a potential causative agent [4]. Demonstration of allergic sensitization (particularly to protein allergens encountered at work) by skin prick testing or serum specific IgE supports the diagnosis of immunologic OA. The diagnosis of irritant induced asthma (eg, RADS) is made retrospectively based on the onset of cough and/or asthma symptoms following high-intensity irritant exposure(s) and demonstration of a positive methacholine challenge test.    

The management, prognosis, and prevention of OA will be reviewed here. The definition, epidemiology, causes, risk factors, pathogenesis, clinical features, evaluation, and diagnosis of OA, and the diagnosis and management of RADS and irritant–induced asthma are discussed separately. (See "Occupational asthma: Definitions, epidemiology, causes, and risk factors" and "Occupational asthma: Pathogenesis" and "Occupational asthma: Clinical features and diagnosis" and "Reactive airways dysfunction syndrome and irritant-induced asthma".)


The key element is to make the diagnosis and remove the subject from exposure as quickly as possible after the onset of symptoms. Occupational asthma (OA) may be cured if this is done rapidly and efficiently. The management of OA requires a combination of avoidance of further exposure to sensitizing agents, reduction in exposure to irritant agents (eg, environmental tobacco smoke, strong fumes and fragrances, extremes of temperature and humidity) and pharmacotherapy based on the severity of asthma. The management of occupational rhinitis, which may accompany OA, is discussed separately. (See "Occupational rhinitis".)


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Literature review current through: Jul 2017. | This topic last updated: Jun 27, 2017.
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