Occupational asthma (OA) is a form of work-related asthma characterized by variable airflow obstruction, airway hyperresponsiveness, and airway inflammation attributable to exposures in the workplace and not due to stimuli encountered outside the workplace . Work-exacerbated asthma (also known as work-aggravated asthma) is defined as preexisting or concurrent asthma that subjectively worsens in the workplace.
OA is triggered by exposure to immunologic or nonimmunologic stimuli . Immunologic OA has a latency period during which the immunologic sensitization develops. Nonimmunologic OA has no latency period and is caused by exposure to high levels of irritants; it is also known as irritant-induced asthma or reactive airways dysfunction syndrome (RADS) [3,4]. (See "Reactive airways dysfunction syndrome and irritant-induced asthma".)
OA accounts for approximately 10 to 25 percent of adult onset asthma [2,5,6]. This implies that investigation of the causal relationship between workplace exposure and asthma is indicated in approximately one of every 5 to 10 subjects with adult-onset asthma.
The evaluation and diagnosis of suspected OA will be reviewed here. The pathophysiology definition, epidemiology, causes, risk factors, and management are discussed separately. (See "Occupational asthma: Pathogenesis" and "Occupational asthma: Definitions, epidemiology, causes, and risk factors" and "Occupational asthma: Management, prognosis, and prevention" and "Overview of occupational and environmental health".)
The clinical history in patients with possible occupational asthma (OA) should include detailed information about the job description and potential exposures to causal agents, in addition to the routine evaluation of adult-onset asthma . The clinical history, while important, does not confirm or exclude the diagnosis of OA, although the negative predictive value is better than the positive predictive value [8-10]. (See "Diagnosis of asthma in adolescents and adults".)