Work-Related Asthma

William G. Hughson

Asthma is a disorder of lung function characterized by widespread obstruction of the airways that (1) varies in severity; (2) is reversible, either spontaneously or as a result of treatment; and (3) is not caused by cardiovascular disease. Work-related asthma is the broad term that refers to asthma that is induced or exacerbated by inhalation exposures in the workplace and includes both occupational asthma and work-exacerbated asthma. Occupational asthma is caused by exposure to airborne dusts, gases, vapors, or fumes in the working environment. Work-exacerbated asthma refers to asthma triggered by various work-related factors in workers known to have pre-existing or concurrent asthma.

ETIOLOGY

Asthma is a common disease. Approximately 10% of people are diagnosed with asthma during their lifetime (i.e., the incidence of asthma). Some cases resolve, but approximately 5% of the population has active asthma (i.e., the prevalence of asthma). Approximately 10% to 15% of cases of adult asthma is either caused or exacerbated by workplace exposures. The frequency of work-related asthma varies widely among occupations and within industries at different levels of exposure. The true occurrence of work-related asthma is probably greater than reported because affected workers often terminate their employment, leaving unaffected survivors. This type of self-selection is common in studies of working individuals that compare morbidity and mortality rates to those of the general population. Employed populations typically have morbidity and mortality rates 10% to 20% lower than the general population, which contains individuals disabled by chronic diseases. This deficit of disease is referred to as the healthy worker effect. Because asthma is common in the general population and the clinical findings in work-related asthma are identical to those of non–work-related asthma, the clinical challenge is to understand the nature and degree of workplace exposures and to make a temporal association between the asthma and occupation. Diagnosis can be difficult, given the inherent variability of asthma and the fact the patient can have early, late, dual, or recurrent late onset of symptoms.

PATHOGENESIS

The pathogenetic mechanisms of work-related asthma can be classified as reflex, inflammatory, pharmacologic, and allergic. Reflex bronchoconstriction involves irritant receptors in the airway that are stimulated by agents such as cold air, inert dust particles, gases, and fumes. The reaction does not involve immune mechanisms and is nonspecific. Many patients have a history of pre-existing asthma. Inflammatory bronchoconstriction begins as a nonspecific reaction following inhalation of high concentrations of nonspecific irritants. Most individuals recover, but a few develop chronic asthma. This condition is often referred to as reactive airways dysfunction syndrome (RADS). Vocal-cord dysfunction characterized by hoarseness, cough, and dyspnea is also caused by irritant exposures, and can be mistaken for asthma. Pharmacologic bronchoconstriction occurs when agents in the work environment exert a specific pharmacologic effect on the lung. An example is cholinesterase inhibition by organophosphate pesticides causing bronchoconstriction because of excessive parasympathetic stimulation.

Allergic bronchoconstriction is the most common cause of occupational asthma. Susceptible workers develop IgE or IgG antibodies following exposure to workplace antigens such as animal or plant proteins. If high-molecular-weight compounds are responsible (e.g., baker’s asthma), individuals who are atopic become sensitized more readily than workers who are nonatopic. However, atopy is not a predisposing factor when low-molecular-weight compounds are involved (e.g., isocyanate manufacturing). Sensitization takes time, and the latency period between exposure and the onset of symptoms can be weeks to years. Several hundred workplace agents have been shown to cause occupational asthma, and the list grows every year. Cigarette smoking doubles the risk of occupational asthma, possibly by recruiting inflammatory cells into the lung where they are available to react with irritants and sensitizers.

DIAGNOSIS

When considering work-related asthma as a diagnosis, two questions must be answered: (1) does this patient actually have asthma and (2) is the asthma related to work. The general approach to diagnosing asthma is discussed elsewhere in this manual (see Chapter 63). Methods for answering the second question include a detailed clinical and occupational history, physical examination, chest radiographs, pulmonary function tests, inhalation challenge tests, and immunologic tests.

The clinical history of the patient with work-related asthma typically reveals shortness of breath, chest tightness, cough, and wheezing at work or within several hours after leaving work. Respiratory symptoms are often accompanied by rhinitis or conjunctivitis. Recurrent attacks of bronchitis

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