Occupational Asthma
DEFINITION
The definition of occupational asthma, much like the definition of asthma itself, has changed over the years; therefore, it is difficult to determine the prevalence of the disorder. According to the current consensus definition,1 patients with occupational asthma have variable airflow limitation or airway hyperresponsiveness, or both. It occurs in response to a specific work environment and not to stimuli encountered elsewhere.
PREVALENCE
Occupational asthma is a part of a larger category of diseases known as occupational respiratory diseases and includes occupation-induced rhinitis and laryngitis, tracheitis, bronchitis and bronchiolitis, chronic obstructive pulmonary disease, lung cancer, and interstitial diseases such as fibrosis and granuloma formation.2 Physicians and the lay public are aware of other occupational lung disorders such as silicosis and asbestosis (see “Occupational Lung Disease” in Section 12), but occupational asthma is the most prevalent occupational lung disease in industrialized countries.
The incidence of occupational asthma also varies with specific exposures. Occupational asthma has been reported in 8% to 12% of laboratory animal workers, 7% to 9% of bakers, and 1.4% of health care workers exposed to natural rubber latex. Even these percentages vary significantly depending on the study cited. Farmers, painters, plastic and rubber workers, and cleaners (window cleaners, chimney sweepers, and road sweepers) are at greatest risk for developing asthma.3
PATHOPHYSIOLOGY
Like childhood asthma, occupational asthma is the result of interactions between multiple environmental and genetic factors. Some of the known environmental factors include the route, duration, and intensity of exposure and the substance (or agent) to which the person is exposed. Using the definition of Mapp and coworkers,1 occupational asthma can be divided into immunologic causes (associated with a latency period) and nonimmunologic causes. Agents associated with an immunologic cause can be further divided into high-molecular-weight (HMW) agents, usually allergens such as proteins from laboratory animals, flour, or plants, and low-molecular-weight (LMW) agents, usually chemicals such as isocyanates, biocides, or drugs.
Occupational Asthma with a Latency Period
The pathogenic mechanisms of LMW agents are less well understood; however, there appear to be several mechanisms, both immunologic and nonimmunologic, that can lead to occupational asthma. LMW agents probably act as haptens, combining with human proteins in the respiratory tract to become complete immunogens. Atopy and smoking are not risk factors for occupational asthma caused by LMW agents, as they are for occupational asthma caused by HMW agents. Some of the better-studied agents include isocyanates and plicatic acid. Isocyanates are found in paints and are involved in the manufacture of plastics, rubber, and foam, and plicatic acid is the causative agent in asthma caused by western red cedar. Specific IgE for isocyanates or plicatic acid is found in only a small percentage of patients with documented disease. However, the detection of specific IgE may be a marker of exposure and not of disease.4
Activated T cells also play an important role in the pathogenesis and in the inflammation of occupational asthma as they do in other forms of asthma. Bronchial biopsies of patients with occupational asthma induced by isocyanate or red cedar show many activated T cells.5,6 Several recent studies have also shown associations between HLA class II antigens and various types of occupational asthma.7
Box 1 shows some of the more common causes of occupational asthma associated with a latency period.
Occupational Asthma Without Latency
The mechanisms of IrIA or RADS are also poorly understood. IrIA is a nonimmunologically induced asthma that occurs without a latency period. It typically occurs after a brief, high-intensity inhalation exposure followed by the acute onset of persistent respiratory symptoms and ongoing airway hyperresponsiveness. It is postulated that extensive denudation of the airway epithelium occurs, resulting in airway inflammation due to the loss of epithelium-derived relaxing factors, exposure of nerve endings leading to neurogenic inflammation, and nonspecific activation of mast cells with release of inflammatory mediators and cytokines.8 Ammonia, chlorine, and sulfur dioxide are the most common causes of IrIA, although the list is extensive.
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