Occupational asthma has been defined as asthma due to conditions attributable to work exposures, not to causes outside the workplace. A new review article focuses on current data on pathogenesis, evaluation, and management.
Asthma is common in the general population, including among those in the workforce. Work exposures can cause or exacerbate asthma and can also be associated with asthma variants (e.g., eosinophilic bronchitis and aluminum potroom asthma) as well as symptoms that mimic asthma (e.g., the irritable larynx syndrome). In addition, even non-work-related asthma can affect the ability to work.
• What is sensitizer-induced asthma?
Occupational asthma can be caused by a specific workplace sensitizer, defined as an agent that induces asthma through a mechanism that is associated with a specific immunologic response. Occupational sensitizers are commonly high-molecular-weight agents (>10 kD, usually a protein or glycopeptide) that can cause production of specific IgE antibodies and typical allergic responses. Once a person is sensitized, very low exposures can induce asthma, which is often associated with rhinoconjunctivitis. It would appear that almost any protein that becomes airborne and inhaled might be a potential cause of occupational asthma. Low-molecular-weight occupational chemicals can also cause sensitization and, subsequently, asthma. A few have been associated with the production of specific IgE antibodies, such as complex platinum salts used in platinum refineries or the manufacture of catalysts. However, most low-molecular-weight chemical sensitizers induce asthma through mechanisms that are poorly understood, despite a phenotype suggesting sensitization. Diisocyanates are important sensitizers that are used in the production of rigid or flexible polyurethane foam; they are also used as hardeners in urethane spray paints and adhesives. Diisocyanates have been the most common cause of occupational asthma in many industrialized areas. Most chemical sensitizers have highly reactive side chains.
• What is irritant-induced occupational asthma?
Irritant-induced occupational asthma is a term used to describe occupational asthma that occurs from exposure to agents considered to be airway irritants, in the absence of sensitization. In 1985, diagnostic criteria for the reactive airways dysfunction syndrome, a severe form of irritant-induced asthma, were introduced. Subsequent reports have modified the initial, stringent diagnostic criteria for this syndrome and use the term “irritant-induced asthma” to include cases with induced airway symptoms and an onset after one or more high-level exposures. This category also includes cases with less immediate responses to exposure, with the recognition that these latter cases have less diagnostic certainty.
Morning Report Questions
Q: What is the epidemiology of occupational asthma?
A: Occupational asthma has been reported in up to 5 to 10% of workers exposed to most known agents. In addition to the inherent sensitizing potency of a given agent in the workplace, the level of exposure influences the rate of sensitization, as shown with both high-molecular-weight sensitizers such as animal proteins (in persons who work with laboratory animals) and flour proteins (in bakers) and low-molecular-weight sensitizers such as diisocyanates. A systematic analysis of population attributable risk showed that an estimated 16.3% of all cases of adult-onset asthma are caused by occupational exposure. There is a discrepancy between the rates of asthma diagnosed by a health professional as being work-related (4.7% of all new asthma cases) and rates that include self-reported cases of work-related asthma (18.2% of all new asthma cases); one possible explanation for the difference is that occupational asthma is underrecognized in clinical practice.
Q: How is occupational asthma best diagnosed?
A: Occupational asthma should be suspected in every adult with new-onset asthma. Although the respiratory symptoms in cases of occupational asthma, such as wheezing, dyspnea, chest tightness, cough, and sputum production, are similar to those in cases that are not work-related, their occurrence is usually modulated by the work-related exposure. A latency period ranging from weeks to years after the first exposure to the sensitizer is observed before the initial onset of work-related symptoms. Sensitizer-induced symptoms begin variably — at the beginning of the work shift, toward its end, or even in the evening after working hours; typically, remission or improvement occurs during weekends and holidays. Rhinitis often precedes lower respiratory symptoms, especially when high-molecular-weight agents incite the asthma. Although a thorough clinical and occupational history must be obtained, a compatible history alone is insufficient for diagnosis and has a low positive predictive value. Investigations should be started as soon as the diagnosis is suspected, preferably while the patient is still working, and should be as comprehensive as feasible, including assessment of clinical symptoms, objective confirmation of asthma, testing for skin or serologic specific IgE antibodies when possible, and documentation of symptomatic, functional, and inflammatory changes in response to exposure to occupational agents (at work vs. away from work or by specific challenge).