Preventing and controlling occupational asthma can be accomplished through comprehensive programs designed to prevent sensitization.
Occupational asthma is now the most common form of occupational lung disease in industrialized countries. In the United States alone, roughly 2% to 5% of asthmatics (about 600,000 persons) have disease attributable to workplace exposure.1 The worldwide prevalence may be even higher, with estimates ranging from 2% to 15%.2 Identified cases of occupational asthma probably represent only a small proportion of all cases of occupational asthma. The diagnosis of occupational asthma is often difficult because of several factors, including multiple potential causes in many industrial environments, variability of symptoms, and unpredictability of onset and persistence of symptoms.
When considered in relation to specific exposures or occupations, the prevalence of occupational asthma varies enormouslyfrom 1% to approximately 100%. The figures depend on a number of variables including: the industrial agent in question; the amount of exposure to the agent; working conditions in general; industrial hygiene measures; engineering factors; climactic influences; economic factors; and host susceptibility. For example, prevalence studies have shown that occupational asthma develops in about 2% to 40% of millers and bakers (because of allergens in flour), in 5% of workers exposed to toluene diisocyanate, and in 100% of power plant workers along the Mississippi (because of sensitization to river flies).1
Occupations associated with asthma include health care; animal handling; working with grains; bakeries; working with red cedar; laboratory work; snow crab and egg processing; manufacturing of detergents containing biological enzymes; working with paints, plastics, and adhesives; working with metal salts; jewelry making; nickel plating; the tanning industry; and soldering.3-6
More than 200 agents have been shown to cause occupational asthma. This number is likely to grow is new chemical agents are introduced into the workplace. Agents that cause occupational asthma include both naturally occurring and synthetic compounds. (Examples are presented in Table 1.) Some authorities divide the agents that can cause occupational asthma into two groups: IgE-dependent and IgE-independent.5 IgE-dependent occupational asthma has a longer latency period between exposure and onset of symptoms than does IgE-independent occupational asthma. Patients allergy histories and whether or not they smoke are important determinants of occupational asthma developing through IgE-dependent mechanisms. Allergy and smoking histories are less important determinants of occupational asthma developing through IgE-independent mechanisms.5
Although the list of etiologic agents for occupational asthma is more than 200 items long and growing, only a few of these agents have been extensively studied. These include diisocyanates, epoxy resins, and wood dusts.6 Diisocyanates are highly reactive chemicals that readily combine with other compounds to form plastics and adhesives, explains Moria Chan-Yeung, MD, of the Department of Medicine at the University of British Columbia in Vancouver. Chan-Yeung is a noted occupational asthma expert. Almost all processes for making molds and cores in modern steel factories use isocyanates. These agents are perhaps the most widely recognized cause of asthma in the workplace. Exposures occur in a number of industries. The prevalence of isocyanate-induced asthma in exposed workers is close to 10%.
Epoxy resins are made from acid anhydrides such as phthalic anhydride, tetrachlorophthalic anhydride, maleic anhydride, and trimetallic anhydride. They have a wide range of application for reinforced plastics, adhesives, molding resins, and surface coatings. They are potent irritants, and it is usually difficult to distinguish between allergic and irritant mechanisms. Roughly 40% of epoxy resin workers develop specific IgE antibodies to anhydride protein, and 20% develop respiratory disease associated with the immunologic reaction.6
Wood dusts are a common cause of occupational asthma. One of the best studied is the red cedar. The causative agent in this wood dust appears to be plicatic acid. Roughly 4% of exposed workers develop asthma.6
The Occupational Safety and Health Administration has set permissible exposure levels (PELs) for some of the agents associated with occupational asthma. These include cobalt, nickel, platinum salts, and certain isocyanates. However, the vast majority of materials causing asthma at work, including latex products, are unregulated.
Assessment of Asthma in the Workplace
The American College of Chest Physicians (ACCP), under the chair of Chan-Yeung, has addressed the increasing clinical and socioeconomic significance of occupational asthma by issuing a consensus statement regarding the assessment of asthma in the workplace.7 When asked why the ACCP issued the consensus statement, Chan-Yeung replied, There was a recognized need to address the problem of asthma in the workplace on a national level. With the prevalence of this disease increasing, we felt it was important to standardize a definition and to establish assessment guidelines. Clearly, workplace triggers represent a significant public health threat. It is hoped that with greater recognition of occupational asthma among RCPs, exposure to known triggers can be better controlled.
The ACCP consensus statement defines occupational asthma as a disease characterized by variable airflow limitation and/or bronchial hyperresponsiveness due to causes and conditions attributable to a particular working environment and not to stimuli encountered outside the workplace.7 Occupational asthma is subcategorized into that occurring with a latency period and that occurring without a latency period. Occupational asthma occurring with a latency period encompasses all instances of workplace asthma for which an immunologic mechanism has been identified and includes most high and some low molecular weight agents. Occupational asthma occurring without a latency period is best illustrated by irritant-induced asthma.
Assessment of occupational asthma includes history and physical examination, exposure assessment, peak expiratory flow (PEF) monitoring, nonspecific challenge testing, and specific challenge tests. The history should be structured to gain an understanding of the circumstances of the onset of asthma as well as temporal relationships between recurrent exposures and disease exacerbations. The occupational history should be very specific. An occupational profile is substantially enhanced by identifying job duties and work site exposures relevant to the development or exacerbation of asthma. According to Chan-Yeung, In addition to identifying potential hazards, the exposure history should assess the qualitative intensity (duration and concentration), frequency, and peak concentration of the exposures.
The assessment of exposures is a critical step in evaluating the contribution of the workplace to a patients asthma. The goals of exposure assessment are to identify the causative agents, minimize future exposures, and prevent the development of further cases of occupational asthma.5 Essential elements of exposure assessment are listed in Table 2.
The ideal treatment for patients with occupational asthma with a latency period is to remove them from exposure, Chan-Yeung explains. Perhaps a worker could be transferred to a job without exposure in the same company. In many cases, people with occupational asthma have to be retrained for another job. In some cases, reducing exposure by improving ventilation may allow a person to return to the same job, although this is not common. When employees have workplace-related asthma, employers should make every effort toward reasonable accommodation by improving the workplace. Most important, any patient with occupational asthma who returns to the same job should have close medical follow-up. According to the ACCP guidelines, patients with occupational asthma who remain on the offending job should be followed closely. Patients who are no longer left exposed should have a follow-up examination every 6 months for 2 years.7
Administrative management includes advising the patient about eligibility for workers compensation and notification of an appropriate public health agency. Voluntary reporting by RCPs is very important in obtaining information on the prevalence of occupational asthma.
The pharmacologic treatment of patients with occupational asthma does not differ from treatment of patients with nonoccupational asthma.7 The recommendations of the National Asthma Expert Panel8 should be followed. These include the stepwise use of pharmacotherapeutic agents that fall into two general classes: long-term control medications used to achieve and maintain control of persistent asthma; and quick-relief medications used to treat acute symptoms and exacerbations (see Table 3).
|Long-Term Control Medications
Most potent and effective anti-inflammatory medication currently available. Inhaled form is used in the long-term control of asthma. Systemic corticosteroids are often used to gain prompt control of the disease when initiating long-term therapy.
Cromolyn Sodium and Nedocromil
|Table 3. Pharmacotherapeutic agents used in the management of asthma.8|
Opportunities for Intervention
The respiratory care practitioner has an important role in the management of occupational asthma. Management involves removing the worker from the trigger. The RCP can help achieve this goal by educating the patient with known or suspected occupational asthma so that recognition of triggers is made possible. Recognition is the first step toward avoidance. By educating patients about possible triggers associated with their occupation, the RCP is providing a greater opportunity for trigger identification.
Surveillance programs are the keystone for prevention. They may identify individuals who are at an increased risk for developing asthma in the workplace and detect disease at an early stage when intervention options are likely to be successful. The most sensitive health surveillance programs currently available include preemployment and periodic examinations, immunologic monitoring, and periodic spirometric surveys.7
Patients with occupational asthma who smoke should be encouraged to stop smoking. Although the role of cigarette smoking in the pathogenesis of occupational asthma is not completely clear, smoking does appear to predispose workers to allergic sensitization.7 An association between atopy, cigarette smoking, and allergic sensitization to a workplace agent is reported for workers exposed to green coffee bean, tetrachlorophthalic anhydride, and platinum salts.7,9,10
The RCP also has a key role in establishing the diagnosis of occupational asthma through the performance of PEF testing. Prolonged PEF testing may be necessary to establish an association between a suspected trigger and asthma. Detailed and accurate records should be kept as spirometry is repeated.
The prevention and control of occupational asthma require more than just the establishment of PELs, because some sensitized individuals may become symptomatic at extremely low allergen levels. Comprehensive programs designed to prevent sensitization should include engineering controls, personal protective equipment, work-practice controls, and medical surveillance.
Despite the increased recognition of asthma in the workplace as a significant public health threat and the identification of numerous chemical triggers, the prevalence is on the rise. Successful treatment of this debilitating condition is predicated on avoidance of the offending trigger(s). The RCP has an important role in the diagnosis and management of occupational asthma and in prevention through patient counseling. Priorities for the future include improved diagnostic, screening, and surveillance methods, as well as better control of exposure.
John D. Zoidis, MD, is a contributing writer for RT Magazine.
1. Alberts WM, Brooks SM. Occupational asthma. Serious consequences for workers and employers. Postgrad Med. 1995;97:93-98, 101-102, 104.
2. Bernstein JA. Occupational asthma. My job is making me sick. Postgrad Med. 1992;92:109-112, 117-118.
3. Chan-Yeung M, Malo J-L. Aetiological agents in occupational asthma. Eur Respir J. 1994;7:346-371.
4. Chan-Yeung M, Lam S. State of art. Occupational asthma. Am Rev Respir Dis. 1986;133:686-703.
5. Chan-Yeung M, Malo J-L. Occupational asthma. N Engl J Med. 1995;333:107-112.
6. Alberts WM, Brooks SM. Advances in occupational asthma. Clin Chest Med. 1992;13:281-302.
7. American College of Chest Physicians Consensus Statement. Assessment of asthma in the workplace. Chest. 1995;108:1084-1117.
8. National Institutes of Health Expert Panel Report 2. Guidelines for the Diagnosis and Management of Asthma. Bethesda, Md: National Institutes of Health; 1997. NIH Publication No 97-4051.
9. Brooks SM. Occupational origin and environmental asthma. In: Rom WN, ed. Environmental and Occupational Medicine. 2nd ed. Boston: Little, Brown & Company; 1992:393-446.
10. Chan-Yeung M. Occupational asthma. Chest. 1990;98:S148-S161.