Occupational Asthma
Laura S. Welch
Asthma consists of reversible airway obstruction. There is no uniform definition of occupational asthma, but most experts would call it a new state of bronchial hyperreactivity secondary to some agent at work [1], or reversible obstruction of the airways caused by inhalation of a substance or material used by a worker or present at his work [2]. Asthma can be a pre-existing disease that is exacerbated by exposures at work, rather than having these exposures as the primary cause; this is not defined as occupational asthma but rather as exacerbation of pre-existing disease. Exacerbation of pre-existing disease is work-related, but I will reserve the term occupational asthma for use as defined above.
Three percent of all Americans have asthma [3], and 5 to 15% of all asthma is estimated to be occupational [4,5]. The talk will present identified causes of occupational asthma, and working case definitions of the disease.
Even though there has been a great deal of research, not everyone will agree on the case definition of occupational asthma. Definitions vary by the study and the instrument used. Questionnaire has been useful for screening, but are less sensitive than methacholine challenge in detecting cases [6]. If pulmonary function is used, as usual definition is a drop of greater than 10% in FEV1 over a work shift, or a greater than 20% drop in peak flow over a work day. It may take repeated measurements in any one worker to detect such a drop, for some react only at the end of a work week.
Much has been written on the mechanism of occupational asthma, and both Dr. Liebowitz and Dr. Karol have discussed this in their presentations; I will not review that in detail here. As an overview, occupational asthma can be allergic or non-allergic. Asthma may develop as a specific sensitivity to one agent (or a family of related agents), or as a response to exposure to non-specific irritants.
There is certainly a major role of the immune system in the development of occupational asthma specific to one agent. In studies of asthma secondary to Western red cedar dust, considered a prototype of asthma from low-molecular weight compounds, investigators have found specific IgE in 40% of cases (but note that it is not detectable in 60%) [4]. Studies of isocyanate-induced asthma have also found IgE in some cases but not all. Many investigators think there is a role for direct histamine release in the lung. But in
addition, there is much emphasis on the role of inflammation in the initiation and continuation of asthma.
The clinical presentation of occupational asthma can consist of an immediate reaction, a late-phase reaction, or commonly a mixture of both types [2,4]. In Western red cedar cases, for example, late asthmatic reactions alone occurred in 44%, both in 49% and immediate reactions alone in only 7%. There was no correlation between development of red cedar asthma and previous atopic status. These findings suggest that the allergic reaction is more complex than IgE alone. In addition, this same study reported that nonspecific bronchial hyperreactivity (as measured with methacholine) correlated strongly with specific reactivity to plicatic acid, and decreased as patients became asymptomatic.
The second syndrome, a response to what we think is non-specific irritation rather than a specific allergy, was described by Brooks [7], and called RADS (reactive airway dysfunction syndrome); characteristics of this group of patients was also described by Tarlo and Broder [8]. Tarlo reported that this syndrome made up 10% of patients coming for evaluation to two centers. In reviewing 15 cases, these individuals has a low incidence of atopic disease, and were more likely to be smokers. These findings need further investigation.
What we know about occupational asthma can help us in beginning research on multiple chemical sensitivity. Study of occupational asthma first and foremost illustrates both the difficulty of developing a case definition, and the important of having one, as well as the importance of standardized measurement. These are basic research concepts, but it has taken many scientists to develop what tests and clinical signs are appropriate for the study of occupational asthma.
An approach for epidemiologic study that has worked with asthma is to use a questionnaire to define cases, and then proceed to a more detailed case investigation. We know that we do not capture all occupational asthma cases with a questionnaire, but this approach is efficient, acceptable, and yields very useful information of the subgroups of asthmatics that have a set of symptoms.
Occupational asthma is one disease for which exposure is part of the case definition. A particular set of symptoms of clinical findings develops in relationship to exposure. I expect that a case definition of MCS will include such a response to exposure as well, and we can use the lessons learned from occupational asthma to guide us here.
Occupational asthma has many causative agents, and more than one mechanism that results in the same clinical presentation. In asthma, there is dearly a role for both the immune system and direct inflammation.
Of particular importance, studies of occupational asthma have taught us about the role of controlled provocative challenges, and the importance of these challenges being performed in a standard fashion in a few specialized centers [9]. The diagnosis of occupational asthma usually does not need a controlled challenge, and such studies serve as a research toll primarily.
Finally, we have learned a great deal about the role of testing for specific antibodies or other tests of the immune system. Research in occupational asthma has shown that great attention must be paid to quality assurance and quality control, and that analyses must be standardized between laboratories [10].
REFERENCES
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2. Brooks, Smart M.: Bronchial asthma of occupational origin. Scand J Work Environ Health 1977; 3: 53-72.
3. Occupational Disease Surveillance: occupational asthma. MMWR 1990; 39: 119-123.
4. Chan-Yeung, M., Lam, S.: Occupational asthma. Am Rev Respir Dis 1986; 133: 686-703.
5. Blanc, P.D.: Occupational asthma in a national disability survey. Chest 1987; 92: 613-617.
6. Bernstein, D.I., Cohn, J.R.: Guidelines for the diagnosis and evaluation of occupational immunologic lung disease: preface. J Allergy Clin Immunol 19; 5: 791-793.
7. Brooks, Stuart M., Weiss, Mark A., Bernstein, I.L.: Reactive airways dysfunction syndrome-case reports of persistent airways hyperreactivity following high-level irritant exposures. J Occup Med 1985; 27: 473-476.
8. Tarlo, S.M., Broder, I.: Irritant-induced occupational asthma. Chest 1989; 96(2): 297-300.
9. Brooks, Smart M.: The evaluation of occupational airways disease in the laboratory and workplace. J Allergy Clin Immunol 1982; 70: 56-66.
10. Grammer, L.C., Patterson, R, Zeiss, C.R.: Guidelines for the immunologic evaluation of occupational lung disease. J Allergy Clin Immunol 1989; 84: 805-813.
