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Tampa, FL
Dr. Alberts is Professor of Medicine, University of South Florida College of Medicine, and Associate Center Director for Clinical Affairs at the H. Lee Moffitt Cancer Center.
Correspondence to: W. Michael Alberts, MD, MBA, FCCP, Interim-Chair and Professor, Department of Interdisciplinary Oncology, University of South Florida College of Medicine, Associate Center Director for Clinical Affairs, H. Lee Moffitt Cancer Center, 12902 Magnolia Dr, Tampa, FL 33612; e-mail: alberts{at}moffitt.usf.edu
Occupational asthma is not a rare disorder. Work-related asthma is now the most prevalent occupational lung disorder in industrialized nations.1 The prevalence is such that if one maintains a high degree of suspicion when faced with a patient of working age who presents with respiratory symptoms, there is a good chance that one will occasionally make this diagnosis.
Just how common is occupational asthma? The prevalence of asthma in the United States has been conservatively estimated to be 3 to 6% of the population. The prevalence of occupational asthma has been conservatively estimated to be from 2 to 5% of all cases of asthma. A recent study found an attributable fraction of asthma related to occupation of 29% in men and 17% in women.2 Five to 15% is the most frequently quoted range.1 If we take a conservative figure of 5% of the population as being asthmatic and say that 5% of the asthmatic population acquired their asthma from the workplace, an estimated 600,000 to 700,000 individuals have occupational asthma in this country. This, of course, is no small number.
A diagnosis of occupational asthma, however, should not be made without ample proof and confirmatory evidence. A documented case has very serious consequences for both the worker and the offending workplace. The worker is faced with either losing his or her job or risking long-term disability with continued exposure. The employer must face the reality that if one worker has occupational asthma, it is likely that others do too. Epidemiologic studies following the identification of an affected worker have usually uncovered a significant degree of unrecognized disease. A single suspected case of occupational asthma should lead to further investigation and confirmation. A well-defined case should be viewed as evidence of a potential health hazard in the workplace that requires modification to prevent future cases. Moreover, if the offending exposure is an essential part of a process, an entire industry may be threatened.
Taken together, while it is important not to miss a diagnosis of occupational asthma, it is just as damaging to make such a diagnosis in error. Underdiagnosis and overdiagnosis can both lead to substantial and avoidable costs to patients, their families, employers, health-care insurance organizations, and society.3 As a result, the diagnostic evaluation of suspected cases must be approached conscientiously.
The clinical diagnosis of occupational asthma is not easy.4 To confidently render a diagnosis of occupational asthma, one must first diagnose asthma (if the patient doesn’t have asthma, he or she doesn’t have occupational asthma). The next step is to establish a work relationship. Although such a relationship may be suspected on the basis of history, objective confirmation is necessary. Commonly, a "stop-resume" work test using serial measures of pulmonary function is used. Serial measurement of nonspecific bronchial responsiveness may be a useful adjunct to the stop-resume work test. A significant decrement in bronchial responsiveness after removal from the workplace is supportive of the diagnosis.
Having confirmed the diagnosis of asthma and having then traced the origin to the work site, the next step is to attempt to identify the specific cause. A careful and detailed review of the patient’s work history is necessary. Complete lists of all materials in the workplace environment to which the patient is regularly exposed should be requested and the material safety data sheets should be obtained. By comparing the potential exposure to a published list of documented etiologic agents, one might narrow the possibilities. A site visit may become necessary and is often enlightening.
Skin testing with common allergens, such as house dust, dander, and pollen, may be useful in determining the atopic status of the patient. Atopy may be a risk factor for some occupational exposures. In a few circumstances, appropriate material is available for specific skin testing. Specific IgE (and occasionally IgG4) antibodies may be detected and measured by radioallergosorbent test and enzyme-linked immunosorbent assay techniques. It must be remembered, however, that both skin testing and serologic testing document exposure and sensitization and therefore do not necessarily confirm a cause-and-effect relationship.
The extent of the workup and the level of evidence required for confirmation depends on the purpose for which the diagnosis is required. If the diagnosis is required for medical/legal purposes, the requirements are usually more demanding and restrictive. A less intensive workup may be appropriate in a screening examination or a surveillance program in the workplace.
If asthma has been confirmed, a work site association has been demonstrated, and exposure to a known sensitizer has been identified, sufficient evidence may be available to confidently make a diagnosis. The workup may end at this point. When more diagnostic precision is required or when there is doubt concerning the source of the patient’s symptoms after the initial workup, a specific bronchoprovocation challenge test may be helpful. In some cases, the specific bronchial challenge may be the only way to establish the diagnosis.
Many consider the specific inhalation challenge test the "gold standard" for the diagnosis of occupational asthma when the result is positive. A study with a negative finding, however, must be interpreted in context. A patient who has been away from the occupational exposure for a period of time may lose sensitivity.5 The period of time varies with the substance and the individual. As a result, a specific bronchoprovocation challenge test should be performed as close to the last occupational exposure as possible. Another factor to consider when interpreting a negative study result is that exposure to multiple substances at work is the norm. The wrong substance may have been chosen to study, or perhaps a combination of substances is required to evoke symptoms. Finally, the method of challenge may not provide the correct exposure. When performed in a laboratory, the challenge is controlled but is, nonetheless, artificial.
In this issue of CHEST (see page 1276), Sastre and colleagues address one aspect of the false-negative specific bronchoprovocation challenge test result: the decline of specific sensitivity with the passage of time since the last exposure. In a group of 22 individuals with suspected toluene diisocyanate- or hexamethylene diisocyanate-induced asthma, the authors identified five subjects who did not show an asthmatic reaction to a specific bronchoprovocation challenge study but did demonstrate a significant increase in nonspecific bronchial hyperresponsiveness (as measured by methacholine challenge testing) when compared to a baseline measure obtained before the specific challenge. In three of these individuals, a second specific challenge test result was positive. Presumably, nonspecific bronchial hyperresponsiveness was increased and specific sensitivity was rekindled by the initial specific challenge. Specific responsiveness then became demonstrable with the second challenge. Had the methacholine bronchial responsiveness not been remeasured, thus suggesting that a second specific challenge should be performed, three individuals would have been inaccurately diagnosed as not having isocyanate-induced asthma. Sastre and coworkers conclude that nonspecific bronchial responsiveness should be systematically assessed before and after specific inhalation challenge in an attempt to minimize false-negative evaluations.
A point to be kept in mind, however, is that the decision to perform a specific bronchoprovocation challenge study should not be taken lightly. These studies are time-consuming, expensive, and not without significant risk. Testing must be done by experienced personnel, usually in a hospital setting, utilizing a well-defined and standardized protocol. Because of these factors, specific challenge testing is not widely available and is infrequently pursued in most clinical circumstances.6 Many feel that specific inhalation challenge testing places the worker at too much risk. As a result, a "preponderance of the evidence" is considered by many to be the "gold standard" in most clinical situations.
Nevertheless, when a carefully considered risk-benefit analysis favors performing a specific bronchoprovocation challenge study, it is mandatory that the results be as accurate as possible. The suggestion by Sastre and colleagues that a second nonspecific challenge should be done after a negative specific challenge result would appear to decrease the number of false-negative studies and should therefore be incorporated into standard specific bronchoprovocation challenge protocols.
References
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