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].



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