a biologically plausible mechanism for an acute irritant exposure resulting in a postponed but long-term effect which is chronic in nature.
Although not without controversy, this type of environmentally induced asthma is similar to airway reactivity in response to pharmacologic agonists. In this regard, there is a common dose-response relationship with high enough exposures causing reactions in all exposed subjects. Since these reactions are not associated with eosinophilia or nonspecific bronchial hyperreactivity, some argue they should not be considered asthma. Regardless, the causative agents are clearly associated with airway reactions such as those represented by byssinosis and the related chronic effects of exposures to cotton dust (or endotoxin).
In both the examination of chronic airflow limitation and the examination of allergic asthma, less effort has been spent on objective characterization of the environmental exposures and more on delineating host factors such as the sensitization status of the individual. The preceding review, however, suggests that many respiratory irritants and toxins affect broad portions of the population. Host factors certainly interact with these agents, but it should be recognized that the following commonly discussed individual risk factors or habits play a more variable role in the non-malignant respiratory diseases than is often recognized.
There is little evidence to suggest that gender or race are important risk factors in differentiating the types of respiratory tract responses to the above agents. Age, similarly, is relatively unimportant except for those of increasing age having increasing probability of experiencing a wider variety of irritant exposure events.
Atopic status appears to be a risk factor for asthma due to some of the high molecular weight agents but does not appear important for many if not all of the low molecular weight agents. The other respiratory conditions do not seem to be affected by atopic status.
Although nonspecific bronchial reactivity is often noted in the majority of patients with occupational asthma, it is not known whether this is a result of the exposure or a predisposing factor. Studies in red cedar asthma suggest that the increased bronchial reactivity is reduced or returns to normal after exposure ceases, suggesting that the reactivity change is a result of the exposure.80 Similar conclusions might be drawn from a recent study comparing subjects responding to cotton dust (with both byssinotic and non-byssinotic symptoms) and asymptomatic workers, which showed nonspecific bronchial reactivity most prevalent among byssinotics