and least prevalent in the asymptomatic subjects. However, when reactivity was examined without respect to symptoms, cumulative cotton dust level was a significant predictor of reactivity.81 Kennedy recently addressed the question of whether nonspecific bronchial reactivity was an acquired or inherent feature of respiratory reactions in persons exposed to non-immunogenic irritant agents.5 She reluctantly concluded that the question remains unanswered, although there is growing evidence that acquired increased bronchial reactivity is of likely importance.
Smoking (a personal habit rather than a host factor) is well described as a risk factor for chronic obstructive bronchitis and chronic airflow limitation (or emphysema). Agents that cause these conditions most probably result in effects which are additive to those of cigarette smoking.82 The fact that all smokers do not experience the same level of risk suggests that smoking, itself, must be interacting with some other host factor in regard to these respiratory outcomes. With respect to asthma, the role of smoking is quite unclear. One hypothesis suggests that increased membrane permeability of smokers allows greater penetration of antigens. However, smoking has not been associated with work-related symptoms among those exposed to such agents as detergent enzymes83 or colophony84 while it has been noted to be related instudies of workers exposed to phthalic anhydride85 and of soy bean workers.86 In contrast, in studies of those exposed to plicatic acid or to isocyanates, asthma was mostly noted in non-smokers.87,88
In this review a variety of materials toxic to the respiratory tract have been examined. The review was not designed to be comprehensive, yet, it was also not unduly selective. In making the selection, agents were included which are commonly considered primarily as acute respiratory irritants, those known to induce extrinsic asthma, those which are related to non-immunogenic bronchial hyperreactivity, those which are most often responsible for slowly developing chronic fibrosis or granulomatous disease, and one which is believed to cause pharmacologic bronchoconstriction. The chronic respiratory effects associated with each of the agents reviewed included several of the general types of chronic respiratory response rather than being limited to only one type of reaction. Now, as a final step in the evaluation of the agents reviewed, an attempt should be made to answer the original three general questions about pulmonary reactions.
The questions and suggested answers are:
Does the occurrence of an acute pulmonary reaction identify an individual at risk for long-term respiratory sequelae? Ample evidence