HE suggestion has been made that chronic airways ob; struction in workers exposed to occupational environmental inhalants is due in great measure to inhalation of : T > cigarette smoke, and less to substances inhaled during the course of a working day (1). The public health implications of this line of reasoning place considerable onus on the worker to be a nonsmoker and place less responsibility on the part of industry to provide a safe and pleasant working environment. In this review, we present theoretical and experimental evidence that inhaled substances are at least as, or even more important, than is cigarette smoke in the etiology of airways obstruction in these workers. We argue that to achieve optimal respiratory health protection in the workplace, a tripartite approach involving workers, industry and regulating agencies is optimal. While smoking may outweigh industrial exposure in the etiology of airways obstruction in workers in individual circumstances, we believe that the evidence for occupationally-induced airways obstruction is strong. For example, in the cereal grain industry, we showed decreased expiratory flow rates in lifetime-nonsmoking grain workers as compared to lifetimenonsmoking community control subjects (2). In young workmen who had been exposed to grain dust for an average of only 2.S years, we demonstrated evidence of peripheral airways obstruction in workmen who were also smokers (3). These data suggested an additive or synergistic action between smoking and dust inhalation (34). In a group of lifetime-nonsmoking grain workers, we demonstrated a greater tendency toward asthmatic airways, as measured by reactivity to inhaled histamine, than could be shown in lifetime-nonsmoking control subjects (5). In a cross-sectional study consisting of a large group of grain workers, matched by age and smoking to control subjects, there were similar increased prevalences of respiratory symptoms and reductions in pulmonary
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