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Vol. 1. Geneva, World Health Organization, 1977,773 pp. 178 CHAPTER 5 CHRONIC BRONCHITIS: INTERACTION OF SMOKING AND OCCUPATION CONTENTS Introduction Coal Silica Cement Grain Polyvinyl Chloride and Vinyl Chloride Welding Sulfur Dioxide Other Exposures Summary and Conclusions References Introduction Occupational bronchitis is defined as the occurrence of bronchitis caused by worksite chemical or physical agents, whether encoun- tered as gases, fumes, vapors, or dusts. Having derived from a crowded field of overlapping and confusing terms, the term "occupa- tional bronchitis" has inherited a certain inexactitude and has been applied with ambiguity. To complicate the issues further, some industrial substances that cause bronchitis also frequently cause other lung diseases, especially the pneumoconioses and asthma, the symptoms of which may mimic those of occupational bronchitis. Studies of these occupational lung diseases have not always differen- tiated clearly between the development of bronchitis and the development of other lung disorders. Hence, this review begins by briefly applying the customary distinctions in terminology to the area of occupationally derived bronchitis. Whether caused by cigarette smoking, industrial agents, or otherwise, "chronic simple bronchitis" denotes the presence of persistent cough with phlegm production not attributable to a specific pulmonary disease such as bronchiectasis or tuberculosis (Ciba 1959; American Thoracic Society 1962). The operational defini- tion of this form of bronchitis provided by consensus groups of American and British investigators 20 years ago has been widely used in industrial and nonindustrial studies: cough and sputum production on most days for at least 3 months annually for 2 consecutive years (Ciba 1959). Fletcher and coworkers (1976) subse- quently demonstrated that this hypersecretory disorder among cigarette smokers can occur independent of airway obstruction and does not of itself lead to an obstructive disorder. Brinkman and colleagues (1972) confirmed these findings in an occupational setting in a more abbreviated study. Mucus production causes morbidity in that it may lead to increased pulmonary infections, but it does not cause significant dyspnea or potentially disabling obstructive dis- ease. "Chronic obstructive bronchitis" often included in the generic term "chronic obstructive pulmonary disease" (COPD), is defined by the presence of airflow obstruction as measured in most occupational studies by the reduction in the ratio of forced expiratory volume in 1 second to forced vital capacity (FEV,/FVC). More recently, flow rates at low lung volumes obtained from the same forced expiratory maneuver have been used to detect dysfunction of the small airways. In contrast to the mere production of cough and phlegm, the presence of obstruction may have important impact on morbidity and mortality (Fletcher et al. 1976). This subject is reviewed more fully elsewhere in this Report. The term "occupational bronchitis" has been used more often to refer to simple bronchitis than to the airflow obstructive disorder 183 because of the widespread notion that many airborne occupational contaminants produce chronic cough and phlegm, but relatively few agents have been found to lead to measurable airflow obstruction or to clinically significant COPD (Parkes 1982; Casey 1983; Kilburn 1980; Morgan and Seaton 1984). Two related criteria have commonly been used to demonstrate the existence of occupational bronchitis in the presence of a specific exposure or in a specific workplace. First, occupational bronchitis is favored if excessive rates of respiratory symptoms are found in workers who have never smoked. The obvious advantage of such a criterion is the elimination of cigarette smoking, which is a major confounding variable in bronchitis. Unfortunately, this approach could fail to incriminate an occupational agent that produces no respiratory effects by itself but causes higher rates of bronchitis among workers who smoke than are attributable to cigarette smoking alone. Second, the entire exposed population-smokers, former smokers, and nonsmokers-may experience higher rates of chronic cough and phlegm production than a similarly constituted unexposed control population. If the population of exposed nonsmok- ers is small, however, only the interactive effects of smoking and the occupational agent of interest may be evaluated. This chapter describes the impact of smoking and occupational exposures on the prevalence of simple bronchitis. Examining the interaction between smoking and hazardous substances, however, requires documenting the ability of industrial agents alone to produce chronic respiratory disease. The additional or multiplicative effects of cigarette smoking can then be described. Emphasis is placed on evaluating the nature and quality of data rather than on compiling a complete list of agents putatively associated with bronchitis. Coal The role of coal dust in the development of chronic simple bronchitis has been examined (Morgan and Seaton 1984; Parkes 19821, and respiratory disease in coal miners is discussed more fully in a separate chapter of this Report. The specific issue of bronchitis and occupational exposure to coal is reviewed briefly in this section. Evidence supports an independent causal relationship for both cigarette smoking and coal dust in chronic cough and phlegm production (Higgins et al. 1959; Saric and Palaic 1971; Higgins 1972; Lowe and Khosla 1972; Kibelstis et al. 19731. In a series of community-based studies in England and in the United States during the 1950s and 1960s Higgins and colleagues (Higgins et al. 1959; Higgins 1972) found an increased prevalence of chronic simple 184 bronchitis in miners and ex-miners, ranging from 1.2 to 6.4 times the rates in nonminer controls. Lowe and Khosla (19721 studied chronic bronchitis among more than 12,000 Welsh steelworkers, about one-fourth of whom were former coal miners. In the absence of cigarette smoking, previous exposure to coal dust increased the rate of chronic cough and phlegm production from 5.7 percent in nonsmoking nonminers to 13.6 percent in nonsmoking ex-miners. Cigarette smoking was somewhat more important than previous exposure to coal in producing chronic simple bronchitis; 16.6 percent of the nonminers who smoked and 25.5 percent of the ex-miners who smoked had chronic bronchitis. Differences in age among the various subgroups did not account for the varying prevalence of symptoms, which appeared to be additive. Saric and Palaic (1971) compared 904 Yugoslav coal miners with 342 control workers of similar socioeconomic status without occupa- tional exposure to dusts, and found that cigarette smoking and coal dust exposure were multiplicative in the production of chronic simple bronchitis. Of the miners who smoked, 32 percent reported chronic cough and phlegm production, compared with 10 percent of the controls who smoked, 8 percent of the nonsmoking miners, and 2 percent of the nonsmoking controls. However, the rates of chronic simple bronchitis for each exposure subgroup, except the workers who smoked, were below other published rates. Increasing coal dust exposure increased the prevalence of chronic simple bronchitis in both smokers and nonsmokers in the studies by Kibelstis and colleagues (1973) and Rae and colleagues (1971). Neither study included groups not exposed to coal dust. Both studies reported a larger effect of cigarette smoking than of coal dust exposure in causing chronic simple bronchitis, but did demonstrate a substantial coal dust exposure effect. One-third to one-half of the nonsmoking American coal miners over the age of 50 reported chronic cough and phlegm production (Kibelstis et al. 1973). Some- what lower proportions (20 to 40 percent) of the nonsmoking British coal miners with tht highest levels of dust exposure suffered symptoms of chronic cough and phlegm production (Rae et al. 1971). In summary, coal dust exposure causes chronic simple bronchitis independent of cigarette smoking. Although the effects are additive, the effect of smoking is somewhat greater than the effect of coal dust exposure in producing symptoms of chronic bronchitis. Silica Early studies showed no relationship between silica exposure and chronic cough and phlegm production. In 1959, Higgins and col- leagues (19593 found no increase in chronic simple bronchitis in British foundry workers and former foundry workers, regardless of 185 duration of employment, compared with community controls with- out dust exposure. In a cross-sectional study, Brinkman and Coates (1962) found no difference in cough and phlegm production in long- term American foundry workers with normal chest roentgenograms and control workers with no dust exposures. More recently, Glover and colleagues (1980) examined 725 Welsh slate workers and former workers and noted no relation between duration of exposure to slate and presence of chronic simple bronchitis independent of pneumoco- niosis. On the other hand, studies of South African gold miners showed an association between silica and simple bronchitis among smoking miners. White miners were compared with age-matched white nonminers in an area where gold mines had a 50 to 70 percent free silica content (Sluis-Cremer et al. 1967). Nonsmoking miners report- ed an 8.2 percent rate of chronic simple bronchitis, which did not differ from the 6.7 percent rate found among nonsmoking nonmin- ers. However, 50.5 percent of the miners who smoked had chronic cough and phelgm production, almost twice the 28.0 percent found among the nonminers who smoked. Hence, silica dust alone ap- peared not to cause symptoms of simple bronchitis, but magnified the effects of smoking. Wiles and Faure (1977) also studied white South African gold miners and found that they had an increased prevalence of bronchitic symptoms in the absence of cigarette smoking and that there was an additive effect among the workers who did smoke cigarettes. Among the nonsmokers with the lowest dust exposure, no workers had chronic cough with phlegm, but 15 to 20 percent of workers with the highest dust exposures had these symptoms. Twenty-five percent of smokers in the low dust category reported bronchitic symptoms. Among the miners who smoked, 50.5 percent suffered from chronic cough and phlegm production, demonstrating a simple additive effect. A cross-sectional study of 931 Swedish long-term foundry workers with varying exposures to silica was published in 1976 (Karava et al. 1976). Less than 4 percent of the study population had evidence of silicosis on chest x ray. Two percent of the nonsmokers exposed to lesser amounts of dust reported simple chronic bronchitis compared with 9 percent of the nonsmokers with high dust exposure, but the difference was not significant (p>O.lO). However, 16 percent of the smokers exposed to slight or moderate levels of dust had chronic cough and phlegm production, significantly less than the 30 percent of smokers with high dust exposure (p