Document gD85vmVzqyzeEvyyQmxpaQV99

dvgree and duration of asbestos exposure. Table 2 shows tK.it the smoking groups were similar in age. With respect to duration of asbestos exposure, nonsmokers and current smokers were similar but exsmokers averaged eight years more of work at the plant this difference being statisti cally significant. With respect to cumulative asbestos dose, the same pattern appeared: current smokers were similar to nonsmokers, but exsmokers had an average indpx which was 40 to 55% higher than the average index for the other two groups Although these differences may be mifiortdnt, they are not statistically significant by two different methods of analysis. When the men were distributed according to both cumulative dose of asbestos and cigarette habit the prev alence of plaques read by W.W. varied with respect to both factors (Table 3). The data suggest that the preva lence of plaques is high in exsmokers at any asbestos dosage but that in nonsmokers and current smokers the prevalence increases with increasing asbestos dose. Un fortunately. cross-classification by the two factors results in cells with very small numbers. However, if the data in the two lower asbestos dose categories are combined, then plaqups were found in 6 of 21 nonsmokers and cur rent smokers compared with 6 of 7 exsmokers. This differ ence is statistically significant at the 0.05 level using sig nificance limits for the fourfold table test based on the hypergpometrical distribution.* The findings were similar for plaques read by L.C. but the differences were not as clear-cut and were not statistically significant at the 005 level Oiscussion Several investigators have noted an association be tween pleural thickening and smoking in workers exposed to asbestos In a large survey of English naval dockyard workers exposed to chrysotile. amosite, and crocidolite, P C Harries et al! found pleural thickening in 2.7% of 5.552 nonsmokers. 4 9% of 12.798 smokers, and 6.4% of 4.990 exsmokers The prevalence of pleural thickening tended to fall slightly with increasing cigarette dosage In recent published reports of the studies of these dockyard workers. Rossiter et al'* have provided more details for segments of this population In a sample of 1.2IX) men who were aged 50 to 59, pleural thickening was separated into diffuse disease and. plaques.1 Only the presence of plaques was related to the duration of expo sure to asbestos and there was an excess of plaques in ex smokers (29 5%) compared with the prevalence in smokers (23 9%) and in nonsmokers (231%) The preva lence of pleural calcification was different 8 8% among nonsmokers. 3 5% among smokers, and 61 % among exsmokers A nine-year (1966-1975) follow-up study of 253 dockyard workers* found increases in the prevalence of diftuM- pleural thickening, almost entirely limited to those men who had stopped smoking after 1966, and of pleural plaques, with the greatest increase (from 10% to 23%) in smokers, but little change in the prevalence of calcified plaques Hillcrdal' reported a study of pleural plaques in chest s-r.i\ surveys of the general population in the Swedish *f m -ail . 4 V nMttilii l.ilelrs lilli III |H* IIEI 1*1 Journal ol Occupational Medicine/Vol. 23. No. 6/June 1981 Table 3. -- Prevalence ol Pltunl Plaquis (Read by W.W.) by Estimated Cumulative Dose ol Asbestos and Cigarette Habit in Men Aged 40 or Over. Asbestos Dose and Cigarette Habit Asbestos index under 20 Nonsmoker Current smoker Exsmoker Asbestos index 20-59 Nonsmoker Current smoker Exsmoker Asbestos index 604 Nonsmoker Current smoker Exsmoker Total No. ot Men In Croup No. ol Men with PliQuei 5 6 1 * 3 5 6 4 6 7 45 1 2 t 2 5 2 5 5 24 county of Uppsala. Of 492 men with plaques. 354 were in terviewed and it was found that 79% were or had been smokers. The expected frequency in men of the same age and occupation is 55%. In a survey of 197 Swedish asbes tos workers. Hedenberg et al* found pleural plaques in 30% of 103 smokers and 19% of 94 nonsmokers Thus, there is general consistency between the reports from England and Sweden and the data reported m the present study, especially with respect to exsmokers in those studies in which these have been separated from current smokers Unfortunately the studies cited from the literature have no information on the possible confound ing of this relationship by degree of asbestos exposure The data in this study suggest that there may be some confounding While the association between the preva lence of plaques and smoking was somewh.it stronger than that between plaques and cumulative .ishetos dosage, it must be remembered that the estimates oi dosage were crude. It is uncertain whether the finding of 40 to 55% greater asbestos exposure in exsmokers could account for a prevalence of plaques which w.is more than double that in the other groups Conclusions an- nStrained by the small number of workers in this mw-Mig.i tion. A clear-cut answer to the question as to whi ther tinassociation between plaques and smoking is spurious mil require a much larger research effort, preferably in a cohort study. The hypothesis that smoking is a factor m the path> genesis of asbestos-related pleural plaques is a plausible one despite the fact that the mechanism by which inhaled asbestos fibers produces fibrous plaques in the parietal pleura is unknown Smoking is detrimental to sarious aspects of pulmonary function although the effect on the clearance of particulate matter is not clear7 A recent study by Cohen et al* shows, by the use of inhaled mag netic dust (magnetite), that long-term dust clearance is impaired in smokers: 50% retention compared to 10% in nonsmokers It might well be that once smoking has damaged the clearance mechanisms, cessation of smok ing could be more harmful in this type of defense than continued smoking because the short-term otter t of c iga rette smoking is to enhance deep hromhi.il clearance transiently in some people* and smokers mav bi-u.midependent on this effect to maintain clearanie Hus 429 8004 2039