Document a1YgkL0Q17gg5qX49zLE1mqxy

STOOUSSGi Pleural Plaques and Cigarette Smoking in Asbestos Workers William Weis* MD** Richard Levin, and Lawrence Goodman, MJ>. In a survey of 45 men aged 40 or over who had worked five yean or more in an asbestos manufacturing plant, the prevalence of pleural plaques was studied with respect to age duration of asbestos exposure, estimated cumulative asbestos dose, and smoking habit Plaques were found in 30 to 53% of the men, depending on die interpretation of the chest film reader. Cigarette habit appeared to be the most important factor; the prevalence was lowest in not*smokers, intermediate in current smokers, and particularly high in exsmokers. There was some confounding of this relationship by estimated cumulative asbestos dose but such confounding did not seem to be sufficient to explain fully the relationship between the prevalence of plaques and smoking habit Both /actors must be considered in studies of the risk of pleural plaques in asbestos workers. I n a previous report Weiss and Theodos' described the results of a 1975 chest x-ray survey in two asbestos pro ducts manufacturing plants. Plant A had used only chry solite asbestos throughout its history while Plant B had used both chrysolite and amosite from 1950 to 1964 but only ehrysotile before and after this period. The preva lences of both pulmonary fibrosis and pleural disease were higher in Plant B. Cigarette smoking was a factor in the prevalence of pulmonary fibrosis and perhaps also of pleural disease at Plant B. Pleural thickening was found in only one of 10 nonsmokers and in 42% of the 30 current and exsmokers of cigarettes at Plant B. This difference was not quite statisti cally significant (p m 0.074 by Fisher's exact testL but it has stimulated further investigation of the problem by the authors. This paper analyzes the results of the 1977 and 1978 surveys with respect to the relationships between the prevalence of pleural plaques in men aged 40 or over and the factors of age, duration of asbestos exposure, esti mated cumulative dose of asbestos, and cigarette habit tnm tlit Onimh of Occuoiiwul Mfdxw Dmmw V NWwum Mxfcol Collet* *nd MowmI. 2X North Bo*0 St. FMoMthu. P W0J (0> Wm and Mr itvwl and th* Onan T 0*twit XadWotv (Dr Caodmanl Addmi commurocaoom <o Or. Wma. Journal of Occupational Medicme/Vol. 23, No. 6/Juno 1981 Method A detailed description of the products and processes in Plant B was provided in the previous report.' a summary of which follows. In 1935 this facility was manufacturing asbestos trextiles. compressed sheet packing, paper, millboard, and molded thermal insulations. Textiles were made of ehrysotile asbestos in a dry, dusty process; this operation was discontinued in 1951. Sheet packing was also made only of ehrysotile and. because of milling the asbestos, the operation was dustier before the 1950s than it was in later years. Paper and millboard operations were very dusty prior to 1960. but after 1960 process improvements led to better conditions. Molded insulation was made of ehrysotile from 1935 to 1950; thereafter, amosite. which had to be milled dry, was added to the ehrysotile until manufacture of these products was discontinued in 1964. Ir 1948 the plant began to produce corrugated and mono lithic asbestos cement boards made of ehrysotile and Portland cement Asbestos fiber counts were not made until 1972 but have been generally under 2/cm* in recent years. Because of the lack of counts prior to 1972. die cumulative asbestos exposure (dose) for each employee in this study had to be estimated on a semiquantitative basis. A job in dex was devised at a meeting of the industrial hygienist (R.L) with three foremen who had begun work at this plant between 1941 and 1947. Each job was rated as to degree of asbestos exposure on a scale of 1 to 3 (largest exposure). To take into account the change in conditions over time, job ratings were multiplied by three during the period prior to 1951, by two during the period 1951 through 1963, and by one from 1964 on. The employment record of each man was reviewed and an index of cumu lative asbestos exposure was computed by multiplying the job rating, the period rating and the number of yean worked at each job during each period. The maximum in dex recorded in this group of men was 159. Pleural plaques were noted only in men aged 40 or over. There were 69 such employees eligible for examina tion between 1977 and 1978, and 56 (81%) had 110 kv36X 43 cm postero-anterior chest films during one or both of 427 DOW 06833 ! ST000556S TjM t. -- Pravitencs sf Pleural Plaques by Risdir. Agi. 0iratten el Asbesios Exposure. Estimated Cumulative Out tf Asbestos. and Cigarette Habit in Workers Agtd 40 ar Over. CMraetenstic *?* - years cO-54 55* rears exposes 5-29 30. Cumulative Mia mm 0-19 20 59 60* Ggsrene keen Nensmour Current smoker Eismoaer Total Trevsnnts teem H Sneer Oistnbebee % * % t) nr6JiMy % * PraouiMy Nt. Tatai Ha. 9/aep ICM Squirt) He. Grew (CM Senate) 20 44 2S 56 20' 44 25 56 14 31 14 31 17 31 12 27 if 42 14 31 45 100 9 15 9 16 4 9 11 4 12 24 45 60 30 72 29 64 65 33 42 16 S3 >0.05 <0.05 >0.05 <0 025 6 40 9 36 5 25 12 46 2 14 8 57 7 41 2 17 6 32 9 64 17 36 >0.05 >0.05 >0.05 ^* <o.oS:. these annual surveys. Eleven men who had worked for less than five years at this plant were eliminated to allow for a minimal latent period of five years, leaving 45 in the study The chest films were read by rw* of the authors fW W and L.C.) independently without knowledge of the individual's age, work experience, or smoking habit Pleural plaques were recorded as present when pleural thickening of irregular width was noted along the lateral chest wall, provided it spared the apex and the costophrenic angle, or on the dome of the diaphragm, with or without calcification. A careful smoking history was recorded at each survey. For the purpose of this investigation, each employee was classified according to cigarette habit as a nonsmoker (had never smoked cigarettes), a current smoker, or an ex smoker (had stopped smoking one or more yean ago). The statistical significance of differences was deter mined by calculating exact probability by the binomial distribution or by estimating probability by the t test the chi square test (with Yates' correction when there was only one degree of freedom! one-way analysis of vari ance. or significance limits for the fourfold table test based on the hypergeometnc distribution. Results There was 31% disagreement between the two chest film readen on the presence of pleural plaques. In 11 (24%) of the 45 cases W.W. found plaques when LC. did not and in 3 (7%) LC. found them when W.W. did not This difference was not quite statistically significant at the 0.05 level (p * 0.0574 using the binomial distribution for paired observations). The prevalence of plaques is presented for each reader separately. , Table 1 shows that the prevalence of plaques was $3% for W.W. and 30% for LC. Age was not a factor. The data suggest that both duration of asbestos exposure and cumulative dose of asbestos were factors although, be cause of small numbers, three of the four comparisons did not reach statistical significance at the 0.05 level. However, cigarette habit was found to be an important factor, the prevalence of plaques being particularly high in exsmokers, and the differences were statistically sig nificant for both readers. Only two men had calcified plaques (interpreted in both cases by LC.). One must consider the possibility that the relationship between pleural plaques and cigarette habit was con founded by the other factors investigated, particularly Table 2. - Cempanssa at Cigarette Habit Groups by Agi, Duration at Asbestos Exposure, tab Estimates Cumulative Dost ef Asbestos in Workers Aged 40 ir Over. ChsrKtertsa* *9* - years Mean so. Ysara el Mposure Mean SO. Cumulative ooae meet Mean SO Heesmeesrs H 12 Ctesrens HsMt Current Smeters K-19 53.9 1.97 24.50 12.95 40.90 27.21 53.4 9.11 23.61 14.63 45.32 42.79 Eumaters N.14 56.3 5.17 32.43 9.02 93.30 20.72 1i eamoktravs. etnen: t > 1.41. P> 0.05 eamoktn vs. omora: t - 2.09. < 0.05 exsmokers vs. omen: 1 1.76. p > 0 05 AN0VA* ter 3 groups: F * 1.51. 0 >005 On*-*ay analysis <1 variance 428 Pleural Plaques and Cigarette Smoking/Weiss. Levin, and Goodman DOW 06834 degree end duration or asbestos exposure. Table 2 shows that tne smoking groups ^ere similar in age. With respect to curction of asbestos exposure, nonsmokers and current smokers Mere similar but exsmokers averaged eight vears more orwork at the plant, this difference being statisti cally significant With respect to cumulative asbestos dose the same pattern appeared: current smokers Mere similar to nonsmokers, but exsmokers had an average in dex which was 40 to 55% higher than the average index for the other two groups. Although these differences mav be important 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 anv 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 plaques 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 hvpergeometrical 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 0.05 level. Discussion 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 Hames et al1 found pleural thickening m 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. tn recent published reports of the studies of these dockyard workers. Rossiter et al14 have provided more details for segments of this population. In a sample of 1.200 men who were aged 50 to 59. pleural thickening was separated into diffuse disease and plaques.' 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 m smokers (239%) and in nonsmokers (23.1%). The preva lence of pleural calcification was different: 8 8% among nonsmokers. 3 5% among smokers, and 6.1% among ex smokers. A mne-year (1966-1975) follow-up study of 253 dockyard workers4 found increases in the prevalence of diffuse 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%) m smokers, but little change in the prevalence of calcified plaques Hillerdal' reported a studv of pleural plaques in chest x-ray surveys of the general population in the Swedish >esH*Na IjWm I ll journal of Occupational Medicine/Vol. 23. No. 6/June 1981 Tibia 3. -- Prevalence of Pleural Plaques (Read by W.W.) by Estimated Cumulative Oese ol Asbesies and Cigarette Habit in Men Aged 40 er Over. AtDtstet Oese tne Cigann* Hien Asotsios inoex unerr 20 Nonjmoxer Current smoxer turnover asdcsios inoei 20-59 Nonsmoxer Current smoxtr Eumoxer Asoestos meet 60* Nonsmoxer Current smoker bsmoxer Total Me. el Men hi Grove Nt el Men vim Maeues 51 82 11 3 ._ 1 S2 6S 4 *2 6S 7 tt. S " 24 countv 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 al4 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 in the present study, especially with respect to exsmokers in those studies m which these have been separated from current smokers. Unfortunately the studies cited from the G/? literature have no information on the possible cpnfounding of this relationship by degree of asbestos exposure. The data in this studv suggest that there may be some confounding While the association between the preva- *-- lence of plaques and smoking was somewhat stronger 4-0 than that between plaques and cumulative asbestos 4"r` dosage, it must be remembered that the estimates of ^ 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 was more than double that in the other groups Conclusions are re strained by the small number of workers in this investiga tion A clear-cut answer to the question as to whether the association between plaques and smoking is spurious will require a much larger research effort preferably in a cohort study. The hypothesis that smoking is a factor in the patho genesis of asbestos-related pleural plaques is a plausible one despite the fact that the mechanism by which inhalea asbestos fibers produces fibrous plaques in the parietal pleura is unknown. Smoking is detrimental to various aspects of pulmonary function although the effect on the clearance of paniculate matter is not clear ' A recent ' study by Cohen et al* shows, by the use of inhaled mag netic dust (magnetite) that long-term dust clearance is impaired m smokers: 50% retention compared to 10% m 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 shon-term effect of ciga rette smoking is to enhance deep bronchial clearance transiently in some people* and smokers mav become dependent on this effect to maintain clearance This 429 DOW 06835 co-id exoion an increased frequency of pleural plaques m eximokers because damaged clearance mechanisms unaiced bx continued smoking mav lead to higher "effec- coses of asbestos in the tissues. The clinical significance of a relationship between the prexaierice of pleural plaques and smoking depends on the clinical significance of plaques. The immediate impor tance of these lesions is negligible but there is some sus picion that piaques may be indicators of an enhanced risk of lung cancer1'11 and mesothelioma." With respect to lung cancer risk the evidence is equivo cal Kiviluoto et al" found 700 cases of calcified plaque m 6.000 adults during a mass chest x.-ray survey in Tuusniemi commune. Finland, in 1962. The lung cancer incidence between 1962 and 1977 was almost identical to the incidence in controls without plaques in Maamnka commune 13 and 14. respectively. It may be important to note that this study was limited to calcified plaques, live case-control study of 69 lung cancer cases there was an elevated risk of lung cancer of 28 only when there was pulmonary fibrosis in addition to calcified plaques. Infor mation on smoking habits was not provided. Edge" has reported an increased incidence of lung cancer in 429 older British shipyard .workers with pleural plaques unassociated with pulmonary fibrosa found be tween 1964 and 1971 who were compared with a matched control group of 429 men in another city where there was neither known asbestos exposure nor plaques. After excluding six men with lung cancer who had clinical evidence of tumor at the time observation was begun in the men with plaques, the relative risk was 3.25 (13 cases in the men with plaques compared to 4 in the controls, chi square with Yates' correction * 3.84, p * 0.05). How ever. this comparison is probably invalid because only 231 of the 429 men with plaques were discovered by routine chest films and the remaining 198 were found by clinic or hospital films whereas all 429 controls had routine films. Thus, there was undoubtedly some selec tion bias operating to increase the incidence of lung cam cer m the men with plaques. Comparing only the groups that had routine films, six (2.6H) of 231 men with plaques and four (0.956) of 429 controls developed lung cancer, a difference which is not statistically significant at the 0.05 level Furthermore, half the lung cancer cases in the men with plaques were diagnosed in the first two years of follow-up and therefore these individuals presumably had their tumors at the time observation began. After ex clusion of the early cases, the relative risk, as compared to the incidence of lung cancer in the general population. remained at 1.0 until after six yean of follow-up it rose to 2.1 (6 cases compared to 2.8 expected! which also is not statistically* significant at the 0 05 level. Most importantly, no smoking habit information was available for adjust ment of the relative risk. A similar problem indicating selection bias in the men with plaques operated with respect to the incidence of mesothelioma: most of the cases occurred early in the follow-up period and only two developed after six yean of follow-up. However, mesothelioma is so rare in the general population that even two cases in the men with plaques is suspicious, especially since mesqthelioma is not related to smoking. Thus, at present the prognostic significance,of pleural plaques with regard to the risk of lung canceris doubtful. In the absence of smoking-habit data, no conclusions are warranted. If plaques are related to smoking Is.well as to asbestos exposure and if lung cancer is similarly related, then any association between plaques and lung cancer is likely to be spurious. References I Wens W and Theodos PA: Pleurooulmonarv disease among as bestos workers in relation to smoking and type of exposure. I Ocarp Med 20 341-345. 1978. 2. Names PC. Pointer CE. and Coles Rm. Royal Naval Dockyards Aibestosrs Research Protect. Reoort No. 1. December 197S. 3. R osliter CE and Hames PC U.K. Naval Dockyards' Asbestous Study Survey of the sample population aged SO-59 years. 111 Ind Mfd 24:281-291.1979 4 Rossiter CE. Heath |R. and Harries PC: Royal Naval Dockyards Asbestosis Research Protect. Nme-year follow-up study of men ex posed to asbestos in Devonport Dockyard. I Roy See Med 72:337-344. 1980 S. Hillerdal C. Pleural plaques in a health survey material. Scand / Respir On 59:237.243.1978 4 Hedenberg L. Hermansion L liden MA. and Thunnger C. Directed health survey of workers exposed to asbestos. Ukartrdningen 784151-4152.1978 (Abstract in International Cancer Research Data Sank Cancergram on Environmental and Occupational Caremo. genesis. Series CK02. No. 4. April 1979. p4. National Cancer Institute) 7 Smoking and Health. A Report of the Surgeon Ceneral. U S Department of Health. Education, and Welfare. OHEW Publication No. (PHS) 79-50066.1979. Section 6. pp 4-32 and 4-33. 8. Cohen 0. Arai SF. and Bram ID. Smoking impairs long-term dust clearance from the lung. Science 204:514-517.1979. 9 Albert RE, Peterson HT. Sohnmg DE. and lippmaim M Short term effects of cigarette smoking on bronchial clearance in humans. Areh tnvwen Htslth 31.341-347. 1975. 10 Kiviluoto R Meurman LO. and Hakama M Pleural plaques and neoplasia in Finland Arm NY Aetd Set 330.31-33.1979. II Edge IR Incidence of bronchial carcinoma m shipyard workers nth pleural plaques Arm NY Acad Set 310289-294.1979. f i. msooois 430 Pleural Plaques and Cigarette Smoking/Weiss. Levin, and Goodman ofc36 OO^