Document 2JQjDOJzDag5Bmxrzk7qJJarR

V99S0001S i Pleural Plaques and Cigarette Smoking in Asbestos Workers WittUm Woa, HD; Richard Levin, Mi; and Lawrence Goodman, MX). In a survey of 45 men aged 40 or over who had worked five years or more in an asbestos manufacturing plant the prevalence of pUuni plaques was studied with respect to age, duration of asbestos exposure, estimated cumulative asbestos dose and smoking habit Plaques were found in 38 to 53% of the men, depending on the interpretation of the chest film reader. Cigarette habit appeared to be the most important factor the prevalence was lowest in nonsmokers. intermediate in current smokers, and particularly high in eomokers. 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 factors 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 chrysotile asbestos throughout its history while Plant B had used both chrysotile and amosite from 1950 to 1964 but only chrysotile before and after this period. The preva lences of both pulmonary fibrosa 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 38 current and exsmokers of cigarettes at Plant B. This difference was not quite statisti cally significant (p * 0.074 by Fisher's exact test! 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 r>v 9* Orcnwn at Occuemiut MrttM Dreanxwm el --Oct. "Hwkim MKfccji colki* HntMl. ]X> Non* Iwd St. WaliWWIiu. r 1SI02 (Or W1 and Mr LavrnL rtw Papaitwarw Ommn Xidlogi (Or Caadmanl Stin nmuiaM lo Or Waaa. Journal of Occupational Medicine/Vd. 23. No. 6/June 1981 Method A detailed description of the products and processes in Plant 8 was provided in the previous report* a summary of which follows. In 1935 this facility was manufacturing asbestos tex tiles. compressed sheet packing, paper, millboard, and molded thermal insulations. Textiles were made of chrysotile asbestos in a dry. dusty process; this operation was discontinued in 1951. Sheet packing was also made only of chrysotile 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 chrysotile from 1935 to 1950: thereafter, amosite. which had to be milled dry, was added to the chrysotile 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 chrysotile 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. the 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 |ob was rated as to degree of asbestos exposure on a scale of 1 to 3 (largest exposure). To uke 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 I I I I TiM t. -- Prevalence o< Pieurif Ptaqws by Ruder. Age. Onration of tiMsus Exposure. Eipmstab Cumulatnre Oeu o< Album. end Cigarene Maprt in Workers Agep 40 r Ow OatnMM* H or CMrecionrec____________________Ho. Tom ; - run 10-54 55* iin dooms S 10* Cutnmttvo 00M indae 0-19 20 59 60* Crparella MM Mnifnewr Current amour CumsMT Tow 70 44 75 56 70 44 25 56 14 11 14 31 It 36 12 27 19 47 14 31 45 100 >im*nti it Hum by 4mr __________ J---------------* tf Preeeewy Mo. 6reep fC*i Spoon) ------------------ Li X * ftwutfty * Oreop (CM Souerel 9 45 IS 60 6 30 16 77 4 79 9 64 11 65 4 13 6 7 17 66 74 53 >0 05 <005 >005 <0 075 6 40 9 30 5 ` 75 17 46 7 14 8 57 7 41 7 17 6 37 9 64 17 36 >0.05 >0 05 . >0.05 ^' COOK. ~ these annual surveys. Eleven men who had worked for lets 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 [we of the authors (W 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 costophremc 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 stooped 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 hypergeometric distribution. Results There was 31% disagreement between the two chest film readers on the presence of pleural plaques. In 11 (24%) of the 45 cases W.W. found plaques when LC. did not tnd in 3 (7%) L.C. 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 53% for W.W. and 38% 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 L.C.! One must consider the possibility that the relationship between pleural plaques and cigarette habit was con founded by the other factors investigated, particularly ST00U5565 Table 2. -- Cempsrisaa at Cigarette Habit Qraupt by Ago. OuritiM at Asbestos Exposure, U Esbmtsd Cumutatrve Dais of Aibestts m Workers Aqo4 40 or Oner. Ctarecwwk *9* -- yurs Ml SO Yurt l measure Usan SO ClKKMlatlVS MM MMX Mtan s0 Qno-ray atiaiyus SI vananCO 428 NMMMOOn b 17 53.9 6 67 74.SO 17.95 40.90 77.78 Clporem MaM Current Smuts n m If S3 4 .1t 73 66 14 61 45.37 47.79 EziMtin HmH 563 5.17 37 43 9.07 63.36 29.77 PrebiiMy usmoun re. otnore: 1 * l.ai. p >0 05 mmontn vs otMrt: t - 2.09. 0 < 0.05 oxsmoktrs vo. omore: 1 1.76. p >0 05 AN0VA' lor 3 preun f - 156.0 >0 05 Pleural Plaques and Cigarette Smoking/Weiss. Levin, and Goodman nnssoooiss degree and duration ot asbestos exposure Table 2 shows that :ne 'moving groups were similar m age V\ ith resoect to duration or asbestos exposure, nonsmokers and current smokers were similar but exsmokers averaged eight vears more or 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 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 m 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 m cells with very small numbers However, if the data in the two lower asbestos dose categories* are combined, then plaques were_found m 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 limiLi for the fourfold table test based on the bvpergeometricaI 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 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 in 2.7% of 5.557 nonsmokers. 4.9% of 12.796 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 1.200 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 in smokers (239%) and in nonsmokers (23.1%). The preva lence of pleural calcification was different: 8 8% among nonsmokers. 3 5% among smokers, and 61 % among ex smokers. A nine-year (1966-1975) follow-up study of 253 dockyard workers' found increases in the prevalence of dirtuse 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 Hillerdal' reported a study of pleural plaques in chest x-mv surveys of the general population in the Swedish li.. u .*> I ..hU- Ml I <1 p* WtJI '"*U TiOM 3. -- Prtvittitct of Pteuril Plaques (Read by w W .) Dy Estimated Cumuiativt Ooio of Asbestos md Cigarette Haoit m Mon Ajad 40 r Over tsoettu beta md Ciqarattt him xsoffsios inou unerr jo Honsmoxar Current unOMr Eismoxer Asoettes inou 20-S9 NonsmoMr Current amextr Exsmdxer Asoct!oi men SO* Aontmoxer Current unoxar bsmoxer Tout Ne it Mex m Srexo 5 1 1 3 5 6 4 6 7 45 M. i M XX Mieeei 1 2 1 1 _ 1 2 5 * 2 3 1C. 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 in the present study, especially with respect to exsmokers m those studies m 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 mav be some confounding While the association between the preva lence of plaques and smoking was somewhat stronger than that between plaques and cumulative asbestos 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 was more than double that in the other groups Conclusions are re strained bv 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 oi asbestos-related pleural plaques is a plausible one despite the fact that the mechanism bv which inhaled 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 ot particulate matter is not clear ' A recent study by Cohen et al* shows, bv the use of inhaled mag netic dust (magnetite), that long-term dust clearance is impaired in 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 short-term effect oi 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 journal of Occupational Medicine/Vol. 23. No. 6/June 1981 429 co..Id e'oiain an mcreod frequency of pleural plaques remained at 1 0 until after six years of follow-up it rose to in *\<moi>.ef* because damaged clearance mechanrsms 21 (6 cases compared to 2.8 expected! which also is not unaiced b\ continued smoking mav lead to higher "effec- statistically significant at the 005 level. Most importantly ;nt coses or asbestos m the tissues. no smoking habit information was available for adiust- 'he clinical significance of a relationship between the ment of the relative risk. prevalence of pleural plaques and smoking depends on A similar problem indicating selection bias tn the men the clinical significance of plaques. The immediate impor with plaques operated with respect to the incidence of tance of these lesions is negligible but there is some sus mesothelioma: most of the cases occurred early in the picion that plaques may be ndicoton of an enhanced risk follow-up period and only two developed after six yean of lung cancer'* " and mesothelioma." of follow-up. However, mesothelioma is so rare in the v\ ith respect to lung cancer risk the evidence is equivo general population that even two cases in the men with cal Krviluoto et al'* found 700 cases of calcified plaque plaques is suspicious, especially since mesqthetioma a us 6.000 adults during a mass c^-Jt x-ray survey in not related to smoking. Tuusmemi commune. Finland, in 1962. The lung cancer Thus, at present the prognostic significance,of pleural incidence between 1962 and 1977 was almost identical to plaques with regard to the risk of lung canceris doubtful the incidence in controls without plaques in Maamnka In the absence of smoking-habit data, no conclusions are commune 13 and 14. respectively. It may be important to warranted. If plaques are related to smoking Ikwell as to note that this study was limited to calcified plaques. Irua asbestos exposure and if lung cancer is similirfy related, case-control study of 69 lung cancer cases there was an then any association between plaques and lung cancer is elevated rok of lung cancer of 26 only when there was likely to be spurious. 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 urtassociated with pulmonary fibrosis found be tween 1964 end 1971 who were compared with a References I W*tu W and Theodos PA Pleurooulmonary disease among as bestos workers m relation to smoking and ivoc of exposure. I Occup Med 20 141-345. 1978. 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 = 3.64. 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 196 were found by clime or hospital films whereas all 429 controls had routine films. Thus, there was undoubtedly some selec tion bus operating to increase the incidence of lung can cer in the men with plaques. Comparing only the groups that had routine films, six (2.696) of 231 men with plaques and four (0 996) 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 plaaues were diagnosed in the first two years of tol low-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. 2. Hames PC. Pointer CE. and Coles KM. Royal Naval Dockyards Asbestosn Research Protect. Report No 1. December 1975 3 Rossner CE and Hames PC U K Naval Dockyards Asbestosn Study Survey at the sample population aged 50-59 years. Br I Ind Med 34.281-291.1979 a Rossiter CE. Heath |R. and Hames PC Royal Naval Dockyards Asbestosis Research Protect Nine-year follow-up study of men ex posed to asbestos m Devonport Dockyard. / Roy Soc Med 73.337-344. 1980 5 Hillerdal C Pleural plaques m a health survey material. Scand I Resoir Ors 59257-263,1978 6 Hedenberg L. Hermansion L lidcn MA. and Thunnger C. Directed health survey of workers exposed lo asbestos. Lakamdmngen 7*4151-4152. 1978 (Abstract m International Cancer Research Oata Bank Cancergram on Environmental and Occupational Carcino genesis. Senes CK02. No. a. Apnl 1979, p 6. Nationjt Cancer Imtitute) 7 Smoking and Health. A Report of the Suigeon Ceneral. U S Department of Health. Education, and Welfare. OHEW Publication NO (PHS1 79-50066. 1979. Section 6. ap 6-32 and 6-13 8 Cohen D. Arai SF. and Brain ID. Smoking impairs long-term dust clearance Irom the lung Science 304:S14-S17. 1979 9 Albert RE. Peienon HT. Bohmng DE. and lippmarm M- Shortterm effects ol cigarette smoking on bronchial clearance in humans Arch Environ Healrh 11 361-367. 1975 10 Kiviluoto R Meurman LO and Hakama M Pleural plaques and ncoolasia in Finland Ann NV Acad So 130 31-33 1979 II Edge IR Incidence ol bronchial carcinoma m shipyard workers with pleural plaaues Ann NV Acad So 130 289-29a. 1979 msooois.i 430 Pleural Plaques and Cigarette Smoking/Weiss. Levin, and Goodman