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Part III. Environmental Asbestos Disease ASBESTOSIS AMONG HOUSEHOLD CONTACTS OF ASBESTOS FACTORY WORKERS* Henry A. Anderson, Ruth Lilis, Susan M. Daum, and Irving J. Selikoff Environmental Sciences Laboratory Department ofCommunity Medicine Mount Sinai School ofMedicine The City University ofNew York New York, New York 10029 Equally ubiquitous in the environment as industrial chemical wastes' are inorganic microparticles such as asbestos. The environmental burden of asbestos pollution is a recent phenomenon which has grown with the rapid expansion of asbestos-utilizing industries.2 The health consequences of poorly controlled occupational exposures to chemicals and dusts now found in the general environment have been known in many .instances for well over 100 years.' Reports of overt disease (usually seen only with occupational exposure) among nonoccupationally exposed individuals have frequently been considered medical curiosities when they appeared in the medical literature. However, the full extent of the health risks due to nonoccupalional exposure to toxic agents is not known, for it is uncommon to inquire into the neighborhood residence history or occupation and exposures of a patient's household contacts when investigat ing symptoms of a disease. The effects of such exposures may be mild or subdinical manifestations which are only contributory to a current health problem and their role goes unrecognized. In 1976, we reported on a systematic investigation of one such non-occupational exposure to asbestos dust.4 The group studied consisted of household contacts of workers in an asbestos factory manufacturing amosite asbestos insulation materials between 1941 and 1954. None of those reported had personal occupational exposure to asbestos. Yet 35% had asbestos-associated radiographic abnormalities. A source of home contamination in individua. c;.posut; wr s postulated as resulting from dust adhering to shoes, hair, and workdothes brought home for laundering. Changerooms and company laundered coveralls were not available at this plant. We reported the identification of four pleural mesotheliomas among the family contacts of the 1,664 workers who were employed at some time by the factory. Since that time one additional pleural mesotherlioma death has occurred, raising the total mesothelioma deaths to dale among the group under observation to five. This report extends the continuing clinical investigation of this cohort. Population Studied We are actively investigating the status of household contacts of the 1,664 asbestos workers employed in the factory which produced amosite asbestos products from 1941-1954. The names of household contacts arc obtained from the surviving worker cohort members and from other sources for those already deceased. Once identified as *This research is supported by National Institute for Environmental Health Sciences Grant No. ES 00929 and a grant from the National Cancer Institute, CA 22792. 387 0077-8923/79/0330-0387 SI.75/0 C 1979. NYAS 388 An nals New York Academy of Sciences a possible household contact, a variety of epidemiologic tracing techniques to locate the individual and ascertain his/her current status. Living individm^** invited to participate in periodic medical clinics. Control Population i For comparison purposes in the chest x-ray interpretation, a control populate ' was felt to be appropriate. Urban New Jersey residents currently living in the us, community as the study population were identified from the general medical che^, the facility used to examine the workers and household members. Consecutive dip s, individuals who appeared for routine chest x-rays between January I, 197s ltt December 31, 1976 were selected until age and sex classes similar to the firvi >y, examined household contacts were filled; thus, the age and sex distribution m study group and controls were similar. Clinical records of all controls were rcvirn and only those with no recorded personal occupational contact with asbestos sc included. Only PA films were available for review. No new clinical examination) spirometry were performed on controls. Methods '* The clinical examination includes comprehensive lifetime occupational and rev dentiai histories, past and current medical history, history of current symri.es smoking and respiratory questionnaires, physical examination, 14* X 17* po>tcr>u! tenor, right and left oblique chest x-rays, and spirometry. After each clinic, the chest x-rays of household contacts, factory workers j&r previously identified controls were interspersed and read without knowledge rf exposure category. The ILO U/C Pneumoconioses Classification of 1971 was uiihe by a panel of five experienced readers.5 A consensus interpretation was arrived at rai it is this reading that was utilized for statistical analyses. A film was classified s> abnormal if one or more of the following were recorded: small opacities (combine: rounded and irregular) 1 /0 or more; any lateral wall pleural thickening; any pleurs calcification; pleural plaques on the diaphragm. Although recorded, blunting of costophrenic angles was not included in this i ntlysis. Only abnormalities visible on 1 PA film were utilized. The added utility of the oblique films will be discussed in a Ir.r report. The actual extent and intensity of each household resident's asbestos exposure > unavailable. To help approximate a relative exposure dose index for each hou>eh.i contact, the employment history of the factory worker in whose household hc/d* resided was utilized. The resident worker tor each household is referred to av tbg "index worker." Thus, each household contact was assigned a "duration of exposure' which was equivalent to the length of time lived in the household while a worker actively employed. Similarly, each contact was assigned a year of "onset of cxpo*u:r equivalent to the year in which he/she first resided with an actively employed worker Statistical Analyses Prevalence data were compared by the x1 test. Differences between mean* compared using Student's t-test. P values at less than .05 were considered signifiwe: Statistical analyses were performed with the cooperation of the City University ^ New York Computer Center, using the Statistical Package for the Social Science*' Anderson et al.: Household Asbestosis 389 Results In the six-year period 1973-1978, over 3100 household contacts of the 1664 amosite asbestos factory workers were identified. Of that group, 756 are known to be deceased, and of the remaining 2300+, 771 have been examined in our clinics. During 1975-1976, 326 controls were identified. Ninety-two individuals did not meet the criteria set for inclusion in this analysis. Five household contacts and one control are not included in this report because of current medical conditions which are known to cause the types of x-ray abnormalities seen on their radiographs. The use of the 1LO U/C Classification would thus be misleading. These included three pleural mesotheliomas, one lymphosarcoma (post radiation and surgical therapy), two cases of sarcoidosis (one in a control). In addition, there were two unreadable, under-exposed films and one examinee refused a chest x-ray. Residence histories were carefully reviewed and individuals who were not actually in residence with the index worker at the time he was actively employed, were placed in a separate category. Thirty-three individuals were placed into this sub group. They resided in the household only after the worker had ceased active employment. Occupational histories taken at the time of examination revealed that 51 Table 1 Occupational Exposures to Asbestos among 756 Household Contacts Occupation Direct asbestos trade Brake repair work Dry wall construction Shipyard work Indirect asbestos exposure Other fibrogenic dust exposure Total Number 19 8 1 6 16 1 51 Abnormal X-ray 7 (37%) 4 (50%) 0 4 (67%) 8 (50%) 0 23 (45%) individuals had potential personal past occupational exposure to asbestos. The distribution of occupations of these individuals and the prevalence of radiographic abnormality is shown in Table 1. Thus, 92 of the 771 examined did not meet the criteria for inclusion in the study, which is limited to the 679 household contacts who had lived in the household of an actively employed amosite asbestos factory worker and who themselves had not had an occupational exposure to asbestos or other fibrogenic dust. The age distribution for the study subjects and the control population showed that the controls were slightly older than the household contacts (mean age 48 compared to 45 in the contacts) (Table 2). The distribution of examined household contacts by the duration of their exposure in the home of an actively employed index worker and by the year that they were first exposed is shown in Table 3. Duration of active employment and presumably concomitant active daily household contamination was less than one year for 28% of those examined. In only 5% was index worker employment, with increasing household contamination, 10 or more years. At the time of their examination, all study participants were more than 20 years from onset of their first asbestos exposure. 390 Annals New York Academy of Sciences Table 2 Age Distribution of Household Contacts and Controls at Time of X-Ray Examination Age (y.) 20-29 30-39 40-49 50-59 60-69 70+ Total Number of Household Contacts* 54 (8%) 188 (28%) 196 (29%) 144(21%) 68(10%) 29 (4%) 679 Number of Controls'! 30 (9%) 59(18%) 80 (25%) 83 (26%) 51 (16%) 22 (7%) 325 Mean age of household contacts 45.7 I2yrs. tMean age of controls 48.6 14 yrs. Altogether nearly one-third of those examined were under the age of 40. Two-thirds of individuals had already exceeded 30 years from onset of initial asbestos exposure. Information is not available on the dimensions of the asbestos contamination which remained in the house after the worker changed employment. The prevalence of radiographic abnormalities among the survey participant groups is summarized in Table 4. The control population had a 5% overall prevalence of radiographic abnormalities. Individuals who resided in a household after the index worker's employment period had the second lowest prevalence of abnormalities (12f?) followed by persons in residence (35%) during the index worker's employment. As would be expected, the highest prevalence of abnormalities (45%) was among the household residents with reported personal occupational asbestos exposure. Pleural abnormalities were more prevalent than parenchymal small opacities. When the comparative prevalence of the various types of asbestos-associated radiographic abnormalities was analyzed, it was found that pleural abnormalities were the most prominent (Table 5). Pleural calcifications were present in 8% of the household contacts and were seen in none of the controls. Pleural thickening was present on 19% of the household contact radiographs and only 1 % of the control chest x-rays. Overall, 239 (35%) of the household contacts had one or more abnormalities present compared to 15 (5%) of the control group. These radiographic abnormalities Table 3 Distribution of Household Contacts by Duration of Exposure and Year of Onset of 1st Exposure Year of First Exposure 1941-46 1946-50 1950-55 Total Total Examined 436 113 129 678 <1 Year 124 29 40 193 (28%) Duration of Exposure 1-5 Years 5-10 Years 246 32 68 16 89 -- 403 (59%) 48 (7%) 10+ Years 34 _ -- 34 (5%) 392 Annals New York Academy of Sciences were seen in various combinations (Table 6). Pleural change as the only abnormal on the chest x-ray was seen in 18% of the household contacts. This is compared uX with no pleural changes and only parenchymal small opacities present. In S'; household contacts, both small opacities and a pleural abnormality were pre>cr' Among the controls, small opacities as the only abnormality present was the m,. prevalent (3%). Only one of the controls (0.3%) had both small opacities and a p|ci!r abnormality present. The distribution by profusion of combined small opacities (graded according to ii ILO U/C Classification) among the household contacts and controls is shown Table 7. Only two of the household contacts (0.3%) had a category 2 profusion combined small opacities. Forty-seven of the 114 films with small opacities were in i-.r lowest category, 1 /0. Eight out of the ten control films were coded as having combine small opacities in the lowest category. Pleural thickening and pleural calcification were seen in all extent categoric (Tables 8 and 9). As with the parenchymal abnormalities, the pleural abnormalityin household contacts tended to be classified in the lower ILO U/C categoricHowever, 19 (3%) of household contacts had extensive pleural thickening and IOC had extensive pleural calcification present. Table 5 Prevalence of Asbestos-Associated Radiographic Abnormalities among Household Contacts of Amosite Asbestos Workers and Controls Group Total Examined Houschold contracts Controls 678 325 Small Irregular Pleural Pleural Opacities Thickening Calcification 114(17%)* 128(19%)* 54(8%)* 10 (3%) 4 (1%) 0 Pleural One or more Plaques Abnormalilic- 57(8%)* 239 (35r%>* .2(0.6%) 15 <5'v Prevalence of all types of abnormalities significantly higher in the household contacts th.c the controls, p < .001. The possible effect of increasing duration of exposure as an index of increasing dose was also examined. Among occupational groups, duration of exposure correlatewell with increasing prevalence of radiographic abnormalities. The prevalence oi radiographic abnormalities among the household contacts by duration of exposure ipresented in Table 10. All abnormalities show an increase in prevalence as duration t exposure increases. The category of combined small opacities did not show a statistically significant increase in prevalence with duration of exposure although a trend is apparent. For pleural thickening, not only did the prevalence of the abnormality increase with duration of exposure but also the extent of disease (Taiii i 8). However, this did not seem to be the case for pleural calcification (Table 9). Under occupational exposure conditions, for a majority of workers, a period of clinical latency of approximately 20 years from onset of exposure to appearance ot radiographically detectable asbestos-associated disease has been well documented All household contacts had exceeded the 20 year from onset point at the time of their initial examination. Individuals first exposed between 1941 and 1946 had the highe-i prevalence of abnormalities (Table 11). The group exposed between 1950 and 1954 had the lowest prevalence of abnormalities (22%). The increasing prevalence of radiographic abnormality with longer time since onset of first exposure is most evident 15192730 394 Annals New York Academy of Sciences Table 8 Prevalence of Pleural Thickening bv Duration of Household Contact Duration of Exposure (yre.) <1 1-5 5-10 10+ Total Total Examined 192 403 48 34 677 Extent of Pleural Thickening (ILO U/C Classification) Extent 1 15 (8%) 70(17%) 17 (35%) 7(21%) Extent 2 1 (0.5%) 7(2%) 5 (10%) 6(18%) Total Pleural* Thickening 16 (8%) 77(19%) 22 (46%) 13(38%) 109(16%) 19 (3%) 128(19%) 'Prevalence of pleural thickening significantly higher among those with longer duration <>i exposure. )? - 45 p < .001 df-3. Table 9 Distribution of Pleural Calcification by Extent* and Duration of Exposure Duration of Exposure (y.) <1 1-5 5-10 10+ Total Total Examined 192 403 48 34 677' Grade 1 5 (3%) 12 (3%) 6(13%) 4(12%) 27 (4%) Extent of Pleural Calcification Grade 2 1 (0.5%) 14 (4%) 2(4%) 0 17 (3%) Grade 3 1 (0.5%) 8 (2%) 1(2%) 0 , 10 (2%) AM Grades 7 (4%) 34 (8%) 9(19%) 4(12%) 54 (8%) 'Two individuals with uncertain duration of exposure excluded. tPrevalence of pleural calcification significantly greater among those with longer duration of exposure. X1- 12 p c .01 df-3. Table 10 Prevalence of Radiographic Abnormalities among Household Contacts by Duration of Exposure' Duration of Exposure (yrs) <1 1-5 5-10 10+ Total Number Examined 192 403 48 34 677 Small Opacities 27(14%) 65(16%) 14 (29%) 8 (24%) 114(17%) Pleural Thickening 16 (8%) 77(19%) 22 (46%) 13(38%) 128(19%) Pleural Calcification 7 (4%) 34 (8%) 9(19%) 4(12%) ' 54 (8%) One or More Abnormality 47 (24%) 145 (36%) 29 (60%) 18(53%) 239 (35%) 'Prevalence of pleural thickening, pleural calcification and all abnormalities significant!) higher among household contacts with longer duration of exposure (p < .01). "V , Anderson et al.\ Household Asbestosis 395 Table 11 Prevalence of Raoiographic Abnormauties by Year of Onset of Exposure* Year of Onset of Exposure 1941-1946 1946-1950 1950-1955 Total Total Examined 434 113 129 676* Small Opacities 79(18%) 19(17%) 16(12%) 114(17%) Pleuralt Thickening 98 (23%) 21 (19%) 9 (7%) 128(19%) Pleuralt Calcification 46(11%) 5 (4%) 3 (2%) 54 (8%) One or moret Abnormalities 172(40%) 38 (34%) 29 (22%) 239 (35%) Three individuals with uncertain year of onset excluded. tPrevalence of abnormality greater among those with earlier onset of exposure, (p < .01). for the pleural abnormalities. Statistical significance was not reached for a similar increase in combined small opacities. The relationship of the household contact to the worker was also important (Table 12). Wives had the highest prevalence of abnormalities (48%) and daughters had the lowest (21 h). Mean duration of expesure was the same for all rilr tionship categories. The prevalence of abnormalities was statistically significantly lower among the daughters when compared to the other exposure groups. With only a few exceptions, household contact clinic participants were unaware that they had any asbestos-associated disease. The prevalence of other disease processes was unrelated to asbestos exposure (arthritis, diabetes, hypertension, gout, etc.). The household contacts considered themselves to be in good health; the clinical examinations generally confirmed this. Current symptoms and clinical findings detected among the household contacts examined are summarized in Table 13. Rhonchi were the most common physical findings, not significantly associated with the prevalence of any type of radiographic abnormality. On the other hand, dyspnea, rales, cyanosis and clubbing were signifi cantly more prevalent among those with small opacities and/or pleural abnormalities on their x-rays. Table 12 Prevalence of Radiographic Abnormauties by Household Contact's Relationship to Index Worker Relationship Wives Daughter Sons Siblings Others Total Total Examined 162 224 151 81 61 679 Small Opacities 40 (25%) 15 (7%) 31 (21%) 15(19%) 12(21%) 129(19%) Pleural Abnormality 58 (36%) 34(15%) 47(31%) 22 (27%) 17(28%) 178(26%) Parenchymal and/or Pleural 77 (48%) 46(21%)* 63 (42%) 30(37%) 23 (38%) 239 (35%) Mean Duration of Exposure 2.2 2.4 yrs. 2.4 2.6 yrs. 2.3 2.8 yrs. 2.1 2.1 yrs. 3.6 3.3 yrs. Prevalence of radiographic abnormalities significantly higher among sons than daughters. X1- 19.6 pc.001. 9* : filtfe Vi: i-g::: ;... : V Tp; v: -Hv, 15192732 396 Annals New York Academy of Sciences Discussion We have examined nearly one-third of the living household asbestos contact cohort members. New data confirm and extend our previous observations. The presence of radiographic abnormalities in our study cohort was statistically significantly asso ciated with clinical abnormalities observed, duration of index worker employment and length of time since first exposure. These x-ray abnormalities, which are usually seen only after occupational asbestos exposure, were significantly more prevalent among the study group than a control comparison group. Although the number of examined individuals has more than doubled since our previous report, the overall prevalence of abnormalities has remained constant. It is most probable that our results represent a good approximation of the prevalance of radiographic abnormalities in the total cohort. Table 13 Prevalence of Current Symptoms and Clinical Findings* among Household Contacts by Radiographic Abnormalities'! Radiographic Finding S nail opacities Pleural change Small opacities and/or pleural abnormality Total Number Examined Absent 558 Present 111 Absent 495 Present 174 Absent 435 Present 234 669 Dyspnea 22 (4%) S 11 (10%) 20 (4%) 1 13 (8%) 14 (3%) s 19 (8%) 33 (5%) Rales 23 (<*> t 11 (10%) 18 (4%) 16 (9%) 13 (3%) 21 (9%) 34 (5%) Rhonchi Cyanosis 27 (5%) ' 2 (0.4%; 11 8 10(9%) 2(2%) 26 (5%) 8 11 (6%) 0 s 4(2%) 21 (5%) 8 16(7%) 0 S 4(2%) 37 (6%) 4 (0.6%) Clubbing 2 ,0.47 ) $ 3(3%) 2 (0.4%) 8 3(2%) 1 (0.2%) 4(2%) 5 (0.7%) Ten individuals did not have physical examinations. tPrevalence of abnormality significantly greater among those with radiographic abnormality than those with normal x-rays. ^Significantly different at p < .OS using x1 test. Significantly different at p < .01 using x! test. 8Not statistically significant. The early observation that pleural calcification, which is uncommon in the general population (.02-.S%)*`10 and common in asbestos-exposed populations (30+%)7" suggested that pleural calcification might serve as a marker of past asbestos exposure in non-occupationally exposed groups. This association was first remarked upon by Kiviluoto in I960 when he described an abnormally high prevalence of pleural calcification among residents of a district in Finland in which an anthophyllite asbestos mine and mill had been operating for many years.11 Subsequently, similar observations were made in other countries.,,'l, A survey of factory workers, factory worker household contacts, and factory neighborhood residents reported in 1971 by Navratil described an increased prevalence of pleural calcification among not only the factory workers but the relatives of factory workers and the residents in the neighbor hood of the factory.'* However, both the neighborhood and blood relative groups were small (1SS and 114 respectively). Anderson et al.: Household Asbestosis 397 Our continuing survey extends the observations of these authors and indicates that pleuro-pulmonary disease can occur under the conditions of nonoccupational exposure as experienced in the homes of asbestos workers. Of the household contacts with occupational exposure to asbestos, only 19 were aware that they were or had been working with asbestos. Individuals who reported having done brake repair work in the past, worked in shipyards, or performed general maintenance work involving pipe insulation, had the highest prevalence of abnormal x-rays (more than 50%). Of special interest is the group of household residents who entered the index worker's home shortly after his active employment period had ended. This group of 33 individuals did not show an increased prevalence of small opacities. However, they did have a statistically significantly increased prevalence of pleural abnormalities when compared to the urban New Jersey resident controls. It would appear that pleural changes are a better indicator of environmental asbestos exposure than are parenchy mal small opacities. The proportion of household contacts who had the more classic appearance of asbestosis, with both parenchymal small opacities and pleural abnormalities, was small (Table 6). This again indicates the importance of assessing pleural disease in nonoccupational settings. The appearance of asbestos-associated disease has been shown to depend upon duration and intensity of exposure. The longer and more intense the exposure, the sooner the disease could be expected to appear and, conversely, the shorter and less intense the exposure, the longer the time (latency) before an increased prevalence of disease could be demonstrated. As in occupational groups, increasing duration of exposure was associated with a higher prevalence of abnormalities in our study group. The effects of duration of exposure and time since onset of exposure were most marked for the pleural abnormalities. Individuals with more than ten years of exposure had four times as much pleural thickening and three times as much pleural calcification as individuals with less than one year of exposure. There was less than a two-fold increase in the prevalence of combined small opacities between the two groups. Forty percent of individuals first exposed between 1941 and 1946 had an abnormal x-ray compared to only 22% for those exposed first between 1950 and 1954. The data presented here demonstrate the time dynamics for the appearance of radiographic abnormalities after household asbestos exposure. It appears that there is a longer period of latency between first exposure and appearance of radiologic abnormalities under the condi tions of household asbestos exposure. The observation that sons have twice the prevalence of radiographic abnormalities of daughters is an interesting one. One possible explanation for the difference would be that the sons had a longer duration of exposure. However, it can be seen from Table 12 that the sons and daughters had the same mean duration of exposure. Further investigation of these differences is being made. The observation that nearly one-half of the wives examined had abnormal x-rays is consistent with the hypothesis that the wives would have been most heavily exposed because they were responsible for the laundering of workclothes and resided in the household for the longest period of time. Dyspnea, which is often the initial complaint of occupationally exposed asbestos workers, was present in 10% of individuals with parenchymal small opacities on their chest x-rays compared to only 4% of individuals with normal chest x-rays. No statistical association between dyspnea and pleural changes was seen although a similar trend was apparent. Dry rales, commonly heard in asbestotic patients, were also more prevalent among the household contacts with abnormal chest x-rays. Nine percent of the individuals with abnormal x-rays had rales present on physical examination compared to only 3% of individuals with normal x-rays. Rhonchi, 398 Annals New York Academy of Sciences commonly associated with chronic bronchitis in cigarette smoking, were not signifi cantly associated with the presence or absence of radiographic abnormalities. Club bing and cyanosis, associated with advanced disease, were uncommon and were found in only 5 and 4 individuals respectively. Using only one measure of asbestos effect, the chest x-ray, we have seen in our cohort of household asbestos contacts that x-ray abnormalities characteristically seen only after occupational asbestos exposure, are common. We do not yet know the full extent of the disease risk which will be experienced by this cohort. We do know from our own studies and those of others, that household asbestos contact as well as other environmental exposure is associated with an increased risk of mesothelioma, espe cially pleural mesothelioma.s1,,, In our previous report, we described four instances of pleural mesothelioma from among the total household contact cohort under observa tion. An additional case has been detected. Although tracing is not complete, we have so far recorded slightly over SSO deaths and S of them are due to pleural mesothelio ma. Vianna and Polan recently reported a retrospective study of 52 cases of mesothe lioma among women in New York State, 1967-73.19 Using occupational histories gathered on the women's husbands and other household residents, they were able to calculate a relative risk factor of 10 for residents in the home of a worker in an asbestos related industry. Nine of the 52 cases reviewed had only household contact with asbestos. Completion of the mortality survey of our conort and continued prospective observation will help determine the extent of risk for malignant diseases which attends such household asbestos contact exposure. The widespread use of asbestos and the subsequent release of fibers' into the environment did not occur on a large scale until the mid-1940s. While the disease risk among the occupationally exposed workers during that period has already become apparent, we can expect that household contacts may not begin to manifest the possible effects of that exposure until 30 or more years from onset. In the next years we should begin to learn whether the levels of asbestos exposure experienced by groups such as the household contacts we have under observation will be sufficient to cause disabling disease other than mesothelioma. It is essential that clinicians become aware of the significance of pleural disease unaccompanied by evidence of parenchymal fibrosis. In such cases, possible history of exposure to asbestos should be sought and the individual notified of the existence of the abnormality. Acknowledgments We are grateful for the valuable assistance given by our colleagues in the Environmental Sciences Laboratory in conducting the clinical studies and interpreting the chest x-rays, to our field survey stafT, including Mrs. Dorothy Perron, Mr. Charles Nolan, Mrs. Rayla Margoles, Mrs. Stella Przybyla and Ms. Shirley Levine. We wish to thank Mrs. Selma Annenberg and Mr. Sidney Sibcl for the preparation of tables and manuscript and Mr. James Fulmer for his assistance in the tabulation of the data. References I. Environmental Quality-1977: The eighth annual report of the Council on Environmental Quality. U.S. Printing Office, Washington, D.C. December 1977. Anderson el al.: Household Asbestosis 399 2. Selikoff. 1. J., W. J. Nicholson &. A. M. Langer. 1972. Asbestos air pollution. Arch. Environ. Hlth. 25:1. 3. Hunter, D. 1975. The Diseases of Occupations. The English Universities Press Ltd. Fifth Edition. 4. Anderson, H. A., R. Lilis] S. M. Daum, a. S. Fischbein & I. i. Selikoff. 1976. Household contact asbestos neoplastic risk. Ann. N.Y. Acad. Sci. 271:311. 5. ILO U/C International Classification of Radiographs of Pneumoconioses 1971. 1972. Occupational Safety and Health Series. International Labour Office, Geneva. 6. SPSS. Statistical Package for the Social Sciences. Second Edition. N. NiE, C. H. Hull, J. G. Jenkins, K. Steinbrenner, D. H. Bent. 1975. McGraw-Hill Book Company. New York. 7. Selikoff, I. J. 1976. Asbestos disease in the United States, 1918-1975. Rev. Fnnc. Mai. Resp. 4:7. 8. Floyd, C. & R. H. Hepburn. Calcification of the pleura. Am. Rev. Tuberc. 40:215. 9. Neef. W. 1963. Bciseitige Pleuraverkalkungen im Alter. Roentgenfortschr. 99:632. 10. Marsova. D. 1964. Beitrag zur Atiologie der Pleuraverkalkungen. Z. Tuberk. 121:329. 11. Siecal, W_, A. R. Smith & L. Greenburg. 1943. Report on study of talc miners and millers in Sl Lawrence County, N.Y. Indust. Bull. 22:434,468. 12. Kiviluoto, R. 1960. Pleural calcification as a roentgenological sign of non-occupational endemic anlhopyllite-asbcstosis. Acta Radiol. Supp. 194: L 13. Zolov, C,, T. Bourilkov & L. Babadjov. 1967. Pleural asbestosis in agricultural woikcrs. Etwinn. lies. 1:287. 14. Meurman, L. 1966. Asbestos bodies and pleural plaques in a Finnish series of autopsy cases. Acta. Path. Microbiol. Scand. 181:1. 15. Yazicioglu, S. 1976. Pleural calcification associated with exposure to chrysolite asbestos in southeast Turkey. Chest 70:43-47. 16. Navratil, M. & F. Trippe. 1972. Prevalence of pleural calcification in persons exposed to asbestos dust, and in the general population in the same district. Environ. Res. 5:210. 17. Newhouse, M. L. St H. Thompson. 1972. Mesothelioma of pleura and peritoneum following exposure to asbestos in the London area. Brit. J. Indust. Med. 22:261. 18. Baris, Y. I., M. Artvinli & A. A. Sahin. 1979. Environmental mesothelioma in Turkey. This volume. 19. Vianna, N. J. & A. K. Polan. 1978. Non-occupational exposure to asbestos and malignant mesotheliomas in females. Lancet 1: 1061-1063.