Document nK1y67GywBkR84LZRZV7BJLR
REVIEWS ON ENVIRONMENTAL HEALTH
VOLUME 11, NOS. 1-2, 1996
Pleural Mesothelioma and Household Asbestos Exposure
Joachim Schneider, Kurt Straif and Hans-Joachim Woitowitz
Institut undPoliklinikfur Arbeits- und Sozialmedizin der Justus-Liebig-Universitat Giessen Auhveg 129/III35385 Giessen, Deutschland
SUMMARY
This article discusses the development of asbestos-induced malignant mesotheliomas after non-occupational environmental exposure to asbestos through contact with occupationally exposed household members. In our policlinic, we have seen six fatal pleural mesothelioma cases (five wives and one son of asbestosindustry workers) with no history of occupational asbestos exposure. In five women, a causal relation was established between the fatal disease and inhalation of asbestos fibers while cleaning the contaminated work-clothes and shoes of their husbands at home. The son I had also been exposed to asbestos throughout | his childhood during daily visits with his father ! at the workplace.
INTRODUCTION
Asbestos-induced mesothelioma (No. 4105 of the German Ordinance of Occupational Diseases (BeKV) is one of the most frequently compensated occupational cancers III. Malignant mesothelioma is specifically regarded as a " signal tumor" of previous exposure to asbestos in the workplace HI. To our knowledge, causes other than asbestos and the comparably bio-persistent mineral-fiber Erionite have not been found /3,4/. Mesothelioma is considered a marker for non-occupational asbestos exposure as well /5,6/.
Asbestos-induced mesotheliomas have been described in the vicinity of asbestos mines in South Africa /7,8/, Canada 191, Australia /10,11/, and Cyprus /12/. Industrial asbestos manufacture also presents a significant health risk to the environment. In Saxony /13/, and especially in the HamburgBergedorf area, the incidence of mesothelioma
Freund Publishing House Ltd., 1996
cases was significantly increased in areas that are close to industrial asbestos emitters /14-17/. Many reports have emerged from Turkey /18-20/, the northwestern part of Greece /21/, and Corsica 1221, 1231 about the endemic incidence of diffuse malignant mesotheliomas, caused by environmental exposure to asbestos or Erionite through soil erosion. In certain regions of central Anatolia, pleural-mesothelioma incidence figures of up to 216 per 1,000,000 inhabitants have been recorded, although the expected mesothelioma incidence in the general population was very low. The estimate of an annual mesothelioma mortality rate of 1 to 8 per one million inhabitants /24-26/ relates to about one mesothelioma death per 1000 to 10,000 deaths from all causes. An article by Grossgarten and Woitowitz /6/ presents an overview of asbestosinduced pleural mesotheliomas that are linked to indoor inhalation by household contacts.
PATIENTS AND EXPOSURE CRITERIA
In our policlinic, we have seen asbestos-induced tumors in members of households where at least one worker had been occupationally exposed to asbestos. Between 1986 and 1994, five women and one young man (one patient's son), with no occupational history of asbestos exposure, died of asbestos-induced mesothelioma. Their ages ranged from 42 to 68 years (Table 1). The diagnosis was always confirmed by histology on specimens obtained from clinical biopsy or autopsy. Detailed job histories revealed that neither the women nor the son had ever worked in an asbestos factory. Asbestos exposure was exclusively through residential inhalation of asbestos from contaminated work clothes or shoes that were brought home from the workplace by the husband. Throughout his childhood, the son had regularly delivered a hot
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Table 1. Asbestos-induced pleural mesothelioma in six wives and one son of asbestos-industry workers
Patient
G.J. E.L. H.B. M.L. G.K. H.J.* *Son of G.J.
Bom
1923 1925 1926 1931 1933 1946
Died
1986 1993 1994 1987 1992 1992
Length of household exposure 1950-59 1961-84 1954-71 1969-76 1964-74 1950-59
Latency (years)
Occupation of household contact
35 Insulation-mat manufacturing 31 Turbine revision 38 Roofer (asbestos/cement) 17 Asbestos cardboards 26 Insulator 42 Insulation mats manufacturing
meal to his father at the workplace. From 1950 to 1984, the husbands were employed in different companies that manufactured asbestos mats, asbestos textiles, and asbestos cardboard, or in such occupations as insulators, roofers, or turbinerevision workers who process asbestos products. Thus, the asbestos exposure at such jobs is indisputable. The husbands of two patients, G.K. and G.J., had already developed pulmonary asbestosis. The asbestos-contaminated clothes were not removed in the factory for cleaning but rather were taken home, where the wives brushed them almost daily and hand-washed them once or twice a week. Residential fiber measurements are unavailable. The length of the household exposure was between 7 and 23 years (see Table 1). The latency period (time between onset of the residential asbestos exposure and the development of the disease) varied from 17 to 38 years.
DISCUSSION
For almost three decades, the international scientific literature of environmental and occu pational medicine has published papers describing asbestos-induced diseases in family members of workers who have been occupationally exposed to asbestos 15,61. In the United States, the air concentration of chrysotile was measured in the houses of 13 asbestos miners who usually did not remove work clothing after working in the factory. About 75% of the air measurements in such
households fell between 50 and >2000 ng/m3 chrysotile 1211. For comparison, only 32 to 65 ng/m3 chrysotile was measured in the homes of residents who were not employed in the mines. Measurements were also taken from the area where the work clothes were cleaned in an American asbestos textile factory. Between 10,000 and 80,000 (median 30,000) asbestos fibers of a length L >5 pm/m3 air were found in the "cloth-cleaning area" /28/. Brushing asbestos contaminated work clothes results in asbestos-fiber concentrations of a few hundred crocidolite fibers per cm3 /29/.
In 1989, Huncharek et al. /30/ reported that a shipyard machinist's wife, who had washed his asbestos-contaminated work clothes at home, died of pleural mesothelioma. The post-mortem, lungburden analysis yielded concentrations of chrysotile, amosite, and crocidolite, as well as tremolite, actinolite, and anthophyllite fibers per gram dry lung tissue of the same magnitude as that found in specimens from patients with occupational asbestos exposure.
Bianchi et al. /31/ found ferruginous bodies in the post-mortem lung tissue specimens of 73 mesothelioma patients, of whom 6 were asbestos workers' wives with only household exposure. Between 1,000 and 10,000 ferruginous bodies per gram dry lung tissue were measured in half the wives; as many as 10,000 to 100,000 were reported in one wife. Such concentrations are comparable to those found in 56 former shipyard-industry employees. Measurements showed between 1,000 and 10,000 ferruginous bodies per gram dry lung
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tissue in 20 shipyard workers, between 10,000 and 100.000 in 23 workers, and >100,000 in 10 workers. Low concentrations (<1,000 ferruginous bodies per gram dry lung tissue) were measured only in three shipyard workers and two of their wives.
The special risk for death from pleural mesothelioma in wives of asbestos-industry workers is well known from many international case reports /12,30-46/. The risk of mesothelioma death in household members has also been investigated in epidemiological case-control and cohort studies. In a case-control study in England, Newhouse and Thompson /47/ reported that 9 of 76 malignant mesothelioma patients did not have occupational asbestos exposure. Seven female patients had washed the work clothes of their occupationally exposed husbands and siblings. Two male patients were exposed at the respective ages of 9 and 13 years via their siblings who were working in an asbestos mill. The original publication did not distinguish between occupational and paraoccupational exposure, however. A secondary analysis of household contacts gave a crude odds ratio OR = 16.75, with a 95% confidence interval of 2.0 to 136.78.
In a pairwise-matched, case-control study, Vianna and Polan /48/ described pleural and peritoneal mesotheliomas in 52 New York females. In eight pairs, only the patients (seven wives and one daughter of occupationally exposed men) were exposed while washing asbestos-contaminated work clothes, whereas in one pair only the control was thus exposed. A secondary analysis excluding occupational mesotheliomas resulted in an odds ratio OR = 8.0, with a 95% confidence interval of 1.0 to 64.0. The authors presented the occupation of the male family members as the main risk factor for the disease.
A case-control study of McDonald 151 (n=557 mesothelioma cases) revealed that in eight pairs, only the patients (five during childhood) had been exposed to asbestos via household contacts. By contrast, in two pairs, only the controls had a history of domestic exposure to asbestos. The calculated x2 = 3.03 was not statistically significant (p = 0.08).
A cohort study of Anderson /49/ revealed that from 1941 to 1945, only three mesotheliomas were
diagnosed among 2218 household members of amosite workers. The published data did not specify, however, the expected mesothelioma mortality rate, which should have been close to zero. Further, occupational asbestos exposure after 1945 cannot be ruled out from the information provided in this study.
In a cohort study by Magnani et al. 1501, 1740 female household members were monitored from 1965 to 1988. Overall, 210 deaths occurred versus 229.1 expected deaths. Four patients died of pleural tumors (three were confirmed mesotheliomas), which is significantly more than the expected rate of 0.5 (SMR=600). The 95% confidence interval of the SMR (215.9 to 2028.8) is statistically significant. The studies reviewed here confirm that despite certain methodological limitations, household members--predominantly wives--of asbestos workers, have an increased risk of dying from mesothelioma.
Other reports show that not only wives but also sons and daughters of asbestos workers have a high risk of dying from mesothelioma. In the Anderson cohort study on amosite workers /49/, for example, the three adult patients (a 40-year-old son and two daughters, aged 41 and 51 years /46/) who died from mesothelioma had been exposed to asbestos at home during their childhood.
Glage 751/ published one of the first reports from Germany on malignant mesothelioma, with a demonstration of asbestos fibers and ferruginous bodies, in the lung of an adult whose prolonged household exposure to asbestos had taken place during infancy. The patient was between three and seven years old when she was exposed to the asbestos-contaminated work clothes of her father, who cleaned carding machines. An occupational exposure of the daughter to asbestos was ruled out.
Kane et al. /52/ reported five adults under the age of 40 with pleural mesotheliomas. Residential asbestos exposure happened during childhood, exclusively through their fathers, most of whom were working in the shipyard industry.
Household exposure can begin at a relatively early age 1521. At least 5 of 668 mesotheliomas diagnosed in Canada between 1960 and 1975 and in the United States in 1972 can be linked to a household contact during infancy 191. Konetzke et al. 754/ reported that of seven eight cases of
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asbestos-induced diseases ensuing from asbestos exposure during childhood were attributed exclusively to non-occupational exposures. The published data, however, were not sufficient to determine whether the asbestos-induced diseases were mesotheliomas or merely radiologically diagnosed pleural plaques.
The contaminated work clothes of siblings also poses a risk. Newhouse et al. 1411 mentioned three mesothelioma patients, who at three years of age had been exposed to the clothing of sisters who were working in an asbestos mill. Between 1965 and 1992, many reports of mesothelioma cases that had been linked to contact during infancy with the work clothes of either fathers or siblings or both, were published in the United States (15), Canada (1) , England (5), Germany (2), Sweden (2), Italy (2) , and Australia (1) /9,32,36-37,42,44-47,5152,55-59/; see /60,61/ for overview/. Occupations of the fathers/siblings comprised working in an asbestos-mill /47, an asbestos-factory /57/, an asbestos-cement-factory /56/, and with asbestosproducts /46/; insulators /32,37,38/; cardingmachine cleaner /51/, pipe lagger /55/, foundry worker /58/, steam fitter /40/; glass /52/ and shipyard industry 145,52/ workers; and a railroad)^ worker /44/. Twenty-six patients had been exposed to fathers and eight to siblings.
Several reports have described a family clustering of asbestos-induced malignant mesothelioma in patients with household exposure /62,63/. A review by Dawson et al. /64/ covers 27 families comprising 64 (40 male and 24 female) mesothelioma patients; only 30 patients had a history of occupational asbestos exposure. The exposure of 11 patients was exclusively through household contact, 6 others lived near an asbestos factory, and 17 had no known asbestos exposure. Otte et al. 1651 described three mesothelioma patients in a single family, where family members had helped with packing an asbestos-cement product that was manufactured in a very dusty atmosphere in their home. In another report /58/, a pair of siblings who died of mesothelioma had been exposed to asbestos solely through the workclothes of the father, who worked in a foundry where asbestos textiles were used for heat protection.
Other articles describe mesotheliomas in multiple family members, mainly wives and children, with no
occupational history of asbestos exposure. Krousel et al. 1401 and Li et al. /37, 42/ reported that wives and daughters of insulators died from meso thelioma. Like others, the exposure was due to inhaling asbestos while washing the work-clothes of the husband. During infancy, one daughter had reportedly worn diapers that were made from cotton sacks that had been previously used for storing asbestos.
We can infer from the evidence presented in this case series not only that mesotheliomas caused exclusively by household asbestos exposure are a problem in Germany now but also that such tumors will continue to appear in the future. During the period of reconstruction after World War II, the annual consumption of asbestos in the Federal Republic of Germany increased until the mid-1970s. In 1975 for example, 164,000 tons of raw asbestos were turned into about 1.5 million tons of asbestoscontaining products in various industries 1661. Accurate estimates of how many workers were constantly or occasionally exposed to asbestos during the manufacture and use of asbestoscontaining products are not available, but figures of >800,000 such individuals have been claimed 166/. About 45,000 workers were employed in industries processing raw asbestos, which is a plausible number. A relatively high fluctuation in dusty jobs can be assumed 14/. A valid estimate of household members at risk cannot be given.
In our policlinic, the latency period for the malignancy ranged from 17 to 36 years, which is typical for occupational pleural mesotheliomas /67,68/. The duration of the household exposures-- 7 to 23 years--agrees with the reported range of 2 to 41 years 1411. In England, shorter exposure periods preceding mesothelioma have been reported, but it should be noted that in such cases, the first year of exposure fell between 1912 and 1941, when occupational hygiene standards were rare.
The combination of short exposure periods and the long latency of asbestos-induced diseases underscores the significance of taking a detailed exposure history of mesothelioma patients who claim to have had no occupational asbestos exposure. Such patients should always trigger a suspicion of secondary asbestos exposure through household contact.
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REFERENCES
1. Butz M. Beruflich verursachte Krebserkrankungen. Schriftenreihe des Hauptverbandes der gewerblichen Berufsgenossenschaften. St. Augustin 1990.
2. Woitowitz H-J, Paur R, Rodelsperger K. Das Mesotheliom, ein Signaltumor der beruflichen Asbestsstaubgefahrdung. Dtsch Med Wschr 1984; 109: 363-368.
3. Intematioal Agency for Research on Cancer. Evaluation of Carcinogenic Risk of Chemicals to Man: Silica and some Silicates. IARC Monographs, Vol. 42. Lyon, 1987.
4. Woitowitz H-J. Epidemologie und Prevention des malignen Mesothelioms. Med Klin 1987; 82: 578 581.
5. Gardner MJ, Saracci R. Effects on health of nonoccupational exposure to airborne mineral fibers. In: Non-occupational exposure to mineral fibers, Lyon, France: IARC Scientific Publ. No. 90, 1989; 375-397.
6. Grossgarten K, Woitowitz H-J. Erkrankungen der Pleura durch Asbest und Erionitfaserstaub. Dtsch Arztebl 1993; 90: 708-723.
7. Wagner JC, Sleggs P, Marchandt P. Diffuse pleural mesothelioma in the North-West Cape Province. Brit J Indust Med 1960; 17: 260-271.
8. Webster I. Asbestos and malignancy. South African Med J 1973; 47: 165-171.
9. McDonald AD, McDonald JC. Malignant mesothelioma in North America. Cancer 1980; 46: 1650-1656.
10. Armstrong BK, Musk AW, Baker JE, Hunt JM, Newall CC, Henzell HR, et al. Epidemiology of malignant mesothelioma in Western Australia. Med J Australia 1984; 141: 86-88.
11. Hansen J, DeKlerk NH, Eccles JL, Musk AW, Hobbs MST. Malignant mesothelioma after environmental exposure to blue asbestos. Int J Cancer 1993; 54: 578 581.
12. McConnochie K, Simonato L, Mavrides P, Christofides P, Pooley FD, Wagner JC. Mesothelioma in Cyprus: The role of tremolite. Thorax 1987; 42: 342-347.
13. Anspach M. Sind Pleuraverkalkungen pathognomonisch fur eine Asbestose? Int Arch Gewerbepath Gewerbehyg 1962; 19: 108-120.
14. Dalquen P, Dabbert AF, Hinz I. Zur Epidemiologie der Pleuramesotheliome. Vorlaufiger Bericht iiber 119 Falle aus dem Hamburger Raum. Prax Pneumol 1969; 23: 547-558.
15. Hain E, Dalquen P. Katamnestische Untersuchungen zur Genese des Mesothelioms. Bericht iiber 150 Falle aus dem Hamburger Raum. Int Arch Arbeitsmed 1974; 33: 15-37.
16. Hain E. Untersuchungen iiber gesundheitliche Asbestschiiden in Hamburg (1969-1970). BGA-Schriften 1984; 2: 110-111.
17. Bohlig H, Dabbert AF, Dalquen P, Hain E, Hinz I. . Epidemiology of malignant mesothelioma in Hamburg. Environ Res 1970; 3: 365-372.
18. Baris Y, Artvinli M. Natural mineral fiber-induced chest diseases in Turkey. Arch Immun Ther Exp 1982; 30: 161-168.
19. Yazicioglu S. Pleural calcification associated with exposure to chrysotile asbestos in southeast Turkey. Chest 1976; 70: 43-47.
20. Yazicioglu S, Ilcayto R, Balci K, Yorulmaz B. Pleural calcification, pleural mesotheliomas, and bronchial cancers caused by tremolite dust. Thorax 1980; 35: 564-569.
21. Langer AM, Nolan RP, Constantopoulos SH, Moutsopoulos HM. Association of Metsovo lung and pleural mesothelioma with exposure to tremolitecontaining white-wash. Lancet 1987; 8537: 965-967.
22. Boutin G, Viallat JR, Steinbauer J. Bilateral pleural plaques in Corsica: A marker of non-occupational asbestos exposure, Lyon, France: IARC Scientific Publ. No. 90, 1989; 406-410.
23. Baris Y. Asbestos and Erionite-related chest diseases. Semih Ofset Matbaacilik Ltd. Co. Ankara, Tiirkei, 1987.
24. Becklake MR. Asbestos-related disease of the lung and other organs. Their epidemiology and implications for clinical practice. Am Rev Respir Dis 1976; 114: 187.
25. Cutler SJ, Young JL. Third national cancer survey: Incidence data. National Institutes of Health, National Cancer Institute, Bethesda, MD: DAEW Publ, 1975; 75-78.
26. McDonald JC, McDonald AD. Mesothelioma as an index of asbestos impact. In: Quantification of Occupational Cancer. Banbury Report 9, Cold Spring Harbor Laboratory 1981; 73-85.
27. Nicholson WJ. Tumour incidence after asbestos exposure in the USA: Cancer risk of the nonoccupational population. VDI-Berichte Nr 475, Dusseldorf 1983; 161-177.
28. Curtis RA, Bierbaum PJ. Technological feasibility of the 2 fibers/cc standard in asbestos textile facilities. Am Indust Hygiene Assoc J 1975; 36: 115-125.
29. Browne K. Asbestos-related mesothelioma: Epidemi ological evidence for asbestos as a promoter. Arch Environ Health 1983; 261-266.
30. Huncharek M, Capotorto JV, Muscat J. Domestic asbestos exposure, lung fiber burden, and pleural mesothelioma in a housewife. Br J Indust Med 1989; 46: 354-355.
31. Bianchi C, Brollo A, Ramani L, Zuch C. Asbestosrelated mesothelioma in Monfalcone, Italy. Am J Indust Med 1993; 24: 149-160.
32. Lieben J, Pistawaka H. Mesothelioma and asbestos exposure. Arch Environ Health 1967; 14: 559-563.
33. McEvven J, Finlayson A, Mair A. Asbestos and meso thelioma in Scotland. Int Arch Arbeitsmed 1971; 28: 301-311.
70 J. SCHNEIDER ET AL.
34. Rubino GF, Scansette G, Donna A, Paletro G. Epidemiology of pleural mesothelioma in northwestern Italy (Piedmond). Br J Indust Med 1972; 29: 436-442.
35. Lillington GA, Jamplis RW, Differding JR. Conjugal malignant mesothelioma. New Engl J Med 1874; 291: 583-584.
36. Greenberg M, Davies TAL. Mesothelioma register 1967-1968. Br Am J Indust Med 1974; 31: 91-104.
37. Li FP, Lokisch J, Lapey J, Neptune WB, Wilkins EW. Familial mesothelioma after intense asbestos exposure at home. J Am Med Assoc 1978; 240: 467.
38. Vianna NJ, Maslowsky J, Roberts S, Spellman G, Patton R. Malignant mesothelioma: Epidemiologic patterns in New York state. NY State J Med 1982; 5: 735-738.
39. Hirsch A, Brochard P, DeCremoux H, Erkan L, Sebastien P, DiMenza L, Bignon J. Features of asbestos-exposed and unexposed mesothelioma. Am J Indust Med 1982; 3: 413-422.
40. Krousel T, Garcas N, Rothschild H. Familial clustering of mesothelioma: a report on three affected persons in one family. Am J Prevent Med 1986; 2: 186-188.
41. Wolf KM, Piotrowski ZH, Engel JD, Beekeris LG, Palacios E, Fischer KA. Malignant mesothelioma with occupational and environmental asbestos exposure in an Illinois community hospital. Arch Intern Med 1987; 147: 2145-2149.
42. Li FP, Dreyfus MG, Antman KH. Asbestoscontaminated nappies and familial mesothelioma. Lancet 1989; 22: 909-910.
43 Shepherd KE, Oliver LC, Kazemi H. Diffuse malignant pleural mesothelioma in an urban hospital: Clinical spectrum and trends in incidence over time. Am J Indust Med 1989; 16: 373-383.
44. Maltoni C, Pinto C, Mobiglia A. Mesotheliomas due to asbestos used in railroads in Italy. Ann NY Acad Sci 1991; 643: 347-367.
45. Dodoli D, DelNevo M, Fiumalbi C, Iaia TE, Christaudo A, Comba P, et al. Environmental household exposure to asbestos and occurrence of pleural mesothelioma. Am J Indust Med 1992; 681.
46. Anderson HA, Lilis R, Daum SM, Fischbein AS, Selikoff U. Household-contact asbestos neoplastic risk.. Ann NY Acad Sci 1976; 271: 311-323.
47. Newhouse ML. Thompson H. Mesothelioma of pleura and peritoneum following exposure to asbestos in the London area. Br J Indust Med 1965; 22: 261-267.
48. Vianna NJ, Polan AK. Non-occupational exposure to asbestos and malignant mesothelioma in females. Lancet 1978; 20: 1061-1063.
49 Anderson HA. Family contact exposure. In: Proceedings of the World Symposium on Asbestos, Canadian Asbestos Information Center. Montreal, Canada: 1983; 349-362.
50. Magnani C, Terracini B, Ivaldi C, Botta M, Budel P, Mancini A, Zanetti R. A cohort study on mortality
among wives of workers in the asbestos cement industry in Casale Monferrato, Italy. Br J Indust Med 1993; 50: 779-784. 51. Glage E. Malignes Pleuramesotheliom einer Erwachsenen nach Asbest-exposition im kindesalter. Praxis Pneumologie 1970; 24: 39--45. 52. Kane MJ, Chahinaian AP, Holland JF. Malignant mesothelioma in young adults. Cancer 1990; 65: 1449-1455.
53. Joubert L, Seidman H, Selikoff IJ. Mortality experience of family contacts of asbestos factory workers. Ann NY Acad Sci 1991; 643: 416-418.
54. Konetzke GW, Beck B, Mehnert WH. Uber berufliche und ausserberufliche Asbesteinwirkungen. Pneumologie 1990; 44: 858-861.
55. Champion P. Two cases of malignant mesothelioma after exposure to asbestos. Am Rev Respir Dis 1971; 103: 821-825.
56. Milne JEH. Thirty-two cases of mesothelioma in Victoria, Australia: A retrospective survey related to occupational asbestos exposure. Br J Indust Med 1972; 33: 115-122.
57. Knappmann J. Beobachtungen an 251 obduzierten Mesotheliom-fallen in Hamburg (1958-1968). Pneumologie 1972; 148: 60-65.
58. Martensson G, Siminato L, Mavrides P, Christofides P, Pooley FC, Wagner JC. Malignant mesothelioma in two pairs of siblings: Is there a hereditary predisposing factor? Eur J Respir Dis 1984; 65: 179-184.
59. Hammar SP, Bockus D, Remington F, Freidman S, LaZerte G. Familial mesothelioma: A report of two families. Human Pathol 1989; 20: 107-112.
60. Grundy GW, Miller RW. Malignant mesothelioma in childhood. Cancer 1972; 30: 1216-1218.
61. Wassermann M, Wassermann D, Steinitz R, Katz L, Lemesch C. Mesothelioma in children. In: Wagner JC, ed. Biological Effects of Mineral Fibres, Lyon, France: IARC Scientific Publ. No. 30, 1980; 253-257.
62. Lynch HT, Katz D, Markvicka SE. Familial mesothelioma: A review and family study. Cancer Genetics Cytogenetics 1985; 15: 25-35.
63. Risberg B, Nickels J, Wagermark J. Familial clustering of malignant mesothelioma. Cancer 1980; 45: 2422.
64. Dawson A, Gibbs A, Browne K, Pooley F, Griffiths M. Familial mesothelioma. Cancer 1992; 70: 1183-1187.
65. Otte KE, Sigsgaard TI, KjaerulfF J. Malignant mesothelioma: Clustering in a family producing asbestos cement in their home. Br J Indust Med 1990; 47: 10-13.
66. BMFT-Mitteilung. Humanisierung des Arbeitslebens. Aktivitiiten zum Abbau der Gesundheitsgefahren durch schiidliche Arbeitsstoffe (Asbest). Bonn: 1981.
67. Selikoff J, Hammond EC, Seidman H. Latency of asbestos diseases among insulation workers in the United States and Canada. Cancer 1980; 46: 2736.
68. Woitowitz H-J. Spate Folgeschaden nach Asbeststaubgefahrdung. Med Sach 1986; 82: 19-21.