Document GKpBLV81MkDDZmKagorpOr1jq

FILE NAME: Household Contact (HC) DATE: 0000 DOC#: HC029 DOCUMENT DESCRIPTION: Book Chapter - Household Exposure to Asbestos and Risk o f Subsequent Disease HOUSEHOLD EXPOSURE TO ASBESTOS AND RISK OF SUBSEQUENT DISEASE1 Henry Anderson, Ruth L iiis, Susan Daum, A lf Fischbein and Irvin g J. S elikoff ... Environmental Sciences Laboratory, Mount-Sinai School of Medicine of The City University of New York. New York, 10029 INTRODUCTION Today, everyone living in an industrialized country is exposed to dusts, fumes and chemicals inadvertently released into the environment during manufacturing, processing or use of finished products. Initially, public awareness was focused on the most obvious pollution types and sources, plumes of malodorous smoke and discharge of pollutants into rivers and lakes. A more recent phenomenon is concern that unrecognized and less obvious environmental pollution might pose a significant health hazard to the general public. Largely unrecognized was the contamination of workers' homes, and the resulting exposure of wives and children to toxic materials brought from the work place via contaminated clothing. Insidiously, household residents were exposed to materials used and manufactured by the worker living in the household. It has been known that disease related to toxic industrial substances can occasionally be found among household contacts of exposed workers, as well as among individuals living in the neighborhood of factories producing or using these toxic suostances. Nearly 40 years ago, chloracne was described among family contacts of a chemical worker employed in a polychlorinated biphenyl (PCB) man ufacturing plant (Commonwealth of Pennsylvania, 1935). The PCB responsible for the chloracne came from the worker's contaminated coveralls. His clothes, shoes and even his hands and hair contained enough PCB to cause death among his unsuspecting family. That significant household contamination with asbestos dust brought home on the clothes of workmen can occur has been assumed on the basis of reported cases of pleural mesothelioma in individuals whose only asbestos contact would have been from residence in an asbestos worker's household (Newhouse and Thomp son, 1965). The growing incidence of such mesothelioma cases has focused new attention on the potential health risk, especially neoplastic, associated with en vironmental exposure to asbestos. Besides mortality experience and the appearance of rare "signal tumors" such as mesothelioma, other more readily obtainable means exist to assess whether changes have resulted from environmental asbestos exposure. Thus, few attempts have been made to assess the prevalence of asbestos-associated radiographic abnormalities among household contact of asbestos workmen. 1This investigation has been supported by grants from the National Institute of Environmental Health Sciences, ES 00928 and ES 02553. fifii AH OEri SO re A - O P ^ u a TPCNS s t u d i e d _ ''~'a are n - A srigating m e status of h o u se n o ld co n ta cts or \5 S n asocstos L ' c ,i' ^S ie v e d m a rsctcry wm ch produced amosrte asbestos -redeem from ban .c tQPa ' ' i tr (Cf-.c oO ouiation nas a w e ll-c n a ra c te n z e o clinical anc mcnaim, m .p e r- e-C c1s .rc e me-- nave bee n u n d e r clinical o b se rva tio n by one of us (Irvm g 1%e.,Ko^ ' 0. m ere m e - PC years (S e lik o ff e r a / , 1964, 1972) T a o le sum m er,zes m <T o 'Din exp-enence of the s u b -g ro u p (933) first em ployee from 1941 :c iSoC ' 7,0 cnbm oi c c s e ~ .e c to e x p e c te d deaths due to lung and gastrointesuna, p e n c e uaho-sm i pleum l and peritoneal m esotheliom a and asoestcsis snow me emrac"- o n a p- e x p e rie n c e or m is p o p u la tio n A d d itio n a l analysis has re ve a ie c that w o m e n am'" mis group .-we n s c as itrle as one m onth of e m p lo ym e n t began :c veer a ,,w e a rs .,,emhm gp gears .a te ' 'S e id rn a n er a' 19751 ` AdL- Thu ~WV>J eo a m P csu<vec b e a n s a m o n g rP3 A rre s ile a -pmxcvwc "<7,, ' 5aS Co served ;o P e c e n c e . J ) ' 9 " C e a tr s ' 9-a - excecteo Ccserve-c : J d ' y 3<-.~ae' ^ p,' gp --n'-C X T C 3 J "} - C2` `'',c 'T .(b c 1cr-n,n ' -- w m- a cuestes : C m w ~cr -i--e n o u s 368 63 71 35 13 ic 3 ' 5d ^ ,, 59-4 >55 00 b n 4 ' 3C a _ 9) ' "_i m b-T re sp i'j:o f'y a s e a s a 3 43 "5 Pr mi r r e r a_s'-' 2 86 SC 360 53 c x _ e c ;a c deaths a a s e c upon a g e -s p e a h e a ea tn -ata c a ta c - aw _,6 rs a \ mb.. rpn.es correspcocing years ,,,,ean s m e s ro t ava lla tile out n e s e nave oeer. "are causes a. a e a trs arerai cccuiacor v e n 'P O L AO Pum eTlO D mr c o io p a n s c n p u rp o s e s in the chest x-ra y in te rp re ta tio n a co n tro l popumuo- o ' j ' u a r Dew oersey re s id e n ts w h o lived in the sam e c o m m u n rv as the s u e - ro p u ia t.o n was -dentified from the general m edical clinic at the facuty usee tr exam ine the w o o e rs anc house h o ld m em bers C ontrols were m atenee o r age arm - in n ,ol 0LLrQ. w e r m. v iq w. d a r id o n l y thoo w.rH no Unown pversom. r c r n,,-- ; onai contact w th asoestos w ere included ' ' HOUSEHOLD EXPOSURE TO AS8EST0S 147 METHODS In 1973. we began tracing all the household contacts who could be identified as being resident in the workers' households during the period of their active asbestos employment. All individuals were invited to participate in periodic special clinics established previously for prospective observation of the workers. Examinations included comprehensive occupational and residential histories, past and current medical history, history of current symptoms, smoking and Medical Research Council of Great Britain respiratory questionnaires, physical examination, 14" x 17" postero-anterior, and right and left oblique chest x-rays, and spirometry. The chest x-rays of household contacts, factory workers and controls were intermixed and read without knowledge of exposure category. The ILO U/C Pneumoconiqsis Classification of 1971 was utilized by the authors and a consensus reading reported for statistical analyses. A film was classified as abnormal if one or more of the following abnormalities was recorded: irregular opacities 1/0 or more: any lateral wall pleural thickening; any pleural calcification; pleural plaques on the diaphragm. RESULTS Table 2 gives the distribution of 704 household contacts who have so far undergone clinical examinations by relationship to the index worker. Fifty-six per cent of those examined were children. Occupational and residence histones re vealed that, in addition to household asbestos exposure, 46 individuals had had occupational exposure to asbestos or other fibrogenic dusts. Thirty-two did not live TABLE 2. Distribution Of 704 Household Contacts Of Amosite Asbestos Workers By Relationship To Index Worker Relationship Wives Daughters Sons Siblings Parents Other Total _________ __________________ _______________________ Number Percentage 155 22 0o 222 31 5o 178 25.2 81 11.5% 12 1 7o _56 8 1% 704 in the index household during the workers' asbestos handling employment. The 78 individuals listed in Table 3 did not fit the criteria for inclusion in the study and have been excluded from the following analyses. This report is concerned with the 626 household contacts who had lived in the household of an asbestos worker while he was actively employed in the amosite asbestos factory, and who themselves had not had an occupational exposure to asbestos. 926 control subjects were identified. The age and sex distribution of the sub jects and controls were not statistically significantly different. iii:. 1= . 1 ;ij<l.7,, 1r il it: !j; iii 1i. Hit :f!if rtf .IkV|lt 4M .rR tipi Si > . - .Is., .'ft \? 7 `fi fii . Direct asbestos trade Automobile brake repair Drywall construction taper Shipyard work Other indirect asbestos exposure Other fibrogemc dust exposure Resident in index household after active asbestos employment period Total excluded t a r i a s s , "1'he househ ,d con,ac& ~ i - TABLE 4. Age Distribution Of 626 Household Aabem Contacts Age 20-29 30-39 40-49 50-59 60-69 70- Total Number 43 161 182 136 69 35 626 Percentage 6.9% 25.7% 29.1% 21 7% 11.0% 5.6% s S s S ^ S S s ^ S first exposed 1941-45 1946-54 Total Total# examined 413 (66.0%) 213 (34.0%) 626 lyr. 166 (40.2%) 97 (45.5%) 263 (42.0%) 1-5yrs. 196 (47.5%) 103 (48.4%) 299 (47.8%) 5-10yrs. 30 (7.3%) 13 (6.1%) 43 (6.9%) 10+yrs. 21 (5.1%) o 21 HOUSEH tant act examin of more contam Howevi homes attestin At from oi years f O' associ. 15 (4.6 abnorr T titles v while (fibros most which opacit antly t TABLE " 326 Irx House COfT Comp H-eM% tm 2?- .- v*.' . * -- tan. active daily household examined. In only 10% was amp'oymem. of the asbestos attesting to the persistence of asbestos in the home en 20 years already exceeded 30 *" 2 2 ^ aSTa!fia./eidoTmeP32S6 t S e w w e d ia d sTm.lLr abnormalities. The prevalence ol TABLES. Chest X-ray Abnormalities1 (1973-1976) Among 626 Household Contacts Ot Amosite Asbestos Workers And 326 Comparison Individual^ -- Total number examined Number with abnormal x-rays Household contacts 626 225 (35.9%) Table 7 summanzes lies were the most common No pleu - a|_ificat;on Dresent. Pleural thickening I ihile 8.1% of the study participan rnmoared to 1 2% of control films. The ibrosis) was seen on 19% ot the # smal l irregular opacities tost common abnom aiit/ among trols population nad small Irregular were statistically sign,r,o mtly different. . Household Contacts of Amosite Asbestos Workers and TABLE 7. Chest X-ray Abnormalities Among 626 326 Individuals in a Companson Group Pleural Total thickening examined present Pleural Pleural calcification plaques present________ present Irregular opacities present Household 626 contacts 119 (19%) 50 (8%) 106 (16.9%) .fi I n i ! i s-: 1 r 150 ANDERSON ETAL. . .J abl .8 further examines the prevalence of abnormalities. The predominance of pleural disease is sinking. Of the abnormal films, 54% had only pleural chanqes c S d S t' Tn w 3% o f ^ Sin i th P'eural and Parenchymal abnormalities were^ecorded. Tables 9 and 10 demonstrate that not only was pleural disease more prevalent, but when present was more extensive. Of the 106S showing s n S pie S rifth 0Pi f CI-,eS' nly 2 (1'9%) Wer classified as having profusion category 2 47 (39 h T f "h *S ef a? J ve- fth e 1 1 9 films showing pleural thickenTng,' S h - g l S L S 10 TM mm anS 12 had vefy mlck f,leura TABLE 8. Classification of 225 Abnormal Chest X-rays Of Household Contacts Of Amosite Asbestos Workers Type of abnormality present Plejral thickening only Pleural calcification only . Pleural plaques only More than one pleural change Total with pleural abnormalities only Irregular opacities only Irregular opacities and some pteuraJ change Total with abnormal findings Number 64 16 18 22 120 53 52 225 Percent (28.4%) ( 7.1%) ( 8.0%) ( 9.8%) (53.3%) (23.6%) (23.1%) TABLE 9. ILO U/C Pneumoconiosis Classification of 106 Household Cohort X-rays with parenchymal abnormalities Total with irregular opacities 106 1/0 43 (40.6%) 1/1 58 (54.7%) 1/2 3 (2.8%) 2/2 2 (1.9%) rtnei T 9 occupational groups exposed to asbestos, two factors, duration from onset of exposure and duration of exposure, have been associated with an increase in prevalence of x-ray abnormality. The same relationships were seen in the study fPrnmConc1fSo 7 ab eS 10 and 11 show the distribution of abnormalities by duration of xpos>ir (TM ore than 30 years and less than 30 years). For all the v M rc T S n ^ r df SCnbed' thPrevalence was higher among those with more than 30 T h t nro ^ exposure. The greatest difference is seen for pleural calcification. I L m^ i P. W, on9[ duration from onset had a three times higher prevalence of pleural calcification than that of the group with less than 30 years from onset household exposure to asbestos 153 ing and Duration of Index Worker Exposure in 626 Household Asbestos TABLE 12. Pleural Thickening Contacts____________ 1 yr 10+yrs. Total Number examined 263 299 41 23 626 8 (34.8%) 119 (19.0%) TABLE 13. Distribution Of X-ray Abnormalities Among Household Contacts By Their Relationship To The index Asbestos Worker^------------------------------------ ------------------- Relationship Wives Daughters Sons Siblings Others Total Total number examined 626 Number with abnormal x-ray findings 70 (46 4o) 46 (23.6%) 59 (40%) 27 (35.5%) 23 (41.1%) 225 (35.9%) TABLE 14. Distribution Of Physical Pinamga Total Normal 401 x-rays Abnormal 225 x-rays Total 626 ' = 5.88 p < 02 2X2 - 7 17p < .01 ~3 -x22 = 4 25 p < -05 Rales1 ' 13 (3.2%) 17 (7.6%) 27 (4.3%) Cyanosis2 0 4 (1.8%) 4 (0.6%) Clubbing3 1 (0.2%) 4 (1.8%) 5 (0.8%) ^ individuals with abnormal chest x-ray x-rays. m i I i 'nMI i I ! : . ' ,i . - I *- % ; DISCUSSION Inorganic dusts emitted from industrial sources became a recognized hazard when Kiviluoto described an abnormally high prevalence of pleural calcification among 6,312 residents of a district in Finland in which an anthophyllite asbestos mme and mill had been operating for many years (Kiviluoto, i960). In a contiguous district without an asbestos mine, no such instances of calcification were observed among 7,101 surveyed residents. Subsequently, similar observations were made in other countries (Zolovefa/., 1967; Yazicioglu, 1976; Navratil and Trippe, 1972). Navratil (1972) studied factory workers, neighborhood residents around the workers factory, household contacts of the workers and an unexposed control population. Table 15 summarizes the results of these surveys. All three exposed populations had an increased prevalence of pleural calcifications. TABLE 15. Prevalence Of Pleural Calcifications In Populations With Different Sources Of Exposure To Asbestos In Czechoslovakia1 General non-exposed population Blood relatives of factory workers Number examined 8,133 114 Number with pleural calcification 28 (0.34%) 4 (3.5%) Neighborhood residents of asbestos factory 155 9 (5.8%) Factory workers 755 42 (5.3%) The results of our study extend the observations of these and other investi gators. Pleural and/or pulmonary disease occurring under the conditions of non* occupational exposure experienced in the home of asbestos workers is more common than previously appreciated. Radiographic examinations 1973-1976 of 626 household contacts of amosite asbestos workers found that 225 (36%) individ uals had pleuropulmonary abnormalities characteristic of asbestosis. Consistent with occupationally exposed populations, the prevalence ofabnormalities increased among those with a longer period of active household exposure as estimated by duration of the index workers' length of asbestos employment. The importance of sufficient elapsed latency time, duration from first exposure, was also demon strated. This was most apparent for pleural calcification, which was three times more prevalent among those with more than 30 years from onset compared to those with less than 30 years (10.4% vs. 3.8%). The study begins to demonstrate the time dynamics for the appearance of radiographic abnormalities after this type of en vironmental exposure. Serial observations of this cohort will provide additional information concerning the interaction of length of exposure and lapsed time from onset of first exposure. For environmental asbestos exposure, it appears that a longer elapsed time is required before disease becomes apparent, compared with direct occupational exposure. m I low-lt Se*' antiy popi medi virar rene nom Sud instE inde and 196 the) wor help wid fror PC! a/., ast in ir nec ass der site La; Re Ar Be G E t K k li- J- HOUSEHOLD EXPOSURE TO ASBESTOS 1S5 It is apparent from this study and others that for environmental and other low-level asbestos exposures, the radiographic appearance of disease is predomin antly pleural. Therefore, the presence of pleural changes when seen in the general copulation is of considerable significance and. when present m the absence of other medical causes, possible past asbestos exposure should be investigated. In en vironmental asbestosis, the classical" radiographic appearance of combined pa renchymal and pleural abnormalities is the exception rather than the rule. In addition to the now recognized, increased prevalence of radiographic ab normalities, household asbestos contact carries a risk of developing mesothehoma. Such case reports now total over 50. In a previous report we described four instances of pleural mesothelioma from among the household contacts of the 1,664 index amosite asbestos workers (Anderson et al., 1976). In a recent study by Vianna and Polan (1978), of 52 cases of mesothelioma among women in New York State 1967-1973. nine additional household contact mesotheliomas were reported and they were able to calculate a relative risk factor of 10 for residence in the homes of a worker in an asbestos-related industry. Prospective observation of our cohort will help determine the extent of the malignancy risk which attends such exposure. Household environmental contamination from industrial sources may be more widespread than hitherto suspected. Asbestos is not unique in its ability to escape from the industrial setting in quantities sufficient to cause disease in the community. PCBs lead and beryllium have been demonstrated to cause such disease (Baker er al. 1976; Rice et al., 1978; Eisenbud et al., 1949). It must be recognized that asbestos'will not remain as the only occupational carcinogen to cause malignancies in individuals environmentally exposed. As more industrial substances are linked to neoplastic and other diseases after 20 to 30 year latency periods r,s* f associated household and environmental exposure must be considered. This study demonstrates that environmental contamination from one industrial source of amo site asbestos commonly occurred and resulted in the appearance of charactenstic radiologic changes as well as neoplastic disease. We are grateful for the support of our colleages in the Environmental Sciences Laboratory in the clinical studies, and to our field survey staff, including Dorothy Perron, Charles Nolan, Rayla Margoles, Stella Przybyla, and Shirley Levine. REFERENCES Anderson, H.A.. Lilis. R., Daum. S.M., Fischbein, A.S. and Selikoff, I.J.: Household contact asbestos neoplastic risk. Ann. N.Y. Acad. Set. 27t: 311,1976. . . Baker, E.L., Folland, D.S.. Taylor, T.A., Frank. M.. Peterson. W Lovepy^a, Cox D Housworfr,, J.. Landriaan P.J.: Lead poisoning In children of lead workers. N. Engl. J. Med. 296.260-261,1976. Commonwealth of Pennsylvania: A Preliminary Report of the Dermatological and Systemic Effects o Exposure to Hexachloro-Naphthaiene and Chloro-Diphenyl. Bureau of Industnal Standards, Depart ment of Labor and Industry, Harrisburg, P.A. Special Bulletin 43. M^ rcf1 Eisenbud, M,, Wanta, R.C.. Dustan, C.. Steadman, L.T., Hams, W.G.. and Wolff, B.S.. Non-occupa tional berylliosis. J. Industr.Hyg. 31:282-294,1949. -_,nnhvin*i- Kiviluoto, R.: Pleural calcification as a roentgenologic sign of non-occupationai endemic anthophyllite- asbestosis. Acta Radiol. Suppl. 194:1,1960 __ ., Navratil, M.. Trippe, F.: Prevalence of pleural catcifiction in persons exposed to asbestos dust, and in the general population in the same district. Environ. Res. 5:210,1972. T56 ANDERSON ETAL. NeT,,hm'iSr ; I i ; L ' Th0mSS0n' H" Mesothelioma of Pteura and peritoneum following exposure to asbestos in the London area. Bnt. J. Indust. Med. 22:261-269,1965. Nicholson. W.J.: Recent approaches to the control of'carcinogenic exposure: Asbestos - The "TLV" approach. Ann. N.Y. Acad. Sci. (In press) 1979. Rice, C. Fischbein, A.. Lilis, R,, Sarkozi. L , Kon, S.. Selikoff, I.J.: Lead contamination in the homes of employees of secondary lead smelters. Environ. Res. 75:375-380 1978 t aL H^ L!liS ; a ^ S e lik o ff I.J, Short-term asbestos exposure and delayed cancer risk Proven- _ '`on and Detection of Cancer. Ed. H.E. Nieburgs. Marcel Dekker, Inc., N > . 7-943-690 1976 S * 1964 ^ ' ChurS- Hammond, E.C.: Asbestos exposure and neoplasia. J. Am*Med.^Assoc.^78fl: 22. Selif83-186,'sept11972^' E C " ChUf9, J' : Carcino9enici,y o( amosite asbestos. Arch. Env, Hlth. 25: ,0 aSbeS,0S and ma,i9nam meso,he,lomas" Y a c h | U70S; 3P 47,ri 9T6C'fiCa'iOn assoaa,ed Wlth exposure t0 chryso,lle asbestos in southeast TurkeyZOl9 6 7 " B Unlk0V' T- Babadi0V' L: Pleural asbestosis in agricultural workers. Environ. Res. 7: 287, t Sot Gillie, 1 bestos l on the increas larger t hundre differer cancer that 00 a "sma clarifie produc health recogr tion mt T N Wher mode per K to ast smok the b. due epide mone (197: in Ta lung too fc For exp* likel ' &