Document peR644BgwRObNeMppgZKexj3j

WORLD HEALTH ORGANIZATION INTERNATIONAL AGENCY FOR RESEARCH ON CANCER IARC MONOGRAPHS ON THE EVALUATION OF CARCINOGENIC RISKS TO HUMANS Overall Evaluations of Carcinogenicity: An Updating of IA RC Monographs Volumes I to 42 SUPPLEMENT7 This publication represents the views and expert opinions of an IARC ad-hoc Working Group on the Evaluation of Carcinogenic Risks to llutiians, which met in Lyon, 10-18 March 1987 1987 VINYL CHLORIDE (Group I) A. Evidence for carcinogenicity to Humana (sufficient) Vinyl chloride has been assoeialrd with tumour* of (he liver, brain, lung and haematoiymphopnietic system*. A large number of epidemiological studies'-" and case reports''*" have substantiated the causal association between vinyl chloride and angio sarcoma of the lifer. Several studies also confirm that exposure to vinyl chloride causes other forms of cancer, i e.. hepatocellular carcinoma"'1*'1"*, brain tumours"'1', lung tumours"1*''1 and malignancies of the lymphatic and haematopoietic system"'1*'11. Exposure to polyvinyl chloride dust was associated with an increased incidence of lung tumours in one study; the authors suggested that tupped vinyl chloride monomer was responsible**. Melanoma occurred in excess in one study" but has not been mentioned in others. Slightly elevated risks for gastric1* and gastrointestinal cancer (other than liver cancer)'1 were indicated in some studies, but these were not confirmed in others. I. Evidence for carcinogenicity to animals (sufficient) Vinyl chloride administered orally or by inhalation to mice, rats and hamsters produced tumours in the mammary gland, lung, Zymbal gland and skin and angiosarcomas of the liver1. Similar findings were made in more recent studies"''*, tn one, a combination of oral administration of ethanol and inhalation of vinyl chloride resulted in more liver tumour* (including angiosarcomas) than after treatment with vinyl chloride alone**. JJ C. Other relevnnl data < Chromosomal aberrations were induced in peripheral blood lymphocytes of workers exposed to vinyl chloride at levels of 5-500 ppm (13*1)00 mg/m'). Two studies reported oo negative results for sister chromatid exchanges in exposed workers, while in another study a weakly positive response was found*'. o> 3 -P* RSV 0016705 374 IARC MONOGRAPHS SUPPI EMENT > Vinyl chloride induced chromosomal aberrations, sister chromatid exchanges and micronuclei in rodents exposed in vivo but did not induce mutalion in the mouse spot test or dominant lethal mutations in rats or mice- It alkylated DNA in several tissues of mice and rats exposed in vivo. Vinyl chloride induced sister chromatid exchanges in human lymphocytes in vitro It induced mutation in Chinese hamster cells and unscheduled DNA synthesis in rat hepatocytes in vitro and induced translormation of BAl.B/c 3TJ cells and virus-infected Syrian hamster cells. It induced sex-linked recessive lethal mutations, but not aneuploidy, heritable translocations or dominant lethal mutations in Drosophila. It was mutagenic to plants and to Schitosorcharomyces pombt but not to other fungi; it induced gene conversion in yeast. It caused DNA damage and mutation in bacteria. Vinyl chloride bound covalently to isolated DNA in the presence of a metabolic system**. References IIARC Monographs, 19, 377-438. 1979 'Raxtei. P.J.. Anthony, P.P , MacSween. R.N.M. A Scheucr, P.J. (1977) Angiosarcoma of the liver in Ureal Britain 1963-73. Rr. mrd 7,11,919-921 'Brady..!., I iberaioic. F.. Harper, P., Greenwald. P, Burnell. W., Davies, J N.P., Bishop, M . Polan, A A Viana, N. (1977) Angiosarcoma of the liver: an epidemiologic survey. J. nail Cancer Inst, 59, 1383 1385 *Bailer, P J . Anthony, P P , MacSwcen. R.N.M. A Schcucr, P J. (1980) Angiosarcoma of the liver: annual occurrence and aetiology in Ureal Britain, fir. / ind. Mtd, J7, 213-221 'Baxter, P J (1981)1 he British hepatic angiosarcoma register. Environ. Health Prrspea, 41,1IJ-116 Falk. II. Herbert, J.. Crowley. S . Ishak, K O.. Thoms. LB, Popper. H. A Caldwell. G.G. (1981) Epidemiology of hepatic angiosarcoma in the United States, 1964-1974. Environ Health Prnptct ,41, 107-113 'TMriault. G. A Allard, P. (1981) Cancer mortality of group of Canadian workers exposed to vinyl chloride monomer. J necup, Med., 21,67| -676 Vianna, NJ , Brady, J. A ACardamone, A.T (1981) Epidemiology of angiosarcoma of liver in New York Slate. N.Y. Stale J JMed,6, B9J-B99 Weber. II , Reinl. W A Greiser, E. (1981) German investigations on morbidity and mortality of workers exposed to vinyl chloride. Environ. Health Perspect , 41,95-99 'Forman. I) , Bennett, 8.. Stafford, J A Doll. R. (1985) Exposure to vinyl chloride and angiosarcoma of the liver: a report of the register of cases. Br. J. ind. Med, 42, 730-733 "von Greiser. , Reinl, W. A Wetter, It. (1982) Vinyl chloride exposure and mortality of German chemical workers in compaiison to mortality of non-expnsed chemical workers and PVC workers tGet.) Zhl Arheitsmed, )2, 44-62 "HeMaa*. S S , l.angard. S L A Andersen. A (1984) Incidence nf cancer among vinyl chloride and polyvinyl chloride workers. Be J. tnd. Med., 4l. 25-30 "Gokel, J M , l.kbezeit, E. A Eder, M (1976) Hemangiosarcoma and hepatocellular carcinoma of the liver following vinyl chloride exposure A report of two cases. Virchows Arth. Pathol. Anar. Hittol. 372, 195-203 "Bonneion. G . Champetier, J . Fouinet. i , Guidicelli. H . I.egrand. 3., Duprd, A., Hottein, M , Marly, F A Pahn. M. 11977) Angiosarcoma of the liver and portal fibrosis in vinyl chloride workers. Two cases (Ft.). iVoi/i Ptrsse mdd.,6, 735-742 VINYl. CHLORIDE 373 "Puech. A -M , Fournet, A . laulherc, I.., Faure, J , Cau.fi. A Mallows. J.-M. (1977) Study of hepatic lesions seen in 5 subjects exposed to vinyl chlotide. including .3 cases of angiosarcoma of the liver (F'r.J. Arch Mat. prof., Jd. 787-795 "Rfty, J , Lambert, R A Pialat, J. (1981) Medical surveillance of persons exposed to occupational toxic compounds with late or carcinogenic effects. The llth French case of angiosarcoma of the liver in a PVC worker <l r ). Arch. Mai prof., 42. 403-406 "Pialat. J , Pasquier, B . Pahn. M. A Kopp, N. (1979) Hepatic lesions cawed by vinyl chloride monomer. Study of eight clinicopathologicalcaseilFr.). Arch Anat. t't'tof patho!., 27,361-373 "Ghandur-Mnaymnch, I.. A Gonraler, M S. (1981) Angiosarcoma ol the penis with hepatic angiumas in a patient with low vinyl chloride exposure. Cancer, 47, 1318-1324 "Kobchwrti. D.Ielbach, W K , Ijackner, K. A Hcimanuti. H.|l9tt) Angiosarcoma of the liver and hepatocellular carcinomas induced by vinyl chloride (Get.) Fottuhr. Rirntgrniir., 134,283-290 MVianns, N J, Rrady, J. A Harper, P. (1981) Angiosarcoma of the liver: a signal lesion of vinyl chloride exposure. Environ Health Perspect., 41, 207-210 "Chiappicto, C., Brrtaizi, P A . Baroni. M A Masini, T. (1917) Hepatic angiosarcoma from vinyl chloride. Report of a new Italian case. Med. Lav., A, 333-563 "Janet, DB. A Smith, PM. (1982) Progression nf vinyl chloride induced hepatic fihttvsis t angiosarcoma of the liver fir J. ind Met', 39, 306-307 "Evans, D M.D., Williams, W.J. A Rung, I T.M (1983) Angiosarcoma and hcpaincelMar carcinoma in vinyl chloride workers. Hmnpathobgy, 7, 377-J88 "Mahoni, C., Clint, C . Vicini. F. A Masiru, A. (1984) Two cases of liver angiosarcoma among polyvinyl chloride (PVC) extruders of an Italian factory producing PVC bags and other containers. Am. J. ind. Med., S, 297-302 "Louagic, Y A .Gianeflo, P , Ktstens, PJ. Bonbled. F A llaol, J.G. (1914) Vinyl chloride induced hepatic angiosarcoma Br. J Surg, 71, J22-323 "Langbein, G , Permanctlcr, W. A Dietz, A. (1983) Hepatocellular carcinoma after vinyl chloride exposure (Ger). Dtsrh mrd Wochentchr, 108, 741-745 "Cooper, W.C.(I98I) F.pidemiologk study ol vinyl chloride workers mortality through December 31. 1972 Environ. Health Perspect., 41,101-106 "Buffler, P.A., Wood, S., Eifler, Suarez, L. A Kilian, D J. (1979) Mortality experience of workers in a vinyl chloride monomer production plant J. oervp. Med., 21,193-20J "Fedotova, I V (1983) The incidence of malignant lutnouri among workers engaged in the manufacture ol vinyl chloride and polyvinyl chloride (Russ ). Gig. 7). prof. Zahnl, 4. 30-32 **Waiwetter, R J .Smith, A II.. Falk, H. A Tyroler, H.A. (1981 (Excess lung cancer risk in a synthetic chemicals plant. Environ Health Perspect., 41, 159-163 "Filatova. V.S.. Antonyu/henlo, V.A., Smulevich, V I, Fedotova. I V., Ktyshanovtkaya, N A , Bochkareva, I.V., Goryacheva. (..A. A Bulbulyan. MAf 1982) Blastomogenic hazard of vinyl chloride(clinico-hygienk and epidemiologic study! tRuss ). Gig Tr. prof. Zahol, I, 28-11 ''Molina. O., Holmbeig. B , Elolsson, S., Ilolmlund, l . Moosing. R. A Wesletholm, P (1911) Mortality and cancer rates among worker! in Ibe Swedish PVC processing industry. Environ. Health Perspecl , 41, 143-151 "Hong, C.B., Wintton. I M .. T hoinburg, I. P., Lee. C.C. A Woods. J.S (1981) Follow-up study on the carcinogenicity of vinyl chloride and vinylidene chloride in rats and mice: tumor incidence and mortality subsequent to exposure. J. Toxirol environ Health, 7,909-924 RSV 0016706 376 IARC MONOGRAPHS SUPPI EMENT 7 V.J., Hcndrikscn, CFM, Speck. A J., Til. II.P. A Spit, B.J <l9BI}Mfc*pan Dial loiiciljr study of vinyl chloride in fall, food Cotmet. Toxicol , 19, 317-337 'Hehir, R M . McNamara. B P . Melaugblin. J.. Jr. Willigan, DA.Biet bower. G. AHardisty, J.F. {1981) Cancer induction following iin|le and multiple eaposurcs to a constant amount of vinyl chloride monomer. Environ, Health Eetspeet, 41,63-72 "Maltoni. C.. I.cfemine, G.Cilibeili, A .Cniti, G ACarrcui, 0< l981)Ceicinogenicily bioarsayr of vinyl chloride monomer: a model ol liik assessment on an experimental basis. Environ. Health Pertpeet., 41, 3-J9 'Drew. R T . Boorman.G A., Haseman, J K.. McConnell.E.E.,BuKy, W.M.ft Moore,J.A.(1983) The effect ofaft and eapotureduration on cancer induction by a known carcinogen in rate, mice and hamsters. Toxicol appi Pharmacol, 69,130*130 "Suzuki, V. (1913) Neoplastic effect of vinyl chloride in mouse lung - tower doses and ihor1*ierm eaposure. Environ. Ret. J3,91-103 "Grolh, D. It ,Conte, W.B., Uitand, B M. A Hornirng. R.W. (19111 Effectso( aging on the induction i of angiosarcoma. Environ. Health Pertptc41, 31-57 "Radike, M.J., Slemmer, K L A Bingham, E (1981) Effect of ethanol on vjnyl chloride carcinogenesis. Environ. Health Pertpeet., 44, S9-62 "MJIf Monographt, Suppi 6, 566-569, 1917 ii i '34 ,lancet a?*:-. 3. :;*6 Occasional Survev GENETIC RISXS OF VINYL CHLORIDE Peter F. Infante Joseph K. Wagoner Anthony J. McMichael Richard J. Waxweiler Henry Falk Dtvuton ofSurenilanet, Hazard Ecaiuatwns and Field Siudiet, national Institutefor Occupational Safety and Health, and Bureau of Epidemiatog/. Center for Dictate Control; and School of Public Health, Lnicerstty of Horih Carolina Summary A study of pregnancy outcome among wives of workers exposed to vinyl-chlor- ide monomer ,'v,c.m.) indicated that, in comparison wuh controls, there was a significant excess fetal loss in the group whose husbands had a primary exposure to v.c-H., whereas no differences between the groups were observed before the husbands' exposures. The difference to fetal death-rates for the post-exposure comparisons was a reflection of a greater fetal loss associated with the wives younger-aged husbands. The significant excess did not seem to be the result of bias from interviewers, re spondents, nor from women who had experienced chronic abortions weighting the results, These findings, in conjunction with the demonstration of a mutagenic response via microbial test systems and with observa tions of significant excesses of chromosomal aberrations among workers exposed to v.c.m., raise scientific and public-health concern for the possible genetic risks of v.c.m. to man. In the past year, several reports have indicated that vinyl-chloride monomer (v.c-H.) is mutagenic is micro bial test systems.*'"1 v.c.m. metabolites also have in duced mutations in mammalian ceils.4 Likewise, reports from four countries have shown an excess of chromoso mal aberrations is lymphocytes of workers exposed to v.c-M. compared with controls.'-' However, Purchase et al.T have stated <though no animal data were presented), that the muugemc effects of v.c.m. expressed as chro mosomal aberrations in lymphocytes in humans do not occur in germ cells in mice; they concluded that the potential danger of mutagenic effects on the fetus via sperm seemed unlikely to exist. In a study without con trols, Selikoff observed fetal death-rates among wives of v.c-M. workers that ranged from 7 to 14 per 100 preg nancies.* These rates appear to have been higher than expected.14 To develop further data on this question, pregnancy outcome has been studied among the wives of workers exposed to v.c-h. All current v.c.m. polymerisation and polyvinyl-chlonde (p.v.c.) fabrication workers were in cluded for study together with a similar number of cur rent rubber workers (8^ of all such workers) selected from work areas relatively free from known toxic materials and matched as a group to the v.c.m. workers by age. Group-panidpation rates ranged from 62 to 77%. Data for the wiva of v.c.m. polymerisation workers (primary v.c.m. group) were contrasted with data for the wiva of p.v.c. fabrication and rubber workers ("controls"), who were known to have bad very low or no v.c.m. exposure, respectively. A total of 95 v.c.m. polytcer.sa::cn and 153 rubber ar.d p.v.c. fabri cation workers were interviewed. Paternal age, preg nancy outcome, and estimates fsr the time of concenter of all prsgr.acctes were ascertained by inrervtr* :r. Oct ober, 1974, frerr. caies estptcyed at a rjbeer manufac turing, p.v.c. fabricating, and v.c.m. poiy--er.tir.g facil ity. As pan of a larger survey cf worker health, date at first employment in the 10b categories was determined from company records. Mean paternal age, total number 01 conceptions, total number of fetal deaths .defined as any product of conception not born alive., and fecal deaths per 100 conceptions w ere then computed for each group prtor to and subsequent to the worker's date of employment. No interviews were conducted with workers' wiva and no data were obtained concerning maternal age, except indirectly through paternal age. Since fetal loss is known to increase with ascending parental age, the fetal death-rates for the primary v.c.m. exposure group were age-adiusted to the control group. Table I shows the age-adiusted feta! death-rates for wiva of the primary v.cjw. exposure group venus the control group, both pnor to and subsequent to each group's respective exposures. Among pregnan cies occurring pnor to exposure, fetal death-rates were 6-9<e for the controls versus 6- I'c (age-adiusted) for the primary v.c.M. exposure group. These rata were not significantly different by Maoiel-Haenizei Chi-square testing.11 Among pregnancies occurring subsequent tc the husband's exposure, the difference in frequency of fetal deaths between groups was significant at p<0-05 (^1=4-00, df=l).n Although the underlying dis tributions differed, mean paternal ages were virtually the same--30-4 venus 30-2 years. The significant dif ference between the groups subsequent to exposure was a reflection of a relatively greater fetal mortality-rate as sociated with younger-aged husbands in the prunary v.c-h. exposure group. Among pregnancies occurring subsequent to exposure, the fetal mortality-rates associ ated with husbands 30 years of age and older for the pri mary v.c-h. exposure and control groups were 9/69 (U-O^) and 17/142 (l2-0fe), respectively; whereas, for TASLI I-----W1AM P.VTTB.NAL AC|, OF PUGMANCItt, AMO FITAl OtATW-KATtl SCCOft&lMC TO HtlSAMD S r.C. ISPOSCM -- tO HtUbOBtd t riMIk'l, Nunttgr n fimiiiA Mean pitmAl ift fit canctption vr. Number af fetal ilraiba amenf -r*a N umber of presnAMos Afr-adiuued fetal JeaiBVlOO prcfU a twMM > ofnuri Number of fanuLm .View paiunii fife ucftocepuofl ft.. Number at fetal Qeailu atnobf ia SumMr prtpAAOCI \p-adiuticd fetal Scanty 100 Jrt|l Primary "Cantmu'* * cj. apeeureT 95 :j 0 11 159 i9 24 4 IS 14| 10 4 24 2?J 4-1 JO-2 21 1)9 15 It -Rubber and*, v c. tabnsuoo orl0i. t* c. pciyrneriAAnpo wrtut IfUica ate-adiuiied 10 "oatmi" paup pucrul aft Oiauibuuoo. 'Subsequent to buabaod't eipotur*. the tasucMv w fcul dcatha imaa , waa ufiuSsnUv peaier ia the primary X.. ctpeauie ptw thaa m the "* tmU " r<0 05> or is the ud froup pnor to auabaad'a aapmui* ,<0 02l PF j|t*adiuaia efci-aqwn inunf." RSV 0016707 jHt LANCET, APRIL 3, 1976 735 Ttfti JJ-----MIA* PATEUUL 40K. NTMFW OT PUONANCBS, MB KTAL pUITUTII 1K0ISM TO HClMm't *. (WOfVU UCICDIH puauiicat or wbmek wtth 3 mu gum ferences in recall. Tbe interval, however, was estimated to have bees about two yean leas for controls, stiffen ing that, if a bias did exist, it would have been towards 5* -- Primacy a greatff ascertainment in the control group. In some "Comrata"' v.cjt. fipeaant cases, the worker failed to indicate the ages of his png* IO enjootp', exfonre Meta patooal >p iiniaieptioan.l susoer at fetal deatht asoe| wi,a StmMraf Apt-adnmm feial itatitaalOO prapX SntMeaeai to eaioead a eepwera: vlcae patmai apt at eoeetpuop ,yt.) Susan of fetal Jeatht aatonp wirs 9TTfn4000 Apr-adiuatcd fetal death* 100 pfep4 2J-0 1! 15* 69 )0 2 It 2d) 6-1 26 ) 9 141 )-l )0-S 14 120 10-1 children and in other cases be was unable to recall tbe approximate of his wife's abortion; therefore, the data were analysed to determine the distribution of fetal death-rates among the respondents in each occupational group who did not complete the interview properly. The difference in fetal death-rates between groups was very slight. Finally, the workers may have been subject to bias resulting from prior knowledge of known hazards of vinyl chloride. However, tbe workers themselves did not always know into which of our employment categories they were being allocated. For example, several p.v.c. fabrication workers who were included in the control AubOn tod mx. feMimuee varaai. *,x. prim--u-- *or*em Idw ef*4diused tr "eoamr ptinal aft riiuibtitioe. group thought that they had a primary v.c.m. exposure as a fabrication worker. In addition, the quations regarding pregnancy outcome were contained in a much husbends leu thu 30 veers of age, feial mortality was larger interview-questionnaire, the results of which 14/70 (20-0%) for tbe primary v.c.m. exposure group demonstrated very few significant differences with oo compared with 7/131 (5-3%) for the control group consistent bias for tbe parameters ascertained between ` (these data are not shows ta tables.) the workers with a primary v.c.m. exposure, and tbe Furthermore, intragroup comparisons indicated an other groups. This observation as well as several others increase in age-tdiusted rates for the primary v.c.m. presented above tend to support tbe validity of the exposure group from 6-1% before exposure to 13-8% study. subsequent to the husband's exposure. This difference In summary, a significant excess of fetal loss was also was significant, p<0-02 (yJ5-51, df=l).u Similar observed among wives of workers following exposure to comparison for rates in tbe control group, 6-9% versus V.CJA. The excess did not appear to be tbe result of bias 8 8%, indicated no significant difference. from interviewers or respondents, nor from women who To determine whether women who had chronically experienced chronic abortions weighting the results. experienced abortions might have weighted the results in Several mechanisms by which such fetal loss may arise favour of a higher fetal death-rate in the primary v.c.M. are suggested. Either fetal or maternal toxidty or germ- group subsequent to husband's exposure, pregnancies of cell mutagenesis in the mother through indirect v.c.m. i women who bad more than two abortions were elim exposure from the father might be considered, although inated from the analyses and tbe data were recalcu these mechanisms --"* highly unlikely in view of the lated to determine whether or not the trend was main highly volatile nature of v.C-M.1' Then the findings of tained. The decision to exclude all pregnancies among the present study are taken in conjunction with the prior families associated with more than two abortions was demonstration of a mutagenic response via microbial made without prior knowledge of how these families test systems and observations of significant excesses of were distributed among tbe exposure categories. Tbe chromosomal aberrations among workers exposed to data in table ti show that the trend was maintained. V.CJW., the leading possibility is germ-cell damage in the Prior to exposure, the fetal death-rates in the control father through diren v.c-m. exposure. The increased and primary v.c.m. exposure groups were 6-9% and fetal monalily among wivo of workers subsequent to 3-1% (age-adiusted), respectively, whereas, after expo- v.c.m. exposure now raises serious scientific and public- ' sure, the rates were 6-8% and 10-8%, respectively. Sub health concern for the possible geneuc risks of vinyl sequently, data were eliminated for pregnancies of chloride to man. women who bad experienced, firstly, more than one abortion, and, secondly, more than three abortions, and Requests for repnsu should be addressed to P.F.I.. SM.O.S.H.. Post Office Buildup Room }13. cimmmii. Ohm 4)202, L.S.A. each ume the tread was mmniwH So io rates aznuHCES for controls were observed, whereas a 2-3-fold increase 1 Banach. H.. Mtleviclle. C- Moalsaao, R. Im. J Cmrr If). IS, *14 1 was observed in the primary v.c..H. group subsequent to : Lopncno. N.. Strata. R- VtrancelU. et it. .Muiauea An. id ihe prat, . r exposure. 3. U.. IM. * ffimrl C-. tTfhemwtr. C A. Amt* 19*4. J, To determine whether differences in fetal lots might 4. Huhema. . Barlach. H.. tacta L la[..7 Caaeee. ITT), 14, 4)9. have been the result of one or two interviewen weight ing the results, the data were analysed by individual in J. Duenmaa. A- Hmchbm, K-. Sehkx^. 1. J. AIhmom Aa,. 19TJ. St. 143. 6. FunCraMO. F.. Lassen. B-, Lmdtien. J., Ehiuearg. 1_ Stiara,ta. A. T. OttBnasColhar, S. Ltnibi. If?), u 45. terviewer. Tbe results demonstrated a general trend for ' PuiOam. 1. F H.. (Lehaeaaoe. C. JU Aadenaa. D. ,rri. 19TI, u. 410. each interviewer to report a higher ascertainment S HiDantd. t_ Thita-Evmm. E- Lapubliatad. 9 Selikaft. t. J., N.l.E.H.S. Caafoeact oa Puri* Health Isipliceiiom of Cos- among v.c_h. polymerisation workers than among the POM9U of Platte .Haauiaeiua*. Pinchur*. Sonh CarouAA jut*. lf*4 control group. Further, the possibility was entertained that the inter 10. lofaate. P. F. Am*. .VI'. AaA. ia. ii ihepra*:. 12. Shcpira. S.. Jonet. E- V.. Deasa. T. M -Wi/4*4 C 19*2-40,1. 12. Mantel. N., HicbuD. S J Min. C,np lor 1959.22, *19. val between the date of interview and tbe date of fetal loss might have mnuenced the results through dif 1) toned Stem Emvooseatei Praieeuoa Apenes. anritnp and Mal,wt of icmr iquc tuMtaaeek talk in vinyl chloride. Contract no. 0441-2446. laa. 20.19?4.