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7 8 7 0 19 REQUEST .-OR APPROVAL TO RELEASE PROPRI E T AR V TECHNICAL INfORMAl'ION 1 Risk of Angiosarcoma in Vinyl Chloride Workers as Predicted freni Studies in Rats P. J. Gearing, C. N. Park, and P. G. Watonabe B-/ N . .. N . ------- -- -j'.--------------- dlix-Lcnlnny ,and- An died J?hnnmcolooy------------ .\||D >-A,f.NT<- P `,1'. GS..'- rs = . F P - r-..rrs ,), *. *ted ofrrwTs or Pufu<CATfo*<$ M..! J *iit~ok ron ; > n r -1 a F Or * S v aiuSCRi11 * K. Groves T. Torkelson R&S 101256 P. J. Gehrinj 1803 ii. f O'.i Midland .'I > A! u" A. > V ! , f 4- t D l f' A ' ! IF f * A -*. :'* * age tl- i`E r'it'rf:tp 'o Tox Res Lab HS.E1R 15 May 1978 636-1089 Rush *- r` t * [ *'' r16$TMh\O\oLL^/iQ8 3 .copied is- .midland ?j " 16 . ' s . n R&S 101257 bv P. J. Gear ire, P. G. V.'a tar. a bo Toniccioay Research Laboratory Hea 1 th and Env ir err: onto 1 Research Dew Chen i ca i U . S . A . Midland, Michigan 43640 ana C. NT. Par Computations Research Dow Chemical L' Labora to c: n 64 0 Abbreviated Title: Vir.vi Coloride-Riss Assessment Send Correspondence to: Dr. P. J. Gehrinq Tcnicoloqy Research Laboratory Health and Environmental Research Dow Chemical U.S.A. 130 3 Bui Id inn Midland, Ml 43040 R&S 101258 R&S 101259 RISK C" ANGLCGABCOMA IN VINYL CMLOLILC WOr.KMI'S AS PBNDICTLD FF.OM STCDIF3 IN RA. 73 introduction Exposure of r.its (Mai tom and Lefemino, 1975} ana man (Creech and Johnson, 197-1; Taber3haw and Ga:fey, 1974 ; Makk, o_L a_l, 197(3; and Fox and Collier, 1977) no vinyl chloride (VC) has been associated with the development of hepazic ar.y icsarccma , Numerous studies in rats indicate than it is not VC per so which is responsible for production or an;icsnrecma but rather a reactive metabolite formed from, it in the body (Bartsch, ct_ a_l, 1977; Barbin, et aj^, 197r; Kappus et al, 1970; Malaviolle, c_t rvl, 19. Watar.abe, 1977; Bclt 91 rlc 197 5; and Bolt, et al., 1970) . B ictrans formation of VC in rats is a nonlinear process occurring in accordance with Michaeljs-Menton kinetics: 1) v = VmS/Km + S (Watanabe, cjz a_l, 1976a, 1970b, and 1970c and Bclt c_t ol_ 1970). In this equation, v and Vra are velocity and maximum velocity, respectively, for the bictransform.at ion or VC expressed as ay equivalents VC metabolized daily. S and K m are the concentration of VC being i".haled and the Michaolis constant expressed as i.y VC/i air, respectively. Utilizing the foregoing information, Go'nriny, e_t o_l (19/3) revealed a yood correlation between the probit percent incidence of angiosarcoma in rats exposed to varying concen trations of VC, 4 hr daily, and the amount of vinyl chlorice biotransforned, Vv, yg equivalents VC n*' taro I i ::cd ;jor day. Tho probit equation is: 2) Probit Percent Incider.ee - -1. 62 0*1. 5 4 3 Lea v. This correlation substantiates further the hypothesis that tho induction of ana iosarcce.a is attributable to a biotransformation product of VC, not VC per sc. R&S 101260 Hypothesis ir.g that the bictrar.sf ornati or. of VC is rotates directly to body surface area, Gehrir.q, e_t a_l 1973 deterr.inec th.at the amount of VC transformed to a reaezrve torn by nan on a mass equivalent basis tc rat is: 167 5 :,c 'hr P.c;/:. 3) V ..c/3 hr 800..g/ . t- S,,a, Utilising this relationship together with the ferogeing prebit equation, it was dnternir.ed. th.at ir.cider.ee of hepatic ar.giosaroona in workers exposed to 200 pun should be approximately 11. This incidence is 50-fold higher than that experienced (Fcx and Collier, 1977). Various plausible explanations were put fort!: to explain this difference including greater sensitivity of rats and. inc reus ing latency for developner.t as v decreases. One plausible explanation not mentioned was that in worker populations studied to-date, nnny were exposed for only fractions of their working life. Furthermore for some, the -3- duration since ir.iti-i exposure was likely insufficient for dev elopmor. t of clinical do roc table disease. Recently available is a ccnprer.er.s ivc epidemiciogical study'*' entitled, "Ep'iuemioloc ical Study of Vinyl Chloride 'dor he r s , Final Report". In this study, reasonably detailed infermntio: on 10,173 workers has been obtained for duration of exposure and loosed time since first exposure. Thus, much better information is available now to assess the reliability of the me del of Gearing et a_l, 1973 , for predicting the incidence of hepatic a r.u rasa reema in nan utilising data COiitlCCC'J n rats. This assessment is reported here. In auJ i hr00 other models rcr estimating the incidence have been used for comparison of their reii_oixity for predicting the incidence being experienced by workers exposed to vinyl chloride. R&S 101261 Prepared for Manufacturing Chemists Association, 1825 Connecticut Avenue, N.W., Washington, D.C. 20009, Prepared by equitable Environmental Health, Inc., G000 Executive Dlvd, Suite 303, Rockville, Maryland 20352, January 1978. R&S 101262 1- - ML i'HOCS Four models were selected co analyze their reliability for calea 1 a ting the incidence of hepatic angiosarcoma in rats as function of ,.gVC cquiva 1 an metabolized daily by rats exposed 4 nr/day 5 days/weoh for one year. These models were as foilaw: A) Frob it % Prohit % = a + b(Log v) = -1. 6 2 5 i . 5 4 3 (Log v) 3) Linea: % a + b(v) _? 1.43+0.339 x 10 "(v C) Linear Forced through Oriy. I * bv = 0.3565 x 10~2(v) D) One-Hit Model (Cancer Assessment Croup, National Cancor Institute) % = i-<r-i(v) = l-uxp(-0.38 >: 10"4 :< v) } 100 l'ho constants given for the preceding models were t-.otermined by linear regression analysis and represent the best fit of the data for the incidence of hepatic ar.g iosur coma versus the amount of VC metabolised daily in rats exposed to different concentrations of VC (see Gehring, e_t a_l, 1978) . R&S 101263 The data used to dor ivn cha constants arc given iTable 1. Using the equations derived for the models, the trod 1 ctoe incidence of anaiOoareema for tho groups c: rots exposed to different concentrations of VC wore co leu In tec:. Those results arc shown also in Table 1. Ail four models overprcdict the incidence cf hepatic angio sarcoma in rats exposed to 10,000 ppm VC. This is as expected because this exposure caused excessive mortality unrelated to development of ar.c iosarctma . With respect to the predicted versus experimental incruer.ee of hepatic angiosarcoma experienced by groups or rats exposes to the remaining concentrations cf VC, none o: the tour meders is unequivocally more reliable than any other. Thus, any one cf the four models represents adequately the experimental data, Since no clear preference is discernible, all four models will be used to predict the incidence of hepatic angiesarcemn experienced or to be experienced by workers exposed to vc. \ . *v I*. >. . .* v* . o .* \. . *.j . / . 8 c_ t. r. r *o * . rvs: '.'jt to the: r j'.c-jo vor.-.ers r. r 1u d o 9 5.1'. o: t h e 19 , - * i the rc-emin. ram r.ct n .orie eoneontrn mens ot vinyl chloride tc which i.;._.j-. workers had beer. exposed were nee yuant. Luted, except su:. ^ vC ^ . v a . nnc .ii...\/ "ivu. u..> a.,e lc.\ ^ j ^i .'vs . 8 . o t::t-v. : :xtoU-U'. virxuo (TV.") c:;;osi::o roec :c by the ien:i Conference of Covernmonta1 looser Lai Hyc i on', s rs (ACG:::) :r:;r to 197 2 war. 5C0 pen and subseauont7y 200 per.; until -id.atiox of the Cceuya tior.al Safety an.' health Ace ? ta xaa r 1 cf 1 .: s a Lha:: 1 m ; r. 1971, it is as '-urr.od that evo: there c.x yes or or. subjectively deemed lev wore h i y h . mdeed, it : s reasonable to cm you t the TWA exposures of 200 ppm and create:' for 8 hoars verc ocutter, rather than the exceptions. R&S 101264 T.sb l c i .:c:. Lets tho averay o theoretic o f b 1 i' tra::.". f or:r.u tier. products o L' !< | - 1 .*u to 20 0 or 5 00 ppm for 8 hr via L U l* l he fra etii-r ol their work my lif oc::\\ :vd . Vr.e ucr.or., v, a r.ex nr esse. l: j, 1 c l a Led from, ca_u.it Lea 3 yiv~n in t b*/ t:\'a : r.;U tier, of an ar. r.u;:r.ed 3 3~year wh i c;; , ;; c are ceeurred. i"5 "* 1 1 * d > a o r,' : '0 hr a: . n trod uc tier, mu 1 tie lied ::.;V : r.._: estimated the i;at: ecu i v a L : n t. daily doses cf hiotrans- forma t i an products of VC rcceiv- i by various sue.;roups e: :vi77 workmen ex: 'red to i. . 0 0 -- v; :::u::j:cu me : uor.ee o: :u ::.i e i : a r.u : can reema :, ^ C [. 'w m to L`, / Table 4. Foam i na tion of the data ir. h i s * *. i ' ' " V 1 c ` ' *1 * *> 1 ^ 1 ,to and 0 ov...rosLimaro the in eider, C : -j tic a r.c i o s a r,: c r.\ * e:::: o; fenced bv these workers while Model r un.ivi'os t i.na tos the incidences. Me..: vis C ana C nay cvorp:.'edi.c c LeeaUiO tr.ey do not address either the orryrnncio bictranr :urmatier oi VC or repair o: the looi-r. leading to development ci u r.:: i esa rccr.t hot:: oi which are likely to be distributed normally in human or animal populations or because tin: tine-we i :ktcd-avi rune ex:osures for o i\. a hi > o - e then 2G0 When a TWA of 2CC ppn is utilir.ee. to represent the atmospheric concentration to wh :ch those workers wore exposed, t.-.e predicted influence or ana: esu re :ma e: 10 cases as in.; Model A compares with that ex per i on ce J , 5 cases.. For a sier.ificant number of workers, the time elapsed since initial exposure has yet to reach 11 years, the shortest tine needed for d eve lea: nor. t of ana msarccma in 1 of 5 of the afflicted workers, Table 2. Thun, it may be anticipated that a few additional cases of hepatic a ::a i era ream will occur :h is population. It is oo:a f or u i n : that an epidemic oi oases, as ::as been envisioned bv seme, is not to bo anticipated. R&S 101265 v: 1.1:0, t.n-' 0:: : "r : :::i: a: t: " t a a: ,a r Safety and health Act standard. T: .so eradiations arc shovr. in Table 5 lc: ail :ou: Models. R&S 101267 Medals C ant: L prod i an incidence comparable to that experienced by vorxors exposed to mush higher levels, agar: inndeuuacv because of overuredic tier,. Xc.::i li, although u lixrar -cool, prodic sera resuon.se a: 03.7 gum VC. Thu:, exposures to levels be lev: this are net ureuictoa to in.auco hematic ana icsarcorta . v/hat appears to bo the ruest reliable node 1 (Mode 1 A, j) , t..o 1.. .bonce of horatic ana iesarccna isvl.j x 10 , or 1.5 lusen. in 100,000,000 workers. It is 3i 1 atA- . L i l> us0 of Medels A,- c, a nd D to predic t the i: ic ice nee of he:patie a no:osa rcoma in wor . ' *" c. onposed to 1 ppm VC assumes r.o t'nresiiold or even an inf iv.'C. *- ion. point in tile dose-response curve. A . J ..'-.ary, the use of ..liraal data fur the assessment or 1 s n humans exsesud :o a chemical is not as mvstical as ntiyL -- ' ,* . e* *_ assumed. Dose-lvisviiso data for the induction ies.treo:r.n m rats exposed to various levels o: VC b i c trails forma t ion data have been J ultoJ. to to, roliobly, tho rij> or* .i*;velopir.j xtajIc- Sui'ccr.^. i:%. orxo*i.s ox* oxoo to V 0 . . i c - . . ,n j...t_ *-i- v*- ") `i ^ "V * ;ou_j oo us*, x ; :\ z:\-j axxo jsr..v:'*; oi r: jc: ^-xxo^uro to \f*r <=i \ ' s.L' r : R&S 101268 s 1) herein, A., n. ,;j i i , I!. , i.r. ; y , e. , ~ a a Mn lavei lie, Mcr.:osr.r.c, P.. , ar.J L :vor-:r,i jrjGcr.o-'.T.odu tod to me.t;:cn : frcrr! vinyl brc:ni Je and vinyl chlcri. A i a: : .y a . F. -5 . Ca:r.:r.. , 0 7 , 5 9 6-603. (1973) nr. a F'Olt, ii. M., v;ai:i, H , K.iu fro. uc . -t w , , _ . t t\ , , aaa holt, w. (15' j ) . , /V- - i/ MoLaco: :;r.i c: l vinyl chlcri, !o i :r vitro and in vivc. I'no^, Vci 52, 151-165. to )j o x ,_ , n * .*1. , knee..3, t!. , *j a o n e r , . , ana l50x_, A . (107fc). D i :;:~os i t ic r. of (i,2-^C) vinyl chloride in the rata. Arc::. Toxical. 35, 153-152. )) Creech, j. l. ana Jehneon, M. N!. (1975). Ang icaarcoraa oC liver in the nar.ufacturo of polyvinyl chloride. J. Occur). Med., 16, 150-151. 5) Fox, A. L. and Collier , P. F. ( 1977 ) . : '.urea 1 i ty Oxter ie i".co of worker:; . x pen od to vir.yl c: ; ioriJe rr.on in the : uanufno tare of t .'Olyv i:v.1 chloride in Croat H Frit. J . Ind. Med., 3-1,, 1-10. R&S 101269 fi 30 e </) 6) .'i r _ / i e * , n i `ji,1 f P. Cj . , i* ro o C. (1378) Rocoiu tien cf do no-re.:;.on.re toxic:ty t e r chemical a re.pair inc metabolic jj t iva t ion: Bxnm :.'lo-"vinvl chloride, Tcxicri. Ax ml. Pharmacol. {I cross) 7) Kacpus, II. , Belt, H. >i. , Buchtor , A., and Beit., W. (1976) j^ Liver m.icror.mal uxtake c: ("'C) vir.vi chic::ice ar.d trir,,sf err.iaticr. to croteix alkviatixa metabolites in viere . To:-:: cel. .-Vet I. Fhnrmicei., 37, 8) Me:-;:-;, L., Dclnoro, F., Creech, J. L., Ogden, L. L., Face 11, L. H. , Songster, C. L. , Clanton, J-, Aohr.son, M. N., a::.i Christeghorscn, W. H. (197 6) . Clinical and :::or choice ie effects of heretic ang icon'.eoau in vinyl chloride workers. Cancer, 37, 1-19-163. 9) :! tlac idle, C., Bartseh, 1!., Harbin, A., Camus, A. M-, and .Ton teen no, R. (1973). Mutagenicity of vinyl chloride chioroethy ienoo:-: ide, ch lorcaceta lde'n.yde an.d ehloroo th.anol, Hiechem Bionhvs. P.e-n . C.Vmm., 63, 363- 370. 10} Mnlteni, C. ( 1973). The value o f predictive exper i men onv i r or.men ta 1 carcinogen c'biij * An example: vinyl ch lc Ambio, 4, 18~ 23 . -i' R&S 101271 ll) Multcr.i, C. and dot emi r.e, G. (157 5;. Care ir.cner. ici ty assays of vinyl or. ier ido : Current results. An r>. M.Y. Acad. Fc:., 2440, 1 1-224. 12; "'annuo, L:. , Johansson, A., Rar.el, C., and V.'ach t:r.e i s ter , C. (1974). The rautaeonicity of vir.yl chloride after metabolic activation. Arab i o , 2_, 194-197. 13) Tabersr.aw, 1. R. ar.d Gaffey, W. F.. (1974). Mortality study of workers ir. the .T.anufacfare of vinyl chloride and its col vrv.or s. J. Ocrcuo. Med., 16, 509-513. 14) V.'a ta r.abe, P. G., Me Cowar., G . R . , Madrid, F. 0., Gear i.og , P. J. (197 6a) . Fate o r- 14e., -vmy,l cr. .,l foi;G'.v'::tj inhalation expo sure in rats. Toxicol Pha r:;:ucol ., 37, 49-59. Via tana be, P. G., McGowan, G . R. , and Gehrincj, P (19/ub). F te of ^'C-vinyl chloride after single oral administration in ra! 339-352. Toxicol. Anal. Pharmaco3., 36, 16) Watauabe, P. G., Hofr.or, R. 2. , Jr . , and Gehrimj, P. J. (1976c). Vinyl chloride induced depression of hepatic nor.protein nuifhydryl content and effects on bremosuiohtha leir. (U5P) clearance in rats. Toxicoloev, 6, 1-6 .,WoLnnabo, P. G., :',cnu;ol, J. 11 Pegg, D. G., one Gohrinx, P. J. (1073i lie r.'.n;; r o mo 1e c u1a r binding following exnonuro to vinyl chloride. Toxicol. A op I. PI'.': IT.1..-: col . fin CCOiiS) . R&S 101272 R&S 101273 TABLE 1 - PREDICTED INCIDENCE OF ANGIOSARCOMA Til RATS EXPOSED TO VINYL CHLORIDE USING VARIOUS MODELS VERSUS DOSE (v, ;.<j VC METABOLIZED PIR DAY) COMPARED TO EXPERIMENTAL RESULTS Exposure i `i 10,000 6,000 2 , 500 500 250 50 v, D,,eo/s, eu. ey ,b !j 5 21 54 0 3 5030 3 4 13 24 3 5 739 Experimentaln 14.8 (9/Cl) 21.7 (13/60) 22.0 (13/59) 11.9 (7/59) 6.8 (4/59) 1.7 (1/59)- Mod c1 A Prodic ted 3C Mod cl B Model C Model D 19.0 19.3 17.9 12.1 8.1 .4 20. 0 20 . 5 18.1 11 . 8 8.0 1.4 13.7 19.3 17 . 3 12.2 3.7 2.6 18 . 9 18.6 17.4 12.2 8.8 2.8 u) From Maltoni. jnJ Leleniino (197 5) b) Calculated from eouation v = 570-5 (;:<iVC/4 Hr) S (ii f| / l) 860 ([[',/ ) + S(:kj/.') , where S = 2 . 56 (ucj/ppm/f.) x Exposure, ppm; soo Gehring, ct a 1, 1978 . c) Model A, Probit l = -1.625 + 1.543 I.oy (Dose) ; Model B, Z = -1.48+0.389 x 10 " (Dose); Model C, % - 0.3565 x 10 ^ (Dose); Model D, % = ^ 1 - Cl '' (dose)^100 whGrc 5 - 0.38 x 10 R&S 101274 TAtlLE 2 - INCIDENCE OF ANGIOSARCOMA IN 9677 WORKMEN EXPOSED TO VINYL CHLORIDE^1 Pnou1 a tion 13 8-1 (0.31}d 2339 (0.271 9-16 (0.30) 1 007 (1.0) 67 7 (1.01 3 24 (1.0) Dura tion oE Exposure,Yrs <4 3-9 10-14 1 3-19 20-24 25 + Meat Exposure Dura t i on, Yr s1J 2 7 12 17 22 27 Fraction of Workinq Lifc 0.06 0.20 0.34 0.49 0.63 0.77 9677 Observed Ami i osar cornu s 1 (18 Yr r>)C 0 2 ( 15 f. 23 Yrs) 2 (18 L 1.9 Yrs) 0 0 a) From " Ej ,i deni ol oq j cn 1 Study of Vinyl Chloride Workers", Final Report January 1978, prepared i,y Kqu i tab 1 e Environmental Health, I no . , Roc:l:villc, MD, tor Manu f. ac Lur inj Chemists Association, Wa sh j nq ton , DC. 1)} Assumed moan duration of. exposure. e) Moan duration of exposure divid-'d Ly 35 years. d) Fraction ul population ineucrin<j f irst exposure 13 or more ye.n s prior to study. e) Duration between first exposure and diaqnosis. R&S 101275 TABLE 3 - AVERAGE THEORETICAL BAT KQUT VALENT DAILY DOSES OF BT OTPAKSF0IIMA7I0N PRODUCTS HECK IVED BY A 7 0 KG MAN EXPOSED TO 200 OR 500 PPM VINYL CHLORIDE FOR VARIOUS FRACTIONS OF AN ASSUMED 35-YEAR WORKING LIEU \CO ro tn > M o a n r. :: (-o s 11 r c Deration, Yrn. 2 7 12 17 22 27 Fraction of V.'<rki n<] life 0.06 0.20 0.34 0. '19 0.6 3 0.77 hr Average;! o\ 5 hrsl` (n;."0 500 200 60 200 341 49 1 631 771 38 12 5 213 306 39 4 43 1 a) 1C `/Jill.!/D lir - _S_,i<j/J t- S,.(jA (Fraction of working life) R&S 101276 TABLE 4 PREDICTED DUMBER OF ANG 1OSAECOMAS 1!J V.'ORHMEN EXPOSED TO 500 OH 200 PPM VINYL CHLORIDE 8 IIOURS/DAY, 5 DAYS/WKEK FOR VARIOUS FRACTIOUS OF A 35-YEAR WORKING LIFE VERSUS THE NUMBERS OBSERVED USING BIOTRANSFOKMATION AMD ANGIOSARCOMA INCIDENCE DATA FROM RATS AND FOUR MODELS FOR EXTRAPOLATION Pc.'pu J a L j cm 4 384 23 39 9 4 f. 1007 (.7 7 3 24 9077 Ar,q 1 osar comas Observed 1 0 2 2 0 0 5 Model A 500 2 0 0 0.2 0.0 2 . <1 0 . 8 3.0 1.1 G .8 2 . 7 7.3 3.0 4.9 2.1 25 LO Anqiosa roomas Pr cd i c iLed.b Model U 500 200 Mode1 C 500 200 00 9 . 4 5.9 0 0 J G. 7 10.4 0 u 11 . 5 7.2 4.0 0 17.6 11.0 G . G 0.3 ] tj - 2 9 . 5 4.9 1.3 8.9 5. G 1G 2 79 50 Mode). D 500 200 10.0 G.3 17.7 11 . 1 12.1 7.G 18 . G 11.7 1G . 0 10.1 9.4 5 . 9 84 53 Cl) Observed number of angiosarcomas from "Kpi dcmioiogical Study of vin.-l Chloride Workers", Final ifeport January 1978, prepared by Egui table Environmental Health, Inc., Roc'rvillc, MD, for M..n;u f ac Lur i ikj Chemist:-; Assoc: i a Lion, Washing ton, DC . b) Model A, Probit l = -1. C2 51-1. 543 Log (Dose); Model B, l - -i.<1840.388 x lG~2(Lose); Model C, 1 = 0.35G5 x 10~2 (Dose); Model D, l = (l _~c(c:ose) j 1Q0 w;u,ro p = q.38 x 10~4. The constants in these ModeJ.s were obtained using the biotransformation and angiosarcoma incidence data for rats exposed to vinyl chloride, Gchrir.g, ct al (1978). R&S 101277 TABLE 5 predicted i:;cj ui::ic[-; of alt;ioearcoma m workmen exposed to l ppm VINYL CHLORIDE fi liOURS/DAY, 5 DAYS/L'EEK FOR 35 YEARS USING 1) lOTRAL'RFOUMAT IUH AND AIJGI OS ARCOMA INCIDENCE DATA FROM STUDIES IN RATS J. A) Probit ?, or Lopur i tlu:i Probabil i ty 1.5 x 10_Gb or 1. 5/100 , 00 0,00-J B) Linear Not Forced Throu'.jii Oriyin l .'one predict ed be 1 ow exposures o L 0 C. 7 ppm. ^ O) Linear Forced Throu-jh Or icj in ' 1.7 x 1U"2'. or 1.7/10,000 or 17 1/1,000,00 0 / DJ One Hit (CAG) i.tPj 10"2., or l.y/10,0jt or 1G 9/1 , 00 0,00 0 n lint t" :u i vli 1 mi L daily doue of b i uLr.insforcnt i cm product v;oi'hi;i'.'n exposed for IJ hour:; to 1 pp:u vinyl chloride in V K7 nj; <> G 0 i; <j 1 \. yv.. j/;i in* I Ris Vinyl ChicriJc E:-:irn:jcla-_icr. Ar.'.j io;i rc'.rni Ra t3 H r.s -207ERMS R&S 101278