Document qabzJgYoYZyZG44XOwbLvMKvR

5/25/90 - c: E. 0. DeLoughy i OTNCS OFFICES: WASHINGTON, O. C- DALLAS AUSTIN f! ^G.W.Hart, Esq. BAKER & BOTTS ONE SHELL PLAZA 910 LOUISIANA HOUSTON. TEXAS 77002-AS95 G-45,618 TELEPHONE.(713) 229-123-A FAX: (7131 229 1522 TELEX: 76-2779 May 21, 1990 Mr. G. J. Triplett Senior Regional Counsel Union Carbide Chemicals and Plastics Company Inc. 437 MacCorkle Avenue, S.W. South Charleston, WV 25303 K t C c 1 V c. U _ ,QQn MAY 2 ? iyyu- ^ 0* J* TR1ELEIT Re: No. 87-CV-488; Jerlean Clay vs. Union_Carbide Corporation: In the District Court of Galveston County, 122nd Judicial District Dear Joe: I have enclosed a medical report by Dr. Legator on Mr. Clay for your review in the above case. 229-1179. Should you have any questions, please do not hesitate to contact me at Very/hlly yours, ACS: 1397 Enclosure cc: Ms. Nila Pittillo Union Carbide Chemicals and Plastics Company Inc. 3301 Fifth Avenue South Administration Building 61 Texas City, Texas 77592 Ms. Lee Rosenthal L0867/1397/03CT01 Andrew C. Schirrmeister III privileged and "CONFIDENTIAL MATERIAL SUBJECT TO PROTECTIVE ORDER" UCC 070871  M-C-T INC. ! J TOXICOLOGICAL CONSULTANTS IN THE AREA OF \ ! MUTAGENS-CARCINOGENS-TERATOGENS ! ! I.D, #74 212 4899 i I 70 COLONY PARK CIRCLE GALVESTON TX. 775S1 ! ; TELECOPIER 409 744-6369 ! ! I M.LEGATOR, PRESIDENT ii i \ !i \---------------------------------------------------------------------------------------------------/ April 7, 1990 RL: NO. 07 CV 0400 JL'RLPAN CLAY V UNION CARBIDE I am currently Professor and Director of the Division of Toxicology &t the University of Texas Medical Branch in CnlvcuLon Taxers. My major area of interest is toxicology, end especially genetic toxicology- Genetic toxicology has tp do with the effect of cliornic&lfc. on ou genetic material which could load to neoplasms , reproduce S vr. problems end l.ransfcicsibJe genetic damage to go? mine 1 . col lr.. I was one of Lhe mc.ruboru of the EPA comrni tt.ee or the Health Assoynmont Document fo: Po* ychlor ineted DibenzopDioxins (FPA 190S). 1 om currently a member of the Notional Academy of Science Committee on animal monitoring, t member of the Office of Technology Committee on I Luna n Biological 1 UCC 070872 Morii ten i. uc c member of the Uf'A health ei-tlcts. PLt;r.Ar<tn r<rv:tw PANLu. end g member of the NATIONAL LXDKApy'or MC.DIC7NC SCJCNTIFJC RLV1TW PAULI . ; havo Also been involved in IFr* risk **scc.r.ri.nr.t p/>nc*l which considered potential risk to numerous chemical*; i t<. ludj no Vinyl Chloride. ASSIGNMENT In the* Qhov-st refer&iicvcl case, I was asked to > eview the toxicological eteta having to do with vinyl chloride and livei tumor , the medical records of Causby Clay as well as his exposure to vinyl chloride during his period of employment at Union car* bide. Furthermore. based upon my expertise as a toxicologi*1, I will render an opinion as to the probability of the adverse health effects suffered by the* plaintiffs being caused entirely, or significantly contributed to by exposure to vinyl chloride during the course of his employment at Union Carbide. Appro.at.hj. Tev.mijiplpgy . Ij& Oef ini Lions i 3ri arr effort to make it easier for the court to understand my approach to the evaluation of toxic chew Joels, I am outlining ffsomc; basic assumptions which underlie my toxicological method. Furthermore, 1 will briefly review some of the terms which I use, including the "road to cancer", threshold concepts, arid what i*> known about the. c erci nogunicity of vinyl chloride. Daoed on the 2 UCC 070873 information preconted I will render my opinion, os a toxicolo gist, au to the probability that Mr. Clay's exposure in the workplace contributed or was responsible more likely than not to his neoplasm. !l.h& C'O&.cJ. t.A* C.a.iioer". 1 believe that any amount of any ceicinogen is detrimental to the health of any human ( Ko> animal) who is exposed. Jn at tempt* i ng to undo ;ta no* the manner in which all the factors which are relevant to the human health condition correlate, I analog!?* th< nee; rick present in any human life to a roadway upon which each of uo travel sou - the road to cancer . taoh of us has the potential to develop cancer in the future. Dome of us-, never will: we die from other diseases, accidents, and other causes before our bodies develop tumors. iho manner in which wo traverse this road to cancer is unique to each oho of us, depending on our individual genetic makeup and life experiences. Cach of us; begins life at different points* on our respective ro&ds. to cancer. Wo ere born with certain genetic traits which may initially piece- un et & point on thft road which is significantly "farther down" than the starting points of many UCC 070874 fll(o*r persons. Tor example, biMce born with Down'}* CyncJi omc arc farthoi t'.]ori>2 the road to conce* than most other babicr- who do not have t his genetic coedition. Fcmi] i vr, in which C*r t.e. j n cancevi ere 6 prevailing cause of death, in multifarious forms, arc farther along down the road then families who exhibit no history of cancer death. Individuals who smoke accelerate the rate at whi ch t hey ate moving down tho road to cancer; a person who smokos one cigarette in his or her lifetime does not move as fast n) or,g the road to canter as a person who emokas ten* thousand cigarettes during his ov her 1iftime. Likewise, exposures to catc i nocjeris, whet hen natural (such es carcinogens found in food p: oduc-ls?} commonly occurring (such as found in automobile ex* hauui), c*r as & result of occupational exposure to chemicals such as vinyl chloride, as in the case of Mr Clay. To appreciate how this placed Mr. Clay in the "fast lane", consider that the organ that developed cancer in Mr. Clay, the liver, is precisely one? of the major target organs of this known highly potent human carcinogen.. One important consideration with regard to nr.y "road to cancer*' analogy in how it fits into the toxicologist's under standing of the development of concur in man.. Human beings exhibit a very complex series:, of lifetime interactions with regard to exposure to carcinogens, lifestyle, exposures to dir- A UCC 070875 &, and genetic pre-dispositions, all of which diffei in every individual. I r. tht cast* of Mr . Clay his sm.ki ng up to the early 70*i$ moy have inti Gfit.od his risk to cancer (especially lung career ), but there can be little doubt that hit. prolonged expos-ure to vinyl chloride, (see later section for discussion on this human liver carcinogen), really put him f * in the fast lane*. t-i. Cavci.iipgentih Ng. faf& Thresftold Ii 24, There it; no reeogr.ix&w' safe level for a carcinogen, such as vinyl chloride, frequently, toxicologists and other profession als will engage i r evaluations at determining so called "ro effect levels." 1 do i.ot believe that a no effect level exists for any gcnotcxic agent or carcinogen. As implied by my "rose* to c a Vice v " analogy, 1 do not think it is e< curate ov sensible to conclude. thef e minuscule expos'jrc to & known carcinogen has absolutely no impact on the* current or future* health of the individual exposed. On the contrary, every exposure to every can c iiiog^Tiic. chemical has some incremental effect on present and future health and may play some role in the subsequent develop ment. of a pathological process. In the case of vinyl chloride, however its; potency if- such that exposure even over g fraction of the pet loci that Mr, Clay experienced, would have a significant effect on his fatal adverse health outcome. UCC 070876 VINYL CHLORIDE # A KNOWN HUMAN LIVER (MULTI-ORGAN) CARCINOGEN Vinyl Chloride i s a color lest; gas, with * mild, tweet odor. Moc.t of vinyl chloride made in the U.O. iu used to rri !<? F`VC. h'uxrinu arc exposed to vinyl Chios ide a consequence of it roanuf ec t-ur a , Although there is c. low background rate of this chemical, the- occupational exposure is. usually thousand fold greater than rios'i* occupatioftl exposure. Of the 60"70,000 chemicals wc encounter in our daily liver, approximately 3i> are known human carcinogens*. Vinyl chloride is one of the select group* of known human carcinogens, it is one of the most potent of known human carcinogens, and one of the major organs ir. which it induces neoplasm*, is the liver. It ig & complete carcinogen, that is it initiates as well an promotes the mult, ir tag*; process that 1 sods to cancer. Animal studies support the human data so to the cave j nogenitA y of thiu chemical, and also indicate fundamental information cr to the mechanisms of I action of this synthetic chemical as well as dafinirrig the active metabolites of vinyl chloride which are formed primarily in the liver* . A striking similarity in the disease process er.d the induction of liver cancer was presented by Popper *t. al (01). This compound hav. been known as & human liver carcinogen since the early 70's. Of specific importance to thir c.av.o- is tho fact that this 6 UCC 070877 ccucef. both CMt i nomac and r,ar.omoji in animals and man. Several vcpor ti. in thf 1 itcrfilurc including Di*t2 ct el. ( *8?.). Ivons* et ai. ( *00), Infant* et flJ (*G1), Koischwltz ct *1. C'Oi). end Popper st a ? (01). documented hepatocav ci noff.&s j re duced t*y occ upat i cru-*l exposure to vinyl chloride. The latency pc; iod f r oiv; expose r *. to hop&tocelulai carcinoma with viny chlo ride h6s boon shown to be oven ycai s; ( Dietz et a). . *66), The time from exposure to cancer however can be quite variable de pending on concentration &s well as time of exposure. SUMMARY AND CONCLUSIONS Mr. Clay Ceucby, as a laborer with Union Carbide, was exposed to vinyl chloride from 1960-1900. He stopped smoking in the c-eil v 70's. He died from Hepatocellular Carcinoma (disease cl&^sifiratior. 81700) in 1906. i Vinyl Chloride j? t. well documented human carcinogen, one of the major target organ* is the liver . This chemicai is known to cause both sarcoma- and carcinomas inc 1 uding-hepatocar c i norries . My road to cancel analogy illustrates how a chemical like vinyl chloride integrated into our lifetime exposure pattern can bring us to the end of the road, meaning death from cancer. 7 UCC 070878 MCT-INC-M.LEGATOR-PRES TEL No.409-744-6369 APr . 7.90 12:33 P.09 for the above reasons I boiieve the cinco And resultant death of Mr. Clay Causby fiom thi Amlioncncy, in fill probabili- ty# Biore I i kc J y t he* i > not was tu sc either entirely or was signj f- Ic-antly contributed to by his* exposure to vinyl chloride. This* fxpoMire pr ily occurred during his employment. At Union C*i- bide. UCC 070879 VINYL CHLORIDE HUMAN MEPAT0CARCIN06CN 4 C- 90 / 1. ANTHONY PP. PRIMARY CARCINOMA Of THE LIVER. ANN. R. COLL . SURC.. ENGL. 3 976. 50(4) 205- 292- 2. DOVER U>. ENVIRONMENTAL AGENTS IN THE CAUSE Of HEPATIC MALIGNANCIES. BECKER, C. . AND M. 0. COYC (ED.). CANCER PREVENTION' STRATEGICS IN 71 IE WORKPLACE i SECOND ANNUAL OCCUPATIONAL CANCER- CONFERENCE . SAN FRANCISCO, CALIFORNIA, Ui-A, 3964. XjdSSP. Rf.'KJSPi Jf RE PUBLISHING CORPORATION: WASHINGTON, PI5TRIC3 OF COLUMBIA, USA; CAMBRIDGE, ENGLAND. ISDN 0-09116-441 J.i 0 (0). 1900. 70-02. 3. Chieco P; Nouu^v.ni Pi Moslem' MT; Mailoni C . Quantit&t.i vu histochemistry of bertzaidehyde dehydrogenase in hepatocellular card nomar. of vinyl chi or Ido* treated rate . J Mistoche-m CyLochonr.; VOi. 34, 1SS 2, 1906, P151-S. 4. CHU KC; M1LMAN HA. REVIEW OF EXPERIMENTAL CARCINOGENESIS DY COMPOUNDS RELATED TO VINYL CHLORIDE. CONFERENCE TO RFEVALUATF THl TOXICITY OF VINYL CHLORIDE MONOMER, POtY(VINYL CHLORIDE) AND STRUCTURAL ANALOGS, BET HESOA, MO., USA, MAR. 20-21 , 1900. ENVIRON HEALTH PFRSPCCIl d (0). 1901 (F-fECD. 19G2). 211-220. 6, Diet? A; Langbdn 6> Pcrmariettev W. [Vinyl chloride: induced hepatocellular card noma] . Klin Wochenschr; VOL 63, ISS 7, 1905, P32S-31. 6. EVAN'S 0 MD; WILLIAMS WJ; KUNG I TM. Angiosarcoma and hepatocellular carcinoma in vinyl chloride workers. HIST OF'ATHOLOGY (OXF ); 7 (3). 1983. 377-288. 7. HEKIR RM; MCNAMARA DP; MCLAUGHLIN J JR; WILLIGAN DA; BICKflOWER G; HARDISTY JF. CANCER INDUCTION FOLLOWING SINGLE AND MULTIPLE EXPOSURES TO A CONSTANT AMOUNT Or VINYL CHLORIDE MONOMER. CONFERENCE TO REEVALUATE THE TOXICITY OF VINYL CHLORIDE MONOMER, POLY(VINYL CHLORIDE) AND STRUCTURAL ANALOGS, BCTHCSDA, MD., USA, MAR. 20-23, 1900*. ENVIRON HEALTH PlHSPECT; 41 (O). 1901 (RE CD. 1902). 63 72, . Inf a lit e fT. Gbeer vatic* nr: of the cite-specific carcinogenicity of vinyl chloride to humane*. Environ Health F'crspcct; VOi. 41, )9fU, P6V-94. 9. hoischwit* D; Lelbach WK; Ladner K; Hevmanulz D. [Vinyl chlorido-induced angiosarcoma and hepsto-cellular carcino/r.j of the liver (author*s U&nsl. )j. ROFO; VOL 134, ISS 3, i901 , P2S3* 90. 1C. Lfingbdn Cu Perinanel ter W; Dietz A. [Hepatocellular carcinoma aftei exposuvu to vinyl chloride]. Dtsch Med Wochenschr; VOL 100, JSS 19, 3983, P741-S. 13. MALT0N1 Ci COTTI G. CARCINOGENICITY OF VINYL CHLORIDE IN SPRAGUE DAWLEY RATS AFTER PRENATAL AND POSTNATAL EXPOSURE. MALTONI, C. AND 1.0. SELIKOH (ED.). ANNALS Or THE NEW YORK ACADEMY OF SCIENCES, VOI . 534. LIVING IN A CHEMICAL WORLD: OCCUPATIONAL AND ENVIRONMENTAL SIGNIFICANCE OF INDUSTRIAL CARCINOGENS; INTERNATIONAL CONFERENCE, BOLOGNA, ITALY. **"'Sf"r 'V 10, 1 90S . XXV * I 04 CP. NEW YORK ACADEMY Of SCIENCES*' '* n. A9766- 465- UCC 070880 iri the V'c-rvu ilKIU^U ; . I ' V V . raw-75, 13. P&pj'GV IS: Mellon] Ci Eeiikoff 1 3 . Vinyl chlor ide i nducec! hepatic lciiionr. i r ir.en end rodents. A corner ioon. Liver; VOL. 1 . 3 , 1901 f R7* 20. 14 . kAdiko KJ; Otcmmci KL; Singhem C. Effect of ethanol on vinyl chloride cer ciTiOoei.ee is . Environ Health Pci sped; VOi. 41, 2 901, rev 62. 10. Ocitx I IK; C./>'jii. f*; Komnioi ol J B. Alcohol And C.t< i nos'onc-c; I s . Lc-i>*r Merge n Cieru,, Vol . 12, No. 3, page*;-: 90- 107, 179 ref or one c--c , 19021902 . 16. TAMt30f\f\0 CH. RELATIONSHIP Of VINYL M0NC>MlfiO AND LIVER CANCERS ANGIOSARCOMA AND HEPATOCELLULAR CARCINOMA. SEMIN LIVER 01S; A (2). 1904. 1SO-3C9. UCC 070881