Document 6Brz9aV5XnzzK0mzkzxKqKn6

JOHN PETERSON and SHIRLEY MAE PETERSON, Plaintiffs, vs. UNION CARBIDE CORPORATION, Defendants. SUPERIOR COURT OF NEW JERSEY LAW DIVISION: MIDDLESEX COUNTY DOCKET NO. L-060148-87 ,m DEPOSITION DIGEST OF SAMUEL EPSTEIN DECEMBER 16, 1989 DIGESTED BY: NANCY K. DOCHERTY LEGAL ASSISTANT UCC 089691 y Esae Lines Subject Matter Digest of Testimony DIRECT EXAMINATION CONTINUED BY ROBERT L. HOLLINGSHEAD (Defendant) 4 to 15 X3-24 1-7 Exhibits Epstein 5-17 Extensive discussion held re docu ments Mr. Hollingshead requested from witness during his 12/1/89 deposition. Epstein 5 is a copy of witness' C.V. Epstein 6 is the transcript of witness' deposition from the Strader v. Franklin Elec tric case involving meat wrappers asthma. Epstein 7 is witness' transcript from Starling v. Mc Donnell Douglas case involving nasal sinus cancer following mul tiple exposures including as bestos. Epstein 8 is a letter from an attorney by the name of Ellis E. Neder, Jr., dated 5/14/82. Epstein 9 is a letter and attachment from the law firm of Brown, Connery, et al, dated 2/9/81. The attachment is a re port on John Grasso prepared by witness on 1/21/81. The case Grasso v. BF Goodrich involved VC exposure. Epstein 10 is a letter dated 1/16/87 from the law firm of Brown, Tyrrel, et al, to witness with a 1-page report on Andrew Ski attached. The case involved asbestos exposure and Ski was a co-worker of Starling. Epstein 11 is a letter dated 10/26/84 from the law firm of Philo, Atkinson, et al, to witness re Earle v. Cryovac and involved meat wrappers asthma. Epstein 12 is a letter dated 2/3/84 from the law firm of Philo, Atkinson, et al, to witness re Wall v. Hobart involving meat wrappers asthma. Epstein 13 is a letter dated 12/9/83 from the law firm of Watkins, Boulware, et al, to witness re Strader v. Franklin. Epstein 14 is a letter XJCC 089692 V Page Lines Subject Matter Digest of Testimony dated 12/1/86 from the law firm of Philo, Atkinson, et al, re Sutkaitis v. Goodyear with an attachment of a 2-page report by witness re Mrs. Sutkaitis. It was another meat wrappers asthma case. Ep stein 15 is a letter dated 1/15/85 from the law firm of Smith & Gold stein, re Ferrara v. Tenneco Chem icals with an attachment of a 1page report dated 11/30/85 by witness re Mrs. Ferrara. The case involved VC. Epstein 16 is a letter dated 7/9/81 from the law firm of Bogus & Bogus re Mikyska v. 3F Goodrich involving PVC/VC. Epstein 17 is a letter dated 4/6/79 from the law firm of Stan ley Rosenblatt to witness re Ellias v. Parke Davis and Sprayon with an attachment of witness' 4page affidavit. The case involved VC. (Witness requested that the deposition transcripts in the Strader and Starling cases be returned to him after being copied by Mr. Hollingshead.) 15 8-24 16 1-24 17 1-21 Exhibit Epstein18 Epstein 18 are several pages from the exhibit that had previously been marked as Epstein 4 (witness' preliminary report). The pages had been updated since witness' previous deposition. The update involved the inclusion of six new studies (Byren; Bufler; inter national Agency For Research On Cancer, 1979; Infante, 1981; In ternational Agency For Research On Cancer, 1987 and Doll, 1988). 17 22-24 Exhibit Epstein 19 Epstein 19 is a document entitled 18 1-15 State of the Art on Residual CV and PVC Prior to 1975. 18 16-24 Exhibit Epstein 20 Epstein 20 is a 1-page document 19 1-4 entitled Infante, et al, 1981. -2- UCC 089693 r Pag 20 21 21 22 23 23 24 25 25 26 28 29 30 31 32 Lines Subject Ma-tter Digest of Testimony 9-24 1-4 5-24 1-24 1-8 9-24 1-24 1-2 12-24 1-18 16-24 1-19 17-24 1-24 1-2 Exhibits Epstein 21 and 22 Asbestos/Silica Exposure At Lean Manufacturing Company Tabershaw Supports PVC-Laryngeal Cancer Peterson's PVC Concentrations Unknown Epstein 21 is the new 2-page document entitled State of the Art on VC/PVC Toxicology Prior to 1974. Epstein 22 is the 5-pag document entitled Illustrative Literature on the Toxic and Car cinogenic Effects of VC/PVC in the Respiratory Tract of Exposed Ani mals. (For the record: Epstein 18 and Epstein 22 are the same with the exception that Epstein 18 contains witnesses notations.) Extensive attorney discussion held re the fact witness continually submits supplemental to his pre liminary report. (Mr. Hollingshead requested a copy of the info Levinson supplied to witness re Peterson's work history and exposure.) Witness stated that there was no indication in Peterson's occu pational history that Peterson was exposed to asbestos/silica at Lean Manufacturing Company from 1962-67. Literature suggests there is a relation between asbes tos exposure and laryngeal cancer but not to silica exposure. Witness stated that although there are a substantial number of reports linking PVC exposure to respiratory tract cancers, there is no breakdown citing how many are laryngeal and how many are lung cancers. The only literature support for the proposition that laryngeal cancer had been related to exposure to PVC are the Taber shaw papers. Witness stated due to the lack of monitoring data, Peterson's actual PVC/VC exposure at ATC is -3- UCC 089694 X Page Lines Subject Matter Digest of Testimony 32 6-24 33 1 33 to 37 2-24 1-9 37 10-24 38 1-5 38 7-24 39 1-24 40 1-16 40 17-24 41 1-24 42 1-6 unknown. It is known that Peter son's exposure to PVC occurred largely in the bagging area of ATC. Thermal Degradation Of PVC Witness explained that the thermal degradation of PVC would result in HCL in combination with benzene, carbon monoxide and phosgene, among other materials, when dealing with PVC film. When dealing with PVC pellets and dust, the major source of exposure would be VC. Extensive discussion was held re witness' reference to Davidson's expertise re specifics of PVC thermal degradation. Difference Between PVC Film/Pellets Witness explained that PVC film produces higher levels of residual VC because the VC will constantly evaporate from the film and the film is so thin that the measured levels of VC are minuscular. He further stated that no matter how thermal degradation of PVC occurs, whether it is from the heat seal ing process or the welding pro cess, the amount of VC given off and to what extent it is given off remains the same. Extensive discussion held re various tables witness included in his preliminary report. Exhibit Epstein 23 Epstein 23 is witness' addition to his chart entitled Illustrative Literature on the Toxic and Car cinogenic Effects of VC/PVC in the Respiratory Tract of Experimental Animals. The addition was a re port by Cornish & Abar of 1969 dealing with rats' inhalation of fumes from heated PVC producing interstitial edema and focal -4- UCC 089695 Lines Subj et Matter Digest of Testimony 17-24 1-3 Fibrosis/ Granuloma/ Adenoma 4-22 Any Dust Can Produce Pneumo coniosis 23-24 1-8 Frongia Study Of 1974 10-20 Agarwal & Feron Studies 7-24 1-21 Shortcomings Of Doll Study hemorrhages in the lungs. Witness stated that the disease of fibrosis is basically just scar The disease of granuloma is a chronic inflammatory reaction generally characterized by for mation of nodules and multinucleate giant cells associated with fibrosis. Adenoma is a tumor of the lung which hasn't pro gressed to malignancy. Witness stated that pneumoconiosis is a chronic inflammatory condition of the lung generally associated with fibrosis and granular nodulation and granuloma formation. Any form of dust in high concentrations can po tentially cause pneumoconiosis. Witness stated that the Frongia Study of 1974 involved rats and guinea pigs being exposed in the areas where workers were bagging PVC. The animals, like the workers, developed fibrosis nodu lation granulomas. Witness stated that although the overwhelming majority of PVC test were inhalation studies, two were not. The Agarwal Study of 1978 involved intra-trachial in jection. The Feron Study of 1981 was a gavage study which involved the incorporation of the PVC in the diet. Extensive discussion held re the shortcomings of the Doll Study. Witness stated that the short comings involved Doll's failure to cite critical references re res piratory tract cancers, and al though Doll recognizes lung cancer he didn't reflect his source of -5- UCC 089696 Pag Lines Subi ct Matter 51 23-24 Byren Study 52 1-18 52 19-24 Bufler Study 53 1-6 53 7-24 IARC Report 54 1-18 55 7-24 56 1-4 Digest of Testimony research support. Witness stated that Doll performed a highly selective review of the litera ture, but did not conduct any original research to come to Doll's conclusions. Doll also stated that there was no positive evidence of non-malignant disease despite the vast body of documen tation to prove otherwise. Witness stated that the Byren Study was one of many studies confirming the excess of lung cancer in VC/PVC workers. He further stated that the study was biologically but not statistically significant. Witness stated that the Bufler Study of 1979 was statistically significant because once the study was balanced to take into account smokers, there was an excess of respiratory tract cancers in VC worker. Witness stated that the Inter national Agency for Research on Cancer (IARC) did a report in 1979 depicting a review of the liter ature prior to 1978 on VC/PVC in animals and humans. The IARC stated that VC is a human car cinogen whose target organs are the liver, brain, lungs and haemolymphopoietic system. The report did not include whether or not the larynx was a target organ for VC. Witness stated that if any agency, such as the IARC, was aware of the existence of an unpublished study, they would not include it in their report because they only cite published data from the literature which is available to the scien- UCC 089697 Page Lines Subject Matter Digest of Testimony 56 5-24 Infante Report 57 1-24 58 1-7 58 8-18 IARC 1987 Report 59 to 66 20-24 1-7 Loomis' Report Of 11/2/89 tific community. Not all pub lished studies are subject to peer review. Witness stated that the Infante Report of 1981 is a review of eight studies involving the car cinogenic effects of VC in humans. Seven of the eight studies showed excess risk of lung cancers ranging from 7 to 200%. He explained that the one study that was negative showed a short duration of follow-up limiting the validity of any inferences that could be developed. He further explained that Infante stated that the carcinogenic effects of VC in humans extended beyond the liver and that the brain and lungs should be considered target organs. He stated that respira tory system cancers include laryn geal cancers. Laryngeal cancer is a relatively rare cancer with a figure of 8.5 per hundred thousand where the incidence for lung can cer is more than ten times that. Witness stated that the IARC 1987 Report updated the IARC 1979 Re port. The report stressed that exposure to PVC dust and VC was associated with an increased inci dence of lung tumors. Witness described the various sections of Loomis' report of 11/2/89 that he considered "scien tific rubbish." He felt Loomis' statement that PVC is toxicologically safe and produced only mini mal, non-specific, primary effects during industrial exposure to be nonsense. He did not agree with Loomis' statement that laryngeal cancer had never been documented to have been causally related to 7- UCC 089698 Page Lines Subject Matter Digest of Testimony 67 2-21 68 1-24 69 1-23 69 24 70 1-24 71 1-24 72 to 75 16-24 1-2 Austin 1982-Laryngeal Cancer Asbestos-Cancer PS Present At ATC VC/PVC exposure. Witness stated that any individual acting as an expert to industry received unpub lished data. Witness referred to a reference book that was published in 1982 authored by Schottenfeld and Fraumeni which include a chapter on laryngeal cancer that was authored by Austin, which he included as a reference for his preliminary report. Witness explained that Austin would not have access to the unpublished studies of Tabershaw of 1974-75 because Austin did not work specifically in the VC/PVC field. He further ex plained that Austin's particular chapter re laryngeal cancer is devoid of any comment about VC/PVC. Witness stated that he agreed with Austin re the fact asbestos is a risk factor for cancer including laryngeal cancer. He explained that Austin discussed a wide range of occupations in which excessive laryngeal cancer is found. They included chemical exposures to unspecified chemicals. Other occupational factors included tobacco, alcohol, nickel and mus tard gas exposures. No where in Austin's paper is VC mentioned. Witness went on to say that Austin found elevated PMR in meat cut ters . Witness stated that the pellet form of polystyrene (PS) was present at ATC. Due to frag mentation of the handling of the pellets, dust would be generated thereby causing pneumoconiosis. In order to induce pneumoconiosis, it would depend on the exposure -8- Page Lines Subject Matter 75 20-24 IARC Rankings Of 76 1-24 Carcinogens 77 1-6 77 7-24 Degassing Of 78 1-24 Styrene 79 1-20 Digest of Testimony and the size of the dust frag ments. Particles of 2 microns are 100% respirable, 5 microns are 20 to 30% respirable and 10 microns are non-respirable. Witness stated that he was not aware of any study re a causal relationship between exposure to PS and laryn geal cancer. He further explained that the epidemiological study of Hobson and Jones showed an asso ciation between styrene exposure and laryngeal cancer. Witness explained the IARC listing of carcinogens. Group I is when clear-cut epidemiological data is available for humans. Group II-A is when reasonable epidemiological data is available for humans. Group II-B is when excellent ani mal data is available. Group III is when animal data with no epi demiological data is available and Group IV is basically non-carcinogenic or questionable validity of animal data. IARC frequently stated that valid animal data creates a strong presumption of human cancer risk. Witness further explained that EPA rank ings, in general, reflect the IARC ranking and sometimes EPA refers to the IARC rankings. Witness stated that the styrene monomer is degassed from the PS pellet the same way that VC is degassed from PVC. Additionally, when you heat-treat PS, you will liberate styrene. Witness further stated that PS contained up to 1% of the volatile residual styrene monomer. Higher concentrations of unreacted styrene are released from fresh PS rather than aged PS. He further explained that -9- UCC 089700 Lines Subiect Matter Digest of Testimony 80 to 83 8-24 1-16 83 to 86 17-24 1-2 Peterson's Exposures At ATC Shell Report Bisphenol A Resins when you degas in the air, you will have a progressive reduction in levels of the monomer in the polymer. When you degas in a closed system, there is a migration from within the polymer to the closed dead air space and with the secondary absorption on the surface of the polymer. Witness stated that because of the lack of monitoring data by ATC, he was not able to quote what per centage of exposures Peterson had to any resin in the ATC plant. He is unable to substantiate his assumption that the majority of Peterson's time was spent in the presence of PVC. Witness agreed that one of the reasons that he's assumed that PVC was the main chemical to which Peterson was exposed to, was due to Levinson's original letter dated 4/88 re PVC pellets. Witness discussed various sections of the Shell Report of 1982. He stated that the isopropylidene bisphenol resins are potent pri mary irritants and sensitizers. Various components of the resins that cause this reaction are epichlorohydrin, phenolics and the glycidol ethers. He stated that isopropylidene bisphenol resins and particularly 4.4 isopropyli dene diphenyl are the same as bi sphenol A resins. He is not aware of any literature linking bi sphenol A resins and epichlorohydrin with laryngeal cancer. There is literature that linked them with nasal cancer, lung can cer and respiratory tract cancers and the "respiratory tract in cludes the larynx." -10- UCC 089701 Pag Lines Subject Hatter / Digest of Testimony 86 87 87 88 89 90 90 91 92 92 to 95 3-24 1-5 6-24 1-20 6-24 1-10 18-24 1-24 1-16 17-24 1-10 Interline Reports Witness explained the conclusions of the three Interline Reports. He stated that the data on studies based on experimental or occu pational studies and on a single exposure would understate risk to particular target organs when you expose workers to a wide range of different carcinogens. Peterson's Exposure To Welding Fumes/Emissions Witness stated that it is not known what percentage of welding fumes/emissions Peterson was ex posed to at ATC but it was his opinion that they played a con tributory role to Peterson's laryngeal cancer. "Attendant Complications" Witness explained that the term "attendant complications" referred to various complications that can occur from one disease entity. "Substantially Increased Risk" Witness stated that although he felt that Peterson was at a "substantially increased risk" for developing other cancers from his occupational exposures at ATC, he could not quantitate it. He felt he was at excess risk for respira tory tract cancers because Peter son was exposed to a wide range of pulmonary carcinogens and the fact Peterson had already had cancer in the respiratory tract, his chances of getting another cancer in that same system are substantially increased. Peterson's Cancer Risk Witness stated that due to Peter son's chronic obstructive lung disease, Peterson has a sub stantial increase with relation to cancer above and beyond the general population's one and three risk of getting cancer and one and four risk of dying from cancer. -11- UCC 089702 Pa9e Lines Subject Matter / Digest of Testimony 95 11-24 Austin Report 96 1-24 97 1-14 Witness stated that the Austin Report studied the effects of smoking and alcohol upon laryngeal cancer. Witness did not consider Peterson's smoking in relation to his development of laryngeal can cer because Peterson had stopped smoking one year prior to his employment at ATC. 97 15-24 Selikoff Report Witness stated that the Selikoff 98 1-5 Report studied the synergistic effect of cigarette smoking and exposure to asbestos. Witness had not done researh re Selikoff's claim. 98 10-24 US Surgeon Witness stated that the US General's Report Surgeon General's Report sum marized that there is a progres sive reduction in the risk of developing laryngeal cancer fol lowing cessation of smoking. 101 2-24 Smoking/Laryngeal Witness stated that due to the 102 1-24 Cancer fact Peterson developed his laryn 103 1-9 geal cancer at a much earlier age than the general population's anticipated age of 60-plus, that would tend to minimize the role of Peterson's smoking and maximize the role of his occupational fac tors. He further explained that according to the Surgeon General's Report, smoking and laryngeal cancer is strongly dependent on the numbers and due to the fact Peterson smoked less than one pack a day, he would be considered a light smoker which decreased the relationship between his smoking and laryngeal cancer. 104 17-24 Latency Period- Witness stated that although he 105 6-15 Cigarette Smoking does not mention specifically in his report about latency period of contracting any cancer as a result -12- UCC 089703 Page Lines Subject Matter Digest of Testimony 105 16-24 to 108 1-4 108 5-24 109 1-5 109 6-24 to 112 1-8 113 12-24 114 1-24 115 1-9 No Observable Effect Level For Carcinogens Early V. Late Stage Carcinogens Difference In Latency Periods of exposure to cigarette smoking, he does acknowledge the fact that the longer you follow the VC/PVC workers and the more heavily they were exposed, the incidence of respiratory tract cancer is higher, Witness stated there is no way of setting safe levels for chemical carcinogens because, from a stand point, one molecule on one re ceptor site can create genetic damage which can theoretically be associated with carcinogen ef fects. Witness stated that the risk of Peterson's laryngeal cancer is the same as that of a non-smoker. Witness explained the difference between an early stage and late stage carcinogen. The over whelming majority of carcinogens are considered early stage, the longer you wait, the higher their risk is. Other carcinogens, such as tobacco and estrogen, depend upon continuing exposure. Once removed from that exposure, their risk decrease progressively. It has been noted by the Consumer Products Safety Commission that one hour of exposure to VC can lead to the development of tumors later in life. Witness explained various des criptions of latency periods. Generally, it is the time of ini tial exposure to the time of diag nosis. Other descriptions include the time of initial exposure to the time of death and "sometimes latency is defined more sloppily from the mid-point of exposure." -13- ucc 089704 X Page Lines Subject Matter Digest of Testimony 115 14-24 VC Latency Period Witness stated that it is not 116 1-24 117 1-4 possible to say what VC's la tency period is because most of the epidemiological studies have had an inadequate follow-up. He considers the latency period for VC to commence with the first exposure by the individual. Deposition Concluded -14- UCC 089705