Document omQZeN91356BbrvQ1N6BzdmXE

1 1 STATE OP NEW JERSEY ) ) SS: 2 COUNTY OP MIDDLESEX ) 3 IN THE SUPERIOR COURT OF NEW JERSEY LAW DIVISION} MIDDLESEX COUNTY 4 5 JOHN PETERSON and SHIRLEY MAE PETERSON, his wife, 6 Plaintiffs, 7 vs. 8 UNION CARBIDE CORPORATION, 9 Defendant. 10 ) ) ) ) ) ) NO. L 060148-8? ) Civil Action ) ) ) 11 The continued discovery deposition of 12 SAMUEL EPSTEIN, M.D., taken in the above-ehtit1ed 13 cause before Sandra A. Kasper, a notary public 14 within and for the County of DU Page and State of 15 Illinois, and a Certified Shorthand Reporter of 16 said state, at 303 West Madison Street, Suite 1400, 17 Chicago, Illinois, on the 16th day of December 1989 18 at 10:30 o'clock a.m. 19 20 21 22 23 24 RNW 2068 PATRICIA G. TALAMO COURT REPORTERS, INC. (312) 641-3500 2 1 APPEARANCES: 2 LEVINSON, AXELROD, WHEATON & GRAYZEL, by MR. ALFRED A. LEVINSON, 3 2 Lincoln Highway P.O. Box 2905 4 Edison, New Jersey 08818-2905, 5 On behalf of the plaintiffs; 6 PITNEY, HARDIN, KIPP & SZUCH, by MR. ROBERT L. HOLLINGSHEAD, 7 163 Madison Avenue Morristown, New Jersey 07960, 8 On behalf of the defendant. 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 RNW 2069 3 1 INDEX 2 WITNESS: Examination 3 SAMUEL EPSTEIN, M.D. 4 by Mr. Hollingshead (cont'd.) 4 5 6 7 8 9 10 11 12 EXHIBITS 13 Number Marked For ID 14 5-17 18 15 19 20 16 21 22 17 23 12 16 18 19 20 20 42 18 19 20 21 22 23 24 RNW 2070 4 1 MR. HOLLINGSHEAD: Dr. Epstein, good morning. 2 THE WITNESS: Good morning. 3 MR. HOLLINGSHEAD: As you know this is a 4 continued day for your first deposition and you're 5 still under oath from the first day in New York. 6 THE WITNESS: Yes, of course. 7 SAMUEL EPSTEIN, M.D., 8 the witness on the stand at the time of 9 adjournment, having been previously sworn, resumed 10 the stand and testified further as follows: 11 EXAMINATION (Continued) 12 BY MR. HOLLINGSHEAD: 13 Q. Doctor, I believe at the last deposition 14 there were some items you were going to find for 15 me, and I understand you brought some documents 16 with you today. 17 Would you identify what you brought 18 today? 19 A. Yes. The first is a deposition of 20 Strader, S-t-r-a-d-e-r, versus Franklin Electric. 21 It's ray deposition on a case of meat wrappers 22 asthma. The second is a deposition of myself in a 23 case of Starling versus McDonnell Douglas, and this 24 is a case of nasal sinus cancer following multiple RNW 2071 5 1 exposures including asbestos. 2 The third is a batch of documents 3 relating to cases you asked me to dig out. The 4 first is Grasso versus B. F. Goodrich. If you 5 recall that was a VC case which we talked about 6 last time. It's a report of mine which I kept, a 7 report of January *81, and a letter from the 8 attorneys so you can get all the information from 9 the attorneys. 10 The next is another vinyl chloride case, 11 Ellias, E-l-l-i-a-s, versus Parke Davis and Spray12 on, one word, with a letter from the attorney and 13 an affidavit from me. I was deposed in that rase 14 but I haven't got the deposition.^ ______ , 15 The next is a letter -- the next is 16 another case, a VC/PVC case, called Mikyska, 17 M-i-k-y-s-k-a. I think it's Mikyska versus B. F. 18 Goodrich and possibly Ford -- yes, it is. I think 19 so -- and it's a letter of 1981. It was -- I don't 20 have any other documents in this case. This was -21 I believe I was deposed. I don't think thece was a 22 trial but I don't have any records. 23 The next is a VC case of Ferrara 24 F-e-r-r-a-r-a, versus Tenneco, T-e-n-n-e-c-o; RNW 2072 6 1 letter from the attorney and a preliminary report 2 by myself. I don't believe I was deposed. There 3 certainly was no trial. 4 The next one is a meat wrappers asthma 5 case -- well, actually one, two, three, four meat 6 wrappers asthma cases. The first is Earle, 7 E-a-r-l-e, versus Cryovac, C-r-y-o-v-a-c. The 8 second is Wall versus Hobart, H-o-b-a-r-t. The 9 third is Strader versus Franklin -- that's a bit 10 si1ly of me. 11 The very first document I gave you was 12 the deposition so this is just a letter with the 13 attorney's name, et cetera. 14 The next is Sutkaitis versus Goodyear, 15 S-u-t-k-a-i-t-i-s, which there is a report from me, 16 a letter from the attorney. No deposition to the 17 best of my recollection, no trial. The next is -18 that's -- those are all the meat wrappers asthma 19 cases. 20 The next is a letter from the attorney on 21 the asbestos case -- on another asbestos case. 22 This was a coworker of Starling called Ski, and 23 it's Ski -- and that was a nasal sinus cancer in 24 which asbestos was involved, S-k-i. RNW 2073 7 1 And the final one is a letter from the 2 attorney in relation to the Starling case, and 3 you've got the deposition of the Starling case 4 here. That's the asbestos. 5 (Discussion off the record.) 6 THE WITNESS: Now in addition to that I've got 7 some other tables and some corrected tables from my 8 notebook. The first is a document called State of 9 the Art on Residual VC in PVC Prior to 1975. I now 10 have that in my notebook. It wasn't in the copy I 11 sent you. 12 The next is -- there was a table if you 13 recall in the book I sent you called Illustrative 14 Literature on the Toxic and Carcinogenic Effects of 15 VC/PVC in the Respiratory Tract of Exposed Workers. 16 I have added quite a bit to that so this is a new 17 table for that. 18 The final one is just a table from a 19 paper by Infante et al. 1981 on respiratory tract 20 cancers. 21 MR. HOLLINGSHEAD: Before we mark the 22 documents you provided me with, let me refer to an 23 index that the court reporter gave to me from the 24 last deposition. I had asked her if she would just RNW 2074 8 1 give me a list of items that had been requested. . 2 BY MR. HOLLINGSHEAD: 3 Q. I had requested a curriculum vitae and 4 you sent that to me in the mail? 5 A. Yes. 6 Q. The next item was a list of publications 7 that you have authored over the course of time, and 8 that's also included in the C.V., is it not? 9 A . Sure. 10 Q. Next were formal reports written in the 11 Ellias, Grasso, and Mikyska cases, and you have 12 given those to me today, correct? 13 A. Yes. 14 Q. The next was to provide deposition 15 transcripts of any deposition of yours in those 16 three cases, and I believe you've given us the 17 deposition transcript from the Strader case. 18 Were there depositions taken in the 19 Ellias, Grasso, or Mikyska cases? 20 A. Yes. There's been a deposition taken in 21 the Grasso -- the Grasso case went to trial. So 22 there was a deposition and a transcript of that, 23 neither of which I have. 24 Q. And you don't have the transcripts from RNW 2075 9 1 the Ellias or the Mikyska cases? 2 A. No, I don't have them. The Ellias case 3 didn't go to trial. I was deposed on that. 4 Q. Do you have that transcript? 5 A. No, and the Mikyska -- I can't recall 6 whether I was deposed. I wrote a brief report on 7 it but I can't -- it didn't go to trial. 8 Q. And you don't have a transcript of any of 9 your testimony in that case, deposition or 10 otherwise? 11 A. I'm not sure that I was deposed in the 12 Mikyska case. 13 Q. The next item I had requested was 14 documentation which might include correspondence 15 with the attorneys on those three cases, and I 16 believe you have provided us with some of that? 17 A. Yes. 18 Q. The next request was for any expert 19 reports in any of the cases on asbestos. 20 A. Yes. 21 Q. And you've provided us with what you have 22 on that? 23 A. Yes. 24 Q. And that's all you have with regard to RNW 2076 10 1 that item? 2 A. Yes . 3 Q. The next was for any other expert reports 4 on isopropylidene bisphenol resins. 5 A. The only place where that came in is in 6 the meat wrappers asthma. That was one of the 7 exposures in the meat wrappers asthma cases. 8 Q. And you have given us what you have on 9 that? 10 A. Yes. 11 Q. The next was any documentation regarding 12 your involvement in any of the bisphenol cases. 13 Same thing? 14 A. Yes. 15 Q. The next was any report rendered with 16 respect to the NASAf N-A-S-A, plant worker who 17 apparently had laryngeal cancer. 18 A. I mislead you on that. I was under the 19 impression that one of these was a laryngeal 20 cancer. In fact both are nasal sinus cancers. 21 I still am under the impression that I 22 had an involvement in the laryngeal cancer case due 23 to asbestos, but I searched and spent a lot of time 24 looking in the basement and storage areas. I can't RNW 2077 11 1 lay my hands on it. 2 And I don't know whether it's faulty 3 memory or I was -- as I said before I was under the 4 impression that one of the NASA cases was a 5 laryngeal cancer because I know I did a search of 6 the literature. 7 Q. What did you find during your search that 8 made you conclude they were not laryngeal cancer 9 cases ? 10 A. The documentation is very clear. They're 11 both nasal sinus cancers. 12 Q. Now which were the NASA cases? 13 A. Both the Ski and the Starling. They were 14 both coworkers in a NASA plant in Jacksonville, 15 Florida. 16 Q. The next request was for any reports that 17 you had written independent of the Peterson case 18 relating to the toxic properties of any of the 19 chemicals that may have caused his illness. 20 That would of course be the chemicals in 21 this case and have we covered that? 22 A. Yes. 23 Q. Did you find any reference -- and I had 24 requested this, but did you find any reference to RNW 2078 12 1 information supplied by Mr. Levinson's office 2 regarding Mr. Peterson's exposure to asbestos at 3 the time of his employment? 4 A. No. As I explained last time I had a 5 two-page note from his office specifying the 6 details of this. I incorporated that in the 7 occupational history and then tossed it out. It 8 was an unsigned -- I remember it was a two-page, 9 unsigned piece of paper I got from the office. 10 Q. So I'll follow up on that with 11 Mr. Levinson's office. Very good. 12 Let me ask you -13 A. Can I see the recent curriculum? 14 MR. HOLLINGSHEAD: I have shown Dr. Epstein 15 the C.V. that he provided to me in the mail the 16 past week or so, and I'd like to mark this as 17 Epstein 5. 18 (Whereupon, Deposition 19 Exhibits 5-17, Witness 20 Epstein, was marked for 21 identification.) 22 MR. HOLLINGSHEAD: Dr. Epstein, we have marked 23 the documents that you provided me with today and 24 also the C.V. which you provided me with during the RNW 2079 13 1 week. 2 The C.V. is Epstein 5. The transcript in 3 the Strader case is Epstein 6. The deposition in 4 the Starling case is Epstein 7. We have marked as 5 Epstein 8 a letter from an attorney by the name of 6 Ellis E. Neder, N-e-d-e-r, Jr., dated May 14, 1982. 7 We have marked as Epstein 9 a letter and 8 attachment from the law firm of Brown, Connery et 9 al. dated February 9, 1981. The attachment is a 10 report on John Grasso prepared by Dr. Epstein on 11 January 21, 1981. 12 We have marked as Epstein 10 a letter of 13 January 16, 1987, from the law firm of Brown Tyrell 14 (phonetic) et al. to Dr. Epstein, and attached is a 15 one-page report on Andrew Ski, S-k-i. 16 We have marked as Epstein 11 a letter 17 from the law firm of Philo, P-h-i-l-o, Atkinson et 18 al. to Dr. Epstein on the Earle case, E-a-r-l-e. 19 The letter is dated October 26, 1984. 20 We have marked as Epstein 12 a letter 21 from the same law firm dated February 3, 1984, to 22 Dr. Epstein on the case of Wall versus Hobart, 23 H-o-b-a-r-t. 24 We have marked as Epstein 13 a letter RNW 2080 14 1 from the law firm of Watkins, Boulware, 2 B-o-u-l-w-a-r-e et al. dated December 9, 1983, to 3 Dr. Epstein on the case of Strader versus Franklin. 4 We have marked as Epstein 14 a letter of 5 December 1, 1986, from the Philo law firm on the 6 case of Sutkaitis, S-u-t-k-a-i-t-i-s, versus 7 Goodyear; and attached to that is a two-page report 8 by Dr. Epstein regarding Mrs. N. Sutkaitis. 9 We have marked as Epstein 15 a letter of 10 January 16, 1985, from the law firm of Smith & 11 Goldstein on the case of the estate of Lucy Ferrara 12 versus Tenneco Chemicals; and attached to that is a 13 one-page report dated November 30, 1984, by 14 Dr. Epstein entitled Preliminary Report on 15 Mrs. Ferrara. 16 We have marked as Epstein 16 a letter of 17 July 9, 1981, from the law firm of Bogus & Bogus, 18 B-o-g-o-s, directed to Dr. Epstein on the Mikyska 19 case and attached to that are -- excuse me. It is 20 a three-page letter. There is no attachment. 21 Lastly as Epstein 17 we have marked a 22 letter from the law office of Stanley M. Rosenblatt 23 dated April 6, 1979, to Dr. Epstein on the Ellias 24 case; and attached to that is an affidavit by RNW 2081 15 1 Dr. Epstein of four pages in that same case. 2 Let me put those aside and I will take 3 them home with me and copy them and. Dr. Epstein, I 4 will send back to you as you have requested the 5 deposition transcripts in the Strader and Starling 6 cases. 7 THE WITNESS: Thank you. 8 MR. HOLLINGSHEAD: Now if we can I'd like to 9 turn to the tables that you have provided me with 10 as you've indicated would constitute a change in 11 what appears and what we have previously marked as 12 Epstein 4. 13 I'm looking now at the document entitled 14 Illustrative Literature on the Toxic and 15 Carcinogenic Effects of VC/PVC in the Respiratory 16 Tract of Exposed Workers. 17 BY MR. HOLLINGSHEAD: 18 Q. Can you tell me where the additions 19 appear in that document or the changes? 20 A. We'd have to go over this one -21 MR. HOLLINGSHEAD: Why don't we mark that 22 first as Epstein 18. 23 24 RNW 2082 16 1 (Whereupon, Deposition 2 Exhibit No. 18, Witness 3 Epstein, was marked for 4 identifiction.) 5 BY MR. HOLLINGSHEAD: 6 Q. Just so the record reflects. Dr. Epstein, 7 I understand that you have taken this page from the 8 exhibit -9 A. Not this page. These several pages. 10 Q. -- these several pages from the exhibit 11 that had previously been marked as Epstein 4. You 12 updated them and then unfortunately you discarded 13 the earlier pages; is that correct? 14 A. Yes, having sent both you and 15 Mr. Levinson copies of the original document. 16 Q. Yes, I understand that. I would ask from 17 this point on that any exhibits that are left in 18 your possession remain as they are when they were 19 marked, all right? 20 A. Sure. 21 MR. HOLLINGSHEAD: Mr. Levinson, I do have 22 copies of this table so we will replace it into 23 that report. 24 MR. LEVINSON: All right. RNW 2083 17 1 BY MR. HOLLINGSHEAD: 2 Q. Let's look at this exhibit we have now 3 marked as Epstein 18 and compare it to my copy of 4 what was previously part of Epstein 4, and I would 5 ask you if you could point out the changes for us. 6 A. Thanks, and I will put a tick on these. 7 Q. You don't need to do that. If you can 8 just describe what the changes are. 9 A. Nothing on the first page. 10 Q. On the exhibit we just marked as Epstein 11 18, you put a check mark on the second page to a 12 study by Byren, B-y-r-e-n, and that's a new 13 addition; is that right? 14 A. Yes. There's a new one, Bufler, et al., 15 B-u-f-l-e-r, and a new one. International Agency 16 for Research on Cancer, '79. Then Infante, '81. 17 Q. And that's on page 4. 18 A. Then International Agency for Research on 19 Cancer, page 5 -- that's 1987. And then Doll, '88, 20 page 5. All that's all the additions I have ticked 21 on Epstein 18. 22 Q. Now you have also got a document entitled 23 State of the Art on Residual CV in PVC Prior to 24 1975 . RNW 2084 18 1 Is that a new document or is that an 2 update of something that was in Epstein 4? 3 A. Well, I think these references were -- 4 these people were probably cited in paperwork in 5 Epstein 4, but I just put them in the table to 6 systematize this information. 7 Q. Did you take anything else out of Epstein 8 4? 9 A. No. 10 MR. HOLLINGSHEAD: Can we mark this then as 11 Epstein 19. 12 (Whereupon, Deposition 13 Exhibit No. 19, Witness 14 Epstein, was marked for 15 identification.) 16 MR. HOLLINGSHEAD: Lastly you provided me with 17 a one-page document entitled at the top Infante et 18 al., 1981. 19 BY MR. HOLLINGSHEAD: 20 Q. Can you tell me what that shows? 21 A. It's just a table from his paper on 22 respiratory cancer in workers exposed to VC. 23 MR. HOLLINGSHEAD: Mark that as Epstein 20, 24 please. RNW 2085 19 1 (Whereupon, Deposition 2 Exhibit No. 20, Witness 3 Epstein, was marked for 4 identification.) 5 BY MR. HOLLINGSHEAD: 6 Q. Dr. Epstein, is there another page within 7 Epstein 4 that you think you may have altered in 8 some fashion? 9 A. Yes, I think I made an addition on State 10 of the Art on VC/PVC Toxicology Prior to 1974. I'd 11 like to check on that if I may. 12 Q. I will provide you with the copy that I 13 have. 14 A. One minor thing under the animal data for 15 Viola. I have handwritten in ray copy at the end of 16 the handwritten material in your copy in parens: 17 "At 250 ppm admitted to NIOSH, 1973." 18 Q. I also note that what you did was to 19 retype this page? 20 A. That1s right. 21 Q. What appears in handwriting on the copy 22 that I have, which was marked two weeks ago, has 23 now been turned into print. 24 A. Yes, the Viola '70, the Tribukh '49, and RNW 2086 20 1 the NIOSH '73. 2 MR. HOLLINGSHEAD: Just so we can distinguish 3 one from the other, I want to mark this as a 4 separate exhibit. 5 THE WITNESS: Let me have a copy of it, 6 please. 7 MR. HOLLINGSHEAD: Yes, we will. Let's mark 8 this as Epstein 21. 9 (Whereupon, Deposition 10 Exhibits 21 and 22, Witness 11 Epstein, were marked for 12 identification.) 13 MR. HOLLINGSHEAD: For the record let me 14 describe what we have done. 15 We have managed to put back in its 16 entirety the document that was marked as Epstein 4 17 at the last deposition by taking copies of some of 18 my pages and reinserting them in Dr. Epstein's 19 original copy, and we have taken out of that volume 20 the two new versions of the pages that appear in 21 Epstein 4. 22 And we have marked as Epstein 21 the new 23 two-page document entitled State of the Art on 24 VC/PVC Toxicology Prior to 1974, and we have marked RNW 2087 21 1 as Epstein 22 the now five-page document entitled 2 Illustrative Literature on the Toxic and 3 Carcinogenic Effects of VC/PVC in the Respiratory 4 Tract of Exposed Animals (sic). 5 MR. LEVINSON: Let the record reflect that all 6 the documents that have been offered for 7 identification at this particular deposition of 8 Dr. Epstein both today and on the prior day shall 9 be considered for all purposes as amendments to my 10 answers to interrogatories propounded by 11 Mr. Hollingshead. 12 MR. HOLLINGSHEAD: I note Mr. Levinson's 13 statement. I have some concern, however, that at 14 the last deposition I was provided with new 15 material. I am now being provided with new 16 material today. I don't think it presents any 17 insurmountable problem, but I don't wish' to get 18 into a prolonged discussion about it now. 19 MR. LEVINSON: If you want anything that you 20 haven't been provided with, just let me know and I 21 will try to get it for you. 22 THE WITNESS: I should merely comment that I 23 have been working on these the last few days. 24 MR. LEVINSON: I don't follow what particular RNW 2088 22 1 items that you would like that we haven't provided 2 you with. 3 MR. HOLLINGSHEAD: It's not a question. I 4 have a letter from you, Alfred, of some time ago 5 that says that Dr. Epstein would be relying upon 6 his preliminary report and I should consider it to 7 be final. 8 I then came to his deposition on 9 December 1 and we both were provided with new 10 material by Dr. Epstein which -became a supplemental 11 report -- 12 MR. LEVINSON: Oh, I see. 13 MR. HOLLINGSHEAD: -- which I have now 14 reviewed in preparation for today, and admittedly 15 what he has given us today as anything supplemental 16 is relatively minor but nonetheless it is new 17 again -18 MR. LEVINSON: I see. 19 MR. HOLLINGSHEAD: -- when I thought we were 20 already done with -21 MR. LEVINSON: I see your point. I'm sorry. 22 MR. HOLLINGSHEAD: In terms of discovery, et 23 cetera, there's nothing outstanding that I'm aware 24 of that you owe me. RNW 2089 23 1 MR. LEVINSON: Okay, but let me say this. I 2 will cooperate with you entirely. If after today 3 you want any additional information by written 4 interrogatories, I'll be happy to give them to you. 5 MR. HOLLINGSHEAD: I understand that. I 6 appreciate it. I think we can work through this. 7 Dr. Epstein, let's -- let me hold these 8 for now. 9 At the last deposition, Dr. Epstein, you 10 provided me with a letter from Mr. Levinson to you 11 dated April 18, 1988, which we marked as Epstein 3, 12 and I want to clarify something. 13 That letter contains some information 14 with regard to Mr. Peterson's work history and 15 exposure, but I recall that there was other 16 information supplied to you at some point which I 17 believe you said you either discarded or returned 18 to Mr. Levinson, one or the other. 19 BY MR. HOLLINGSHEAD: 20 Q. Am I correct in that recollection? 21 A. I think you will recall that we discussed 22 this in great detail and I said that the material I 23 received from Mr. Levinson I incorporated in my 24 notes on the occupational history and then RNW 2090 24 1 discarded them. 2 MR. HOLLINGSHEAD: Okay, and you discarded 3 whatever you received from Mr. Levinson. 4 Therefore, Mr. Levinson, you and I when 5 we go back to New Jersey I'd like to follow up on 6 this to try to obtain from you a copy of whatever 7 other information you sent to Dr. Epstein which 8 provided information on Mr. Peterson's work history 9 and exposure. 10 And in particular, Dr. Epstein, if I 11 recall correctly there was information in asbestos 12 exposure in that submission to you by Mr. Levinson; 13 is that right? 14 A. Not in that submission. In a later 15 submission. 16 MR. LEVINSON: Didn't I give you a set of 17 the -- or was that included in Dr. Epstein's? 18 MR. HOLLINGSHEAD: It's in neither place. 19 It's not in 4 and he doesn't have it. 20 MR. LEVINSON: I found it in the office, and 21 the reason I didn't provide you with it was I just 22 assumed it was in this document. 23 MR. HOLLINGSHEAD: No, what is in that 24 document is his handwritten summary in effect -- RNW 2091 25 1 MR. LEVINSON: I'll be happy to give it to 2 you. I've got it right in my file. 3 MR. HOLLINGSHEAD: Dr. Epstein, if you would 4 turn to Epstein 4 and in particular the summary 5 sheet that you labeled O.H., which I understand 6 stands for occupational history, I've had the 7 opportunity now to look over this material. I only 8 have a couple of questions with regard to this 9 document. 10 THE WITNESS: Sure. 11 BY MR. HOLLINGSHEAD: 12 Q. When Mr. Peterson was at Leam (phonetic) 13 Manufacturing Company from 1962 to 1967, you listed 14 that he had no asbestos or -15 A. Silica. 16 Q. Thank you -- silica exposure and then the 17 next item is no, I believe -18 A. No maintenance or cleaning kiln. 19 Q. No maintenance or cleaning kiln, k-i-l-n, 20 and that's underlined. 21 Is there a reason why you made a note of 22 that particular lack of activity on Mr. Peterson's 23 part? 24 A. Sure, because had he done any maintenance RNW 2092 26 1 or cleaning of the kiln, there would have been a 2 possibility of asbestos or silica exposure. 3 Q. You were looking for that as part of his 4 work history? 5 A. Certainly. 6 Q. What would the concern be for either 7 asbestos or silica exposure if you had found it 8 when he was at Leam Manufacturing Company? 9 A. I would have noted it accordingly and I 10 would taken it into account in the assessment of 11 his subsequent medical events. 12 Q. Is there literature, scientific 13 literature or medical literature, to your knowledge 14 relating silica exposure to laryngeal cancer? 15 A. No. 16 Q. But there is with asbestos if I recall 17 your testimony correctly? 18 A. Yes. 19 Q. Have you been able to determine from any 20 source as to not exactly but approximately how much 21 exposure Mr. Peterson had to asbestos while he 22 worked at the ATC plant? 23 A. I described it to you last time in 24 qualitative terms. That's the sum total of the RNW 2093 27 1 information that I have. 2 Q. Turning now to the document that you 3 provided to me at the last deposition which, if you 4 go along in Exhibit Epstein 4, this is a document 5 entitled Factors Incriminating VC/PVC as the 6 Primary Cause of Peterson's Laryngeal Cancer. 7 What caused you to write this particular 8 page which came about after the submission of your 9 preliminary report in this case? 10 A. Well, as I mentioned the preliminary 11 report was a hurried response to a rapid deadline 12 imposed on me by Mr. Levinson and I continued work 13 subsequent to that, and the object of this was to 14 summarize the data with particular reference to 15 VC/PVC, which I felt to be the major factor. 16 Q. What caused you to conclude that the 17 exposure to VC/PVC was the major or as you say 18 on this page the primary causal factor of 19 Mr. Peterson's laryngeal cancer? 20 A. For the seven reasons so stated on this 21 page . 22 Q. Without getting into that at the moment, 23 it is true, is it not, that Mr. Peterson had an 24 exposure to asbestos in at least the first several RNW 2094 28 1 years of his employment at ATC? 2 A. That's not what I said last time. What I 3 said last time was the exposure was primarily in 4 the first six months. Subsequent to the first six 5 months his exposure was extremely minimal; and 6 changing insulation rope that once or so a year on 7 the doors of the asbestos boiler and, in fact, even 8 in the first six months the repairing of the brake 9 lining was not a frequent job and as I said only in 10 the first six months. 11 Q. But it is true that there is literature 12 support for the proposition that exposure to 13 asbestos can result in laryngeal cancer, is there 14 no t ? 15 A. Yes, correct. 16 Q. Is it also true that other than the 17 Tabershaw study that you have indicated that you 18 talked about the last time, there's no other 19 literature support for the proposition that 20 laryngeal cancer has been related to exposure to 21 PVC? 22 A. Well, first of all it's not the 23 Tabershaw. It's three documents. There's 24 Tabershaw, there's Tabershaw and Gaffey, and -- RNW 2095 29 1 unpublished reports, and there's a Tabershaw and 2 Cooper published paper. 3 Q. Including all of the Tabershaw papers, 4 that's the only support that you have put forth 5 for -- literature support for the proposition that 6 there has been a finding of a connection between 7 laryngeal cancer, that specific cancer, and 8 exposure to PVC? 9 A. No, not at all. There is a wide range of 10 reports on respiratory tract oancers -11 Q. My question was the specific cancer of 12 laryngeal cancer. 13 A. Well, you interrupted me. 14 There's a substantial number of reports 15 on respiratory system or respiratory tract cancers 16 which will include laryngeal cancers of which 17 there's no breakdown, so we don't know how many of 18 those are laryngeal and how many of these are lung 19 cancers. 20 Q. But the only study that in fact -- the 21 only studies that in fact talk in specifics about 22 laryngeal cancer would be the Tabershaw studies as 23 you have indicated? 24 A. With that one qualification I have just RNW 2096 30 1 so indicated and with also the qualification 2 there was a coworker of Mr. Peterson, maybe 3 Mr. Wilkinson, who also developed laryngeal cancer. 4 MR. HOLLINGSHEAD: Some of this I appreciate 5 we may have gone over to some extent the last time, 6 but because the interim provided me with the time 7 to read what was new to me the last time I want to 8 go back over a couple of items. 9 In your paragraph 2 of this same document 10 which you produced at the last deposition. Factors 11 Incriminating VC/PVC, et cetera, you talk about 12 Mr. Peterson having been continually exposed to VC 13 from several sources. One of them is high 14 concentrations from degassing of PVC pellets and 15 dust in hoppers, cars, bags, and storage areas. 16 BY MR. HOLLINGSHEAD: 17 Q. Were you ever able to determine the 18 actual concentrations at which he was exposed? 19 A. Well, no. In spite of Union Carbide's 20 recommendation in '74 that the atmosphere should 21 have been monitored to detect levels of VC and 22 prevent injury to workers, Union Carbide failed to 23 do any monitoring whatsoever prior to '74. We have 24 some post '74 monitoring data which I discussed RNW 2097 31 1 with you last time. 2 Q. Do you have information that was provided 3 to you from any source that would indicate that 4 Mr. Peterson was in fact working in the hoppers or 5 cars as you state in this paragraph? 6 A. No, other than the fact that he was a 7 maintenance worker and therefore could have been 8 exposed in any area he went into. 9 Q. All right, but on a regular occurring 10 basis it's your understanding *that his exposure to 11 PVC occurred largely in the bagging area; is that 12 correct? 13 A. Correct. 14 Q. Now is the bagging area different -15 A. Excuse me. That's not the case. In the 16 bagging area but also even after the bagging area 17 from degassing of dust on his clothes -18 Q. No, I asked you where he worked. 19 A. Oh, I see. Okay. 20 Q. Do you have information that he worked in 21 the storage area of the ATC facility? 22 A. You have already asked me about the 23 hoppers, cars, bags, and storage areas. I have 24 responded by saying that as a maintenance worker he RNW 2098 32 1 would periodically be -- go into all areas in the 2 plant requiring maintenance work. 3 Q. I don't want to quibble with you but my 4 earlier question dealt only with hoppers and cars. 5 A. Fine, okay. 6 Q. You mentioned also in the same paragraph 7 that there were high concentrations from thermal 8 degradation of PVC pellets and dust during heat 9 sealing and welding. I believe we went over this 10 last time in a more general context, but since this 11 document is new again I just want to come back to 12 that. 13 The thermal degradation of PVC results in 14 what type of fumes? 15 A. It depends entirely what you're dealing 16 with. If you're dealing with a PVC film, the major 17 degradation products would be HC1 and a variety of 18 other materials ranging from benzene, carbon 19 monoxide, phosgene, et cetera. 20 Q. HC1 is 21 A. Hydrochloric acid or hydrogen chloride. 22 However, when you're dealing with pellets and dust, 23 particularly with the pre '75 pellets and dust, the 24 major source of -- a very major source of exposure RNW 2099 33 1 would be vinyl chloride. 2 Q. 3 source? To what percentage would that be a major 4 A. It's very difficult to say except I 5 indicated that this will depend on a wide range of 6 factors which were discussed with you in extenso by 7 Dr. Davidson. 8 And in the State of the Art on Residual 9 VC in PVC, the actual residual VC levels in the PVC 10 would be an important factor. The thickness of the 11 originating material, the PVC; the size of it, the 12 presence of catalyst, a whole range of physico 13 chemical factors would also influence the release 14 of VC from PVC. 15 One can say that minimally the VC levels 16 would be the levels which you find from degassing 17 absent thermal degradation, but with thermal 18 degradation there would be virtually an 19 instantaneous release of these very high levels. 20 Q. When you talk about, as you just have -21 when you talk about the major components of thermal 22 degradation of PVC pellets resulting in an emission 23 of VC fumes, on what are you relying for that 24 statement? RNW 2100 34 1 A. Well, there's a -- first of all you'll 2 find a note from Boettner in the State of the Art 3 on Residual VC on the emissions of residual VC from 4 PVC and that these are maximal at temperatures of 5 280 to 350. 6 There's a variety of papers. Simmonds et 7 al., '49, talks about as early as 1949 Union 8 Carbide knew that residual VC was released from VC 9 (sic) during processing, calendering, raoldering, 10 and extrusion at temperatures 'from 100 to 200 . So 11 there's a big literature prior to '75 on release of 12 VC from PVC by heat treatment. This was discussed 13 among other things by Dr. Davidson. 14 And as far as the actual levels are 15 concerned, we don't -- I can't provide you with 16 specific levels at ATC because of Union Carbide's 17 failure monitor contrary to its own recommendations 18 in 1974, and I quote: "Resin users must monitor 19 the work space air VC concentrations so that they 20 could take appropriate action to protect their 21 employees". 22 MR. HOLLINGSHEAD: I move to strike every part 23 of that answer. That was not responsive to my 24 question. RNW 2101 35 1 My question deals with the source of your 2 information that on thermal degradation of PVC the 3 major component that is given off is VCM. I 4 believe you have referred to various references 5 that are in your -- that are contained within 6 Epstein 4 on the page entitled State of the Art on 7 Residual VC in PVC Resin to 1975. 8 THE WITNESS: 1975, yes. 9 MR. HOLLINGSHEAD: Now -- 10 THE WITNESS: And the additional point I made 11 was that Dr. Davidson discussed this in detail in 12 his deposition and also in his document. 13 MR. HOLLINGSHEAD: I agree that he did. 14 BY MR. HOLLINGSHEAD: 15 Q. Is it your testimony that upon thermal 16 degradation of PVC pellets as they were at the ATC 17 plant,- the major ingredient that is given off is 18 not hydrogen chloride? 19 A. I didn't say that. I said a major 20 ingredient. 21 Q. I'm asking you what size is the 22 percentage if you know of the ingredient of VCM 23 that is given off upon thermal degradation of these 24 PVC pellets? RNW 2102 36 1 A. I suggest you refer that question to 2 Dr. Davidson. That's more his area of expertise. 3 I'm merely aware that high levels are given off 4 upon thermal degradation. The specifics of this 5 you should discuss with an industrial hygienist. 6 Q. You would rely upon Dr. Davidson's 7 testimony in that regard? 8 A. Among other things. Among that and also 9 the literature. 10 Q. But if Dr. Davidson 'were to give a 11 percentage of the amount of hydrogen chloride as 12 compared to VC that is given off upon thermal 13 degradation, you would accept that as 14 authoritative, wouldn't you? 15 A. This is a straw man. You asked me about 16 major emissions. I said a major emission is VC. 17 I'm certainly not precluding hydrochloric acid. I 18 would think it's very likely that hydrochloric acid 19 is also a major component. 20 We do know that after the calendering, 21 after the welding, Peterson had to leave the room 22 because of the choking and it's clear that 23 hydrochloric acid was given off. I don't think 24 there's any question that hydrochloric acid would RNW 2103 37 1 be given off. 2 You clearly have misunderstood the point 3 that I made: That when we're dealing with PVC 4 film, VC emission is not a major component. HC1 is 5 the predominant major component when it comes to 6 PVC pellets. In addition to HC1 and all the other 7 factors which are given off from PVC film, there 8 will be very high emission levels of vinyl 9 chloride. 10 Q. Why is there a difference between PVC 11 film and PVC pellets to your understanding? 12 A. Well, there's an overwhelming difference 13 for very obvious reasons. There's high levels of 14 residual VC in PVC resins and dust particularly 15 those prior to 1975. 16 And there's very, very low minimal levels 17 in VC film -- in PVC film because of the PVC -- the 18 VC will constantly evaporate from the film and the 19 film is so very, very thin that the measured levels 20 of VC are minuscular. 21 Q. Is this also true with regard to thermal 22 degradation of PVC upon welding, which is also 23 contained within your paragraph? 24 A. Correct. RNW 2104 38 1 Q. So your testimony with regard to what is 2 given off and to what extent it's given off remains 3 the same whether it's from the heat-sealing process 4 or the welding process? 5 A. That's what the report states. 6 Q. That's all I'm trying to find out. 7 In Paragraph 4 on that same page where 8 you talk about VC being a multipotent carcinogen in 9 roads and exposed workers, et cetera, is this a 10 summary of what is contained in your table that 11 appears several pages later or tables with regard 12 to the illustrative literature on the effects of 13 VC/PVC in both animals and workers? 14 A. Sure -- 15 (Discussion off the record.) 16 THE WITNESS: The answer is sure with respect 17 to the respiratory tract tumors. It's no with 18 respect to the multipotent carcinogenicity. 19 The tables that follow deal specifically 20 with respiratory tract effects. The multipotent 21 carcinogenicity is referred to incidentally, but 22 the tables don't deal with the multipotency per se 23 as opposed to respiratory tract per se. 24 RNW 2105 39 1 BY MR. HOLLINGSHEAD: 2 Q. What studies do you rely upon for the 3 multipotency effect that's cited in paragraph 4 of 4 this page? 5 A. These are legion. They're not dealt with 6 in the tables that follow but you'll find them and 7 with references -- some early references under the 8 report on Harry Wilkinson and the attachments, the 9 appendix attachments. 10 Q. So they are contained within the document 11 we have marked as Epstein 4? 12 A. Yes, and also in the two tables there's 13 periodic incidental reference to multipotency. 14 Q. In paragraph 5 of this -- on this page 15 you talked about adenocarcinomas and large cell and 16 differentiated carcinomas in exposed workers. 17 Just so I understand how this relates to 18 the rest of the document, what studies or what 19 particular exposed workers are you talking about in 20 that paragraph 5? 21 A. In workers exposed to PVC dust. 22 Q. And which studies are you referring to? 23 A. There's about four or five studies in the 24 table. RNW 2106 40 1 Q. Contained in the table, right? 2 A. Sure. 3 Q. Then you also refer to laryngeal cancers 4 in VC/PVC-exposed workers, and I'm assuming that in 5 general, without regard to the ATC bagger, in 6 general you're referring to those who were 7 mentioned or studied in the Tabershaw studies? 8 A. Correct. 9 Q. And then the ATC bagger that is mentioned 10 in this paragraph 5 refers to-Mr. Wilkinson; is 11 that right? 12 A. Yes. 13 Q. Now Mr. Wilkinson was both a bagger and a 14 bag room utility worker, so that reference is just 15 to him; is that -16 A. Correct. 17 Q. With regard to the chart that is entitled 18 Illustrative Literature on the Toxic and 19 Carcinogenic Effects of VC/PVC in the Respiratory 20 Tract of Experimental Animals, first let me ask 21 whether or not you've made any changes in this 22 chart. I understand the answer to that should be 23 no, but 24 A. I don't think I have, no. RNW 2107 41 1 Q. Do you want to check it with my copy? 2 A. Might as well take a quick look at it. I 3 don't believe I have. 4 Lucky we did. 5 Q. Is there a change? 6 A. Yes. 7 MR. LEVINSON: What is this the doctor is 8 reviewing? 9 MR. HOLLINGSHEAD: He's looking at my copy of 10 what is contained in the exhibit we marked as 11 Epstein 4, and I have asked if he would compare it 12 with the current copy of Epstein 4 just to be sure 13 he did not change that, and I believe he perhaps 14 has found that he did. 15 THE WITNESS: Yes, there is one addition: 16 Cornish, C-o-r-n-i-s-h, and Abar, A-b-a-r, 1969, 17 dealiag with rats' inhalation of fumes from heated 18 PVC producing interstitial edema and focal 19 hemorrhages in the lungs. 20 MR. HOLLINGSHEAD: Why don't we pull that out 21 and replace it with a copy and we'll mark this as a 22 new exhibit. 23 I'm going to ask the reporter to mark 24 this revised table on experimental animals as the RNW 2108 42 1 next exhibit, and we'll make a copy of the old page 2 and place it back into the book. 3 4 5 6 7 BY MR. HOLLINGSHEAD: (Whereupon, Deposition Exhibit No. 23, Witness Epstein, was marked for identification.) 8 Q. 9 they ? Adenocarcinomas occur in the lung, don't 10 A. Yes. Well, they occur many places. 11 Q. On this chart when it refers to an 12 adenocarcinoma with the designation of AC, is that 13 supposed to indicate any particular location for 14 that cancer? 15 A. Yes, the heading for that as you see is 16 pulmonary effects. That's effects in the lung. 17 Q. What is the disease of fibrosis very 18 briefly if you will? 19 A. It's basically just scarring. 20 Q. And the disease of granuloma? 21 A. It's chronic inflammatory reaction 22 generally characterized by formation of nodules and 23 multinucleate giant cells associated with fibrosis. 24 Q. And what is adenoma? RNW 2109 43 1 A. Adenoma is a premalignant -- or it's a 2 tumor of the lung which hasn't progressed to 3 malignancy yet. 4 Q. Can you describe pneumoconiosis for me? 5 A. Yes, pneumoconiosis is a chronic 6 inflammatory condition of the lung generally 7 associated with fibrosis and granular nodulation 8 and granuloma formation. 9 Q. Pneumoconiosis is normally associated 10 with dust in some form, isn't*it? 11 A. Correct, yes. 12 Q. Can any form of dust cause -- potentially 13 cause pneumoconiosis? 14 A. That's my understanding. 15 Q. Would something even not chemically 16 related, for instance, something such as road dust 17 or dirt cause pneumoconiosis or could it? 18 A. At high concentrations it could, but 19 generally there has to be a -- there's generally an 20 inflammatory role, element to pneumoconiosis. But 21 to all intents and purposes dusts can also cause 22 pneumoconiosis at high concentrations. 23 Q. With regard to the reference to Frongia 24 in 1974, in the comments section there's a comment RNW 2110 44 1 that says, quote, "Exposed with workers bagging PVC 2 (Wagoner, '77)." 3 Can you explain that comment? 4 A. Certainly. This study, the Frongia et 5 al. study, took rats and guinea pigs and exposed 6 them in the area where workers were bagging PVC. 7 So these animals like the workers both developed 8 fibrosis nodulation granulomas. 9 Q. Were any -- strike that. 10 Obviously some of these tests were 11 inhalation studies, correct? 12 A. The overwhelming majority. There were 13 only two that were not in that table. 14 Q. Which two were not and what type of 15 exposure were they? 16 A. The Agarwal, A-g-a-r-w-a-1, et al., '78. 17 This was intratracheal injection. And the Feron et 18 al., '81, was either gavage -- that means putting a 19 tube down into the stomach -- or incorporation of 20 the PVC in the diet. 21 Q. In the chart on the illustrative 22 literature with regard to exposed workers, on the 23 Tabershaw studies on the first page there is a 24 reference in the column entitled Respiratory Tract RNW 2111 45 1 Effects to a #3354. 2 3 A. 4 paper. Could you just explain that for me? That's the code number in the Tabershaw 5 Q. For the individual who was found to have 6 an extrinsic laryngeal cancer? 7 A. Correct. 8 Q. And on the Comments side the note at the 9 end of that lists "respiratory system cancers, ICD 10 equals 160 - 164 . " 11 What does that mean? 12 A. That's an international code for -- 13 tumors internationally are coded with a coding 14 number. That's -- 160 to 164 is respiratory tract 15 or respiratory system. 16 Q. Following that same answer, laryngeal 17 cancer must be Item 161 in the code; is that -- 18 A. Correct, yes. 19 Q. Would you remind me again, please, as to 20 what workers were exposed in the Tabershaw 21 studies? What was their occupation? 22 A. These were basically VC workers to the 23 best of my recollection. 24 Q. At the manufacturing end as compared to RNW 2112 46 1 the bagging or storage end one might say do you 2 recall? 3 A. To be quite frank this is a whole series 4 of 19 industries -- based on 19 industries and I 5 believe they were -- they included PVC. It was a 6 VC/PVC set of studies. 7 Q. Before we leave this particular document, 8 which is the illustrative literature regarding 9 exposed workers, let me ask you about the Doll 10 study which is now one of the 'items on this 11 five-page document. 12 I take it that after we had our first day 13 of deposition you went and located the Doll study 14 because I believe you were not familiar with it at 15 that time. 16 A. Correct. 17 Q. What is it that you found with regard to 18 the Doll study? 19 A. Well, it is summarized in my table if 20 you'd like to give me a copy of my table. 21 Doll reviewed the literature and among 22 other things confirmed the fact that there was an 23 excess of respiratory tract cancers in the exposed 24 workers . RNW 2113 47 1 I should also point out that the Doll -2 with regard to respiratory tract systems, there was 3 a wide range of omissions in the references, 4 critical omissions in the references cited by Doll. 5 He failed to refer to the Waxweiler '76 study, the 6 Wagoner et al. '80 study, the Waxweiler et al. '81, 7 the Wagoner '83, and the Infante '81 studies. 8 As far as respiratory tract cancer, I 9 would categorize it as once over lightly with 10 omission of the critical documentation. In spite 11 of that, he recognized higher risks for lung cancer 12 in heavily exposed workers. 13 Q. What conclusions or findings did he come 14 to other than that? 15 A. Well, he -- it was a review of the whole 16 area of the epidemiology of VC/PVC and I quote 17 here: 18 "No positive evidence of a hazard 19 of nonmalignant disease or any type of 20 cancer other than angiosarcoma of the 21 liver has been found except possibly 22 for a small hazard of lung cancer when 23 exposure was heavy. 24 "There are, however, consistently RNW 2114 48 1 higher risks in the subgroups of men 2 in the U.S. and U.K. series in which 3 occupational hazards would be more likely. 4 That is, men employed for more than ten 5 years exposed to higher than average 6 concentrations or observed more than 7 twenty years after first exposures. 8 "The mortality from lung cancer 9 has been rising throughout the period 10 of observation." 11 I should also note that Doll's 12 conclusions on the lack of evidence of other 13 diseases besides angiosarcoma of the liver and lung 14 cancer and nonmalignant disease are in striking 15 contrast to a wide range of governmental studies in 16 the United States, in striking contrast to the 17 conclusions of innumerable international experts 18 representing academia, industry, labor, and 19 government and a branch of the WHO dealing with 20 cancer; namely, the International Agency for 21 Research on Cancer. 22 So Doll is way out on left base in this 23 area, and some of the additional references that I 24 cite in the amended table -- for instance, the IARC RNW 2115 49 1 '87 and the IARC '79 -- indicates how isolated Doll 2 is . 3 I also note that the Doll paper is also 4 characterized by an absence of reference to any 5 source of research support. This is particularly 6 interesting as Green College where Doll works has 7 been partially financed by industry including 8 Monsanto and this is to me of particular interest. 9 It is customary when you write scientific articles 10 based on research of one kind -or another to cite 11 source of research support. 12 So not only is he way out on left base -13 field in reference to some of the references I 14 cited, not only does he fail to cite critical 15 references such as Waxweiler et al., he also 16 recognizes the lung cancer but also he doesn't 17 reflect his source of research support. 18 Q. He found -- if I recall the paper right, 19 he found that there was a specific hazard of 20 angiosarcoma of the liver to men -- for men 21 occupationally exposed to vinyl chloride, correct, 22 and he also -23 A. That was found twenty, thirty years 24 before -- RNW 2116 50 1 Q. Well, he's not finding anything original. 2 He's doing a review of the literature, isn't he? 3 A. He's doing a partial -- a highly 4 selective review of the literature. 5 Q. By that I only wanted to indicate for the 6 record that he was not conducting original research 7 as I recall the paper. 8 A. Correct. 9 Q. Is there a listing in the Doll report as 10 to -- or the Doll paper as to .other occupational 11 hazards that men exposed to vinyl chloride may have 12 had? 13 A. He says there's no positive evidence of 14 nonmalignant disease. 15 Q. And you take issue with that statement 16 based upon the studies that you have supplied to me 17 in the course of two days of your deposition? 18 A. It's a statement that is in total 19 contrast to a vast body of documentation. 20 Q. Can I see the table again. 21 A. Sure. 22 MR. HOLLINGSHEAD: Now the other new papers 23 that were included on here -- if we can just take a 24 moment to find them. Off the record. RNW 2117 51 1 (Discussion off the record.) 2 MR. HOLLINGSHEAD: For the record in looking 3 at what we have marked this morning, there's some 4 confusion. Apparently I have marked the same 5 exhibit twice. Both Epstein 18 and Epstein 22 are 6 the same with the exception that Epstein 18 has the 7 check marks that Dr. Epstein put on the new 8 references for this table, which is what I am 9 turning my attention to now. 10 THE WITNESS: Turn to page 2 -- 11 MR. HOLLINGSHEAD: This is the first new 12 reference and this is -- 13 THE WITNESS: Byren et al., '76. 14 merely an excess of lung caner. That's 15 BY MR. HOLLINGSHEAD: 16 Q. Were you not aware of Byren prior to the 17 deposition two weeks ago? 18 A. Yes, sure, I was aware of that. 19 Q. Is there a reason why it was not cited at 20 that time? 21 A. No particular reason. The table wasn't 22 claimed to be totally comprehensive. 23 Q. What can you tell me about the Byren 24 study? RNW 2118 52 1 A. it was nearly one of many studies 2 confirming the excess of lung cancer in VC/PVC 3 wo r ke r s . 4 Q. Do you recall -- this document appears to 5 indicate it was an SMR study? 6 A. Yes. 7 Q. Do you recall what the expected 8 proportion would have been as compared to the 9 actual proportion -10 A. You mean the observed to the expected? 11 Q. Yes. 12 A. No, I don't recall. 13 Q. Was it significant do you know, 14 statistically significant? 15 A. I'm not sure. I doubt it. It's 16 biologically significant but probably not 17 statis-tically significant. 18 Q. What's the next one? 19 A. Bufler et al., '79. This was a 20 statistically significant excess of respiratory 21 tract cancers in VC workers and particularly in 22 more heavily exposed workers, and this was a 23 particularly important paper because the excess of 24 respiratory tract cancers persisted after RNW 2119 53 1 adjustment for smokers. 2 Q. That means that once somebody balanced 3 the study to take into account smokers, there was 4 still a statistically significant excess of lung 5 cancers -- I'm sorry, respiratory cancers? 6 A. Yes, correct. 7 The next is International Agency for 8 Research on Cancer, '79. This is a review of the 9 literature prior to 1978 on VC/PVC in animals and 10 humans. The report was prepared by a working group 11 of twenty international experts representing 12 academia, industry, labor, and government together 13 with the Secretariat of the IARC, which as I 14 mentioned before is a branch of the World Health 15 Organization dealing specifically with cancer. 16 First of all they stated vinyl chloride 17 is a human carcinogen. Its target organs are the 18 liver, brain, lungs, and haerao-lymphopoietic 19 system. This incidentally is in striking contrast 20 to the contrary and isolated statements of Doll. 21 IARC goes on to say there's no evidence 22 there's an exposure level below which there's no 23 increased risk of cancer in humans. IARC also goes 24 on to -- there's a statement that IARC reviewed the RNW 2120 54 1 literature demonstrating fibrotic lung changes, 2 pneumoconiosis, and reduced lung function in 3 workers exposed to PVC dust. 4 Q. Dr. Epstein, when you see the phrase 5 target organs or you use it yourself, how do you 6 employ that phrase? 7 A. When you talk about multipotency, that 8 means that a carcinogen can induce tumors in a 9 variety of organs. Then generally one lists what 10 the predominant organs are and you refer to them as 11 target organs. 12 Q. And the IARC report in '79 lists liver, 13 brain, lung, and haemo-lymphopoietic? 14 A. Yes. 15 Q. Did the report conclude whether or not 16 the larynx was a target organ for vinyl chloride? 17 A. There was no discussion of larynx, no 18 reference to larynx. 19 Q. What is the next new one that you have 20 listed? 21 A. In this connection you may recall that 22 the only publication by Tabershaw would have been 23 the Tabershaw and Gaffey paper on general 24 occupational medicine which to the best of my RNW 2121 55 1 recollection only referred to one laryngeal 2 cancer. The other industry studies were never 3 published and IARC only deals with published 4 studies The next it Infante '81 -- 5 Q. Could we hold that for a second? 6 A. Sure. 7 Q. If an agency such as IARC was aware of 8 the existence of an unpublished study, would they 9 include it in your experience? 10 A. In general the answer is no, they would 11 no t. 12 Q. Is there a reason for that? 13 A. Because they only cite published data 14 from the literature which are available to 15 scientists, the scientific community. 16 Q. Published studies would go through some 17 form of peer review, would they not? 18 A. Not necessarily. 19 Q. NO? 20 A. Some do, some don't. Depends what 21 journal it is. All you can say is unpublished 22 studies certainly don't have any peer review. 23 Q. And therefore are they considered less 24 authoritative by members of the medical or RNW 2122 56 1 scientific community? 2 A. Not necessarily. They can vary in 3 quality. Some may be highly reliable. Others may 4 be highly manipulated. 5 Q. What is the next new study? 6 A. Infante '81. This is a review and seven 7 of eight studies which he reviewed showed -- quote/ 8 "showed excess risks of lung cancers ranging from 7 9 to 200 percent." Data from two of the studies 10 suggested a qualitative dose-response relationship 11 between exposure and lung cancer risk. 12 In the one remaining study, which was 13 negative, the short duration of followup limited 14 the validity of any inferences that could be 15 developed. 16 The epidemiological evidence -- Infante 17 summarizes by saying the epidemiological evidence 18 demonstrates that the carcinogenic effects of VC in 19 humans extend beyond the liver. The brain and the 20 lungs should also be considered target organs. 21 And workers exposed to VC demonstrated a 22 significant excess of mortality for lung cancer, 23 and in fact he also stressed the sensitivity of the 24 epidemiological studies reflecting small cohorts RNW 2123 57 1 and inappropriate methodologies, et cetera. 2 Q. With regard to a study such as this one, 3 which is a review I will note, or with regard to a 4 paper such as this one that talks about an excess 5 of lung cancers, does that have particular 6 significance in your mind with regard to the 7 Peterson litigation and the fact that Mr. Peterson 8 contracted laryngeal cancer? 9 A. Well, it only has it insofar as that 10 respiratory tract or respiratory system cancers 11 include laryngeal. If a study specifically refers 12 to lung cancer as opposed to respiratory tract 13 cancers, its relevance would only be an expression 14 of the fact that the respiratory tract per se 15 including the lung is sensitive to these 16 carcinogenic effects. 17 The other point of course that should be 18 made is that lung cancer is very, very much more 19 common than laryngeal cancers and one would not 20 expect -- and if indeed these studies are 21 insensitive to even common cancers such as lung 22 cancer, the sensitivity to relatively rare cancers 23 would be of a very low order. 2 4 Q. Laryngeal cancer is one of those that are RNW 2124 58 1 relatively rare? 2 A. Yes . 3 Q. I think you gave a figure of 8.5 for 4 hundred thousand? 5 A. Superb. 6 Q. What's the incidence for lung cancer? 7 A. More than ten times that. 8 Q. The next new item on the table? 9 A. The next new one is IARC 1987 and this 10 updated the IARC '79. 11 And this is a report reported by a 12 working group of 35 international experts including 13 the Secretariat of IARC and basically stresses 14 again the multipotency of vinyl chloride; stresses 15 again, and several studies confirm, that exposure 16 causes lung tumors. Exposure to PVC dust was 17 associated with an increased incidence of lung 18 tumors too. 19 Q. In your -- 20 A. Excuse me. Something else was 21 handwritten on this one which is not on that -22 Q. Tell me what it is. 23 A. Under Doll -- you have it. I beg your 24 pardon. RNW 2125 59 1 Q. So the two exhibits seem to be exactly 2 the same? 3 A. Yes. 4 Q. In the exhibit we marked as Epstein 4 you 5 have a number of literature references actually in 6 their entirety in the back of the volume. 7 Are these new items that we've been 8 talking about contained in the report as it exists 9 now? 10 A. The references in the back relate to 11 larynx cancer, not necessarily to these. You may 12 recall last time I brought with me batches of cards 13 on my VC/PVC references. 14 MR. HOLLINGSHEAD: If you would, staying with 15 Epstein Exhibit 4 -16 MR. HOLLINGSHEAD: Do you mind if I break for 17 a seco-nd? 18 (Discussion off the record.) 19 BY MR. HOLLINGSHEAD: 20 Q. Turning to that portion of Epstein 4 in 21 which is contained Dr. Loomis's report of November 22 2, 1989, could you turn to that. 23 A. Yes. 24 Q. You have a certain amount of underlining RNW 2126 60 1 and a couple of what I would consider to be 2 exclamation points that you made in the margin. 3 Could we turn to the underlining and the 4 exclamation points. 5 A. Yes. 6 Q. Did the exclamation points mean anything 7 other than the fact that it's something to be 8 emphasized? For instance, do you disagree with the 9 statement that's made at that point in the report? 10 A. It could range from-astonishment to 11 incredulity. 12 Q. Why don't we turn to page 2 where a 13 couple of them appear. There are three sections 14 that are underlined on page 2. The first seems to 15 be underlining and a notation on your part. 16 Is there anything of significance to that 17 underlining? 18 A. No, that was simply confirmation of my 19 under -- that underlining that -- it said that 20 prior to his employment at ATC he had no specific 21 occupational exposure to any industrial chemical. 22 This is consistent with ray understanding and also 23 with Davidson's understanding. 24 Q. The next underlining talks about him RNW 2127 61 1 working most of the time in the vinyl packaging 2 room. 3 A. Again consistent with my understanding 4 and Davidson's understanding. 5 Q. The next underlining is a section which 6 contains the exclamation point, so tell me the 7 significance of that. 8 A. I would characterize that as a rubbish -9 statement as total scientific rubbish. He says PVC 10 is toxicologically a very safe compound but by, 11 according to literature, industrial exposure 12 produces only minimal nonspecific primary effects. 13 Q. He then goes on to talk about 14 unpolymerized vinyl chloride coming out of the -15 from which the PVC -- sorry. 16 It then goes on to talk about 17 unpolymerized vinyl chloride. 18 Does that straighten out any of the 19 concerns you have with regard to the earlier 20 statement on PVC? 21 A. No. The statement that PVC is 22 toxicologically very safe and produces only minimal 23 nonspecific pulmonary effects I characterized as 24 scientific rubbish. Whatever he may say afterwards RNW 2128 62 1 is another matter, but that statement is rubbish. 2 Q. The next page contains an underlined 3 section which also has exclamation points. Can you 4 talk about that for a minute? 5 A. That again is scientific nonsense. 6 There's general knowledge about the possible 7 tumorigenic properties of VC as well as the federal 8 regulatory act that didn't come about until almost 9 seven years after Peterson was initially employed 10 at ATC in 1974. There's substantial information on 11 this going back to minimally 1970 and possibly also 12 as early as 1965. 13 Q. And support for your statement can be 14 found throughout your report and the various 15 studies you have referred me to? 16 A. I would think these are discussed in 17 various places, yes. 18 Q. I'm only seeking now to go back over 19 things we've done before. 20 In the next section you've made some 21 handwritten notes in the left-hand margin. Let's 22 go through that for a moment. 23 A. Yes. Davidson estimates that up to 10 24 ppm vinyl chloride before 1975. RNW 2129 63 1 Q. Was there a statement by Dr. Loomis that 2 was inconsistent with that? 3 A. I didn't have an exclamation mark there. 4 Q. I'm just trying to figure out your code. 5 What's the reason for the comment there? 6 Just to remind yourself as to what Dr. Davidson had 7 said? 8 A. Because the Loomis document is 9 misleading. The -- first off, when he refers to 10 samples that were obtained showed less than .1 to 11 maximum .45, this is untrue. Three to 4 ppm were 12 demonstrated in the breathing zone of the bag room. 13 And even in 1975 his statement that 14 weighted average concentrations were .68 and .76 is 15 untrue. Levels over 1 ppm were found. There's 16 also no recognition of the high potency of vinyl 17 chloride including carcinogenicity at the lowest 18 level tested; namely, 1 ppm. 19 Q. Was that the Maltoni? 20 A. Correct. There was also one other study, 21 an ovarian study, which I refer to in mice and rats 22 with carcinogenic effects of 1 ppm and there's no 23 consideration of PVC dust. There's a substantial 24 literature on the carcinogenicity of PVC dust such RNW 2130 64 1 as the Wagoner, Waxweiler, IARC studies. we are on 2 page 4 now. 3 Q. On page 4 there's one underlined section 4 with a couple of -5 A. Yes. Laryngeal cancer has never been 6 documented to have been causally related to 7 exposure to VC or PVC is nonsense. He hasn't 8 obviously read the industry studies. 9 Q. The only one that specifically links 10 laryngeal cancer are the Tabershaw studies, 11 correct? 12 A. Tabershaw studies, correct. Lastly it's 13 only in Velez's report that exposure to asbestos is 14 suggested. This makes it clear that he has no 15 knowledge at all on pathology and radiology because 16 just by looking at the X-ray report on Mr. Peterson 17 it's clear that he had asbestosis. 18 Q. Do you know that he had it? 19 A. I have no idea. I presume that you and 20 Union Carbide furnished him with all the necessary 21 documentation and medical reports. 22 Q. Wouldn't you also have to assume that I 23 had it as well? 24 A. You had the medical reports. RNW 2131 65 1 Q. Yes, I had the medical reports. 2 A. And if you nad the medical reports you 3 had the X-ray report. The medical reports clearly 4 state that there was calcification. There was -5 you don't have to look at the X ray. The medical 6 reports state clearly there's calcification. 7 Page 5; "I am unable to find a single 8 report in the literature on laryngeal cancer." We 9 discussed that already. "In humans VC is believed 10 to be associated with accounts only of the rare 11 tumor angiosarcoma of the liver." I characterize 12 that again as scientific rubbish and hopeless 13 ignorance of the field in which presumably he's 14 acting as an expert. 15 Q. Going back to the first statement, the 16 only published article on laryngeal cancer would be 17 the on-e Tabershaw study. The other two are 18 unpublished, correct? 19 A. That's right, but he doesn't say -- he 20 doesn't talk about the published literature. He 21 says "in the literature," which includes 22 unpublished data. 23 Q. How does one get unpublished data? 24 A. By acting as an expert to industry, as a RNW 2132 66 1 consultant to industry, presumably industry files 2 will become available to you. Furthermore, these 3 unpublished data have been widely circulated. 4 The unpublished reports of Tabershaw have 5 been widely circulated and have been referenced in 6 various places in the published literature 7 particularly by government in government reports. 8 Q. You have a chart in here on meat wrappers 9 asthma as I recall? 10 A. A couple of tables, -yes. 11 Q. In particular there is one entitled 12 Chronic Meat Wrappers Asthma, Illustrative 13 Quotations on Irreversibility and another on Meat 14 Wrappers Asthma, Illustrative Statements on 15 Prevention and then there's another one looks like 16 a continuation of the statement on prevention. 17 Would you just indicate for me. 18 Dr. Epstein, the significance of the meat wrappers 19 asthma literature for the laryngeal cancer case 20 that Mr. Peterson presents. 21 A. I would say none. The only reason I put 22 it in was because you expressed an interest in any 23 cases before which I had been involved on PVC film. 24 I was responsive to your interests. RNW 2133 67 1 Q . Oh, I see. 2 Could you turn to the section on the 3 literature, the Austin 1982 document. 4 A. Sure. 5 Q. What is this compilation? How would one 6 refer to this? Is this a review of laryngeal 7 cancer? 8 A. Well, this is in the book by -- multi9 authored book edited by Schottenfeld and Fraumeni, 10 S-c-h-o-t-t-e-n-f-e-l-d, and F.raumeni, 11 F-r-a-u-m-e-n-i. There's a chapter on laryngeal 12 cancer and this chapter was authored by Austin and 13 this is just extracts of material from that 14 chapter. 15 Q. Do you consider it to be authoritative? 16 A. I would say yes on the whole. It's a 17 once over lightly but it's a pretty good basic 18 source. 19 Q. Was this published in '82? 20 A. Yes, it's a textbook -- it's a reference 21 book rather than a textbook. 22 Q. What was the year of the Tabershaw study 23 that indicated an existence of a laryngeal cancer 24 and a relationship with PVC? RNW 2134 68 1 A. About '74, '75. In the published one I 2 believe there was only reference to one cancer. 3 Q. To the laryngeal? 4 A. Yeah. The other two unpublished studies 5 contained reference to the two others. 6 Q. Unless I've missed it, when I read the 7 Austin paper there was no mention of the Tabershaw 8 study. 9 A. You're right. As I stated before in that 10 one published paper there was .only one laryngeal 11 cancer. You wouldn't expect it to be referred to. 12 Q. When were the unpublished studies of 13 Tabershaw? 14 A. '74 and '75. 15 Q. And presumably Austin would have had 16 access to the unpublished literature? 17 A. I doubt it. 18 Q. Why is that? 19 A. Because he doesn't work specifically in 20 the VC/PVC field. Had he worked specifically in 21 the VC/PVC field, he would have known about it. 22 Q. Had he known about it would you have 23 expected him to include Tabershaw in this review? 24 A. He might well have done so. RNW 2135 69 1 Q. Why would he not have -- in your opinion 2 why would he not have included the reference to the 3 one Tabershaw study that was published? 4 Was it not statistically significant 5 because it was only the one finding? 6 A. First of all, it's obviously not 7 statistically significant. The question is whether 8 it's biologically significant and one wouldn't in 9 fact ascribe biological significance to one 10 cancer. 11 But when you're dealing with three and 12 four laryngeal cancers, which we are now, then it 13 becomes more biologically significant and also 14 taking into account the fact that in several of the 15 VC/PVC studies the results are reported as 16 respiratory system cancers or respiratory tract 17 cancers, which would include laryngeal cancer. So 18 this particular chapter wouldn't reflect the 19 specific information on laryngeal cancer and VC. 20 Q. And that would account for the fact that 21 the entire paper is devoid of any comment about PVC 22 or VC, correct? 23 A. Correct. 24 Q. Austin lists asbestos as a risk factor at RNW 2136 71 1 on occupational factors the major risk factors as 2 being tobacco, alcohol, asbestos, nickel, and 3 mustard gas exposures. Would you -4 A. Yes, I have underlined those for you. 5 Q. Thank you. It helped me to find them but 6 I even read those sections that were not 7 under1ined. 8 A. Oh, bravo. 9 Q. Would you agree with his conclusion that 10 those are the major risk factors? 11 A. They are major risk factors. He doesn't 12 say "the" major risk factors. He said they are 13 major risk factors. 14 Q. If there were other major risk factors 15 would you have expected him to include it in his 16 paper ? 17 A. He does. He discusses them in increased 18 mortality of organization, with air pollution, in a 19 variety of occupations in which no particular 20 breakdown of chemical exposures has been 21 identified. Additionally even in meat cutters he 22 notes an elevated PMR was found. I should have 23 underlined that for you. 24 Q. I saw that too. RNW 2138 72 1 A. Sorry, I didn't underline it. 2 MR. HOLLINGSHEAD: I see you're also marking 3 the exhibit. Let the record reflect that 4 Dr. Epstein has underlined that portion of the 5 Exhibit Epstein 4 under Occupational Factors 6 talking about meat cutters. Off the record. 7 (Discussion off the record.) 8 MR. HOLLINGSHEAD: Dr. Epstein, let me ask you 9 to look at your report in this case which was 10 entitled Preliminary Report 9/13/89 and which we 11 marked as Exhibit Epstein 2 on the last occasion we 12 were together. Starting on page 7 there's a 13 discussion with regard to polystyrene. I would ask 14 you to turn to that. 15 BY MR. HOLLINGSHEAD: 16 Q. What form of polystyrene is it that was 17 present at ATC if you know? By that I mean whether 18 it pellet or powder. 19 A. To the best of my recollection they were 20 pellets. Let me see if I have a notation on that. 21 I don't have a notation on that. 22 Q. For the record I think I can represent to 23 you that they were pellets to the best of my 24 knowledge. That's also your recollection? RNW 2139 73 1 A. That's my impression but I don't have a 2 notation, however, on that. 3 Q. At the end of the first paragraph on 4 polystyrene you talk about exposure of animals to 5 PS, meaning polystyrene, dust induces 6 pneumoconiosis. 7 Do you know if that was with -- strike 8 that. 9 Do you know what study that was that 10 demonstrated that? 11 A. To be frank I don't and I would think 12 this is unfortunate that I didn't reference that. 13 Q. Would it be one of those references at 14 the bottom of the page? 15 A. I would imagine so, yes. 16 Q. Are you aware whether or not there's any 17 study that indicates that polystyrene pellets give 18 off dust and thereby cause pneumoconiosis? 19 A. Well, if you have pellets you'll 20 certainly get dust from the pellets. 21 Q. How do you get dust from the pellets? 22 A. From fragmentation. From handling of 23 pellets you'll generate dust. 24 Q. So your view would be whether the study RNW 2140 74 1 is with regard to powder or pellets of polystyrene 2 you would still get dust and therefore would likely 3 get pneumoconiosis? 4 A. It depends. 5 Q. Depends on the exposure and the size of 6 the dust fragments? 7 A. Yes, certainly. 8 Q. What micron size of dust would you need 9 in order to induce pneumoconiosis? 10 A. Well, dust would have to be respirable 11 and the particles of about 5 microns are 20 to 30 12 percent respirable, 10 microns is nonrespirable, 13 and 2 microns are about 100 percent respirable. So 14 in that range. 15 Q. Is there any study you are aware of that 16 with regard to polystyrene that shows a direct 17 causal relationship between exposure to polystyrene 18 and laryngeal cancer? 19 A. No. There's a study on styrene which 20 shows association with laryngeal cancer, Hobson and 21 Jones. 22 Q. What was the exposure do you recall in 23 Hobson and Jones? 24 A. To styrene. RNW 2141 75 1 Q. Were these animals? 2 A. No, that's an epidemiological study. 3 Q. 4 recall? What were the levels of exposure do you 5 A. I don ' t recall. 6 Q. Do you recall who, in terms of the 7 subject of the study, who was being studied? 8 A. Yes, workers, the exposed workers. 9 Q. Do you know what level they were being 10 exposed? 11 A. You just asked me that. I said I don't 12 know. 13 Q. Do you know in what end of the 14 manufacturing -- 15 A. I don't recall. 16 Q. -- business they were in? 17 A. The reference will give you all that 18 information. 19 Q. Yes, thank you. 20 How does IARC list their -- come up with 21 a list of carcinogens? 22 You've indicated here that you have -- at 23 the bottom you say styrene is ranked as a group 24 II-B carcinogen. RNW 2142 76 1 Is that a listing of the probable human 2 carcinogens ? 3 A. Well, it's a ranking of carcinogenicity 4 in which human and animal data are taken into 5 account. 6 Q. What are the rankings that IARC puts on 7 carcinogenicity? 8 A. Group I: when you have clear-cut 9 epidemiological data. II-A and II-B: II-A is 10 where you have reasonable epidemiological data. 11 Q. In humans? 12 A. Epidemiological is humans. II-B is -13 and you can have a II-A where you have excellent 14 animal data. II-B is animal data without -- is 15 very good animal data. Ill is animal data with no 16 epidemiological data. That's basically -- and IV 17 is ba&ically noncarcinogenic or questionable 18 validity of animal data. 19 Q. Group I again is known carcinogenicity? 20 A. One again is unequivocal epidemiological 21 data in humans, and IARC frequently states that 22 when you have valid animal data this creates a 23 strong presumption or basis for presumption of 24 human cancer risk. RNW 2143 77 1 Q. Do these rankings line up with the EPA 2 rankings? 3 A. Put it the other way around. EPA 4 rankings in general reflect the IARC although not 5 necessarily, and sometimes EPA refers to the IARC 6 rankings. 7 Q. Does styrene monomer pass from the pellet 8 to the air and if so can you tell me how and under 9 what conditions? 10 A. Sure. It's degassed in the same way as 11 VC is degassed from PVC and, additionally, when you 12 heat-treat polystyrene you will liberate styrene. 13 This is discussed in the first paragraph of page 7. 14 Q. Is there a residual level of styrene 15 contained within the pellet similar to PVC? 16 A. Yes, I refer you to sentence 2, paragraph 17 1, and. sentence 3. 18 Q. Sentence 2 indicates that polystyrene 19 contains up to 1 percent of the residual -- of the 20 volatile residual styrene monomer. 21 Is it your understanding that that is the 22 maximum that is contained within the pellet? 23 A. I haven't frankly looked at the early 24 literature to find whether there were higher levels RNW 2144 78 1 but these are references in '79 and '83. Whether 2 the levels at the time Peterson were (sic) exposed 3 were higher, I don't know. 4 Also we do know that to have high 5 concentrations of unreacted styrene released from 6 fresh polystyrene, the high concentrations are 7 released. That was known as early as 1968. 8 Q. Mr. Peterson was not exposed to 9 relatively fresh polystyrene, was he, to your 10 knowledge? 11 A. Polystyrene comes from UC. 12 Q. Right, but it was shipped from Texas, 13 wasn't it? Isn't that part of your information? 14 A. Yes. So what? 15 Q. When you talk about fresh polystyrene -16 A. As opposed to aged polystyrene. You and 17 I are aged. When we were born we were fresh. 18 Q. When polystyrene is first manufactured 19 it's fresh, correct? 20 A. Fresher than two weeks later. But in 21 addition to that I should point out to you that 22 when you degas a monomer from the polymer, the 23 monomer particularly in closed conditions such as 24 in a vat, et cetera, will adsorb itself on the RNW 2145 79 1 polymer. 2 So it really doesn't make much 3 difference. You'll have the adsorbed monomer on 4 the actual polymer as opposed to contained within 5 the polymer as when you have it under closed stored 6 conditions. 7 Q. So what you're saying is when it's 8 degassed out of the pellet, it then clings to the 9 outside of the pellet and that's what you referred 10 to as adsorbed? 11 A. No, that's not what I said. I said when 12 it is degassed under closed conditions such as in a 13 car or a vat or a box. When you degas in the air 14 you will have a progressive reduction in levels of 15 the monomer in the polymer. 16 But when you degas in a closed system, 17 essentially what's happening is that there's a 18 migration from within the polymer to the closed 19 dead air space and with the secondary adsorption on 20 the surface of the polymer. 21 Q. With regard to the Hobson and Jones study 22 which according to your paper demonstrated a major 23 excess of laryngeal cancer, I take it by the 24 reference to 3/0.5 that your expected rate of RNW 2146 80 1 cancer was .5 and the actual occurred cancer was at 2 rate 3? 3 A. Yes, in other words a six-fold increase 4 in workers exposed to polystyrene in the total 5 cohort; and when it comes to the subcohort of men 6 under the age of 45, the ratio then becomes 7 twenty-fold excess of laryngeal cancers. 8 Q. Do you know the amount of styrene or -9 well, the amount of polystyrene that Mr. Peterson 10 was exposed to? 11 A. No. 12 Q. Do you know the levels of the exposure? 13 A. Union Carbide failed to monitor -14 Q. The answer is no -15 A. I haven't finished -- and Golub 16 (phonetic) wasn't requested by ATC or Union Carbide 17 to monitor. Therefore, we have no information. 18 Q. Then I take it the answer to my question 19 is no? 20 A. Yes, the answer was no. 21 Q. Do you have information as to what 22 percent of Mr. Peterson's time was spent with 23 regard to either bagging polystyrene or in any 24 other way being around polystyrene as compared to RNW 2147 81 1 the amount, of time he spent with the PVC? 2 A. Well, he didn't spend time specifically 3 with -- he worked in tne bagging room. 4 If I may rephrase your question, it could 5 be posed as what percentage of the total polymers 6 entering into the bagging room were polystyrene as 7 opposed to polyvinyl chloride. I don't know -8 Q* I'll accept that question and you can 9 answer that one. 10 A. The answer is I don'.t know, but it's a 11 good question once rephrased. 12 Q. But the germ of it was good too. 13 A. 14 that. Dr. Davidson may have information on 15 Q. I only wish to establish what information 16 you have at the moment. 17 other information. I appreciate he may have 18 With regard to that same form of 19 question, do you have any understanding as to what 20 percentage of Mr. Peterson's time was spent -- off 21 the record. 22 (Discussion off the record.) 23 MR. HOLLINGSHEAD: Dr. Epstein, let me 24 withdraw that and rephrase the question. RNW 2148 82 1 BY MR. HOLLINGSHEAD: 2 Q. Do you have any information that would 3 tell you what percentage of time Mr. Peterson spent 4 on bagging any of the other resins in the ATC plant 5 as compared to PVC? 6 A. With due respect, as you know perfectly 7 well Mr. Peterson never bagged or was employed as a 8 bagger so I can't answer that. 9 Q. I will rephrase the question. 10 What percentage of time did he spend in 11 the bagging room when isopropy1idene resins were 12 being bagged do you know? 13 A. I don't know. I don't know whether they 14 were being bagged at the same time as PVC, whether 15 they were being bagged in separate batches. I just 16 don't know. 17 ft. You have acted on the assumption in this 18 case that the majority of Mr. Peterson's time was 19 spent in the presence of PVC, have you not? 20 A. That is an assumption but I regret to say 21 that I haven't substantiated that assumption -22 well, I know that the vast amounts of VC/PVC were 23 bagged. I went into the amounts in terms of bags 24 per day and pounds per day. I don't have the RNW 2149 83 1 equivalent information for polystyrene. 2 Q. Mr. Levinson's original letter to you in 3 April of 1988 that we have marked as Epstein 3 only 4 talks about PVC pellets if I read it correctly; am 5 I right ? 6 A. Correct. 7 Q. And that's one of the reasons why you've 8 assumed throughout your efforts in this case that 9 PVC was the main chemical to which Mr. Peterson was 10 exposed; is that -11 A. I believe this to be the case, but I will 12 prior to trial attempt to find out the percentage 13 of polystyrene and the other resins which were used 14 and the amounts used. That's provided this 15 information is available. If it isn't perhaps you 16 will pass this on to Mr. Levinson. 17 Q. With regard to the isopropylidene 18 bisphenol resins discussion which begins on page 8, 19 you indicate that bisphenol is a potent primary 20 irritant and sensitizer, and you go on to talk 21 about other things from the Shell (phonetic) 22 r epo r t, 19 8 2 . 23 Is there a particular ingredient in the 24 isopropylidene bisphenol resins that makes it a RNW 2150 84 1 primary irritant and sensitizer? 2 A. Well, there's various components. 3 Epichlorohydrin -- epichlorohydrin is certainly an 4 irritant and a sensitizer. Over and above that 5 there's a variety of other volatile components 6 particularly phenolics and the glycidol ethers 7 which are sensitizers too. 8 Q. I think I asked you the last time but 9 let's put it in context for today's deposition. 10 You have referred to isopropylidene 11 bisphenol resins and I think in particular to 4.4 12 isopropylidene -13 A. I'm sorry. I beg your pardon. What was 14 that? 15 Q. You have referred to isopropylidene 16 bisphenol resins and particularly 4.4 17 isoprapylidene diphenyl, have you not? 18 A. Yes. 19 Q. Do you understand those materials to be 20 the same as bisphenol A resins? 21 A. Yes. 22 Q. And is it your understanding that 23 epichlorohydrin is present in the bisphenol A that 24 was in existence at the ATC plant? RNW 2151 85 1 A. That's my understanding. 2 Q. Is it the epichlorohydrin that in fact is 3 the primary ingredient in making it a potent 4 irritant and sensitizer? 5 A. Well, that's the result -- the literature 6 on epiclorohydrin and also glycidol ethers as 7 irritants and sensitizers particularly 8 epichlorohydrin. 9 Q. Are you aware of any literature that 10 shows a causal relationship between bisphenol A 11 resins and laryngeal cancer? 12 A. I am unaware if there is any literature 13 on this. I know there's literature on respiratory 14 tract cancers including lung cancer and nasal 15 cancer. 16 Q. And that's referred to in the references 17 down at the bottom? 18 A. Yes. 19 Q. Are you aware of any literature showing a 20 causal relationship between epichlorohydrin and 21 laryngeal cancer? 22 A. No. As I said before, there's literature 23 on respiratory tract cancers and the respiratory 24 tract includes the larynx. There are references on rN\N 2^52 86 1 nasal cancer and lung cancer but I haven't seen any 2 on laryngeal cancer. 3 Q. What are the conclusions in the Interline 4 reports that are the first two references at the 5 bottom of the page? 6 A. There are a couple of reports, two or 7 three reports, by Interline and the very first 8 report demonstrates an excess of lung cancer, 9 respiratory tract cancer, and one of the subsequent 10 reports limited the statistical validity of the 11 earlier reports. 12 But again the interest of these agencies 13 with regard to laryngeal cancer is any agent that 14 is a respiratory tract irritant will certainly 15 increase the susceptibility of the larynx to agents 16 that can induce laryngeal cancer, and there's a 17 possibility of synergistic and interactive effects. 18 When you're dealing with a whole complex 19 of chemicals of this kind, the effects on any 20 particular target organ can differ very 21 substantially from the effects of exposure to a 22 single chemical. 23 Therefore, the data on studies based on 24 experimental or occupational studies based on a RNW 2153 87 1 single exposure would understate risks to 2 particular target organs which would be seen -3 which would develop when you expose workers to a 4 wide range of these different carcinogens, toxic, 5 and irritant agents. 6 Q. With regard to the welding emissions, 7 which is a discussion commencing on page 9 of your 8 report, what is your understanding as to how much 9 exposure Mr. Peterson had to welding fumes or 10 welding emissions while he was at ATC? 11 A. We know he welded. The amount of time he 12 spent on welding on a percentage basis every day I 13 don't know. The statements to the best of my 14 recollection are during welding he would sometimes 15 cough and choke and have to leave the room, but I 16 can't tell you the percentage of time he spent on 17 welding as opposed to other activities. 18 I'm not sure these data are available 19 although you might check with Union Carbide or ATC 20 on this to see whether they kept such records, 21 which I doubt. 22 Q. What makes up welding fumes? 23 A. First paragraph will -- gives you a 24 fairly comprehensive -- or attempts to give you a RNW 2154 88 1 fairly comprehensive statement of what can be 2 generated. 3 Of course you have to include in this 4 thermal degradation of any polymers which are on 5 contaminated surfaces such as polyvinyl chloride or 6 polystyrene which would result in release of the 7 residual monomer or the adsorbed monomer such as 8 vinyl chloride or styrene. 9 Q. Without regard to the thermal degradation 10 of PVC or polystyrene -- and by that I'm asking you 11 to assume that a particular welding episode or 12 series of welding episodes took place where there 13 was no thermal degradation because those materials 14 were not present on the metal that was being 15 welded -- is it your opinion that the welding fumes 16 that are given off during the welding process 17 contributed in some fashion to Mr. Peterson's 18 laryngeal cancer? 19 A. I would say that it's likely they played 20 a contributory role. 21 MR. HOLLINGSHEAD: Why don't we stop there. 22 (Whereupon, a luncheon 23 recess was taken until 24 1:15 p.m. this day.) RNW 2155 89 1 AFTERNOON SESS ION 2 (Whereupon, the deposition 3 in the above-entitled cause 4 was resumed at 1:15 o'clock 5 p.m. this day.) 6 MR. HOLLINGSHEAD: Dr. Epstein, directing your 7 attention to page 1 of your report which has been 8 marked as DC-2 as I recall, you talk on the first 9 page particularly in numbered paragraph 3 that 10 Mr. Peterson is at future risk of developing 11 progressive chronic obstructive lung disease and 12 attendant complications. 13 SAMUEL EPSTEIN, M.D., 14 the witness on the stand at the time of recess, 15 resumed the stand and testified further as follows: 16 EXAMINATION (Continued) 17 BY MR.. HOLLINGSHEAD: 18 Q. Can I ask you what you mean by attendant 19 complications? 20 A. Sure. First of all for progressive 21 chronic obstructive lung disease there's a variety 22 of complications that can occur from this. One is 23 just death from progressive respiratory failure. 24 And when you have obstructive lung RNW 2156 90 1 disease particularly in association with 2 restrictive disease you can get right heart 3 failure; and because the -- from tne right 4 ventricle you have a pulmonary artery going to the 5 lung, as you get increased resistance in the lung 6 because of fibrosis you can get gradual -- what's 7 called corpulmonale, c-o-r-p-u-l-m-o-n-a-l-e, with 8 progressive right heart failure. Then of course 9 increased incidence of respiratory infections, 10 pneumonia, et cetera. 11 Q. Can you quantify for me the increased 12 risk that Mr. Peterson does have to the development 13 of progressive chronic obstructive lung disease and 14 attendant complications? 15 A. I think that I should defer on this to 16 Dr. Velez. This is more his background. I can 17 only balk in general terms about this. 18 Q. Would you also defer on the first 19 sentence of paragraph 4 which talks about 20 Mr. Peterson being at future risk of developing 21 other cancers from his past occupational exposures 22 at ATC? Can you quantify that list? 23 A. As far as asbestos is concerned, I think 24 Velez has already done this for asbestos. I think RNW 2157 91 1 he talks about a five-fold increase in risk of lung 2 cancer. I can't quantify this in relation to the 3 whole mix of chemical carcinogens. I would say 4 he's at substantial excess risk for a variety of 5 reasons . 6 First of all he has excess risk for 7 respiratory tract cancers, particularly lung cancer 8 now, for two reasons. He's been exposed to a wide 9 range of pulmonary carcinogens, and these I've 10 tabulated for you in a table in Appendix 2 which of 11 them are carcinogenic to the larynx and which are 12 carcinogenic to the lung. 13 Secondly we know that once you get a 14 single primary in one site in the respiratory 15 tract, your chances of getting another cancer in 16 that same system are substantially increased and 17 that the second cancer can occur at a long time 18 subsequent to the diagnosis and treatment and cure 19 of the first. 20 Then of course you have the total 21 impossibility of developing any form of 22 quantitative prediction because of the multiple 23 interactions between these different carcinogens, 24 and then you've got carcinogenic effects at other RNW 2158 92 1 sites. 2 So I would say that he is at 3 substantially excess risk of future cancer with 4 particular reference to lung cancer but also 5 cancers at other sites. 6 Q. But when you use the phrase 7 "substantially increased risk" or "substantially 8 excess risk," you don't have a particular percent 9 age in mind as to what that substantial risk -10 increased risk is? 11 A. No, I can't quantitate it. But 12 substantially increased risk is more than 13 sufficient to justify the need for lifetime medical 14 surveillance and also justifies, creates a valid 15 basis of fear of the development of such risk and 16 of such future cancers. 17 Q. In your opinion to a reasonable degree of 18 medical probability can you say that Mr. Peterson 19 will in fact contract some additional cancer in the 20 future? 21 A. No, I can't say that. All I can say is 22 he is at substantial excess risk both of which 23 justify as I say two things. One, the need for 24 medical surveillance and the fear of such risk of RNW 2159 93 1 such eventuality -- eventualities. 2 Q. When a certain -- when chemicals are put 3 in combination, which is also referred to I suppose 4 as syne r gism -- 5 A. No, excuse me, they're not. The effects 6 could be -- you could have interactive effects of 7 various kinds. You can have theoretically a 8 negative association or you could have a positive 9 association. 10 The positive association could be 11 additive, could be simply the sum of the individual 12 carcinogenic effects. Or it could be a synergistic 13 which could be a multiplicative. So the effect 14 could be a multiplicative effect. 15 Q. In some combinations of chemicals would 16 one chemical act -- or can one chemical act as an 17 inhibitor upon other chemicals? 18 A. Theoretically, yes. 19 Q. You say theoretically. Have you not seen 20 that circumstance? 21 A. There's some experimental evidence along 22 these directions, but I don't know of any evidence 23 as far as humans are concerned. All the human data 24 point in the direction of either additive or RNW 6 94 1 synergistic interactions. 2 Q. When you talk about Mr. Peterson having a 3 substantially increased risk with regard to both 4 progressive chronic obstructive lung disease and I 5 think you also said the same thing with regard to 6 developing other cancers, what are you comparing 7 that risk to? 8 In other words if you have a 9 substantially increased risk, you have to be using 10 some baseline risk to begin with I would imagine. 11 So what are you comparing the risk to? 12 A. Well, I'm frankly -- as far as the 13 obstructive lung disease I'm not comparing it to 14 the general population because the general 15 population doesn't have in general a risk of 16 chronic obstructive lung disease. 17 What I'm saying is compared to his 18 present status. In other words there's a 19 substantial probability that there will be 20 deterioration in his medical status. That's what 21 I'm saying with relation to the chronic obstructive 22 lung disease. 23 With relation to cancer, as far as 24 cancer's concerned, however, I would say as RNW 2161 95 1 compared with the general population. 2 Q. So if I recall your testimony correctly 3 from the first day, you're using a risk -- a 4 general risk of 25 percent to 33 percent for the 5 population at large and you're talking about a 6 substantial increase on that risk? 7 A. Yes. There's a 1 in 3 risk of getting 8 cancer, which is as you say 33 percent, and 1 in 4 9 risk of dying from cancer, which is the general 10 population. 11 Q. I read the Austin paper which is included 12 in your report -13 A. Abstract. 14 Q. Whatever it is that appears in Epstein 4, 15 when I read that there was a considerable 16 discussion with regard to the effects of smoking 17 and alcohol upon a laryngeal cancer. 18 You have stated on page 2 of your 19 report -- and if I'm interpreting it correctly you 20 are suggesting that the fact that Mr. Peterson has 21 not smoked since 1968, which was twelve years 22 before he developed laryngeal keratosis and sixteen 23 years before he developed laryngeal cancer, is a 24 factor that you have taken into consideration. RNW 2162 96 1 Can you tell me why in your mind the fact 2 that he had not smoked in that period of time 3 should not be considered more strongly than 4 apparently you have in this report? 5 A. Yes, I can give the U.S. Surgeon General 6 as one of several references showing the effects of 7 the risks associated with light smoking firstly and 8 secondly the cessation of a prolonged duration of 9 smoking cessation. 10 These are two factors which make the role 11 of tobacco to say the least minimal on the 12 relatively small amount he smoked, but far more 13 importantly is the prolonged duration of smoking 14 cessation. 15 Q. He was smoking, however, at the rate of 16 one pack per day -17 A. Yes. 18 Q. -- when he first started employment with 19 ATC; is that not correct? 20 A. Yes, from the age of about 17 to 39. 21 Q. I'm sorry, say that again? 22 A. From the age of about 17 to 39 he smoked 23 about one pack a day, and you may recall that he 24 started work at ATC actually about the age of 38 so RNW 2163 97 1 it was just about the first year. 2 Q. You just looked at your list. When did 3 he first start at ATC? 4 A. I have a note that he started at the age 5 of 38; 38 to 44. 6 Q. Do you have a reference as to what year 7 that was? 8 A. Yes, 1967. So '67 -- if he was born in 9 '29, that's about 38. Am I right or am I off a 10 year? 11 He was born in April 1929 and he went to 12 work at ATC in 1967, in June '67. So what's April 13 '29 to June '67? That's two months and -- it's 14 more like 37. I won't rub it out and change it. 15 Q. Are there studies that talk about a 16 synergistic effect of cigarette smoking and 17 exposure to asbestos? 18 A. Oh, yes, sure. 19 Q. Is there a synergistic effect when those 20 two exposures are present? 21 A. Yes -- well, there's an element of 22 controversy on this. Selikoff has published 23 extensively on this. Wagoner has claimed that the 24 evidence for this is less persuasive. I don't have RNW 2164 98 1 a position on this. ' 2 Q. You do not? 3 A. No. My general understanding would veer 4 more towards the Selikoff position but I haven't 5 researched this in detail. 6 Q. Is this an area you would defer to 7 Dr. Velez on? 8 A. Yes, I think so. I think Velez has 9 looked at asbestos more closely than I have. 10 Q. Are there any studies to your knowledge 11 that talk about smoking -- cigarette smoking and 12 its impact on laryngeal cancer that also discuss 13 the concept or the effect of the cessation of 14 smoking? 15 A. Yes, sure. The U.S. Surgeon General's 16 report summarizes various studies on cessation of 17 smoking. You'll find that quoted in extracts on 18 that under the section laryngeal -- Larynx Cancer. 19 Q. Would you tell me what your recollection 20 is of the Surgeon General's report? 21 A. Sure. Basically there's a progressive 22 reduction in risk following cessation of smoking. 23 By the time you reach about ten or eleven years or 24 so, the risks are virtually normal. RNW 2165 99 1 Q. Is that with regard to virtually all 2 possible effects of smoking? 3 A. No, not at al1. 4 Q. Perhaps I'm confusing you. 5 In terms of your answer are you talking 6 about an elimination of virtually all risk of 7 contracting cancers as a result of smoking? 8 A. I was referring specifically to larynx 9 cancer. Similarly it relates to lung cancer. The 10 situation as far as cardiovasoular disease and 11 cancers at other sites in which smoking plays a 12 role I don't know. 13 I think as far as cardiovascular disease 14 there is such an effect although the specifics of 15 the timing I don't know. As far as other sites at 16 which smoking is a risk factor, although much less 17 of a risk factor than for lung or larynx, I don't 18 know. I haven't looked up those data. 19 Q. Are you aware of any studies that show a 20 causal relationship between cigarette smoking and 21 laryngeal cancer? 22 A. Oh, yes. 23 Q. Are you aware of any studies that talk 24 about the latency period for the onset of the RNW 2166 100 1 laryngeal cancer as a result of smoking? 2 A. May well be in the -- I should think the 3 U.S. Surgeon General's report deals with it. I 4 don't offhand recall. 5 Q. You don't offhand recall What the latency 6 period might be or -7 A. No, except that in general we do know 8 that Peterson got his laryngeal cancer at a much 9 earlier age than is known in the general 10 population; and as we know that smoking as -- that 11 one of the major risk factors for laryngeal cancer 12 in the general population is smoking, the fact that 13 Peterson got his lung cancer at a much earlier age 14 would also imply that the latency for smoking and 15 laryngeal cancer is a much longer one. 16 For instance if you turn to Table 2 of 17 the Austin, you see that by far the most -- the 18 highest incidence of laryngeal cancer is above the 19 age of 60. Now Peterson got his laryngeal cancer 20 in the 50 to 54 age bracket and his laryngeal 21 keratosis he got even before that. 22 So one would say that Peterson got his 23 laryngeal disease at a very, very much earlier age 24 than one would have anticipated from factors other RNW 2167 101 1 than occupational. 2 Q. I'm sorry, I'm not following what 3 implication you draw from the fact that he had 4 contracted his cancer at an earlier age than the 5 general population. 6 A. I'm saying that in the general population 7 one of the major risk factors is smoking, and in 8 the general population the maximal incidence of 9 laryngeal cancer is the age of 60-plus. 10 And if you'll recall* Peterson got his 11 laryngeal cancer at a very much earlier age. In 12 fact he got it at the age of 54. But in fact even 13 at the age of 49, which was five years before that, 14 he had developed laryngeal keratosis. 15 Q. And what inference do you draw from that? 16 A. I would say this is just one of many 17 factors all of which tend to minimize the role 18 of -- one of many factors which tend to minimize 19 the role of smoking and to maximize the role of 20 occupational factors. 21 Q. Wouldn't this table set forth by Austin 22 include smokers both active and former -23 A. Sure. 24 Q. -- in the general population? RNW 2168 102 1 A. Sure. It would reflect the general 2 population, yes, but the fact is that as we know 3 that smoking is a very strong risk factor, 4 particularly smoking in relation to alcohol, I 5 would say that the greatest impact of smoking would 6 appear to be in the age of 60-plus. It's difficult 7 to take it very much further than that. 8 Q. Even for someone who began smoking at the 9 age of 17? 10 A. Sure. He smoked about a pack a day which 11 would make him a relatively light smoker. If you 12 turn to the Surgeon General's report, you'll find 13 the relationship between smoking and laryngeal 14 cancer is strongly dependent on the numbers. 15 For instance, if you turn to Figure 21 16 you'll see that for males who smoked cigarettes of 17 under a pack a day, it's relatively small compared 18 to people who smoke four packs a day. And again if 19 you turn to Table 20 you'll find this laid out 20 again. For people who smoke under a pack a day, 21 it's lower than a half of people who smoke four 22 packs a day. 23 Q. Does the Surgeon General list a light 24 smoker as someone who smokes one pack a day? RNW 2169 103 1 A. I don't know the Surgeon General's 2 definition, but under one pack a day is certainly 3 light compared to four packs a day and the data 4 here are listed for four packs a day. 5 But you have two factors: One, the 6 amount he smoked and, two, the duration of 7 cessation which is given in figure 23; and you can 8 see by eleven years the risks are the same as the 9 general population. 10 Q. Somewhere in your report you indicate -11 page 4 of your report you talk about a latency 12 period of nineteen years. 13 A. That's for angiosarcoma of the liver. 14 There have been various figures from 19 to about 21 15 seems in most of the literature to be the average 16 latency for the angiosarcoma of the liver. 17 Now the angiosarcomas of the liver are 18 associated with relatively high exposures, so when 19 you're dealing with much lower exposures you would 20 expect a much longer latency. 21 Q. Just so the record is clear, the latency 22 period is for the effect of angiosarcoma of the 23 liver but -24 A. Excuse me. That's from the time of RNW 2170 104 1 initial exposure to the time of diagnosis. 2 Q. I understand that. I want to make the 3 record clear. 4 It's the latency period from the first 5 exposure to cigarette smoking, correct? 6 A. You've got me -- I don't understand what 7 you're talking about. 8 Q. Let me find the reference -9 A. Just say that -- oh, do you mean duration 10 of cessation of smoking? 11 Oh, page 2 discusses that. 12 Q. I'm confused. I was referring to page 4. 13 There is a reference to nineteen years, but it's 14 the average latency period from first exposure to 15 diagnosis -16 A. Of angiosarcoma, yeah, sure. 17 Q-. -- of angiosarcoma. So there is nothing 18 in your report that talks about latency period of 19 contracting any cancer as a result of exposure to 20 cigarette smoking except as referred to if at all 21 in the Surgeon General's report? 22 A. Well, the Surgeon General only -- parts 23 that I quoted here only deal with laryngeal 24 cancers. As far as lung cancers are concerned I RNW 2171 105 1 don't have any material here. 2 There's a dose response relationship with 3 very high levels of smoking and particularly when 4 you smoke starting from the age of ten or so, 5 latency is shorter. 6 But one of the points about the 7 respiratory system cancers and respiratory tract 8 cancers are that the longer you follow these 9 people -- the VC/PVC workers -- up, the higher is 10 the rate of lung cancer. 11 This is stated in several of the 12 references in the table; that the incidence of 13 respiratory tract cancer is higher in those. A, 14 that have been more heavily exposed and, B, that 15 have been followed up for longer periods. 16 Q. Do you believe that you can have a no 17 observable effect level for a carcinogen? 18 A. What? All one can say is there is an 19 overwhelming body of information in the literature 20 that we don't know any way of setting safe levels 21 for chemical carcinogens. 22 Q. Why is that? 23 A. This is an analysis of the literature; 24 and as far as vinyl chloride, for instance, is RNW 2172 106 1 concerned, even at the lowest levels to which it's 2 been tested -- which vinyl chloride has been 3 tested, namely 1 ppm, carcinogenic effects have 4 been found. 5 Carcinogenic effects have been found also 6 with exposure to vinyl chloride for one hour, one 7 hour. 8 Q. What is the concern? Is -9 A. Can I move on? I want to say -10 Q. I'm sorry. 11 A. In addition to the experimental evidence, 12 we have evidence from human beings showing that 13 very low levels of exposure are associated with 14 major increased risks. For instance, people living 15 in the vicinity of VC/PVC plants have an excess 16 risk of angiosarcoma of the liver. 17 In fact, calculations were developed to 18 the effect that even at the part per billion -- 20 19 part per billion level, the risks of angiosarcoma 20 are significantly increased. These are parts per 21 billion. 22 So -- but that again is consistent with 23 the experimental data that we have and the human 24 data that we have that any exposure confers finite RNW 2173 107 1 risk. The higher the level of the exposure, the 2 greater is the risk. 3 Q. What is the reason for that concern? Is 4 it that a single molecule of a carcinogenic 5 material can cause cell damage and as a result of 6 that lead to a tumor? 7 A. Well, that with due respect is a reductio 8 ad absurdum because a part per billion level of 9 vinyl chloride is equivalent to billions of 10 trillions of molecules, billions of trillions; for 11 instance, maybe some region of 10 to the power of 12 15. That's quadrillions of billions. So we're not 13 really dealing with a one molecule. 14 All one can say is at the lowest level 15 tested in animals there's still carcinogenic 16 effects; and even at the lowest levels of possible 17 exposure to humans, such as an accountant working 18 in a plant without ever going to the workplace 19 still gets a carcinoma of the lung, people living a 20 few miles away from a VC/PVC plant still get 21 angiosarcoma of the liver. 22 From a theoretical standpoint one could 23 say that theoretically one hit, one molecule on one 24 receptor site, can create genetic damage which can RNW 2174 108 1 theoretically be associated with carcinogenic 2 effects. But these levels -- even the very low 3 level of a part per billion is associated with 4 millions of trillions of molecules. 5 Q. Cigarette smoking has a carcinogenic 6 effect, does it not? 7 A. Correct. 8 Q. Would there not be a similar concern for 9 extremely low levels of exposure to cigarette 10 smoking? 11 A. Absolutely right. A person who smokes 12 one cigarette a day has more risks of getting lung 13 cancer than a person who smokes no cigarettes a 14 day, no question. 15 Q. Mr. Peterson was exposed to that 16 carcinogenic chemical, if I can call it that -- 17 A. Well, mix of chemicals. 18 Q. How so? 19 A. There's a vast mix of chemicals in 20 tobacco smoke. 21 Q. I'm sorry -- 22 A. From the age of 17 until the time he went 23 to work at ATC, but as I say that he had stopped 24 smoking for about eleven years or so before he RNW 2175 109 1 developed his laryngeal cancer; and based on the 2 analysis of all available data by Winder (phonetic) 3 and by the U.S. Surgeon General, the risk of his 4 laryngeal cancer is the same as that of a 5 non smo ke r. 6 Q. Assume for a moment that Mr. Peterson had 7 been exposed to VC for approximately a twenty-year 8 period and then had moved on to different 9 employment and thereby had a cessation of exposure 10 to VC. 11 Would you believe after -- for some time 12 after the cessation of that -- strike that. 13 Would you believe that Mr. Peterson would 14 be at risk for the contraction of cancer for the 15 rest of his life from that exposure to VC? 16 A. Nice try. In fact his risks would 17 progress and would become greater the longer he 18 lived. 19 Q. Why is that? 20 A. I was hoping you'd ask that. 21 There's an enormous difference between 22 what's called a late stage carcinogen such as 23 tobacco where the carcinogenic effects of tobacco 24 depend on the -- until you reach an irreversible RNW 2176 110 1 point, depend upon the continuing exposure. 2 In other words once you remove somebody 3 from the exposure to tobacco, their risks decrease 4 progressively. You see the similar effects with 5 women with endometrial cancer from estrogens, from 6 estrogen replacement therapy. The moment you 7 remove them off from their estrogen replacement 8 therapy, their risks of endometrial cancer shoot 9 way down. 10 When it comes to the overwhelming 11 majority of carcinogens, which we call early stage 12 carcinogens, the longer -- very often with these 13 people the longer you wait, the higher is their 14 risk. 15 You see this -- as far as respiratory 16 tract cancers are concerned, the highest rates of 17 respiratory tract cancers are on people who have 18 been followed up for a long period of time; and 19 Infante and others, however, have pointed out the 20 insensitivity of many of the epidemiological 21 studies insofar as people haven't been followed up 22 long enough. 23 Doll in fact also, even in spite of all 24 the criticisms I've made about the Doll study, is RNW 2177 111 1 forced to recognize that the risks of lung cancer 2 are greater in those who have had a longer period 3 of observation. 4 Q. In essence you're telling me that all 5 carcinogenic materials do not have the same impact 6 on the body and therefore do not raise the same 7 concerns? 8 A. Well, your language is your business. 9 What I'm saying is that when it comes to tobacco 10 there is a very marked decrease in risk 11 proportional to the cessation. When -- the period 12 of cessation from smoking. 13 There are a few other carcinogens that 14 fall into that category which are called late stage 15 carcinogens. For the overwhelming majority of 16 carcinogens, however, you're faced with a lifetime 17 risk ance you've been exposed. 18 In fact, you can have just one exposure 19 for one hour only with vinyl chloride and then get 20 tumors later in life as we know from the Consumer 21 Products Safety Commission studies on vinyl 22 chloride with mice and rodents. 23 So once you have initiated a carcinogenic 24 effect, these risks will last for a lifetime and RNW 2178 112 1 the longer you follow people up, the greater will 2 be the number of cancers you will uncover. 3 To give you one example for the asbestos 4 which we are discussing here, the asbestos risks, 5 you can be exposed for five years -- a period of 6 five years and then no more. Then the risks don't 7 really become very serious until about a thirty8 year period later. 9 Q. Is asbestos known as an early stage 10 carcinogen or a late stage -- 11 A. An early stage carcinogen. 12 Q. And that would make it similar to -13 A. Vinyl chloride and the other carcinogens 14 he was exposed to, the other occupational 15 carcinogens. 16 Q. So that an exposure to asbestos 17 theoretically on one occasion carries with it a 18 greater 19 A. A greater risk than no exposure. 20 Q. -- risk than no exposure? 21 A. Well put, yes. 22 Q. But that risk with regard to asbestos 23 continues for the rest -24 A. For lifetime. RNW 2179 113 1 Q. -- of the person's life? 2 A. Correct. And the same with vinyl 3 chloride and polyvinylchloride. 4 MR. HOLLINGSHEAD: I'll move to strike that 5 response as not responsive to the question. To be 6 more precise, I move to strike the last portion of 7 that answer as not being responsive to the 8 question. 9 Let's take a short break. 10 (Short recess.) 11 BY MR. HOLLINGSHEAD: 12 Q. Dr. Epstein, just going back to the 13 latency period discussion for a moment, normally is 14 the latency period given from first exposure to a 15 carcinogenic material or from last exposure? 16 A. Latency is often defined in very -17 neither. 18 Q. Why don't you tell me how you define 19 latency period and from what point in time do you 20 count the latency period? 21 A. Latency is defined in different ways by 22 different authors. Let me just tell you what these 23 are. 24 Generally latency is defined from time of RNW 2180 114 1 initial exposure to the time of the diagnosis of 2 the particular adverse effect. That's one. 3 Sometimes latency is defined, however, from the 4 time of initial exposure to the time of death; and 5 that is a little sloppy because the time -- when it 6 comes to fatal cancers like lung cancer, it doesn't 7 really make any difference. You simply add one or 8 two years on. 9 But when it comes to other cancers of 10 which you can have prolonged remissions or even 11 cures like laryngeal cancer, latency defined from 12 time of initial exposure to death for laryngeal 13 cancer would be a ridiculous thing because you have 14 a 50 to 60 percent cure rate for laryngeal cancers. 15 So those are two of the forms: from time 16 of initial exposure to the time of diagnosis is one 17 or to the time of death is a second. And sometimes 18 latency is defined more sloppily from the midpoint 19 of exposure. 20 But I would say that the best way of 21 defining latency is from initial exposure to 22 diagnosis bearing in mind that this isn't a 23 particularly good definition because initial 24 exposure may not reflect the period of maximal RNW 2181 115 1 expos ure. 2 But when you're dealing with an 3 individual when you can characterize different 4 exposure levels, one could refine it. But when 5 you're dealing with a population and an 6 epidemiological study, the only real way to handle 7 these data are from times of initial exposure to 8 times of diagnosis and that's generally the way 9 latency is defined. 10 Q. We may have discussed this over the 11 course of the two days and, if so, I'm sorry to 12 raise it again but -13 A. Sure. 14 Q. -- do you have a latency period in your 15 mind as to vinyl chloride? 16 A. Well, we talked about it in relation to 17 angiosarcoma of the liver. When it comes to 18 respiratory tract cancers, clearly the latency is 19 longer in general. 20 This is stressed in the various 21 references I have given in the table where it talks 22 about the lung cancer rates are particularly high 23 in those with longer periods of observation and 24 longer duration of followup. RNW 2182 116 1 And also it's reflected in comments of 2 Infante and others that most epidemiological 3 studies are insensitive because it's not an 4 adequate latent period -- followup. In other words 5 people haven't been followed up for a longer period 6 of time. 7 What one does seem to see with vinyl 8 chloride is at relatively high exposure levels you 9 get angiosarcoma and the average latency is about 10 nineteen, twenty years or so. With lower exposure 11 levels you get a shift in the target organ from 12 angiosarcoma to other sites, and the latency is 13 much greater than twenty years. 14 Q. Do you have a range in mind? 15 A. No, it's not possible to say this because 16 most of the epidemiological studies have had an 17 inadequate followup. But you see the longer you 18 observe these people, the higher the lung cancer 19 rates become -- the higher the respiratory tract 2 0 cancer rates become. 21 Q. In any event, whether it's angiosarcoma 22 of the liver or some other carcinogenic effect, 23 you're looking at a latency period that is 24 commenced with first exposure generally? RNW 2183 117 1 A. Yeah, that's the proper way of looking at 2 it. 3 Q. And that's the way you look at it? 4 A. Yes, sure. 5 MR. HOLLINGSHEAD: That's all I have. 6 Dr. Epstein. Thank you very much. 7 THE WITNESS: Fine. Thank you. 8 FURTHER DEPONENT SAITH NOT... 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 RNW 2184 118 1 STATE OF ILLINOIS ) ) SS : 2 COUNTY OF DU PAGE ) 3 4 I, Sandra A. Kaspar, a notary public 5 within and for ^he County of Du Page and State of 6 Illinois, do hereby certify 'that heretofore, 7 to-wit, on the 15th day of December 1989, SAMUEL 8 EPSTEIN, M.D., personally appeared before me at 303 9 West Madison Street, Suite 1400, in the City of 10 Chicago, in the County of Cool? and State of 11 Illinois, a witness in a certain cause now pending 12 and undetermined in the Superior Court of Middlesex 13 County, New Jersey, wherein John and Shirley Mae 14 Peterson are plaintiff and Union Carbide 15 Corporation is defendant. 16 I further certify that the said witness 17 was first duly sworn to testify the truth, the 18 whole truth, and nothing but the truth in the cause 19 aforesaid; that the testimony then given by said 20 witness was reported stenographically by me, in the 21 presence of the said witness, and afterwards 22 reduced to typewriting by computer-aided 23 transcription, and the foregoing is a true and 24 RNW 2185 119 1 correct transcript of the testimony so given by 2 said witness as aforesaid. 3 I further certify that the signature of 4 the witness to the foregoing deposition was waived 5 by agreement of counsel for the respective parties. 6 I further certify that there were present 7 at the taking of this deposition the attorneys as 8 hereinbefore noted. 9 I further certify that I am not counsel 10 for nor in any way related to .the parties to this 11 suit, nor am I in any way interested in the outcome 12 thereof. 13 In testimony whereof I have hereunto set 14 my hand and affixed my notarial seal this 22nd day 15 of December 1989. 16 __ , CSR 17 Notary Public, Du Pafge County, 111. 18 I CT-Tir.lAL ScAL 19 j SANOfV. A K.ASPAR i NOTARV italic STATE Or ILLINOIS j MV COKKISSIOU EXP MA X 24, i 902 20 21 22 23 24 RNW 2186