Document Y335yg7k9NY9pY0BD47xpO68

1 CAUSE NO. 17958-JG01 2 3 JAMES BOREN AND GINGER ) IN THE DISTRICT COURT OF BOREN ) 4) VS. ) BRAZORIA COUNTY, TEXAS 5) THE DOW CHEMICAL ) 6 COMPANY, ET AL. ) 239TH JUDICIAL DISTRICT 7 ********************************************************** 8 ORAL DEPOSITION OF 9 GERHARD K. RAABE, MD OCTOBER 6, 2004 10 ********************************************************** 11 12 13 14 15 16 17 ORAL DEPOSITION OF GERHARD K. RAABE, MD, duly sworn, produced 18 as a witness at the instance of the Plaintiff, was taken in the 19 above styled and numbered cause on the 6th day of October, 20 2004, from 10:05 a.m. to 4:12 p.m., before Valerie B. Corrales, 21 CSR, Certified Shorthand Reporter in and for the State of 22 Texas, reported by machine shorthand, at the offices of 23 THOMPSON & KNIGHT, LLP, 333 Clay Street, Suite 3300, Houston, 24 Texas, pursuant to the Texas Rules of Civil Procedure and the 25 provisions stated on the record. 1 1 A P P E A R A N C E S: 2 3 FOR THE PLAINTIFFS: Mr. Lance H. Lubel 4 Mr. J. Robert Black HEARD, ROBINS, CLOUD, LUBEL & GREENWOOD, LLP 5 500 Dallas, Suite 3100 Houston, Texas 77002 6 Tel 713-650-1200 7 FOR THE DEFENDANT THE DOW CHEMICAL COMPANY: Mr. Jonathan Shoebotham 8 THOMPSON & KNIGHT, LLP 333 Clay Street, Suite 3300 9 Houston, Texas 77002 Tel 713-654-8111 10 Ms. Katherine L. Rhyne 11 KING & SPALDING, LLP 1730 Pennsylvania Avenue, NW 12 Washington, DC 20006-4706 Tel 202-626-3743 13 14 15 16 17 18 19 20 21 22 23 24 25 2 1 INDEX 2 PAGE 3 Appearances.................................. 2 4 GERHARD K. RAABE, MD 5 Examination by Mr. Lubel............ 6 Examination by Mr. Shoebotham....... 156 6 Examination by Mr. Lubel............ 162 7 Signature and Changes........................ 172 8 Reporter's Certificate....................... 173 9 10 EXHIBITS 11 NO. DESCRIPTION PAGE 12 1 Plaintiffs' Second Amended Notice of 6 Intention to Take Oral and/or Videotaped 13 Deposition of Gerhard K. Raabe, MD and Subpoena Duces Tecum 14 2 The Nature of Chromosomal Aberrations 22 15 Detected in Humans Exposed to Benzene 16 3 Various articles 24 17 4 An update of mortality among chemical 34 workers exposed to benzene 18 5 Cause-specific mortality among employees 38 19 of a Texas-based chemical manufacturing facility, 1940 through 1996 20 6 Mortality Among a Large Cohort of Chemical 39 21 Manufacturing Employees 22 7 A Half-Century of Cause-Specific Mortality 39 Experience of Chemical Manufacturing 23 Employees 24 8 A Half-Century of Cause-Specific Mortality 39 Experience of Chemical Manufacturing 25 Employees (thicker version) 3 19 2 3 10 4 5 11 6 12 7 13 8 9 14 10 15 11 16 12 17 13 18 14 19 15 20 16 17 21 18 22 19 23 20 21 24 22 23 24 25 25 Cell-Type-Specific Leukemia Analyses in a Combined Cohort of More Than 208,000 Petroleum Workers in the United States and the United Kingdom, 1937-1989 54 An industry wide mortality study of chemical workers occupationally exposed to benzene. II Dose response analyses 60 Handwritten notes 106 Medical records 106 Benzene and the Dose-Related Incidence of Hematologic Neoplasms in China Deposition and Trial List, Dr. Gerhard K. Raabe 171 116 Curriculum Vitae 117 Materials sent by Mr. Shoebotham's office 117 Frank Parker's Dose Estimate 120 Affidavit of James Boren 121 Correspondence with Mr. Shoebotham 121 Leukemia -- Acute Myeloid (Myelogenous) and Adult Acute Myeloid Leukemia (PDQ) Treatment Health Professional Version 123 Acute Myelogenous Leukemia articles 124 Cancer Epidemiology and Prevention 125 Risk of acute myeloid leukaemia and multiple myeloma in workers exposed to benzene 132 Leukemia Risk and Relevant Benzene Exposure Period - Re: Follow-up Time on Risk Estimates, Am J Ind Med 42:481-489, 2002 Leukemia Risk Associated With Low-Level Benzene Exposure 132 134 4 1 26 2 3 27 4 28 5 29 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 Update of a prospective study of mortality 135 and cancer incidence in the Australian petroleum industry Benzene Exposure and Leukemia 138 Various articles 139 Benzene and Lymphohematopoietic 162 Malignancies in Humans 5 1 (RAABE Exhibit No. 1 was marked.) 2 GERHARD K. RAABE, MD, 3 having been first duly sworn, testified as follows: 4 EXAMINATION 5 QUESTIONS BY MR. LUBEL: 6 Q. Please state your full name. 7 A. Gerhard Karl Raabe. 8 Q. Where do you reside? 9 A. New Hope, Pennsylvania. 10 Q. Who hired you in this lawsuit? 11 A. Mr. Shoebotham. 12 Q. On behalf of what company does he represent? 13 A. Dow. 14 Q. Dow Chemical Company? 15 A. I'm not sure of the specifics of that. 16 Q. Have you ever heard of Dow Chemical Company? 17 A. Yes. 18 Q. Have you ever done any work for them? 19 A. Not that I recall. 20 Q. And I'm not talking about just in a lawsuit capacity. 21 I'm talking about have you ever done any consultation or 22 consulting work with them? 23 A. I don't think so. 24 Q. Do you -- do you know anybody that's employed by Dow 25 Chemical Company? 6 1 A. Yes. 2 Q. Who are they? 3 A. Currently employed? 4 Q. Yes, sir. 5 A. Jim Collins, Greg Bond -- but I have not seen him in 6 many years. I think he's still employed. 7 THE REPORTER: You think he is what? 8 THE WITNESS: I think he's still employed. I'm 9 sorry. 10 A. That's -- that's what comes to mind as we speak. 11 Q. (By Mr. Lubel) Are there any people that you do not 12 believe are still working for Dow Chemical that you've had 13 relationships with in the past? 14 A. Yes. 15 Q. Who are they? 16 A. Dr. Ralph Cook. That's the one that comes to mind. 17 Q. How do you know Jim Collins? 18 A. I've known Jim for a number of years. He was 19 considering taking a position with Mobil at one time. And I 20 believe he went to Monsanto. And I knew him when he was 21 Director of Epidemiology at Monsanto. And we've continued our 22 relationships over the years. 23 Q. Have you served on any committees or subcommittees 24 with Mr. Collins? 25 A. Yes. 7 1 Q. Which committees or subcommittees? 2 A. Dr. Collins and I were both on the American 3 Industrial Health Council's Epidemiology Committee. And we -4 we both are fairly active in the American College of 5 Epidemiology. So I see him there periodically, but we're not 6 on any committees together. 7 Q. Have you ever seen Dr. Collins at any American 8 Petroleum Institute or CMA meetings? 9 A. No API meetings. I don't think so at CMA. 10 Q. Any other industry organizations or trade groups for 11 which you recall seeing Dr. Collins at? 12 A. Yes, one other. We -- there was a group that we had 13 in the '80s called the Epidemiology Forum, and we participated 14 in the some of those meetings. 15 Q. Epidemiology Forum? 16 A. Yes. 17 Q. Is that group still together? 18 A. Don't actually know. It was an ad hoc group that 19 would meet about once a year. 20 Q. Was it petroleum or petrochemical company people? 21 A. It was epidemiologists that worked for essentially 22 industry, not particularly any industry -- specific industry. 23 Q. When is the last time you've spoken to Dr. Jim 24 Collins? 25 A. I -- probably -- the most recent time was probably 8 1 fall of 2003. 2 Q. What was the nature of that visit? 3 A. We had dinner together during one of the American 4 College of Epidemiology meetings. 5 Q. Was the dinner that you had business related or 6 purely personal? 7 A. No, just personal. 8 Q. Have you had any conversations with Dr. Collins about 9 the benzene studies in China? 10 A. I did ask him about that at dinner, whether Dow was 11 participating. 12 Q. Is that the extent of y'all's conversation about 13 that? 14 A. Yes. 15 Q. So you would not have shown the POWERPoint 16 presentation regarding the benzene China studies to 17 Dr. Collins. Correct? 18 A. No. 19 Q. Is that correct? 20 A. Yes, that's correct. 21 Q. Nor any other Dow people? 22 A. Not -- yes. No other Dow people that I'm aware of. 23 Q. So the only communication between, at least, yourself 24 and any Dow people regarding the Chinese benzene studies was 25 the few moments that you spoke to Dr. Collins at that dinner 9 1 about it. Correct? 2 A. Yes. 3 Q. And at least nobody on your behalf nor did you send 4 any written communications to anybody at Dow concerning the 5 benzene studies in China. Correct? 6 A. Not that I'm aware of. 7 Q. Is Dow Chemical participating in any form or fashion 8 in the benzene studies in China? 9 A. I don't know what the current status is. They 10 weren't when -- as of the time we spoke. 11 Q. Did Dr. Collins give you any indication as to why Dow 12 was not participating when y'all had that dinner? 13 A. I'm not sure if he knew. 14 Q. Did he voice any concerns or objections to you about 15 the design of those studies? 16 A. No. We didn't talk about them that long. 17 Q. Your conversation with Dr. Collins -- or 18 conversations, plural, I should say -- did not go to the extent 19 of getting into the actual study design, those types of things. 20 Correct? 21 A. No, not at all. 22 Q. Are you familiar with the study design? 23 A. No, sir. 24 Q. The Chinese study. 25 A. Basic -- the basic concepts that were being discussed 10 1 in 1999 but not since then. 2 Q. When were you first approached about the 3 industry-funded Chinese benzene studies? 4 MR. SHOEBOTHAM: Objection, form. 5 A. It was in -- first approached? I'm not sure if... 6 Q. (By Mr. Lubel) How did you become introduced to the 7 fact that they were considering the studies? 8 A. Well, during that period of time, I was actively 9 involved with the American Petroleum Institute on their health 10 and safety committee. We were interested in what were the 11 research opportunities that could provide more information on 12 health effects of benzene. And that was an evolutionary 13 process that went on several years before China became more 14 focussed. 15 Q. Who started the discussions about there needing to be 16 a study in China on benzene funded by industry? 17 A. I don't think there was any single individual. I 18 think the group of industry toxicologists and epidemiologists 19 and other professionals trying to explore is there any place in 20 the world where you can do additional research to better 21 understand the health benefits. 22 Q. And you recall our -- generally our discussion when I 23 deposed you in the James Cowey case, I believe, in -- around 24 December of 2003. We had a brief discussion about the Chinese 25 benzene studies. Correct? 11 1 A. Yes. 2 Q. And at that time you had told me that one of your 3 responsibilities for the American Petroleum Institute was to go 4 out and show different companies a POWERPoint presentation 5 regarding the studies. Correct? 6 A. I think that somewhat misstates what I said or at the 7 very least what I -- what I -- what I meant. I gave -- as 8 chair of the committee, once we decided on the approach, I gave 9 what I believe are two presentations at API meetings that had 10 -- had industry management types of different levels present. 11 Q. Who prepared the POWERPoint presentations that you're 12 referring to now? 13 A. Well, it was just essentially one presentation. And 14 part of it, I took input from Dr. Wong and Dr. Schnatter and 15 possibly even Dr. Irons. And collectively we came up with a 16 set of slides that described the general thoughts of what we 17 were trying to accomplish. 18 Q. And this was presented to the executives that had 19 appeared on behalf of the industry at the meeting or 20 presentation? 21 A. I don't remember the levels of the executives, but I 22 think that's probably true. They were API meetings. It would 23 have been petroleum representatives. 24 Q. And when were those present -- when was that 25 presentation made? 12 1 A. I don't know the -- the months. Probably 1999. 2 Q. Who are the stakeholders regarding the benzene 3 Chinese -- China studies? 4 A. I don't understand what you mean by stakeholders. 5 Q. You've never seen the term "stakeholders" referenced 6 in the documents of the committee that is responsible for the 7 industry-funded Chinese studies regarding -8 A. I've never seen that term used, no. 9 Q. Who are the companies that have funded those studies 10 to date? 11 A. I don't know the current list. I -- at the time all 12 I can tell you is -- is who -- who were heading -- heading to 13 funding when I left the industry. 14 Q. Who was that? 15 A. Exxon-Mobil, Shell, Chevron. I think those are the 16 only ones that, at the time I was leaving, had probably even 17 then not made formal commitments but seemed to be committed to 18 funding some portion. 19 Q. How about BP? Were they part of that group? 20 A. Don't recall. 21 Q. And did you have conversations with Patrick Beatty 22 about these studies? 23 A. Well, Patrick was a member of the health products 24 stewardship committee, but the studies had not started when I 25 left -- when I left the industry. 13 1 Q. Who designed the protocol for the studies? 2 A. I can tell you who the primary investigators were: 3 Dr. Otto Wong for the epidemiology components, Dr. Richard 4 Irons for molecular biology, and they had -- they were 5 assembling an advisory committee to help work out details. 6 Q. And is Dr. Irons in charge of the study or just a 7 part of it? 8 A. Just a part of it is my understanding. I mean, when 9 you say "in charge of," I'm talking the principal investigator. 10 I mean, I don't know how the project's managed at all. 11 Q. Would you agree that one of the purposes behind the 12 benzene study in China being sponsored or funded, if you will, 13 by industry was to understand the health effects of low level 14 benzene exposure? 15 A. Yes, that was one of the objectives. 16 Q. And another objective was to refute information that 17 had come out of the Australian Institute of Petroleum's health 18 watch study that was released in 2001? 19 A. That was not an objective that I'm aware of since it 20 came out two years after when I was working on that project. 21 Q. That was not an objective that you recall being 22 discussed by the American Petroleum Institute or its members? 23 A. Well, we weren't trying to refute anything. We were 24 trying to improve the state of the science and the -- protect 25 our workers. So the -- without knowing what the results of the 14 1 studies were, it's hard to imagine what -- what it would all be 2 used for. 3 Q. Well, do you recall that part of the purpose of this 4 study was to gain a quantifiable understanding of the 5 relationship between benzene exposure and potential associated 6 cancer risks? 7 A. Yes. Definitely. 8 Q. And one of the reasons -- or would it be a fair 9 statement that the primary reason that China was picked as the 10 location for these studies was because they had a unique study 11 environment, including databases documenting exposure? 12 A. Yes. I mean, ultimately that's -- that's one of the 13 reasons it became a favorable location. 14 Q. Do you know anything about the databases? 15 A. No. Not -- not -- only very general, not particular. 16 Q. Well, what was it about the databases in China that 17 made that location, if you will, unique to study benzene and 18 the effects of cancer? 19 A. Well, I'm not sure -- "unique" sounds like the only 20 place in the world. We -- we -- we started out by asking the 21 question whether -- where were there places where benzene 22 exposures were high enough that you could develop a range of 23 exposures and still identify cases. The databases around 24 Shanghai and -- and -- and some other places in China, they 25 have a -- essentially an epidemiologic surveillance registry 15 1 that, amongst other things, reports new cases of -- new cancer 2 cases and new leukemia cases, and it's tied into the region 3 which is very, very large, so the opportunity to collect a 4 number of cases over a short -- relatively short period of time 5 existed. 6 Q. And, in fact, didn't the organization acknowledge 7 that Shanghai was a unique study environment because there was 8 a range of exposure levels? 9 A. Yes. They did a site -- some individuals did a site 10 visit, and they felt it was -- offered a lot of opportunities. 11 Q. I take it that there was an agreement between these 12 companies that agreed to fund the studies and the 13 investigators. Would that be a fair statement? 14 A. I left the industry before anything formal was 15 established. I don't know. 16 Q. Would it surprise you that members of the companies 17 such as Chevron, Texaco, and Exxon-Mobil that had funded the 18 Chinese benzene studies that were being performed by Dr. Wong 19 and Dr. Irons and others, that they had the right to get 20 essentially data as the study was ongoing to review 21 information? 22 MR. SHOEBOTHAM: Objection, form. 23 A. I have no knowledge about that. 24 Q. (By Mr. Lubel) Would that surprise you? 25 MR. SHOEBOTHAM: Objection, form, calls for 16 1 speculation. 2 A. I don't -- I know nothing about it. 3 Q. (By Mr. Lubel) Let me ask you this: From an 4 epidemiological standpoint, is that appropriate for the 5 investigators to send data as the study is ongoing and not 6 completed to review the information? 7 MR. SHOEBOTHAM: Objection, form. 8 A. I've worked on a number of industry-sponsored studies 9 looking at multiple segments. It's not unusual for the 10 investigators to report in quarterly or semiannual or annual, 11 depending on the duration of the project, progress reports that 12 would say the number of cases that are identified or the -- the 13 total number of -- in the cohort at this time or in each 14 distributions, but these would be all demographics. They would 15 not have any outcome information in them. 16 Q. (By Mr. Lubel) What about laboratory results from 17 tests? Would that be appropriate from an epidemiological 18 standpoint for -- on an ongoing basis before the study has been 19 completed and reports have been drafted to furnish that 20 information to the companies that are essentially pouring 21 billions of dollars into the studies? 22 MR. SHOEBOTHAM: Objection, form. 23 A. I've not seen the protocols, so I don't know what 24 type of information we're talking about. It's just 25 speculation, so I -- I can't answer that. 17 1 Q. (By Mr. Lubel) But as a general rule, I mean -2 well, you're an epidemiologist, correct, by trade? 3 A. Yeah. 4 Q. As a general rule, is it appropriate for the 5 investigators to send reports of laboratory results for tests 6 that are being done in association with the study to the 7 companies that are funding the -- the study and before the 8 study is complete? 9 MR. SHOEBOTHAM: Objection, form. 10 A. I don't know what type of laboratory tests we're 11 talking about. If it's exposure related type of information 12 on -- on the set of data being collected, it -- it could make 13 sense. I don't know what we're talking about. 14 Q. (By Mr. Lubel) Let me ask you -- let -- let's do it 15 this way then: What type of information is appropriate for the 16 investigators to share with the sponsoring or funding companies 17 before the study's ever completed, as it's ongoing? 18 MR. SHOEBOTHAM: Objection, form. 19 A. I've never participated in a study that had molecular 20 biology components to it, so I have no experience to speak from 21 in that area. 22 Q. (By Mr. Lubel) Are you -- have you been privy to the 23 various committees that have been created concerning the study 24 and membership organization, things of that nature? 25 A. No. No, I have no information. 18 1 Q. Are you familiar with the American Petroleum 2 Institute's responsibilities with regard to this 3 industry-funded study in China? 4 A. Vaguely as it was evolving in 2000. 5 Q. What's your understanding of API's responsibility? 6 A. Well, as it was evolving at that time, they were 7 going to provide administrative support for the project in the 8 sense of handling the building and organizing oversight 9 committee meetings, things like that. 10 Q. Including negotiating agreements with investigators? 11 A. I -- I think part of the activity was they would -12 they would write the contracts with part of the administrative 13 component. 14 Q. Were you aware that one of the reasons behind this 15 study was to determine whether benzene causes all forms of AML 16 or only certain subtypes? 17 A. That was one of the objectives of the -- the 18 research. Or is, I guess, an objective of the research. I -19 I would use the word "confirm" what we believed to be already 20 the substate of the science. 21 Q. Which is what? 22 A. That benzene is only associated after high doses and 23 long duration with certain forms of acute myelogenous. 24 Q. Which forms? 25 A. Well, most typically M7 -- those with five to seven 19 1 dilutions. 2 Q. Those the only ones that benzene causes? 3 A. By far the most frequent. There -- there are 4 other -- some other chromosomal abnormalities and 5 translocations that -- that have been associated but of lower 6 frequency. 7 Q. Which one? 8 A. Those are reviewed by -- pretty well by Zhang. 9 Q. Let me ask it this way: Is there any chromosome 10 abnormalities that you believe are not related to benzene 11 exposure? 12 A. Based on my reading of the literature, which is still 13 emerging, inverse 16 is not related to benzene, and 14 translocation 15, 17 of the form that Mr. Boren has is not -15 or it does not appear to be related to benzene. 16 Q. And do you have studies that state that translocation 17 15 and 17 is not related to benzene? 18 A. There is a fair amount of epidemiology about 19 promyelocyte leukemias that the world generally concludes that 20 there are no known environmental or occupational associations. 21 I mean, there are some statistical associations here and there, 22 but -- but benzene is not on any of those lists. 23 Q. I'm just asking you if you brought with you today 24 studies that conclude that benzene cannot cause translocations 25 of chromosomes 15 and 17? 20 1 A. No, I have not. 2 Q. Have you brought with you any studies that state in 3 conclusion that benzene exposures can't cause translocation or 4 breaks in 16? 5 A. Well, actually, let me rephrase even the answer to 6 the first question. I have brought paper with me that examines 7 the various frequencies and types of -- of translocation and 8 chromosomal breaks that are associated with benzene. And you 9 do not see clear. The statements are all made in the positive 10 of what you see. Okay? And what you don't see are the -- are 11 any translocations of 15 and 17 without lots of other 12 chromosomal abnormalities associated with it. And you don't 13 see any inverted 16s probably at all. But these are reviews of 14 all the chromosomal abberations detected in humans exposed to 15 benzene. 16 Q. Will you pull those studies out, if you've got one? 17 A. That one. That one actually reviews the benzene. 18 MR. LUBEL: Stickers. 19 THE REPORTER: That one actually what? I'm 20 sorry. What did you just say? 21 THE WITNESS: That paper was specific to what 22 has been observed in benzene. 23 MR. LUBEL: And we're going to mark what you 24 just called that paper as Exhibit 2. Okay? 25 (RAABE Exhibit No. 2 was marked.) 21 1 A. Yeah. It's the paper by Zhang and Martyn Smith is 2 the last author. 3 Q. (By Mr. Lubel) Before you move to the next paper, 4 can you show me where in this paper these authors reach the 5 conclusion that translocations of 15 and 17 are not related to 6 benzene exposures? Or can't be related to benzene exposures. 7 A. Well, I -- I stated that these papers are in the 8 affirmative. They -- they are reporting what has been seen. 9 Q. I understand you said that. Now I'm asking you: Can 10 you find for me in that article the location where they say -11 A. No, you cannot. 12 Q. -- it can't cause it? 13 A. No, you would not. 14 Q. In any of the studies -- you've done studies on 15 benzene. Correct? 16 A. Yes. 17 Q. They've been published? 18 A. Yes. 19 Q. In any of your studies, did you conclude that the 20 translocations 15 and 17 can't be related to benzene exposures? 21 A. As some of these papers criticizing our epidemiology 22 portray is that we have not -- it's only in the last several 23 years that the appreciation of the cyto -- cytogenetics and the 24 subspecies, the subclassifications of AML, is very important. 25 So the -- pretty much all the epidemiology and certainly the 22 1 epidemiology that is exclusively dealing with mortality studies 2 just can't do that. 3 MR. LUBEL: Objection, nonresponsive. 4 Q. (By Mr. Lubel) My question, Dr. Raabe, is: In any 5 of the studies that you performed on benzene, did you make any 6 statement or draw a conclusion that is in written form that 7 benzene exposures cannot cause the chromosome translocations of 8 15 and 17? 9 A. None of our studies had a subtype available. So the 10 answer is no, we did not. 11 Q. Now, you also referenced chromosome damage to 16. 12 Correct? 13 A. Invert -- inverted 16. 14 Q. Inverted 16? 15 A. That's an M4. That's not related to Mr. Bolen. 16 Q. You call that an M4? 17 A. Well, it's -- it is a form of M4. Pure inverted 16 18 is the marker generally for classified -- classification of M4. 19 Q. Does Exhibit No. 2, which you've told us addresses 20 translocations 15 and 17, also address inverted 16? 21 A. It addresses what has been found in benzene-exposed 22 workers. 23 Q. Right. Now, I interrupted you from your process of 24 gathering the other articles on this issue. So I'm going to 25 give you -- 23 1 MR. LUBEL: Let's take a short break so you can 2 pull those out, if you don't mind. 3 THE WITNESS: That's fine. 4 (Recess from 10:35 a.m. to 10:41 a.m.) 5 Q. (By Mr. Lubel) Have you pulled the studies we talked 6 about before the break? 7 A. Yes. I pulled the studies that I think are related 8 to the discussion of what can cause acute promyelocytic 9 leukemia and what is known about secondary benzene or other 10 chemical-induced leukemia. 11 MR. LUBEL: Can we mark those as Exhibit 3, all 12 of them? 13 THE WITNESS: Yes, that's fine with me. 14 (RAABE Exhibit No. 3 was marked.) 15 Q. (By Mr. Lubel) Do any of the studies that we've 16 marked as Exhibit No. 3 that you've brought with you today 17 conclude that benzene exposures cannot cause APL? 18 A. The very first one, for example, concludes that there 19 are no known -- it -- it reviews what is known about the 20 occupational and therapy related and other possible etiologies 21 for -- may we call it APL? 22 Q. (Mr. Lubel nods.) 23 A. APL. And draws the conclusion that it -- that there 24 are currently no known associations. 25 The second paper examines a number of risk 24 1 factors associated with a large study of APL in -- in Italy -2 I believe it's Italy -- and concludes that while they find a 3 few associations, none of them were related to trades or crafts 4 that would be thought to have potential for benzene exposure. 5 The last one is another case control study of 6 acute promyelocytic leukemia. And it -- the only association 7 it finds is related to shoe making in Italy and weak 8 associations with radionuclide exposure and hair dyes. 9 The last -- the next paper is therapy-related 10 acute promyelocytic leukemias, discusses what appeared -- what 11 makes APL very unique in that even secondaries look pretty 12 similar to the -- the primaries in terms of their treatment 13 outcome and things like that and discusses the types of 14 materials that are potentially capable of causing secondaries. 15 And benzene, at least in terms of exclusion, does not seem to 16 fall into those categories. 17 And the last paper is a -- is a review paper of 18 what's known about secondary myelodysplastic syndromes in 19 leukemias not specific to APL. 20 MR. LUBEL: Objection, nonresponsive. 21 Q. (By Mr. Lubel) My only question, Dr. Raabe, is: In 22 Exhibit No. 3, can you pull out the section in any of these 23 studies that conclude that benzene does not cause APL? 24 A. No. 25 Q. Exhibit No. 1 is a copy -- copy of your deposition 25 1 notice. I take it that Mr. Shoebotham, on behalf of his client 2 Dow Chemical, forwarded that before you got here today? 3 A. Yes, sir. 4 Q. Have you brought all the materials that you're 5 relying upon for your opinions? 6 A. Yes. I believe generally these are the ones that 7 would be directly responsive to my opinions in Mr. Boren's 8 case. 9 Q. Have you brought with you the POWERPoint presentation 10 that you used for the benzene studies in China? 11 A. No, I have not. 12 Q. Do you still have it? 13 A. It's still on my desktop, yes. 14 Q. Is there any particular reason you hadn't -- have not 15 brought that? 16 MR. SHOEBOTHAM: I filed an objection to that 17 section of the duces tecum yesterday. 18 Q. (By Mr. Lubel) Is there any particular reason you 19 have -20 MR. SHOEBOTHAM: I advised Dr. Raabe there was 21 an objection that I filed. 22 Q. (By Mr. Lubel) So based upon recommendations of 23 Mr. Shoebotham, you've not brought it. Correct? 24 A. Correct. 25 Q. Is there anything proprietary or secretive about the 26 1 POWERPoint presentation? 2 A. No. Other than it's not related to anything about 3 Mr. Boren. 4 Q. Isn't the Chinese studies about acute leukemias? 5 A. It's a series of studies that have just begun. And I 6 don't know the timeline, but I wouldn't expect any results for 7 three to four or five years. So it's difficult to imagine how 8 anything about those studies could relate to Mr. Boren. 9 Q. Aren't there statements -10 A. Unless it's historically. 11 Q. Don't you make statements in the POWERPoint 12 presentation about AMLs? 13 A. Yes. 14 Q. That's not related to Mr. Boren? Isn't he an AML? 15 A. But the statements are that we want to have more 16 additional study on dose response for AML. But that's not 17 going to happen for years. 18 Q. Well, in fact, the purpose behind the study, at least 19 one of the purposes, is the fact that industry has been plagued 20 with a lack of evidence on whether there's a threshold for 21 benzene and AMLs. Correct? 22 A. No. 23 Q. Isn't that the reason they're going to China to find 24 the threshold? 25 A. No. 27 1 Q. That's not part of the purpose of the study is to 2 find out if there's a threshold for benzene exposure for which 3 no effect can be seen? 4 A. Right now there is only -- there are very few cohorts 5 and only one that has been deemed acceptable for use in risk 6 assessment which is dose response analysis. And one of the 7 objectives of the -- of the Chinese studies is to conduct at 8 least one additional study, if not more, that would -- could be 9 used to assess whether what we have out of the Pliofilm cohort 10 is correct. 11 Q. So you were not aware that one of the primary 12 objectives of the benzene industry-funded China studies was to 13 assess whether there's a threshold level of benzene exposure 14 for which no effect can be seen? 15 A. Well, we have one study of that form to date. 16 Certainly one of the -- when I say "dose response analysis," a 17 consequence of dose response analysis would address the 18 question: Are there levels of benzene exposure for which there 19 is no increased risk of leukemia? We have one study that we 20 use in the United States that gives us data on that. And it 21 would be nice to have some other well-designed, well-conducted 22 studies. 23 Q. And is that the -- one of the main objectives of the 24 Chinese benzene study is to determine what threshold, if any, 25 there is? 28 1 MR. SHOEBOTHAM: Objection, form, asked and 2 answered. 3 A. There's an epidemiology component that will also -4 that hopefully will address dose response analysis, but there's 5 also an enormous molecular biology component that hopefully 6 will provide new science and insight on to the course of 7 occupationally-related benzene-induced disease, not just AML. 8 Q. (By Mr. Lubel) So if I've got, you know, documents 9 from this -- these group of companies that are funding this 10 study in China on benzene that suggest that one of the primary 11 reasons that this study is being put together is to make a 12 determination of the dose response relationship between benzene 13 exposures and effect, you just disagree with that? 14 A. I thought I just said that is one of the objectives. 15 Q. And the companies that fund this study hope that this 16 research may establish that there is an absolute threshold for 17 benzene-induced hematological disorders below which there's no 18 effect. Correct? 19 A. I don't know what they hope. It would -- certainly 20 would be a -- if true, it would -- if true and confirmed in 21 those studies, would be -- it might very -- I think everyone 22 would feel happy if we had more data on that subject. 23 Q. And you were aware, were you not, that at least the 24 two primary reasons behind the study, as you testified in the 25 Cowey case, was to defend the companies in benzene-related 29 1 litigation, number one; and number two, to have documented 2 proof that helps the companies in a regulatory setting? 3 A. That misstates my testimony in that -- in that case. 4 Q. In the Cowey case? 5 A. Yes, it does. 6 Q. You didn't say that in the Cowey case? 7 A. What I said in the Cowey case is we went through a 8 long list of reasons for doing those studies: worker 9 protection, more insight on dose response, more insight on 10 course of disease. We went through a very long list. 11 You asked me then what would be some of the 12 benefits of having data that supported, you know, what -- what 13 we currently believe already exists. I mentioned the -- that 14 it would have impact on some of the regulatory issues. 15 You badgered me some more about litigation, and 16 at that point, I acknowledged that that could be a consequence. 17 But it was not and never was an objective of those studies. 18 Q. Well, you'd agree that we can go back and look at 19 your testimony in the Cowey case -- it's about ten months 20 old -- and we can see what was said. Correct? 21 A. Yes. 22 Q. And you stand by the opinions -- statements you gave 23 in that testimony under oath. Correct? 24 A. Yes. 25 Q. Are you relying on any information from Dow Chemical 30 1 in this case for your opinions? 2 A. Some of the information that supports my opinion 3 comes from some of the epidemiology studies done in the 4 Freeport operations, yes. It's not a -- I don't exclusively 5 rely on it, but it supports my opinion. 6 Q. Let me ask you this: Are you relying upon any of the 7 published studies by Ott or Bond, any of that work? 8 A. Well, we -- they're of historical interest because 9 they -- they provide some limited information on -- on the risk 10 of leukemia from benzene-exposed workers out of the Midland 11 operation which was a totally different operation than where 12 Mr. Boren worked. 13 Q. What were they studying in Midland? 14 A. Very similarly they -- the initial studies were all 15 designed to look at the health of the workforce at the plant. 16 Q. They weren't studying benzene exposures only? 17 A. Well, they focussed down on benzene exposures. 18 Q. So you're telling me they were looking at all 19 malignancies in that study? In -- in the Midland studies that 20 were published by Ott, Bond, and others. 21 A. Well, the published studies are focusing in on 22 benzene. 23 Q. Have you seen any unpublished studies that focussed 24 on something else? 25 A. I have a recollection that there -- that there must 31 1 have been -- I mean, they're nested within a cohort. So I have 2 this recollection that they must have conducted a -- a study 3 that looked at all cancer mentality and then drilled down. But 4 offhand, I don't remember the citation. 5 Q. Can you pull for us the Dow-Midland studies that you 6 have with you today -7 A. Yes, sir. 8 Q. -- please? 9 A. Freeport. That's Midland. 10 MR. LUBEL: Jonathan, what -- what is your 11 objection to the POWERPoint presentation? Is it privilege or 12 what's your objection? 13 MR. SHOEBOTHAM: My objection is stated in the 14 objection that was filed yesterday. My recollection is that 15 the grounds were -- were primarily relevancy. But I think 16 there may have been some other grounds. I would just rely on 17 the written objection that we filed before the deposition 18 began. 19 Okay. Let's take a break. I'll be right back. 20 MR. LUBEL: Can I continue asking him questions? 21 MR. SHOEBOTHAM: What's that? 22 MR. LUBEL: Can I continue to ask him questions? 23 MR. SHOEBOTHAM: Just wait a second. 24 (Recess from 10:56 a.m. to 11:01 a.m.) 25 Q. (By Mr. Lubel) Dr. -- 32 1 A. I've given you two -- two papers from Midland. 2 Q. You actually gave me one, and the lawyer here gave me 3 the other one. Correct? 4 A. That's correct. 5 Q. That was -- the 2003 version was not within your 6 stack of documents. Correct? 7 A. I didn't bring all the Dow documents with me. 8 Q. And as you've told me, you're not relying upon any of 9 these articles for your opinions in this case. Correct? 10 A. Not as they relate to Mr. Boren, no. 11 Q. Do you recall whether or not in the '86 published 12 article from the Dow Chemical personnel whether or not they 13 found a significant excess of AMLs in the benzene-exposed 14 population in Midland? 15 A. I don't recall if it's statistically significant. 16 I'm looking through the paper. 17 My quick examination of the paper suggests that 18 they don't speak to acute myelogenous leukemia, that they just 19 report results for leukemia. And I don't see statistically 20 significant -- statistical significance even for the low 21 leukemia. 22 Q. So you don't see a specific reference to the subtype 23 of leukemia called AML. Correct? 24 A. I don't see that in this paper. 25 Q. All right. And you're referring to the '86 version 33 1 of the Dow Chemical study in Midland? 2 A. Correct. 3 Q. All right. Do you have -- when you flip through 4 there, do you see any reference to what the chemical exposures 5 were to those benzene-exposed workers as far as levels? 6 A. Yes. In this paper they had -- they had -- for 7 the -- all leukemias, they attempt to classify them in three 8 different exposure ranges of accumulative exposure. 9 Q. What are those ranges? 10 A. If I'm reading it correctly: 0 to 499, 500 to 999, 11 and greater than a thousand. 12 Q. Okay. And have you seen references to there being 13 excess leukemias of the AML variety at the Dow Chemical plant 14 in Midland at exposure levels in the approximate range of 25 15 parts per million? 16 A. I don't recall. 17 Q. You've never seen that? 18 A. I... 19 Q. That you can remember? 20 A. I just don't recall. 21 Q. At any rate, you didn't see any reference in this 22 article -23 MR. LUBEL: And we'll go ahead and mark this as 24 Exhibit 4. 25 (RAABE Exhibit No. 4 was marked.) 34 1 Q. (By Mr. Lubel) -- to AML specifically. Correct? 2 You just -3 A. No, I didn't. I -- I just now did not read the text. 4 But in terms of the tables that I was looking at, I didn't see 5 any AML specific tables. 6 Q. And as you sit here, you don't recall there ever 7 being a reference in any form or fashion in Exhibit 4 of this 8 Dow Chemical study about AMLs specifically? 9 A. You're going to make me read the paper. I mean, I 10 just don't recall -11 Q. Read the abstract. You need to go no further than 12 the first paragraph. 13 A. Ah. Good. Thank you. 14 Q. What does it say? 15 A. It says that the leukemias they observed were all 16 AMLs. 17 Q. And that there was a significant excess, correct, in 18 that same category? 19 A. Yes. But it's not presented that way in the table. 20 So it must be the -- the significance analysis must be in the 21 text -- in the body. 22 Q. Did they break down the subtypes of AML in this 23 study? 24 A. No. It's a mortality study, and it's unlikely that 25 that data would have been available. 35 1 Q. In your benzene study, did you break down the 2 subtypes of AML? 3 A. No, we did not. 4 Q. In any of Dr. Wong's longstanding benzene research, 5 did he break down the subtypes of AML? 6 A. Once again, these are mortality studies, and it's 7 unlikely he would have had that information. So I don't 8 believe he has. 9 Q. Does Dr. Irons, in any of his work -- have you seen a 10 breakdown of subtypes of AML regarding what types he thought 11 were related to benzene and what types he didn't? 12 A. I don't routinely follow all of Dr. Irons' work. So 13 I -- I -- I can't answer to what he may have done. 14 Q. In the Rinsky work, was there a breakdown of the 15 subtypes? 16 A. No. 17 Q. In the China work that has been written about by 18 Hayes, Yin, and others, did they break down AML subtypes? 19 A. No. 20 Q. Is it generally accepted within the international 21 scientific community that benzene exposures can cause AML? 22 A. At expo, the -- the descriptive epidemiology we have 23 to date at high exposures of long duration can cause AML, yes. 24 Q. So at this date, there is general acceptance amongst 25 the international scientific community that some benzene 36 1 exposures can cause acute myeloid or acute myelogenesis 2 leukemia. Correct? 3 A. Yes. 4 Q. Otherwise known as acute nonlymphocytic leukemia? 5 A. That may include a few other categories, but 6 basically, yes. 7 Q. And the title of Exhibit No. 4 -- this is the Dow 8 study from '86. Correct? 9 A. Yes. 10 Q. Is "An update of mortality among chemical workers 11 exposed to benzene"? 12 A. Correct. 13 Q. And as you've pointed out for us, this involves 14 Midland, Michigan plants? 15 A. Correct. 16 Q. Have you seen any published study that involves the 17 Freeport, Texas plant? 18 A. Yes. 19 Q. And benzene workers? 20 A. They're not quite conducted exclusively to -- to 21 benzene. 22 Q. What I'm trying to find out is if you've seen a 23 comparable study of benzene workers regarding the Dow-Freeport 24 plant? 25 A. Well, the -- the -- the studies of Freeport that I've 37 1 seen don't show an excess of leukemia. And it -2 Q. Can you show me those studies? 3 A. Well, here's the -- Burns and Carson is a 2003 4 update. It's the most recent that relates to Freeport. And 5 then there are -- there's an '85 and then the published and 6 unpublished version. 7 Q. If you'd pull those out, we'll go ahead and mark them 8 all. 9 So you've handed me a stack of articles that you 10 believe relate to Dow-Freeport specifically. Correct? 11 A. Yes. 12 MR. LUBEL: We're going to mark -- mark them 13 different numbers. 14 A. Well, Freeport and the -- and the few of them include 15 other Texas operations, but -- but they all include Freeport as 16 best as I can see. 17 Q. (By Mr. Lubel) All right. The first one I'm going 18 to mark as Exhibit No. 5, and it's titled "Cause-specific 19 mortality among employees of Texas-based chemical manufacturing 20 facility, 1940 through 1996." Correct? 21 A. Yes. 22 (RAABE Exhibit No. 5 was marked.) 23 Q. (By Mr. Lubel) Does this article -- well, we know by 24 its title, it doesn't specifically address benzene workers. 25 Correct? 38 1 A. Correct. 2 Q. Is there any section of this article that addresses 3 specifically benzene workers? 4 A. I don't -- no, there's not -- no special analysis for 5 benzene-exposed workers. 6 Q. All right. And I'm going to ask you essentially the 7 same series of questions as we go through. The next article 8 you handed me I'm going to mark as Exhibit No. 6. 9 (RAABE Exhibit No. 6 was marked.) 10 Q. (By Mr. Lubel) As we can tell from this article, 11 benzene is not referenced in the title. Correct? As it was in 12 the Midland study? 13 A. Correct. This -- this is titled, "Mortality Among a 14 Large Cohort of Chemical Manufacturing" Workers. 15 Q. Does that study address benzene workers specifically? 16 A. No, it does not. 17 (RAABE Exhibit Nos. 7-8 were marked.) 18 Q. (By Mr. Lubel) Same question for Exhibit 7? 19 A. No, it does not. 20 Q. Same question for No. 8, Exhibit 8? 21 A. No, it does not. 22 Q. Do 5, 6, 7, or 8 -- any of those studies that we've 23 marked as exhibits -- have a breakdown for the form of leukemia 24 called acute myeloid or acute myelogenous leukemia? 25 A. I've not exhaustively gone through all the text, but 39 1 I don't believe that -- at least in the tables, that they 2 specifically discuss AML. 3 Q. Do you have any knowledge regarding the number of AML 4 cases out of the Dow Chemical-Freeport plant? 5 A. I don't believe I've seen any data. 6 Q. And I'm not limiting it to data. Has Mr. Shoebotham 7 or anybody that represents Dow Chemical kind of under the table 8 told you: This is how many acute myelogenesis leukemias we had 9 at Dow-Freeport? Anything like that? 10 MR. SHOEBOTHAM: Objection, form. 11 A. No, they have not. 12 Q. (By Mr. Lubel) Have you seen the Otto Wong study 13 that was done on approximately nine plants in the mid '80s? 14 A. Yes. 15 Q. Do you know whether Dow was a part of that study? 16 A. I believe they were. 17 Q. I've, I think, seen the same study you're referring 18 to. And would it surprise you if there is no reference made 19 specifically to Dow within the study? 20 A. No. 21 Q. That would not surprise you? 22 A. No. 23 Q. Why not? 24 A. My understanding of the agreements for participation 25 were that the individual company data would not be identified. 40 1 Q. Is that common for industry-funded studies? 2 A. Yes. Well, it's common for industry-wide studies 3 whether they're funded by industry or not. 4 Q. Not to identify the plant that's being studied -- or 5 plants? 6 A. It's not typical. 7 Q. So when we look at the Otto Wong study from the mid 8 '80s regarding these nine chemical plants or petrochemical 9 plants, you would not expect to see the identity of those 10 plants contained or listed by the author of the study? 11 A. Correct. 12 Q. Have you seen any of the data that was shipped by Dow 13 Chemical to Otto Wong regarding their plant and what diseases 14 they had out there? 15 A. No, I've not. 16 Q. Are you familiar enough with that study to know that 17 it was not a study that addressed specifically benzene workers? 18 A. Are we talking about the -- what is often called the 19 CMA? 20 Q. (Mr. Lubel nods.) 21 A. The study that Otto -- Otto Wong participated in? 22 Q. In the mid '80s? 23 A. Yes. 24 No. The objective was to have one population of 25 benzene-exposed workers and one population of nonexposed 41 1 workers. 2 Q. So you're saying that that was a benzene-specific 3 study? 4 A. It was -- the attempt was, yes. 5 Q. And do you recall whether or not in that study Otto 6 Wong broke out subcategories that included references -7 subcategories within leukemia that included references to the 8 types of leukemias, such as AML? 9 A. I'm not sure in the original report, but I think it's 10 on the subsequent reports. You get whether there's some 11 information on AMLs versus other cell types. 12 Q. And do you recall whether that was ever -- ever 13 further broken down to provide subtypes within AML such as M3 14 or M4? 15 A. It wouldn't have been available. 16 Q. So it wouldn't list that? 17 A. No. 18 Q. And we won't know from reading the published material 19 by Otto Wong specific information as to Dow Chemical recording 20 the number of AMLs out of that plant. Correct? 21 A. I don't believe you'd be able to ease that out. 22 Q. Where would you get that information? Do you -- do 23 you know whether or not that information would have been 24 provided to Dr. Wong? 25 A. I... 42 1 Q. Just from the general standpoint of an 2 epidemiologist. 3 A. From the general standpoint, I believe Dr. Wong would 4 have known what the different submissions were; in other words, 5 what companies were submitting what data. 6 Q. Have you seen an update from that study? 7 A. There has not been one to my -- my knowledge. 8 Q. Did you read the deposition I took of Dr. Collins, 9 the Dow Chemical Director of Epidemiology? 10 A. Yes. 11 Q. Did you recognize and appreciate that when I asked 12 him why there had not been an update of that study specific to 13 the Dow-Freeport plant, his response to that was: There was no 14 need for it, because we had the studies coming out of 15 Dow-Midland, and those exposures were substantially similar to 16 Dow-Freeport? Did you see the conversation? 17 MR. SHOEBOTHAM: Objection, form. 18 A. I don't recall it specifically. Are you -- but are 19 you implying that Freeport was the group that went into 20 Dr. Wong's? 21 Q. (By Mr. Lubel) I wasn't. 22 A. No. But that's what -- more or less what you just 23 said. 24 Q. Well, what was Dow -- is it your understanding that 25 the Wong study in the mid '80s that you've also called the CMA 43 1 study or some refer to it as the CMA study, that that included 2 Dow-Freeport or was that Dow-Midland or do you know? 3 A. I don't know. 4 Q. It doesn't say in the study? 5 A. But it -- in your previous question to me, you 6 characterize Dr. Collins' answer, which I don't recall being 7 that, that we -- we didn't need to do Freeport because -8 because we had other data on Midland. 9 Q. I think you're right. Let me see if I can rephrase 10 it. 11 I understood Dr. Collins when he gave his 12 testimony under oath -13 A. I don't recall it in that detail. 14 Q. Yeah. So let me just give you -15 A. I'm not -- I'm not prepared to actually debate that 16 with you. 17 Q. Let me give you basics; that is, I understand 18 Dr. Collins to have stated that Dow-Freeport didn't need to be 19 studied any more than it had been because Dr. Wong had studied 20 it when he did the mid '80s report. 21 A. Okay. I don't -22 MR. SHOEBOTHAM: Objection, form. 23 A. -- recall that. 24 Q. (By Mr. Lubel) All right. Well, that's number one. 25 Number two, do you agree or disagree, if this is a correct 44 1 interpretation of Dr. Collins' testimony, that it would not be 2 necessary to study Dow-Freeport specifically regarding benzene 3 workers if you've got reliable data from Dow-Midland benzene 4 workers if the exposures are substantially similar? 5 MR. SHOEBOTHAM: Objection, form. 6 Q. (By Mr. Lubel) Do you agree with that statement? 7 A. I can't agree -- agree or disagree. Because each 8 occupational medicine department or epidemiology group would 9 have different criteria for what studies to update, when to 10 update them. And I don't have enough specific information to 11 agree or disagree with Dr. Collins' statement. 12 Q. Let me ask you this: When -- when Dow started 13 studying the benzene workers in Michigan, would it be a fair 14 assumption that they knew that they had benzene workers down in 15 Texas at Freeport? 16 MR. SHOEBOTHAM: Objection, form. 17 A. I don't now how they're -- I think it would probably 18 be a fair statement, but I don't know how they're organized, 19 whether the epidemiology group at corporate knew the locations 20 of all the different material, the production facilities, 21 and -- and what they made. 22 Q. (By Mr. Lubel) Had you been in the epidemiological 23 department back in the late '70s for Dow Chemical -- let's say 24 you were the director -- would you have recommended that just 25 the Dow-Midland benzene workers been studied, or would you have 45 1 recommended bring in the Dow-Freeport benzene workers to study 2 them all? 3 MR. SHOEBOTHAM: Objection, form. 4 A. There -- there's no simple answer to that question. 5 Q. (By Mr. Lubel) What's the complicated answer? 6 A. Well, the complicated answer is you would tend to 7 start where you had what you perceived to be the best data 8 available to start. And then based on -- based on what you 9 learned in that study and what you knew from industrial hygiene 10 at your other facilities, you could -- depending on what other 11 priorities you had -- benzene is not the only material Dow -12 Dow makes -- make decisions as to what level of detail and how 13 frequently and what -- what do you want to study next. 14 So you just can't say, you know, if I -- what -15 you just can't estimate what their decision process was. 16 Q. Well, you'd agree that in the field of epidemiology, 17 it's generally accepted amongst people that do what you do that 18 the power of the study can have an impact on the conclusions? 19 A. Yes. Well, not -- not -- would have no impact on the 20 conclusions. Would have impact on the -- how strongly you 21 could extrapolate the results. The conclusions would still be 22 just as valid whether it's a big study or not. It's just 23 whether or not they would apply broadly. 24 Q. But generally speaking in the field of epidemiology, 25 you'd like to study more people than less. Correct? You'd 46 1 like to have a bigger size? 2 A. As long as bigger is as manageable as the next level 3 down, yes. 4 Q. So from an epidemiological standpoint, generally 5 speaking, if all else is equal, it would have been better for 6 the Dow people when they're studying benzene workers to study 7 all the benzene-exposed workers which would include the 8 Dow-Freeport people? 9 MR. SHOEBOTHAM: Objection, form. 10 Q. (By Mr. Lubel) True? 11 MR. SHOEBOTHAM: Objection, form, calls for 12 complete speculation. 13 A. It goes back to my earlier answer. I don't know what 14 the underlying motivation was to do the Midland study. So 15 whether to include Freeport or not, I just can't -- I have no 16 way of knowing what -- what -- what would've worked there. 17 Q. (By Mr. Lubel) As you sit here today, you don't know 18 whether there's ever been a benzene workers study of the 19 Dow-Freeport people. Correct? 20 A. I have not seen any material on that. 21 Q. Has anybody told you that there has been a study to 22 that effect? 23 A. No. 24 MR. SHOEBOTHAM: You're talking about other than 25 Wong's study? 47 1 MR. LUBEL: He doesn't know that Wong's study 2 is. Nobody does because it's not in the published literature. 3 MR. SHOEBOTHAM: He testified that -- that the 4 Freeport population was part of the Wong study. 5 THE WITNESS: I didn't. Collins did. 6 MR. LUBEL: He doesn't know. 7 THE WITNESS: Well, he said Collins did. 8 MR. LUBEL: He said he doesn't know. 9 THE WITNESS: I just -10 MR. LUBEL: Raabe's not willing to take that 11 leap of faith as he sits here right now. Right? 12 THE WITNESS: I don't -- I mean, I was at some 13 of those meetings, and I don't recall what Dow's submission 14 was. So if -- if Dr. Collins says it was Freeport, I -- I 15 accept that. I'm not trying to argue with it, but I don't 16 recall that, and it's not -- wouldn't be in the papers. 17 Q. (By Mr. Lubel) Was Dr. Collins there at that time, 18 in those meetings? 19 A. No. 20 Q. He wasn't even working for Dow, was he? 21 A. No. 22 Q. He was at Monsanto? 23 A. No. And I -- and I don't recall who the Dow -- Dow 24 representative was at those meetings. 25 Q. Well, what plants were studied? 48 1 A. I don't -- I don't know. 2 Q. If you're at the meetings? 3 A. Well, I mean, I know -- I know of one plant that was 4 studied. 5 Q. Your plant, Mobil? 6 A. Yes. 7 Q. Any others? 8 A. Any others? 9 Q. That were studied other than Mobil and maybe Dow. 10 A. The only plant-specific information I recall is -- is 11 Mobil. Mobil. 12 Q. And what did Mobil supply to Dr. Wong? 13 A. Every -14 Q. In the way of information. 15 A. To my understanding, because it was -- it was done by 16 others, it was all of the -- we have a very distinct olefins 17 and aromatics production plant in Beaumont. So all of the 18 production people with potential benzene exposure were provided 19 as the exposed group, and an unrelated plant -- and I can't 20 even remember what it -- what it was. It wasn't a refinery. 21 It was something totally different provided the, quote/unquote, 22 nonexposed portion of the cohort. 23 THE REPORTER: Of the what? 24 THE WITNESS: Of the cohort. 25 MR. LUBEL: Nonexposed cohort. 49 1 Q. (By Mr. Lubel) Did Mobil supply Dr. Wong with the 2 exposure information that he was supposed to rely upon? 3 A. It wasn't done quite that way. Do you mean -- ask me 4 a question. 5 Q. Sure. Did Mobil have exposure information for the 6 people that were being studied? 7 A. Yes. 8 Q. Did they supply that information to Dr. Wong? 9 A. No. 10 Q. Who did they supply it to? 11 A. I -- an exposure dictionary -- job exposure matrix 12 was established. And the exposures were appended to the 13 matrix. So we would have submitted a matrix of the job titles 14 with timelines and exposure information. The raw data was not 15 sent to -- to Dr. Wong. 16 Q. Who interpreted the raw data to assemble these 17 matrixes -- matrixes that were actually sent to Dr. Wong? 18 A. Industrial hygiene and plant personnel at the 19 Beaumont facility. 20 Q. And what were the exposure levels at Mobil? 21 A. Very low. 22 Q. How low? 23 A. I think the highest was about four or five ppm. 24 Q. Over what period of time? 25 A. The plant was built in the early '60s, so it was from 50 1 the start of the plant to whenever the cohort cutoff date was, 2 which was '78 or '80, something like that. 3 Q. So about 20 years? 4 A. I'd have to go back and look at the cutoff pit dates, 5 but... 6 Q. At any rate, do you recall whether Mobil had actual 7 monitoring data that went back to the beginning of the plant, 8 1960 or so? 9 A. They had grab samples in some of the early dates, and 10 then later, different qualities of -11 Q. When did they move on from grab samples to actual 12 monitoring of workers? 13 A. Don't recall. 14 Q. Was the progression of exposure information that 15 Mobil had, did it start off with grab samples and then move to 16 area monitoring and then move to personal -- personnel 17 monitoring? 18 A. No. It was technology driven. In other words, in 19 the very early days, there were -- well, that was my 20 understanding. You didn't have the -- any reasonable 21 capabilities to get reliable data on -- on individuals with any 22 routine process. I mean, there were certainly technologies, 23 but -- but... 24 Q. When did that start? 25 A. I don't remember. I'm not -- I'm not familiar with 51 1 state of the art issues in industrial hygiene monitoring. But 2 it was not -- it was some time shortly after that, because 3 there were -- there were data in the mid '60s that started to 4 be personnel. 5 Q. How was the grab sample taken to your knowledge? 6 A. Don't know. Just described to me as a grab sample. 7 Q. Well, how was the information -- the exposure 8 information translated, if you will, from the grab sample to 9 the individual worker in the study? 10 A. I can only speak generally on the process. Generally 11 what was done was the job matrix had a combination of location 12 and tasks and information on -- on the task. And the location 13 would be assembled, whatever they had in the time periods. And 14 then it would be interpolated and assigned to that task in that 15 time period. 16 Q. And who would perform that responsibility? 17 A. Combination of industrial hygiene and plant 18 personnel. I don't know specifically who was involved. 19 Q. So Mobil employees would assemble this information 20 and then send it to Dr. Wong in some type of spreadsheet. Is 21 that -22 A. Yeah, that's a fair -23 Q. -- accurate? 24 A. -- fair summary. 25 Q. Is that generally what's been going in these -- at 52 1 these studies that we've seen on benzene over the last 25 or 30 2 years? 3 A. No. 4 Q. Has it changed? 5 A. Yes. 6 Q. In your '95 study that you and Dr. Wong have 7 published -- do you recall that study? Is it around '95? 8 A. Give me the subject matter. 9 Q. On benzene. 10 A. The -- our review of the refinery workers? 11 Q. Right. 12 A. Yeah. Okay. 13 Q. How did y'all receive exposure information for the 14 refineries that were the subject of the study? 15 A. Okay. That study does not have benzene-specific 16 exposure information in it. 17 Q. You did not receive any benzene information? 18 A. That study summarizes all of the cell type specific 19 leukemias observed in all the different refinery cohorts. 20 Q. Does it reference -21 A. It references -22 Q. -- M3s? 23 A. No. 24 Q. So it doesn't get into that level of detail? 25 A. Correct. 53 1 Q. The subtypes of AML, for example? 2 A. Correct. 3 Q. Y'all broke down leukemias to the like AML, CLL, CML? 4 A. ALL. True. 5 Q. That type of breakdown? 6 A. Correct. 7 Q. So the refinery study is not a benzene-specific 8 study, if you will? 9 A. The -- the summary tables of cell type specific apply 10 to refinery workers. There are -- there's considerable other 11 data and other studies that are discussed in the text, but 12 those tables are not specific to benzene. 13 Q. Can you pull that study out? 14 MR. LUBEL: Can we take a short restroom break? 15 MR. SHOEBOTHAM: Sure. 16 (Recess from 11:35 a.m. to 11:44 a.m.) 17 (RAABE Exhibit No. 9 was marked.) 18 Q. (By Mr. Lubel) Exhibit No. 9 is the study that you 19 pulled out that you and Dr. Wong authored? 20 A. Yes. You know, a case -- case study. 21 Q. It's frequently referred to as the '95 study? You 22 have -23 A. Not by me. 24 Q. You've published other stuff? 25 A. Yes. 54 1 Q. But in '95, it was the only one you published on that 2 area. Right? Benzene? 3 A. Well, there are two versions of it that are 4 essentially identical: one in '95, one in '96. 5 Q. What is the difference between them? 6 A. One -- there's no substantive difference between 7 them. Slightly different discussion because it was being 8 written after the '95 symposium, and it appeared in the 9 Environmental Health Perspectives. There's no real difference. 10 Q. I only need to read the Exhibit 9 version -11 A. Yes. 12 Q. -- to find out -13 A. Exactly. 14 Q. -- how you -15 A. Exactly. 16 Q. -- what you believe. Okay. Now, what -- y'all 17 actually listed the actual plants that are studied in your '95 18 study? 19 A. Correct. 20 Q. How did you get permission to do that when apparently 21 Otto Wong couldn't get permission to list the chemical plants 22 in the mid '80s study that he did? 23 MR. SHOEBOTHAM: Objection, form. 24 A. The -- the cohorts themselves were already published 25 previously. They did not have cell type specific information. 55 1 So who the cohorts were was sort of general knowledge. The 2 actual cell type specific analysis does not show the company. 3 Q. (By Mr. Lubel) In the '95 study that we've marked as 4 Exhibit No. 9, did you do an individual plant-by-plant 5 investigation? 6 A. That -- only to the extent that each individual 7 cohort provided us the specific number of person years and the 8 specific cell types that they observed. So we cal -- so we 9 could calculate the -- the cohort specific cell -- leukemia 10 cell type, SMRs. 11 Q. In other words, did you get exposure information from 12 each plant? 13 A. No. 14 Q. Did you get exposure information as a whole for all 15 the plants? 16 A. No. 17 Q. Exposure was not part of the study. Correct? 18 A. Only to the extent that they were all classified as 19 refinery workers. 20 Q. Yeah. But you don't know, for instance, what the 21 exposures were to the -- to the workers in the Amoco plant? 22 A. Correct. 23 Q. Or the Chevron plant? 24 A. Correct. 25 Q. Or any particular plant other than Mobil where you 56 1 worked? 2 A. Correct. 3 Q. But you do know -- and I take it it's reported in 4 your study that we've marked as Exhibit No. 9 -- the number of, 5 for instance, AMLs at Dow? Not Dow. At Shell? 6 A. At one time we did. 7 Q. Is that reported in this study? 8 A. The number? 9 Q. Per plant. 10 A. Well, the number per plant is, but not -- it doesn't 11 identify which plant. So I can tell you that -12 Q. Why not? 13 A. Because the -- for the companies to agree to let us 14 summarize it this way, they asked us to code the identity. 15 Q. I understand that you wouldn't mention the name of 16 the person that died of AML in the study. I'm just saying why 17 wouldn't -- for instance, let's say Texaco had eight AMLs over 18 the period of the study -- let you reference how many AMLs they 19 had? 20 MR. SHOEBOTHAM: Objection, form. 21 A. I don't -- I don't recall the specifics on a 22 company-by-company basis. But since the objective was to 23 summarize all the petroleum workers that we could, it was 24 easiest for us to get participation by saying we would not show 25 the specific number of AMLs for any individual cohort or plant. 57 1 So, I mean, it was us telling them that, and the 2 few companies that I recall that were having heartache suddenly 3 had less heartache. 4 Q. (By Mr. Lubel) So what -- I mean, as part of this 5 study that you and Dr. Wong did on the refineries, you did not 6 look at each individual leukemia case and look at their 7 particular exposures. Correct? 8 A. Correct. 9 Q. Nor did you look at -- in general at the exposures of 10 the benzene workers at each of those plants? 11 A. Well, all refinery workers would have benzene 12 exposure at higher rates than background populations. So this 13 was just summarizing refinery workers -14 Q. Did you -15 A. -- in that context. 16 No, we did not do individual specific benzene 17 unit analysis. 18 Q. But you didn't get data from the different 19 benzene-containing units for Amoco or Chevron or any of the 20 other particular plants and analyze the data that way? 21 A. Correct. 22 Q. Now, this study did not find a significant excess of 23 AMLs? 24 A. In refinery workers, correct. 25 Q. Right? 58 1 There's more than this study that does not find 2 an excess of AMLs to the benzene-exposed population. Correct? 3 This isn't the only one? 4 A. No, that's correct. But it -- I mean, it summarizes 5 some of the cohorts it did find early -- early excesses of 6 leukemia in refinery workers. 7 Q. But you're not taking the position under oath that 8 just because a study or a number of studies does not find an 9 association in that study population between benzene and AML, 10 you're not saying that stands for the proposition that there is 11 no link? 12 A. No. 13 Q. That wouldn't be good science, would it? 14 A. No. One would have to examine the body of the 15 science and considerable information specific to the 16 individual to -- to associate the two. 17 Q. And it's still good science in your opinion when you 18 look at the body of the science to say that there is a link for 19 certain benzene exposures to acute myelitis leukemia. Correct? 20 A. Correct. 21 Q. Even though there are some studies that don't find an 22 association? 23 A. Well, presumably those are -- the reason for all of 24 that is because the exposures are low. 25 Q. Well, but irrespective of the exposures, the fact 59 1 that a particular study does not reflect an outcome that's 2 reflected in other studies does not mean that the outcome found 3 in the other studies ain't true. Right? 4 A. You have to examine the study in the context of what 5 information it provides and where that information fits with 6 the others -- the other published studies. 7 (RAABE Exhibit No. 10 was marked.) 8 Q. (By Mr. Lubel) Is Exhibit No. 10 the Otto Wong study 9 that you brought with you, at least one version of it, that 10 you've also or previously called today the CMA study? 11 A. Yes. 12 Q. And there's -- there's two versions of this? There's 13 one and two? 14 A. No. There just -- there -- there -- I wouldn't use 15 the term "versions." Paper one describes the general findings 16 from the cohort, who the population studied, what they did, 17 blah, blah, blah. And paper two is specific to the dose 18 response analysis that was conducted for benzene. 19 Q. And this particular study is the study that we were 20 talking about previously about -- Wong did the study of a 21 number of plants, but the study itself doesn't tell you which 22 plants were studied. Correct? 23 A. Correct. 24 Q. Now -25 A. May I see this just briefly? 60 1 Q. Yes. And you know something about that study because 2 you participated in meetings about it. Correct? 3 A. Yes, I did. 4 Q. As a Mobil employee. True? 5 A. Yes. Thank you. 6 Q. Now, it was your recollection that the way this study 7 worked was that the companies assembled exposure data in-house 8 and then supplied a summary of that to Dr. Wong in his capacity 9 as investigator? 10 A. Based on the protocol that was developed for the 11 study on how to do that. 12 Q. So who designed the protocol, if you know? 13 A. Well, Dr. Wong, I believe Dr. Tabershaw was involved 14 early on, and Dr. Abraham Lillianfelds (phonetic) was an 15 advisor. So some combination resulted in a process. 16 Q. So they designed the protocol for the study. 17 Correct? 18 A. I believe that to be correct. 19 Q. And then somehow that protocol would've been 20 communicated from those people to the -- the chemical companies 21 or refineries, whenever the companies were in issue? 22 A. Right. Assignments were given for... 23 Q. But generally speaking as you recall the way it 24 worked, at least for Mobil -- you can't speak for the other 25 companies. Correct? 61 1 A. Correct. 2 Q. For Mobil, industrial hygiene people and other staff 3 assembled exposure information that they had for the Beaumont 4 plant and then put that in some type of summary chart and sent 5 that to Dr. Wong? 6 A. Correct. 7 Q. Did you ever see that information? 8 A. At the time I believe I did, yes. 9 Q. Since this was a mortality study, you're looking at 10 death certificates. Correct? 11 A. Correct. 12 Q. You ought to -- not do what's frequently called a 13 morbidity or incident study? 14 A. There was no way possible to conduct such a study. 15 Q. So you -- the investigator relies on the information 16 in the death certificate as being accurate and reliable. 17 Correct? 18 A. Well, it is because the expected information is 19 calculated the same way. 20 Q. My point is, though, if whoever fills out the death 21 certificate puts the wrong disease on there, then that's a 22 problem that you may not know about? 23 A. Epidemiologically it's not a problem, because if -24 because all -- you're comparing to large populations where the 25 same errors are likely to occur. So while the absolute numbers 62 1 of cases may -- could possibly shift if you had additional 2 information, the resulting observers expect the SMR is 3 considered a perfectly scientifically valid number. 4 Q. Even if you're talking about a rare disease? 5 A. In a general sense unless you believe that, you know, 6 regionally or locally there's, you know, some reason to believe 7 that -- that there is a bias on one side and not the other. 8 Q. But, I mean, you could take a real rare disease where 9 you wouldn't even expect to see many in either the study cohort 10 or in the control group, and if one -- if one death certificate 11 were to be mislabeled and not have that particular rare disease 12 on there, it could have an influence on the interpretation of 13 that study. Correct? 14 MR. SHOEBOTHAM: Objection, form. 15 A. Unlikely. 16 Q. (By Mr. Lubel) But you're not willing to go out on a 17 limb and say, "For all diseases, it matters whether or not the 18 people filling out the death certificates are doing so 19 accurately." You're not willing to make that jump, are you? 20 That it never matters whether the information on the death 21 certificates are reliable or not? 22 MR. SHOEBOTHAM: Objection, form. 23 A. Obviously accurate information on the death 24 certificates is -- is -- is important to these studies. 25 Q. (By Mr. Lubel) Now, for the CMA study that we've 63 1 marked as Exhibit No. 10, did you receive drafts of this before 2 it was published? 3 A. The process wasn't that way. There was a -- Otto 4 could do whatever he wanted on the publication. 5 Q. I'm just asking you -6 A. Dr. Wong. 7 Q. -- in advance -8 A. No. What I'm saying is that there is an unpublished 9 report that was handed to CMA. And that -- that report was 10 communicated immediately to the government. We never saw a 11 draft. I mean, we made comments on what Otto -- what Dr. Wong 12 provided. And I don't know whether there was any changes made, 13 but the report -- the first report that we saw was the report 14 that was sent to OSHA and NIOSH when we first saw it. 15 Q. Well, let me ask you -16 A. But the publication was totally independent of that. 17 Q. Let me do it this way: You referenced an unpublished 18 report? 19 A. Correct. 20 Q. And then you referenced a published report which we 21 see is Exhibit 10. Right? 22 A. Correct. 23 Q. Do you know if the unpublished report looks anything 24 different than the published report? 25 A. It's going to be much thicker because it has lots of 64 1 information that you'd never get into in a published report. 2 One's unpublished analysis tends to have a lot of tables that 3 essentially look at the populations, the age distributions -- a 4 number of things that are not always likely to show up in the 5 published version of the report. 6 Q. Well, what -- what version does the peer reviewers 7 look at? The unpublished or the published version? 8 A. They look at whatever the author sends to the peer 9 reviewers. 10 Q. Okay. In this case, do you know which version they 11 got? 12 MR. SHOEBOTHAM: Objection, form, calls for 13 speculation. 14 Q. (By Mr. Lubel) Have they got the unpublished or the 15 published version? 16 A. Well, it's clearly unpublished when you send it to 17 the peer reviewers. 18 Q. I understand that. But the thicker version, did the 19 peer reviewers get the thicker version or do you know? 20 A. Don't know, but that would be very uncommon in 21 epidemiologic activity. 22 Q. Do you know who peer reviewed this? 23 A. Peer review was a -- is a -- I'm looking for a 24 word -- a confidential process. One does not know who peer 25 reviews your studies. It's up to the editors who they want to 65 1 send it to. 2 Q. Okay. Well, before this study was published, the CMA 3 study -- by the way, CMA refers to the Chemical Manufacturing 4 Association? 5 A. Yes. 6 Q. Did -- did Dr. Wong's work get sent around to, for 7 instance, reputable scientists to examine his work before he 8 sent it out for publication? 9 A. Dr. Wong's unpublished report that he submitted to 10 CMA as part of the contract was sent to NIOSH, OSHA, made 11 generally publically available to whoever wanted to read it. 12 Q. But in -- in particular, do you know if Dr. Wong's 13 work was sent specifically to scientists to review his work? 14 A. I... 15 Q. To edit it or to tell him what changes ought to be 16 made or anything? 17 A. I don't know. Not to my recollection. 18 Q. Now, before the published work -- strike that. 19 Before the unpublished version, the one that you said was the 20 thick version -21 A. Can we call it the final report? Because that's what 22 it -- what it is: the final report. 23 Q. My question is: Did you ever see any draft reports? 24 A. No. 25 Q. I'm not talking about just you. I'm talking about 66 1 anybody at the CMA. You're saying they never saw a draft 2 report? 3 MR. SHOEBOTHAM: Objection, form. 4 A. I don't believe they did. 5 Q. (By Mr. Lubel) So nobody within the CMA had the 6 right, as you recall it, to review Dr. Wong's analysis or his 7 assessments before the final report was completed and sent to 8 the people at OSHA and whoever else asked for it? 9 MR. SHOEBOTHAM: Objection, form. 10 A. I don't recall there being a draft for comments that 11 was not the report that was made immediately available to 12 anybody who wanted it. 13 Q. (By Mr. Lubel) But you recall CMA people making 14 comments about Dr. Wong's paper and writing. Correct? 15 A. After the report was -16 Q. Before he could fix it? 17 MR. SHOEBOTHAM: Objection, form. 18 A. Well, it was not so much fix it. The contract 19 process that was in place at that time resulted in Dr. Wong 20 providing a report that would be distributed. And I don't 21 recall there being like a comment period in the report. That's 22 all I'm saying. 23 Q. (By Mr. Lubel) Was that not common within industry 24 organizations such as the CMA for there to be a period of time 25 for people within the organization to review and potentially 67 1 make comments on the studies? 2 A. Normally, in my experience in -- in -- in 3 industry-wide cohort studies, it's typical for the industry to 4 have it for a month or two to provide comments back to the 5 investigator, and the investigator, at that point, can either 6 take the comments or not and then issue his final report. But 7 there is a -- a window of -- of opportunity for the -- for the 8 contractor to provide comment. 9 Q. And you don't think that happened for the Wong CMA 10 study? 11 A. Correct. 12 Q. Is that something that he requested not be a part of 13 the process? 14 A. Don't know. 15 Q. Well, surely the industry would want to have that 16 ability to make comments. Correct? 17 MR. SHOEBOTHAM: Objection, form. 18 A. I -- I don't know how that process emerged. 19 Q. (By Mr. Lubel) When did the -- the study was 20 apparently published in -- around the '86 time period? 21 A. Yeah, I think it was submitted probably around that 22 time. Submitted in August, '86. 23 Q. When did that study start? 24 A. I think discussions for who would participate 25 probably started around probably 1980 or maybe earlier. 68 1 Q. So the study lasted five or six years? 2 A. No. 3 Q. No. How long? Before the final report was 4 published, how long did it take? 5 A. Well, there is a final report, and then there's a 6 published paper from the report. 7 Q. When did the work start in relationship to when the 8 final report was done? Did it start in the late '70s? I mean, 9 when did this start? 10 A. When I speak to the final report, I'm talking the 11 report that we were just discussing that goes -- the thicker 12 report that goes to -13 Q. I'm with you. I'm with you. 14 A. Okay. I think that was probably completed -- I don't 15 know when the project started, because it was already starting 16 -- started when I joined industry -- joined Mobil. I think 17 it's -- the -- the -- the unpublished final report probably was 18 issued '84, in that timeframe. '84, '85. 19 Q. And do you know whether the work had started in the 20 '70s at some point? 21 A. Don't know. 22 Q. Do you know how Dr. Wong was brought in to -- to do 23 this work? How he was chosen? 24 A. No. No, I don't. 25 Q. Do you know what Tabershaw's relationship to the 69 1 study was? 2 A. I believe that -- that early period, Dr. Wong worked 3 for Dr. Tabershaw. 4 Q. What kind of epidemiologist is Dr. Tabershaw? 5 A. Well, into that -- we're now going into a very early 6 era. Dr. Tabershaw was an occupational physician that went 7 into epidemiology in the '60s and did a lot of historical work 8 with various occupational groups. 9 Q. I take it that he was picked to run this CMA study 10 because of his reputation in the field? If you know. 11 A. I can only speculate. I don't know. 12 Q. Does he have -- does he enjoy a good reputation in 13 the field of epidemiology? 14 A. I'm hesitating only because I'm trying to think. I 15 think he's passed away, but... 16 Q. When he was alive, did he enjoy a great reputation -17 A. Yes. 18 Q. -- in the field of epidemiology? 19 A. Yes. Epidemiology had to be done with calculators in 20 that day, so what he did with the technology available was very 21 good. 22 MR. LUBEL: Good time for the lunch break? 23 MR. SHOEBOTHAM: Sure. 24 (Recess from 12:08 p.m. to 1:03 p.m.) 25 Q. (By Mr. Lubel) Did you have a good lunch? 70 1 A. It was satisfactory. 2 Q. Good. 3 The POWERPoint presentation regarding the China 4 studies that you said was sitting on your desk back at home, 5 have you forwarded a copy of that to Mr. Shoebotham to review? 6 A. No, I've not. And it's not sitting on my desk. 7 Q. I thought you said on your desk? 8 A. On my desktop computer. 9 Q. It's in your computer. 10 Have you talked to Mr. Shoebotham about what 11 information is provided in the POWERPoint presentation? 12 A. Very superficial. 13 Q. What did you tell him? 14 A. I said it outlines the broad objectives for the 15 research program that we were trying to -- trying to fund in 16 China. And that's about the level of detail it was. 17 Q. Did you tell Mr. Shoebotham that any of the 18 information contained therein was confidential or subject to a 19 confidentiality agreement? 20 A. Never came up. 21 Q. Did you tell Mr. Shoebotham that anything on the 22 POWERPoint presentation contained some trade secrets or 23 proprietary information? 24 A. No. 25 Q. Are you taking the position that any of that 71 1 information is proprietary or trade secret? 2 A. No. 3 Q. Is there anything particularly secret about it to 4 your knowledge? 5 MR. SHOEBOTHAM: Objection, form. 6 A. Not that I'm aware of. 7 Q. (By Mr. Lubel) Have you done any work regarding 8 benzene exposures and skin absorption? 9 A. I've tracked the debate over the years between 10 Dr. Paustenbach and some of the NIOSH scientists, but I've not 11 done any work myself. 12 Q. From a toxicological standpoint, you hadn't run tests 13 on any animals in that regard, have you? 14 A. No, I've not. 15 Q. Have you seen any Dow Chemical studies that address 16 the issue of how much benzene can be absorbed through the skin? 17 A. I don't recall. 18 Q. Have you seen any studies done by the Chemical 19 Manufacturers Association or the API on that issue? 20 A. Definitely no for CMA. I don't recall if API ever 21 did any of that work. 22 Q. As you sit here, given the number of years that 23 you've been involved in the -- what I call the benzene debate, 24 have you seen or can you recall any literature that you believe 25 addresses in a reliable fashion benzene exposures and what can 72 1 be absorbed through the skin? 2 A. It is quite a large body of literature out there. I 3 have not looked at it, so I can't offer any opinions on that. 4 Q. That's not something you're prepared to do for this 5 particular case at this time. Correct? 6 A. Correct. 7 Q. Do you recall if Mobil ever ran any studies on that 8 issue of how much skin absorption there could be from benzene 9 exposures? 10 A. As you know, Mobil had a fairly active benzene 11 research program. I don't recall the general absorption 12 specifically, though. 13 Q. Do -- do any of the literature that you've brought 14 with you today, did you -- I take it you didn't bring any 15 literature here today that addresses specifically any opinions 16 you intend to offer on skin absorption for benzene? 17 A. No, I didn't bring any literature. 18 Q. Do you recall discussions within the CMA about the 19 Dow cytogenetic studies that had come out in the late '70s? 20 A. Not at CMA, no. 21 Q. Do you recall a fellow by the name of Epstein? He 22 may have been with API. 23 A. The name Epstein sounds familiar, but I don't recall 24 it with any association to API, no. 25 Q. Do you recall any discussions within the API 73 1 regarding the Dow cytogenetic studies concerning benzene 2 exposures? 3 A. I don't recall. 4 Q. So you don't recall the CMA as an industry 5 organization having a broad problem with the Dow cytogenetic 6 studies in the late '70s? 7 A. I was not that close to the CMA activities, so I -- I 8 don't know what -- what they were up to. 9 Q. I've seen your name -- name on some of the CMA 10 meetings, but it appears to me -- and correct me if I'm wrong 11 -- that the times that you would appear on behalf of Mobil Oil 12 Company would be when the regular members didn't show up? 13 A. That's probably correct. 14 Q. And how do you pronounce -- is it Bue -- Buell 15 (phonetic)? 16 A. Can I see the... 17 Q. I don't have the one with -- let me find the one with 18 his name on it. 19 A. I think I know who we're talking about, but I'm 20 blocking on his name now. John Behun? 21 Q. I don't think that's it. 22 A. I think it -- I think that was him. 23 Q. Was he the regular member as you recall it? 24 A. Yes. 25 Q. What does the RMA stand for? 74 1 A. The RMA? 2 Q. I see that referenced in some of the CMA documents 3 saying that the API and the RMA need to get together to... 4 A. I don't know as we sit here today. 5 Q. I also saw a reference to the Wong CMA studies that 6 we referred to earlier being a ten-plant study. Can you 7 explain why it is that the published literature reflects 8 something less than ten plants? 9 A. Only -- yes, I can. 10 Q. Will you? I'm waiting. 11 A. But without any specifics, my understanding was that 12 there were a number of plants, not all CMA members, that were, 13 I think, originally approached, but not all of them ultimately 14 participated. 15 Q. Did they back out? 16 A. I don't know the circumstances. 17 Q. I also see a fair amount of discussion about the 18 different plants, collecting the plant data on exposures and 19 then sitting down with a group to discuss it. Do you know 20 anything about that? 21 A. I recall participating in one such meeting, yes. 22 Q. What do you recall from your meeting? 23 A. Well, the objective was to -- there were two 24 difficulties in trying to come up with summary metrics. One 25 was relating to peaks: How does one characterize a peak? How 75 1 does one even know when they occur? And that's been an issue 2 inside epidemiological research for -- forever and still is. 3 So there were several discussions as to how to 4 set the peaks and -- and -- and what -- what metric would make 5 sense scientifically. 6 And the other objective was to, I think, try and 7 decide what the range of the cut points would be. In other 8 words, is there under one? I'm not saying that that's -- what 9 I'm giving you here now is the sort of discussion but not -10 not specifically. You know, is it we've got one category under 11 five and five to ten? 12 So it was trying to make some sense of the 13 distribution of the numbers and how to categorize them. That's 14 my recollection of the meeting I participated in. 15 Q. Why wouldn't that have been a decision by the 16 investigators as opposed to the -17 A. I believe the investigators were -- well, at least, I 18 believe the investigator was present during part of that. 19 Q. But why would -- why wouldn't the investigator make 20 the decision on how the exposures were classified as opposed to 21 having, you know, the industry make the decision? 22 A. Well, the industry -- I don't think the industry did 23 make the decision. I think it -- it was a -- the meeting was a 24 group thing as to how to remember the -- the protocol set out 25 that there'd be a job exposure test specific matrix that would 76 1 be -- that would be mapped. Each company would map the 2 exposure methods to that test matrix. The test matrix would be 3 rolled up into jobs. 4 And as a consequence of all that, I think -- you 5 know, Otto needed -- I mean, people -- this hadn't been done 6 very frequently before, so this was a somewhat new activity, 7 and how to do it was a -- was partially just discussed in a 8 broad setting. It wasn't an industry decision as to how to do 9 it. It was what are our choices and which ones make sense. 10 Q. But ultimately there was a uniform rating for each 11 exposure classification. Correct? Or job? 12 A. No. Well, I'm not sure if we're communicating here. 13 What there was is there was a set of categories that each 14 company would map their task into. 15 Q. Like, give us an example of what you're -16 A. Well, let's say there was a task of drumming. 17 THE REPORTER: Of what? 18 THE WITNESS: Drumming. D-R -19 A. And so -- so there was a drumming on the task list. 20 Now, you may or may not have had any drummers in your cohort, 21 but there was a drumming task. But if you had drummers, you 22 would have to assign an exposure category to drumming. 23 Q. (By Mr. Lubel) Per plant or for all the plants? 24 A. Per plant is my -- my recollection. 25 Q. Then that's what I was driving at was -- so your 77 1 understanding is each plant assigned a value for that job 2 classification? 3 A. A long time ago, but I think that was at least part 4 of the initial process. I don't recall the specifics. 5 Q. Now, at least in theory, each plant would look at 6 exposure data that they had learned about before the meeting 7 and take that information and use it as the number that they 8 used for that job description. Correct? 9 A. That's my presumption. 10 Q. So Mobil may have one number for drumming and Dow may 11 have a different number and Union Carbide may have a different 12 number and on down the road. Correct? 13 A. I -- could well be, yes. I mean, I don't know 14 specifically, but makes sense. 15 Q. But you wouldn't anticipate that each company would 16 have the same number for a particular job classification for 17 that exposure, would you? 18 A. Well, there was no reason to think that they would be 19 that dissimilar in a particular time period. But, you know, 20 remember, they're putting it into categories. So, I mean, if 21 they started out with 2.1 and mapped it into two, I -- you 22 know, I don't know. 23 Q. But the raw data that the person or staff at Mobil, 24 for instance, that they used to come up with the -- this 25 exposure classification was not given to the investigators 78 1 themselves. Correct? 2 A. I don't -- I don't recall it being given to the 3 investigator. They did site visit the facilities first. I'm 4 sure they've seen it in the general discussion sense, but I 5 don't believe that they were actually provided copies of that. 6 Q. Do you recall the site visits? 7 A. Before my time. 8 Q. So you don't know what actually took place in their 9 site visits? 10 A. No. And when I say "before my time," I don't mean 11 before my time joining Mobil, but before I got active into the 12 project. 13 Q. So when you talk about summary metrics, what are you 14 referring to? 15 A. Well, it's a -- it's a jargon term in epidemiology. 16 What I'm referring to is the fact that -- that a body of 17 industrial hygiene data would be summarized as either to a mean 18 or median or geometrically. In other words, someone -- you 19 would make a set of decisions that this is how we're going to 20 summarize that data for this observation or this task in either 21 context. 22 Q. Who performs that? 23 A. Typically industrial hygiene person. 24 Q. And then they provide that information to the 25 investigator? 79 1 A. Well, they would work together so that they'd make 2 sure everybody -- the investigator needs to understand very 3 well how it was done so that he can interpret it properly when 4 he uses it. So it's a team effort, but the lead is from 5 industrial hygiene. 6 THE REPORTER: From where? 7 THE WITNESS: Industrial hygiene. Sorry. 8 Q. (By Mr. Lubel) There's going to be a number of 9 communications between the individual company and the 10 investigators. Correct? 11 A. At various times in the process, yes. 12 Q. They're going to be faxing back information to each 13 other and mailing them information and sitting down and having 14 meetings and things of that nature. Correct? 15 A. Not on a daily basis and not even frequently on a 16 monthly basis, but there will be need for clarification of 17 materials, yes. 18 Q. And at some point there's going to be a document from 19 Mobil or whoever the studied plant is to the investigator. 20 There's going to be a written document that's sent to them. 21 Right? 22 A. Not necessarily. 23 Q. How do they get the exposure information? 24 A. Oh, you mean at the end of the process? 25 Q. Whenever. 80 1 A. I mean, a lot of those meetings are face to face. 2 Q. But they have to hand them something? 3 A. Yeah. 4 Q. They don't just verbally say, "Hey, our exposure 5 levels are this"? 6 A. No. I can only speak for Mobil. But at the end of 7 the process, a spreadsheet-like table was sent to the 8 investigator. 9 Q. And have you ever seen those spreadsheets for Mobil? 10 A. I recall seeing it, you know, 30 years -- 25 years 11 ago. 12 Q. Has that information been trashed to your knowledge? 13 MR. SHOEBOTHAM: Objection, form. 14 A. Don't know. Have no knowledge. 15 Q. (By Mr. Lubel) Do you recall what the recordkeeping 16 or destruction policy was for Mobil regarding how long to keep 17 the information that was sent for the studies to the 18 investigators? 19 MR. SHOEBOTHAM: Objection, form. 20 A. I know what the general record retention policy for 21 Mobil was in that time period, but what they -- when you've 22 added on what they did with the investigators, I'd have -- I 23 have no knowledge. 24 Q. (By Mr. Lubel) What was the general policy? 25 A. I think it was five years at that time. 81 1 Q. They would destroy the documents? 2 A. I don't know. I'm just telling you what the policy 3 was. 4 Q. But what did you do with the documents that you had 5 that were over five years old that related to epidemiological 6 studies? Did you tell them -- did you send them down to the 7 trash department to set a fire or whatever they do with them -8 MR. SHOEBOTHAM: Objection, form. 9 Q. (By Mr. Lubel) -- or how did you treat that? 10 A. By the mid '80s, we had adopted a policy of long term 11 record retention for study specific materials. 12 Q. Well, do you recall on the Cowey deposition that you 13 gave nine or ten months ago that you referenced a 1964 Mobil 14 that for the first time had been unearthed and I think you used 15 the words surrendered to the Provost Umphrey firm? Do you 16 recall that? 17 A. Yes. Because I had only recently come across it 18 myself. 19 Q. Where did you find it? 20 A. When -- I found it because there were some library 21 documents that Exxon did not take. And one of my former staff 22 members down in Virginia said: Got some stuff. And there's 23 some folders that you -- you know, it was clearly somewhat 24 epi-related kind of stuff. Should we -- what -- what should we 25 do with it? They don't want it. And then -- so I asked him to 82 1 just send -- I think it was one box worth of stuff -- send it 2 up to me, because it was reprints and things like that. 3 Q. What did you do with the box? 4 A. Well, a number -- a fair percentage of it was 5 reprints of papers that I coauthored, so I put those in my own 6 reprint file. And some of it I had no idea what it was, made 7 no sense to me. I threw that out. And the study I found and I 8 kept. 9 Q. And -- and -- and do you still have that study? 10 A. The 1964 study -11 Q. Right. 12 A. -- that was referenced right here? 13 Q. Can you send that to Mr. Shoebotham so I can see it? 14 MR. SHOEBOTHAM: Well, we -- I've objected -15 MR. LUBEL: To that? 16 MR. SHOEBOTHAM: -- to the production of that 17 study. There's a written objection filed with regard to that. 18 Q. (By Mr. Lubel) What's the -- what's the -- the 1964 19 study about? 20 A. It's an investigation conducted, as best as I can 21 interpret from reading it, by statisticians from Metropolitan 22 Life Insurance Company looking at the mortality patterns of 23 Mobil employees during that period of time or prior -- you 24 know, obviously prior to '64. 25 Q. Was it ever published? 83 1 A. No. 2 Q. So the Met Life study was sent to Mobil and that's 3 how it got in the file that went in the box that was sent to 4 you. Right? 5 A. Yes, I think that's probably fair to assume. 6 Q. So have you sent that 1964 study to Mr. Shoebotham to 7 look at? 8 A. No. 9 Q. Is there anything proprietary about that study? 10 MR. SHOEBOTHAM: Objection, form, calls for 11 speculation. 12 A. Proprietary is a -- is a -- something that 13 epidemiologists don't... 14 Q. (By Mr. Lubel) Is there any trade secrets in it? 15 MR. SHOEBOTHAM: Objection, form, calls for 16 speculation. 17 A. I don't think so. 18 Q. (By Mr. Lubel) Is there any Mobil processes 19 described in it -20 MR. SHOEBOTHAM: Objection. 21 Q. (By Mr. Lubel) -- I can go steal the -- from the 22 study and go build my own Mobil plant and make a bunch of 23 money? 24 MR. SHOEBOTHAM: Wait a second. 25 Q. (By Mr. Lubel) Is there anything like that in there? 84 1 MR. SHOEBOTHAM: Objection, form, calls for 2 speculation. 3 Q. (By Mr. Lubel) Is there? 4 A. I didn't see anything that -- what I would be -5 question as a trade secret. 6 Q. Does it identify by name the individual employees of 7 Mobil? 8 MR. SHOEBOTHAM: Objection, form. 9 A. No, I don't believe so. 10 Q. (By Mr. Lubel) Does it identify by social security 11 number any individual employees? 12 A. No. 13 Q. Give any of their home addresses of where these 14 people live that have these problems? 15 A. No. 16 MR. SHOEBOTHAM: Objection, form. 17 Q. (By Mr. Lubel) Well, you've -- you've produced it to 18 the Provost Umphrey law firm. Correct? 19 A. In a Mobil-related case, yes. 20 Q. Right. A benzene case? 21 A. Specific to a -- a Mobil facility, yes. 22 Q. But it had to do with benzene, I mean? 23 A. Well, the report doesn't, but the -- it's not a 24 benzene-related report. 25 Q. Okay. But you produced it in a benzene-related case? 85 1 A. I was asked to produce all the Mobil documents 2 relative to studies conducted by Mobil. 3 Q. But the -- the underlying case was an alleged benzene 4 case as opposed to a car wreck or something? 5 A. Yes. 6 MR. LUBEL: So what's your objection, John? 7 MR. SHOEBOTHAM: My objection was stated in the 8 objections that we filed yesterday. 9 MR. LUBEL: How do you know? You haven't seen 10 the document. How do you know what to object to? 11 MR. SHOEBOTHAM: Well, I've objected to it. 12 Q. (By Mr. Lubel) Did you discuss with Mr. Shoebotham 13 the specifics of the report? 14 A. No. I said it was a Metropolitan Life Insurance 15 report. It has no bearing on -- on -- on any benzene-related 16 matters that I can see. 17 Q. Did it address any benzene-related diseases like 18 leukemia? 19 A. No. 20 Q. No leukemias were referenced in it? 21 A. In that era of time, it was predominantly cancer and 22 heart disease. And there were few -- a few major cancers 23 discussed. 24 Q. What does that mean, "a few major cancers"? 25 A. Well, I mean, there were -- my -- my only 86 1 recollection was colon cancer, lung cancer is discussed; 2 there's a -- in other words reported. I don't even recall 3 whether there was any leukemia reported in the study. I don't 4 think so. It was more focussed on heart disease in workers, 5 cardio -- cardiovascular risk. 6 Q. Was this information considered by Dr. Wong when he 7 did the CMA study or do you know? 8 A. It would have been quite irrelevant, but I -- I can't 9 imagine that he had even seen it. 10 Q. Wasn't he looking at the mortality of people that 11 worked at the plant from all causes, essentially? 12 A. This is a report. This is not a data sect. 13 Q. But it's talking about mortality. Right? 14 A. I'm sorry, I don't -- yes, the report is talking 15 about mortality, but I don't understand the... 16 Q. Wasn't Wong's study on mortality of Mobil and other 17 plant workers? 18 A. I'm sorry. Now we're getting -- what study are you 19 talking about? 20 Q. The CMA study. 21 A. No. The CMA study was specific -- had a very 22 specific protocol that was not about general mortality 23 experience. 24 Q. Okay. So you're saying that the CMA Wong study did 25 not address, for instance, lung cancer? 87 1 A. It did in benzene-exposed workers. 2 Q. So it just looked at benzene-exposed workers? 3 A. What we've been calling the CMA study only assembled 4 cohorts of benzene-exposed workers and nonbenzine-exposed 5 workers for comparison as -6 Q. As the control group? 7 A. Yes. And the mortality of the benzene-exposed cohort 8 was fully enumerated in those reports. But it -- but it -9 well, I already said it relates to those workers from those 10 companies that were presumed to be benzene exposed. 11 Q. Well, you don't plan on throwing away the 1964 study. 12 Correct? 13 A. No, I don't. 14 Q. Have you ever seen an answer to the question that was 15 posed by the CMA: Do prior exposure to benzene at toxic 16 concentrations make individuals more sensitive to subsequent 17 exposures? 18 A. I'm not familiar with that statement. 19 Q. You ever seen an answer to that question? 20 A. No, I don't -- well, no, not -- not -- I mean, 21 there's been discussions that I can -- without just, you know, 22 being specific. It's a question. And it's a researchable 23 question that we continue to have. 24 Q. Has it been researched? 25 A. I -- in some settings, probably. 88 1 Q. Do you know the answer to the question from the 2 research that's available? 3 A. No. 4 Q. You spoke about peak exposures earlier. Do you 5 recall that? 6 A. Yes, sir. 7 Q. Which exposures are more dangerous: the low level 8 chronic exposures or the peak exposures? Or do we know the 9 answer yet? 10 A. We don't really know the answer yet. The -- the -11 with all the epidemiology, we can reliably develop. The state 12 tends to focus on continuous exposures; and therefore, the 13 metrics are expressed in ppm years. 14 Q. Do you know if the -- the industry-funded China 15 studies that's ongoing, if it's seeking to address that issue 16 of what matters more: the peak exposures as compared to the 17 chronic low level exposures? 18 A. I don't know. 19 Q. Was that an issue that you thought was going to be 20 addressed back when you were involved in '99? 21 A. Well, I think it was certainly known that it was -22 would have been a -- it would be nice to have. But you always 23 come back to the issue: Can you measure peak exposures 24 reliably in a fashion that can be used in an epidemiologic 25 investigation? 89 1 Q. Who is Paul Cheney? Apparently he went to a meeting 2 for you of the CMA variety. 3 A. Paul Cheney, as I recall, was the plant contact of 4 the data gathering in Beaumont. 5 Q. Why were some of the plants in the CMA Otto Wong's 6 study plant-wide studies and some of them were not? Does that 7 make any sense? 8 A. Yes. I understand the question. 9 The answer is that for Mobil, for example, the 10 whole plant was an olefins aromatic plant, so pretty much 11 excluding administrative personnel, all of the plant would have 12 been considered benzene exposed at some level. Other 13 facilities that were quite large would only contribute data 14 from the -- from their BTX units or however they define their 15 benzene subgroup. 16 Q. For instance, Dow, do you know what areas they chose 17 to include in the Wong study? 18 A. I have no knowledge. 19 Q. Did you ever see the Dow exposure information that 20 was submitted to Wong? 21 A. I don't believe so. 22 Q. Did the companies not share the information that they 23 were sharing with the investigator? 24 A. Only to the extent that we would be sitting here 25 around the room and trying to decide how to summarize it. I 90 1 mean, you might say, Well, I've got this, this, this, and 2 you've got that, that, that, but not -- not in writing that I'm 3 aware of. 4 Q. The summary itself for the raw data was shared 5 between companies. Is that a fair statement? 6 A. Yes. 7 Q. I see some reference to discrepancies between tapes 8 submitted and the cohort listings? 9 A. I believe you, but I don't remember any of it. 10 Q. And I'm focussed on what is meant by "tapes." What 11 are they talking about? 12 A. Oh, I know what that answer is. In that era, there 13 were magnetic tapes being shipped. 14 Q. They contained information? 15 A. Well, you know -- do you know -- do you know what I 16 mean by mag tape? 17 Q. I've heard of it, but I -- is it like a microfilm? 18 A. You're not old enough. 19 Q. Is it microfilm like at the library? 20 A. No, no, no. No. Before diskettes, CDs, and things 21 like that, all of these computer analyses were done on big 22 mainframe computers. And these were magnetic tapes that were 23 about 12 inches in diam -- in diameter. And -24 Q. It's the old version of a disk today? 25 A. No. Then -- we had disks back then, too. But they 91 1 were so big and so cumbersome that they were not used to 2 transport data. They were used on the computers themselves. 3 Q. Okay. Do people call you Jerry in those meetings -4 in those meetings? 5 A. Probably. 6 Q. Who was Dr. Stille, S-T-I-L-L-E? 7 A. I think it's pronounced Stille, but I actually don't 8 even remember who that is. I don't remember. 9 Q. Theodore Stille from the TOMA. I think it's 10 Tabershaw Occupational Medicine -11 A. Associates. 12 Q. Right. 13 A. I don't recall. 14 Q. Well, TOMA was the group that was the investigator 15 for the CMA study. Right? That's who Wong worked for, wasn't 16 it? 17 A. I -- I just don't recall if the company name was 18 TOMA, but -- but now that we've said it four times, TOMA, yes, 19 it probably was. You are correct. Didn't ring a bell when we 20 first talked about it. 21 Q. And TOMA representatives, whether they be 22 Dr. Tabershaw himself or Dr. Stille or Dr. Wong or whoever 23 there was as their representative, was actively involved in the 24 CMA meetings. Correct? 25 A. I don't recall that. I... 92 1 Q. You don't recall seeing them at meetings? 2 A. I wasn't at every meeting. 3 Q. At the ones you were at, do you recall seeing them? 4 A. I recall some meetings with Dr. Wong, and I recall a 5 few very early meetings with Dr. Tabershaw, but I don't recall 6 much of any other staff. 7 Q. You recall a fellow by the name of Hazleton? 8 A. No. 9 Q. Do you recall the five-day study? 10 A. No. 11 Q. Do you recall a 90-day benzene toxicology study to be 12 conducted at Hazleton Laboratories? 13 A. Ah, Hazleton Laboratories, yes. They -- there were a 14 number of benzene tox studies going on in the varying places 15 around -- around the United States and around the world during 16 that whole period. But I don't recall the purpose of the 17 90-day study. Although when you say 90-day, it sounds like 18 it's a subchronic study. 19 Q. Well, do you recall the CMA asking Dr. Hazleton to 20 revise his draft final report? 21 A. I have no recollection of that. 22 Q. Do you recall there being a lot of problems with the 23 data that was -- that the plants had put together to give to 24 Otto Wong for the CMA study? 25 A. I don't recall. 93 1 Q. Is it a true statement that analysis of urinary 2 phenols was not considered to be a sensitive indicator of 3 benzene exposure at low levels? 4 A. That's a true statement to my understanding. 5 Q. What is the appropriate weight of medically-monitored 6 benzene exposed workers today? 7 MR. SHOEBOTHAM: Objection, form. 8 A. I am not familiar with what's currently being done. 9 I mean, the urinary phenol was part of the OSHA for high -10 high exposures expected to be over 10 ppm. And then CBCs, 11 blood test, was the surveillance -- surveillance activity at 12 the time when I left the industry. 13 Q. (By Mr. Lubel) Were there problems with looking at 14 the phenol levels for benzene-exposed workers? 15 MR. SHOEBOTHAM: Objection, form. 16 A. They're only predictive at high exposures. And then 17 that test has to be conducted within a reasonable period of 18 time after the exposure. 19 Q. (By Mr. Lubel) Within 24 hours? 20 A. I don't recall. It's not my area. 21 Q. Do you recall the CMA having meetings with the 22 authors of the IARC monograph on benzene? 23 A. I have no knowledge of that. 24 Q. Would that surprise you? 25 A. No. 94 1 MR. SHOEBOTHAM: Objection, form. 2 Q. (By Mr. Lubel) Talking about before the report was 3 finalized, the monograph? 4 A. Whole monographs are written in residence in a week. 5 And there are typically industry observers that are there to 6 provide technical information into the process. But -- so I 7 don't know what you're specifically speaking to. 8 Q. Have all of your studies been cohort studies on 9 benzene? 10 A. Oh, benzene, yes. Well, the ones related to the 11 refinery workers that are related potentially to benzene have 12 all been cohort studies. 13 Q. Have you ever done a case control study? 14 A. Yes. 15 Q. Under what circumstances? 16 A. We did a case control study of workers exposed to 17 asbestos. 18 Q. Why did you do a case control study as opposed to a 19 cohort study? 20 A. Because you can develop a lot more detailed 21 information on a smaller number of cases and controls than is 22 typically feasible for a very large cohort. 23 Q. So what study is better for benzene exposures? A 24 cohort or case control study? 25 A. Depends on what the objective of the study is. 95 1 Q. Under what circumstances would a case control study 2 be better than a cohort study for benzene exposures? 3 A. Typically in a case control study, you can get more 4 refined exposure information on the cases and controls. 5 Q. How do you get better information? Because they're 6 alive? 7 A. No. That's a different element of the design. You 8 just asked case control versus cohort. No, because you -- you 9 now have the ability to identify very specific job history 10 information. You can go to the medical records and get smoking 11 history information. You can directly -- you know, you have 12 just more opportunity to get more refined exposure and 13 lifestyle and individual data on smaller numbers. 14 Q. Why can't you do that on a cohort study? Because the 15 number -- the group's larger? 16 A. It's just typically -- trying to do that on 7,000 17 current and former workers just becomes technically and 18 logistically -- one can never say impossible, but so difficult 19 that -- that you -20 Q. Practically impossible? 21 A. -- you -- that you go to the nested case control 22 design. 23 Q. Would it be a fair statement that the case control 24 design would provide more reliable specific detail than the 25 cohort? 96 1 A. That depends on the individual study and how it's 2 conducted. 3 Q. But everything else is equal, you'd expect to get 4 more detail out of the case control design than the cohort 5 design. Right? 6 A. I -- I -- I don't think you can make generalities 7 that broadly. It depends on the size of the cohort relative to 8 the size of the case control setting. 9 Q. Well, Dr. Collins, on behalf of Dow, objected to the 10 China study being done by Wong and Irons that we've been 11 talking about at some length today. And as I appreciate what 12 he said, his primary complaint was the design of the study. 13 And I -- did you read that when you read his testimony? 14 MR. SHOEBOTHAM: Objection, form. 15 A. I -- I read the same words that you did. My take 16 away was that he was -- that he was speaking as an 17 epidemiologist that liked cohort studies and nested case 18 control studies within cohort studies. And that would not be 19 feasible in the typical China setting. 20 Q. (By Mr. Lubel) To do a cohort study? 21 A. Unless you were going to do the -- all of Shanghai, 22 it would not be feasible. 23 Q. Well, the study that was performed by Hayes & Yin and 24 others in China, were those case control or cohort studies? 25 A. Those were cohort studies of multiple -- multiple 97 1 different facilities, which is part of the reason why nobody 2 can quite understand how to interpret that study. It 3 generated -- generates a lot of confounding information in the 4 exposure setting. 5 Q. That's because they looked at too many factories? 6 A. Well, they've got painters; they've got chemical 7 workers; they've got pesticide workers. And yes, ostensively, 8 they may have shared some element of benzene exposure across 9 those, but nowhere in those studies do they account for all the 10 confounding exposures that are not measured. So if you were a 11 pesticide worker and at any given time benzene was one level 12 and pesticide was another, they're correlated. 13 Q. But that's one of the inherent problems with the 14 cohort study is trying to get the specifics that you're 15 referring to. Right? 16 A. That's why every -- each study has a different set of 17 objectives. 18 Q. So the -- the industry-funded study that's ongoing 19 right now by Irons and Wong, that's a case control study. 20 Right? 21 MR. SHOEBOTHAM: Objection, form. 22 Q. (By Mr. Lubel) As you understand it? 23 MR. SHOEBOTHAM: Calls for speculation. 24 Q. (By Mr. Lubel) No. It's a cohort study. Right? I 25 didn't mean to say case. Isn't it a cohort study? 98 1 A. My understanding of what Dr. Wong's piece is is a 2 case control study with knowledge of the individual plants from 3 which the cases are coming. I don't have any information on 4 the molecular biology piece of what Dr. Irons is -- I don't 5 know where Dr. Irons' cases are coming from. 6 Q. So it's your understanding that the China study, at 7 least the part you're familiar with, is going to be a case 8 control study? 9 A. In its basic design, yes. 10 Q. And Dr. Collins' objection to that was he preferred a 11 cohort study. Is that what you understood him to say? 12 MR. SHOEBOTHAM: Objection, form. 13 A. I can't get into Dr. Collins' head. I mean, it was 14 just a one liner, and -- and... 15 Q. (By Mr. Lubel) What does one line say, is what I'm 16 getting at? What did he testify to? 17 MR. SHOEBOTHAM: Objection, form. 18 A. He said he prefers a cohort study. 19 Q. (By Mr. Lubel) How are they going to assemble the 20 exposure evidence from the China study? 21 A. I don't have firsthand knowledge on how it's being 22 done. I mean secondhand knowledge of how it's... 23 Q. From your '95 studies, how did you assemble the 24 benzene exposure information? 25 A. Well, the papers that I believe you're referring to, 99 1 we had access to the Pliofilm cohort directly. We had the -2 the raw data. And the refinery studies, as you recall our 3 earlier discussion, we did not have exposure data specific to 4 the leukemias. 5 Q. Did you have two '95 studies? 6 A. Dr. Wong has one that he's by himself on, and then 7 there's the one that we have been referring to where we're both 8 coauthors on. There's tables in that paper that talk about 9 dose response for benzene that are generated out of the 10 Pliofilm cohort, not the refinery cohorts. 11 Q. You talking about Exhibit 9? 12 A. Yes. 13 Q. But you -- your study in Exhibit 9 was not a study of 14 the Pliofilm cohorts, was it? I thought it was refinery 15 workers? 16 A. No. It discusses table ten in the paper. There's a 17 very large section in the paper that discusses what we know 18 about dose response and what we know about case control studies 19 of different specific leukemias, subtypes and basic subtypes. 20 Q. But I thought Exhibit 9 was a refinery worker study? 21 A. Half of it, yeah. I mean, the -- the -- the -- it 22 reports the refinery workers and then discusses what all is 23 known about leukemia in a subtype, specific analysis, as it 24 relates to benzene and refinery workers. 25 Q. All right. Now, for the Pliofilm portion of it, 100 1 where did you get the exposure information? 2 A. Dr. Wong received a copy of the Pliofilm cohort with 3 the Rinsky exposure estimates and the Paustenbach exposure 4 estimates. 5 Q. Who did he get them from? 6 A. That I don't recall. 7 Q. Did you ever see them? 8 A. Yeah. 9 Q. Did you ever analyze that data? 10 A. Out of the analysis, I saw some of the tables. 11 Q. What's the volume of exposure data that we're talking 12 about? Are we talking about a box or ten pages of -13 A. No. That cohort has been so extensively studied and 14 documented that the cases are already assigned accumulative 15 exposures and under -- there's three major exposures: Rinsky, 16 Infante, and Paustenbach. And those have already been 17 summarized as individual numbers on each case. 18 Q. I understand that. There's actually articles on 19 them. Right? 20 A. Yeah. Lots. 21 Q. But have you seen the raw data, is what I'm asking? 22 The raw exposure data. 23 A. No. 24 Q. From the Pliofilm cohort? 25 A. I have not. 101 1 Q. Has Wong seen it to your knowledge? 2 A. No. I believe he's -- no, I don't know. I don't 3 know that actually. 4 Q. So when you or Wong -- strike Wong. 5 When you are involved in an article that talks 6 about the Pliofilm exposures, you're interpreting the summary 7 of the data as supplied from the -- from the Rinsky materials, 8 from the Infante materials, and from the Paustenbach materials. 9 Correct? 10 A. Yes. 11 Q. Now, who wrote the first article on the Pliofilm 12 cohort? 13 A. Peter Infante. 14 Q. And it was followed by Rinsky. Correct? 15 A. Several versions of it. 16 Q. And then Paustenbach? 17 A. Paustenbach. Well, no. 18 Q. Crump & Allen? 19 A. You're confusing risk assessments using that data 20 from the epidemiology studies using that data. 21 Q. Well, let's stick with the epidemiological studies. 22 A. Okay. 23 Q. What's the -24 A. First Rinsky, Paustenbach -- excuse me. That's 25 incorrect. Paxton then -- then another update by Rinsky. 102 1 Q. Where does Infante fall in that? 2 A. He was not involved in any of the updates except 3 maybe a courtesy fourth or fifth author on the first Rinsky. 4 THE REPORTER: With what? I'm sorry. 5 THE WITNESS: Courtesy fourth, fifth author -6 fourth or fifth. 7 A. I don't recall where he is, but he's near the end of 8 the author list. 9 Q. (By Mr. Lubel) But the original study was done by 10 Infante. Correct? 11 A. Without detailed exposure estimates, correct. The 12 original cohort mortality study. 13 Q. And then Rinsky followed Infante. Correct? 14 A. Yes. 15 Q. With a study? 16 A. Correct. 17 Q. And he provided exposure information in the study. 18 Correct? 19 A. Correct. 20 Q. How did Rinsky, if you know, locate the exposure 21 information? 22 MR. SHOEBOTHAM: Objection, form. 23 A. NIOSH industrial hygienists reconstructed estimates 24 for that cohort and people in that cohort. 25 Q. (By Mr. Lubel) Where did they get the estimates for 103 1 that cohort? 2 A. From data available in -- in the original cohort. I 3 mean, it was -- it was data that had already been collected 4 that -- but had not been analyzed. 5 Q. Collected by Infante but not analyzed? 6 A. I don't -- the government -- government does their 7 studies differently. They hire lots of subcontractors that go 8 out and see the things. So I don't really know specifics 9 beyond what I just told you. But it was already in their 10 possession either through their contractors that were 11 assembling the data or their own. 12 Q. Here's why I'm asking you: There's at least three 13 theories of the Pliofilm exposures. Correct? 14 A. Not theories. They're three estimates that are -15 that only two -- two of which tend to be used today. 16 Q. But they're different, is my point. 17 A. But there's three different ones. 18 Q. They're not -- there's three different ones, is my 19 point. They don't all agree? 20 A. Correct. 21 Q. So what I'm trying to find out is how Rinsky got his 22 data and then how Paxton the got his data and then how 23 Paustenbach got his data, if you know. If you don't know, just 24 say you don't know. 25 A. Okay. I don't know how Rinsky got his data. 104 1 Paustenbach, who helped Paxton assemble that update, got the 2 records under freedom of information from the federal 3 government. So that's how they got the data. 4 Q. Do we know if Rinsky had that same data? 5 A. Yes. 6 Q. So basically what Paustenbach and Paxton did was is 7 they came up with a different estimate based upon at least in 8 theory the same data that Rinsky had? 9 A. Correct. 10 Q. And do we know whether the data that they all had was 11 actual exposure monitoring, you know, an employee wearing a 12 badge, or whether it was grab samples or whether it was area 13 monitoring? Do we know that kind of detail? 14 A. I don't recall it, but there are published papers 15 that discuss that. 16 Q. Okay. Do you recall whether that was one of the 17 weaknesses with the study was the -- how the estimates were 18 made and what they were based on? 19 A. The big -- the biggest debate or differences between 20 the estimates refer to what the exposures were during the end 21 of the war years. The very early part of the cohort are where 22 the big differences -- well, the difference is enough to change 23 the ppm year distributions -- occur. That I do recall. 24 Q. And in summary is the primary issue in that regard 25 that the Paustenbach camp takes the position that because it 105 1 was the end of the war years, the plants were going at full 2 capacity, if not in excess of full capacity, and therefore 3 you'd expect higher exposures than what Rinsky had estimated? 4 A. I don't recall the specific arguments. I have not 5 looked at them in years. 6 MR. LUBEL: Okay. Can we take a short break, 7 John? 8 MR. SHOEBOTHAM: Sure. 9 (Recess from 1:57 p.m. to 2:09 p.m.) 10 Q. (By Mr. Lubel) I'm going to mark some exhibits from 11 the documents you brought with you today. Okay? 12 A. That's fine. 13 (RAABE Exhibit Nos. 11-12 were marked.) 14 Q. (By Mr. Lubel) Number 11 is out of your file. Can 15 you identify that for me? 16 A. Just a few shorthand notes that I took along the way 17 discussing James Boren. 18 Q. Is that all the notes that you have for this case? 19 A. Yes, sir. 20 Q. Thanks. Are you relying on anything in your notes 21 for your opinions? 22 A. Well, the notes state that -- yes, I am. 23 Q. Which ones? 24 A. Well, he was a pipefitter/welder. He's got an AML-M3 25 with the only cytogenetic abnormality being T15:17 106 1 transportation. He was a smoker and at the end of his -- when 2 he left the petrochemical industry he started a boot/shoe 3 repair shop. I mean, it's just pertinent facts of his history. 4 Q. Did you get that from his deposition? 5 A. Yes, I believe. 6 Q. The notes that we see in Exhibit No. 11? 7 A. Yeah. 8 Q. So you read Mr. Boren's -9 A. Well, his -10 Q. Did you read Mr. Boren's deposition? 11 A. Yes. Yes. I mean, I got the diagnostic information 12 and some other documents. 13 Q. Medical records? 14 A. Yes. 15 Q. Is it safe for a person to stick their hands in pure 16 benzene every day for three years? 17 A. It's probably unwise. 18 Q. Why? 19 A. I can't imagine anybody actually doing it, because 20 benzene is so defatting to the skin that they would have had 21 cracked skin. They would also increase their potential 22 exposure. 23 Q. And why would it be unwise to stick your hands in 24 benzene every day for several years? Pure benzene, from a 25 health hazard standpoint? 107 1 A. Well, I don't believe anybody would, but the reasons 2 for that is that it would so severely defat the skin, they 3 would have severe skin problems, one; two, they would begin to 4 accumulate some inhalation exposure and some dermal exposure to 5 benzene. 6 Q. And what would be their hematological risk to those 7 exposures? 8 A. I can't comment on that. 9 Q. Why? 10 A. Because I've not attempted to do an evaluation on the 11 inhalation of dermal exposures specific to that scenario you 12 just said. 13 Q. But you've been an epidemiologist for a number of 14 years working specifically on benzene issues. Correct? 15 A. Yes. 16 Q. And in all the years that you've been doing this, 17 have you ever seen the question posed as to whether or not it's 18 safe for somebody to stick their hands in pure benzene? 19 A. I think I agree it's -- well, safety is -- I -- when 20 you use the word "safety," I start to balk, but it's certainly 21 not something that should be done. 22 Q. Would you as a -- you're a medical doctor, too. 23 Correct? 24 A. No. Doctor of Public Health. 25 Q. Right. In your role as an epidemiologist that knows 108 1 a fair amount about benzene and the health hazards associated 2 with benzene, if you had been approached by Mobil Oil, for 3 example, and said, "Hey, we've got pipefitters and other crafts 4 running around here washing their tools in benzene every day, 5 pure benzene, what do you think about that, Dr. Raabe?" what 6 would you have said to them? 7 A. Stop it immediately and don't let it continue. 8 Q. Back to my initial question which is: Have you ever 9 seen the question posed as to what the exposure levels are for 10 somebody that sticks their hands in benzene? 11 A. No. 12 Q. Would it surprise you if the industry organization, 13 the Chemical Manufacturers Association, actually posed that 14 question? 15 A. No. 16 Q. Do you know if it was ever answered? 17 A. I don't know. 18 Q. If it was answered, you don't recall what the answer 19 is. Correct? As far as what the exposure levels are? 20 A. I don't recall either part of that process, that they 21 asked it or that an answer was ever developed nor did I see an 22 answer. 23 Q. But as you sit here as an expert that Mr. Shoebotham 24 hired, you may be able to make general comments about whether 25 it's wise or unwise for a worker at any time to stick their 109 1 hands in benzene, whether it be for a day or three years, but 2 you don't feel as though you're in a position to address 3 whether or not that type of exposure could lead to a 4 hematological disease? 5 A. I would look to other scientific disciplines to give 6 me a dose estimate that I could put into context with what we 7 know about dose responses for benzene-induced disease. 8 Q. What discipline would you go to for that information? 9 A. Probably a combination, depending on the level of 10 expertise. Industrial hygiene would be part, someone with 11 familiarity with dermal exposure. Could be the same person or 12 it could be someone else. 13 Q. Who are you thinking of that knows something about 14 dermal exposures? 15 A. Well, it could be toxicologists in combination -- a 16 toxicologist in combination with an industrial hygienist, or it 17 could be an industrial hygienist with that kind of training. 18 Q. Have you ever consulted specifically with somebody in 19 that area that specializes in dermal exposures to benzene? 20 A. No, I have not. 21 Q. Do you know if anybody has? 22 A. In the world? 23 Q. Anybody that you know that has done so. 24 A. I know John Spencer has done work in that area. 25 Q. In what regard? 110 1 A. Well, I'm aware he's done some work with liquid 2 wrench, and I'm also aware that he has done some work in this 3 case. 4 THE REPORTER: Who? Done some work with who? 5 MR. LUBEL: In this case. 6 THE WITNESS: In this case. 7 THE REPORTER: Before that who did you say? 8 THE WITNESS: With liquid wrench. 9 Q. (By Mr. Lubel) Have you talked to John Spencer about 10 his opinion in this case? 11 A. No, but I've seen a one-page summary of exposure 12 information. 13 Q. And does his one-page summary of exposure information 14 address exposures to a person that sticks their hands in 15 benzene every day for a number of years? 16 A. The piece of the document that I have, if there's 17 more of it, does not speak to that. 18 Q. Does or does not? 19 A. Does not. 20 Q. Okay. Have you talked to Mr. Shoebotham about 21 whether Mr. Spencer is going to create a document that 22 addresses that exposure? 23 A. No, I have not. 24 Q. As you sit here today, do you know whether that 25 exposure is sufficient to cause leukemia? 111 1 A. Mr. Parker also came up with some estimates that 2 ostensively included derma. I have not seen any background 3 material on those -- on those calculations, but the number he 4 comes up with is substantially below the 200 ppm years that the 5 literature suggests is the lowest level where increased AML 6 risk occurred. Significantly occurred. 7 Q. Well, Rinsky's and White's data back in the early 8 '80s came up with data that suggested 10 parts per million 9 could increase the risk of leukemia. Correct? 10 A. That is total leukemia. 11 Q. Pardon me? 12 A. I believe you're talking about total leukemia versus 13 acute myelogenous leukemia. 14 Q. All right. You've seen the Rinsky data and you've 15 even seen the EPA 1998 breakdown on it where they have a table 16 in there that talks about increased relative risk of AML 17 specifically from exposures in the 40 part per million to the 18 200 part per million range? 19 A. I would have to go back and look at them. What I'm 20 thinking of is Rinsky's updated paper where he doesn't see 21 statistically significant increase risk for leukemia until 22 approaching 400 ppm in his most recent update. 23 Q. What update was that? 24 A. 2002. 25 Q. What did the previous update say? 112 1 A. It was statistically significant in I believe the 200 2 range as well. 3 Q. Not in the 40 to 200 part per million range? 4 A. I don't recall. 5 Q. Well, surely you're aware that there are peer review 6 published articles that address risk of AML being significantly 7 increased by exposures to benzene less than 200 parts per 8 million. Correct? 9 A. There are several papers out there, yes. 10 Q. One of those is the Hayes, Yin article regarding the 11 China studies done by the National Institute of Health and the 12 Chinese equivalent. Correct? 13 A. Hayes has a few tables that address exposures that are 14 lower than 200 parts per million. 15 Q. In fact less than 10 parts per million. Correct? 16 A. I don't recall that as being statistically 17 significant. 18 Q. In what level do you recall him taking the position 19 that it was statistically significant? 20 A. I don't recall. We would have to pull the paper and 21 start looking at it. 22 Q. Do you think the Hayes and Yin article is in here? 23 A. You have two piles of my papers. 24 Q. That's mine. 25 A. Oh. Yes, it should be, unless we've already pulled 113 1 it out earlier. I don't think. The Hayes paper should be 2 there. 3 Q. Give it back to you? 4 A. I have the paper. 5 Q. Let's mark that as Exhibit No. 13. You can go ahead. 6 I'll just write on it in just a second. Thanks. 7 A. I'm waiting for a question. What... 8 Q. Oh, you found the Hayes and Yin article? 9 A. Yes. 10 Q. What's the date of it? 11 A. 1997. 12 Q. There was a 2000 version, wasn't there? 13 A. Not of the new -- this is the most recent 14 epidemiologic update. 15 Q. I recall talking to you in the Cowey case about the 16 -- was it 2000 or 2001? 17 MR. BLACK: 2000. 18 Q. (By Mr. Lubel) -- 2000 Hayes and Yin article. It's 19 the one that specifically addressed MDS and NHLs? 20 A. Oh, the -- the one that essentially responds to some 21 of the criticisms? 22 Q. I don't recall that that was the nature of it, but... 23 A. I didn't bring that with me. 24 Q. At any rate, looking at the article that you have, do 25 you recall that there was statistically significant excesses of 114 1 what I think they categorized as acute nonlymphocytic leukemias 2 at low level benzene exposures? 3 A. The cumulative -- yes, there is. 4 Q. Do you remember what the -- you've got a chart, so -5 A. Right. Looking -- make the record easy. Looking at 6 table two, the first statistically significant risk occurs in 7 the category 40 to 99, and it's also significant in the 8 category over 100 ppm. 9 Q. 40 to 99 parts per million? 10 A. Yes. 11 Q. And is that for AML specifically? 12 A. AMLL. 13 Q. Which is acute nonlymphocytic leukemia? 14 A. Correct. 15 Q. What would that include other than AML? MDS? 16 A. No, it would not include MDS. It would include a few 17 subtypes that are slightly different than AML. 18 Q. And I take it from the testimony that you've given 19 previously that you still believe that benzene exposures at the 20 right level can induce myelodysplastic syndromes, otherwise 21 called MDS? 22 A. Yes. 23 THE REPORTER: I need just one second. 24 MR. LUBEL: Sure. 25 (Discussion off the record.) 115 1 Q. (By Mr. Lubel) Do you believe that the levels that 2 are required for there to be a benzene-induced MDS are the same 3 that are required for a benzene-induced AML? Or do you think 4 they're different benzene exposures? 5 A. I don't -- they're probably similar but not exact. 6 Q. Which one is lower? 7 A. Depending on the nature of the MDS, probably MDS may 8 be a little lower. 9 Q. Do you know where you're going with that, or you're 10 just saying, "I think it's lower and I'm not sure where"? 11 A. I think it's lower and I'm not sure where. 12 Q. Fair enough. 13 MR. LUBEL: Do you have a paper clip? 14 (Discussion off the record.) 15 Q. (By Mr. Lubel) In your file I see a deposition and 16 trial list that I'm going to mark as Exhibit No. -17 MR. LUBEL: What are we on? 18 THE REPORTER: Fourteen. 19 Q. (By Mr. Lubel) -- 14. 20 A. Yes, that's what that is. 21 (RAABE Exhibit No. 14 was marked.) 22 Q. (By Mr. Lubel) Is that something you created? 23 A. Yes. 24 Q. Is it updated? 25 A. Best as I can. 116 1 (RAABE Exhibit No. 15 was marked.) 2 Q. (By Mr. Lubel) Exhibit 15 is a copy of your 3 curriculum vitae? 4 A. Yes. 5 Q. Who are you employed by right now? 6 A. I'm principal scientist for a company that I own 7 called Health Risk Sciences. 8 THE REPORTER: Health what? 9 THE WITNESS: Risk Sciences. 10 Q. (By Mr. Lubel) Do you have any employees? 11 A. No. 12 Q. You're the -13 A. I'm the only full-time employee. 14 Q. I take it your wife helps? She is the chairman of 15 the board? Come on, be honest? 16 A. She does good Xeroxing. 17 Q. I'll be sure and send her a copy of this. 18 (RAABE Exhibit No. 16 was marked.) 19 Q. (By Ms. Lubel) All right. What is Exhibit 16? 20 A. 16 is a list that I believe to be correct of 21 materials sent to me by Mr. Shoebotham's office. 22 Q. Okay. Are you relying on all of the information 23 contained within Exhibit 16 for your opinions? 24 A. No. 25 Q. Can you put a check mark next to the stuff you're 117 1 relying upon? 2 A. When you use "relying upon," do you mean -- I'm not 3 sure I understand what relying on -- when you use the term. 4 Q. Something you may sit down in front of the jury if 5 this case ever gets to trial and say -6 A. And make statements from? 7 Q. Yeah. 8 A. Okay. 9 Q. Exactly. 10 A. I don't recall offhand the medical -- where I pulled 11 those medical records from, so I'm just going to check the 12 medical records that are listed here. Possibly need it. 13 May I just ask -14 Q. Yes. 15 A. -- him to confer with me? 16 Q. Sure. 17 (Discussion off the record.) 18 Q. (By Mr. Lubel) What you have done at my request here 19 is on Exhibit 16 you've checked off the stuff out of the 20 materials you've been provided by the defense lawyer, 21 Mr. Shoebotham, that you know at least as of right now that you 22 intend to potentially use at trial if asked any questions? 23 A. Potentially. 24 Q. I'm not trying to be tricky, but you have marked a 25 section that says "Documents Produced by TDCC," and then it's 118 1 got a bunch of Bates numbers, 1 through 2,534? 2 A. I believe those are -- you will see I checked -3 there are a couple of other submissions of the same type that I 4 checked. Some of those include -- the ones I'm thinking of 5 mostly are the whole variety of studies conducted by Dow that 6 were -7 Q. What kind of studies are they? 8 A. We discussed -- I mean, I brought a few of them with 9 me. It's essentially the production -- all the studies that 10 that they did relevant to benzene and relevant to Freeport and 11 Midland. 12 Q. And are you including toxicological studies? 13 A. No. 14 Q. Even if they are within these Bates numbers, you're 15 not using those for your opinions. Right? 16 A. Own -- like when you say toxicologic, you mean purely 17 animal study? 18 Q. Right. 19 A. No, I wouldn't be using those. 20 Q. Like fish. 21 A. I would not be using them. 22 Q. Are there any particular Dow studies that we've not 23 already talked about in your deposition that you're relying 24 upon for your opinions? 25 A. Well, we didn't specific -- I believe we numbered 119 1 them all, but we didn't discuss all of the Freeport updates. 2 Q. Other than those, the ones we've marked as exhibits 3 here in the deposition. I'm trying to get you to think about 4 stuff that we don't have in front of us here at the deposition? 5 A. Possibly going -- I possibly may need to go back to 6 some earlier Midland -- Midland papers, doctor's original 7 papers, for example, but I don't know at this time. 8 Q. Okay. Are you relying on Dr. Natelson's deposition? 9 A. Not directly. I checked it only when he makes 10 statements that I support and agree with. 11 Q. Do you agree with all the statements he made in his 12 testimony under oath? 13 A. I don't remember all the statements, but I probably 14 don't agree with every single one. 15 Q. Do you remember the ones you disagree with? 16 A. Not specifically, no. 17 Q. Do you remember any of the disagreements you have 18 with Dr. Snodgrass' deposition? 19 A. His -- the draft I received was very difficult to 20 read, so I have not really comfortably reviewed all of that 21 yet. 22 (RAABE Exhibit No. 17 was marked.) 23 Q. (By Mr. Lubel) Exhibit 17 is the John Spencer 24 exposure information that you've received so far? 25 A. As well as Frank Parker's estimates, yes. 120 1 Q. But who prepared the document to your knowledge? 2 A. I don't know who prepared the document other than it 3 contains the estimates from Frank Parker and the estimates that 4 I have been told are John Spencer's. 5 Q. Who told you they were the estimates for Spencer? 6 A. I believe I got that out of reading the Natelson 7 deposition and was -- I believe it was confirmed by 8 Mr. Shoebotham. 9 Q. So you have not spoke to Mr. Spencer about this case? 10 A. No, I have not. 11 (RAABE Exhibit No. 18 was marked.) 12 Q. (By Mr. Lubel) And then Exhibit 18 is the affidavit 13 of my client that Mr. Shoebotham sent you. That's in your 14 file. Correct? 15 A. Yes. 16 Q. I take it you've relied upon that for exposure 17 information. Correct? 18 A. I relied on it only to the extent that it's an 19 allegation by Mr. Boren of what he did. 20 Q. But it's information that you in your capacity as an 21 epidemiologist has to look at in order to make an assessment? 22 A. Yes. 23 Q. In addition to depositions and other things? 24 A. Yes. 25 (RAABE Exhibit No. 19 was marked.) 121 1 Q. (By Mr. Lubel) Exhibit 19, if you'll just generally 2 summarize what that consists of? 3 A. These are essentially, for the most part -- well, 4 correspondence between Mr. Shoebotham and myself and for the 5 most part our transmittals or plan to meet announcements, and 6 the last item attached to it is the notice of the deposition. 7 Q. Thanks. In Rinsky's 2002 article that you brought 8 with you, did he give different exposure information from what 9 he had in the previous versions, '81 and '87? 10 A. No. The cohort is terminated so the NIOSH estimates 11 that he used in the original study are the same ones being used 12 today. 13 Q. Do you know how he got different exposure 14 information, or did he get a different exposure information? 15 A. There was no more -- there is no -- the plant is 16 closed. There is no more exposure. 17 Q. Did he interpret the exposure information differently 18 in the 2002 version, or did he just have an update of 19 additional information that changed the numbers? 20 A. He updated the mortality of the cohort using the same 21 exposure information. 22 Q. And that gave him different numbers, if you will? 23 A. It gave him additional cases. 24 Q. So his 2002 paper, if you will, on the Pliofilm 25 cohort does not invalidate his '81 or his '87 version of the 122 1 paper. Correct? It's different? 2 A. No, it doesn't invalidate it. 3 Q. It's just different? 4 A. It's just the most recent information on the cohorts 5 mortality. 6 Q. I'm going to show you some information. You can tell 7 me what you're using it for. The American Cancer Society, 8 Leukemia -- Acute Myeloid (Myelogenous), what are you using 9 that for? 10 A. I'm using that for a general description of leukemia 11 and acute myeloid leukemia in this country. 12 Q. So you're not using this article specifically for 13 things like latency periods and that kind of stuff. Right? 14 A. Right. 15 Q. Same question with the National Cancer Institute 16 article, pages 1 through 39, that you brought with you? 17 A. General epidemiology of leukemia and acute myelitis. 18 Q. I'm going to mark these series of articles as one 19 exhibit, No. 20. Okay? 20 A. That's fine. 21 (RAABE Exhibit No. 20 was marked.) 22 Q. (By Mr. Lubel) If we get to an article where there's 23 something other than general background information about 24 leukemia you're using, will you tell me? Stop me, please. 25 A. If I recall it at the time, yes. 123 1 Q. The Estey article on Acute Myelogenous Leukemia? 2 A. This one discusses -- begins to discuss in more 3 detail cytogenetic abnormalities and those that are potentially 4 related to secondary or environmental exposures. 5 Q. All right. We're going to go ahead and mark that as 6 Exhibit 21. 7 (RAABE Exhibit No. 21 was marked.) 8 Q. (By Mr. Lubel) Does that article exclude 9 translocations 15 and 17 from being benzene induced? 10 A. It doesn't speak directly to the benzene. 11 Q. What does it speak to? 12 A. As -- if I'm recalling it correctly, it discusses 13 what is -- what is known about the -- well, it talks about the 14 basic epidemiology of M3, and it -- I believe it also talks 15 about therapy related and does discuss latency, age, some of 16 the -- related to therapy related or types of -- it doesn't 17 speak specifically to benzene. 18 Q. Does it speak indirectly to benzene? Is the word 19 "benzene" in here? 20 A. I don't believe the word "benzene" is in there. 21 Q. Okay. Move on to Exhibit 22 which appears to be an 22 article titled Acute Myelogenesis Leukemia by Seiter, 23 S-E-I-T-E-R, and others? 24 A. Yes. 25 Q. What are you using that for? 124 1 A. Same as the previous article. 2 Q. Okay. Can we keep that as part of 21 then? 3 A. That's fine with me. 4 Q. How about the next one, Cancer Epidemiology? 5 A. That's just general epidemiology. 6 Q. Keep part of 21 too or is that a different category? 7 A. It's not specific to APL. It belongs more with the 8 general epidemiology. 9 Q. Is there any particular section in what I'm going to 10 mark as Exhibit 22, Cancer Epidemiology and Prevention, Second 11 Edition, that you're using for your opinions in this case? 12 A. Depending on what I'm asked, I may refer to it for 13 what are known risk factors for acute myelogenous leukemia. 14 (RAABE Exhibit No. 22 was marked.) 15 Q. (By Mr. Lubel) What are the known risk factors that 16 are generally accepted in the scientific community? 17 A. Radiation, a variety of chemotherapeutic drugs, and 18 in some special circumstances some viruses, and of course 19 benzene in high dose, long duration. 20 It's getting late in the day, but that's the 21 ones that come to my mind right now. 22 Q. Those are the ones you typically see in a textbook. 23 True? 24 A. Yes, generally. 25 Q. There may be articles out there that suggest that 125 1 there's other risk factors. True? Like smoking? 2 A. Yes, smoking. Very good. Thank you. 3 Q. You don't typically see smoking in the textbooks but 4 that doesn't mean that smoking can't be related to AML? 5 A. Well, the surgeon general has recently concluded that 6 it is. 7 Q. Well, that's my point, though. 8 A. Yes. 9 Q. Just because it's not mentioned in an -- every 10 epidemiology textbook doesn't mean that there aren't articles 11 out there that are sufficient to say otherwise? 12 A. Well, once again, individual articles would not do 13 it. It would have to be a body of literature. The paper that 14 we're talking about here, this chapter on leukemia, summarizes 15 through '96 the state of the science about risk factors and 16 epidemiology of leukemia. 17 Q. Well, of the known risk factors, let's go through 18 them. Smoking. Did smoking contribute to cause Jimmy Boren's 19 leukemia? 20 A. It may have confounded or contributed to his disease, 21 yes. 22 Q. You say "may have." Based upon reasonable scientific 23 principles, what is your opinion as to whether smoking 24 contributed to cause in whole or in part his leukemia? 25 A. As it applies to M3s, we don't have a lot of data. 126 1 But it is -- and depending on -- and he didn't smoke that -- in 2 the scheme of things, his pack years are not that high, if 3 correctly reported. So I sort of view it as perhaps 4 contributing to but probably not causing directly. In other 5 words, at most it's contributing, it's adding, but I don't... 6 Q. Well, that's how cancer works. Very seldom can you 7 pick one thing and say that's what caused it. Right? 8 A. Unless you have very specific dose -- dose 9 information. 10 Q. But, I mean, if a person is exposed to multiple 11 carcinogens, the theory that's taught in medical schools is 12 that each and every exposure to those carcinogens can take you 13 down the path of cancer? 14 A. Well, I hope they're not teaching that in medical 15 schools today, but -- because that's a gross oversimplification 16 and probably incorrect in many parts. 17 Q. Is that incorrect? 18 A. It's very specific to which cancer you're talking 19 about. In other words, making it as a generalization is -- is 20 potentially... 21 Q. Well, let's take smoking, for example, with Jimmy 22 Boren. You're willing to say that it perhaps contributed to 23 cause his leukemia, but you won't say that you are of the 24 opinion that it was a cause. Not the sole cause. You won't 25 say that it was a cause of his leukemia. Correct? 127 1 A. I reserve -- I guess I'd want to say I want to 2 reserve that, because I plan to go back to the primary papers 3 that the surgeon general cites and read those. I have not read 4 those all. Right now I'm willing to say that it contributed, 5 but how strongly I make that statement, I think I'll have to 6 reserve my opinion. 7 Q. Based upon papers that you didn't have before you 8 today. Correct? 9 A. Well, based on papers that I have not been able to 10 retrieve yet. 11 Q. You don't have them here at the deposition? 12 A. Correct, but I don't have them anywhere either. I 13 have got to get them. 14 Q. Well, the second risk factor that you referenced for 15 AML was radiation? 16 A. Yes. 17 Q. Did radiation contribute to cause Mr. Borne's 18 leukemia? 19 A. Based on the information I have of his work history, 20 I would say no. 21 Q. Because you don't see any evidence of exposure to 22 radiation before his diagnosis of leukemia. Correct? 23 A. Correct. 24 Q. Do you see any evidence that would suggest that one 25 or more viruses contributed to cause Mr. Boren's leukemia? 128 1 A. I don't have enough information to write any 2 conclusions on virus. 3 Q. One way or the other. Correct? What information 4 would you need? 5 A. I don't think it plays for Mr. Boren, but in some 6 other lymphomatic diseases I would like to know more about 7 farming and animal husbandry and HIV and -- you know, there are 8 a number of -- I didn't see any virus markers in any of his 9 medical history that would be related. 10 Q. See evidence that would cause you to suspect or opine 11 that Mr. Boren had previous chemotherapy treatment that caused 12 his leukemia? 13 A. I have not seen anything in the records. 14 Q. We can rule that out. Correct? 15 A. Yes. 16 Q. And we can rule out the radiation. Correct? 17 A. Based on the data available to date, yes. 18 Q. And at least based upon the information you received 19 on Mr. Boren's to date, we can rule out viruses for now? 20 A. Yes. 21 Q. What we're left with is smoking, which you want to 22 look at the surgeon general opinions before you make a final 23 opinion on that. Correct? 24 A. Yes. 25 Q. And then I take it that it's your opinion that 129 1 benzene didn't contribute one iota to Mr. Boren's leukemia. 2 Correct? 3 A. Pretty much everything I have read says that the form 4 of M3 he has is a spontaneously-occurring leukemia and is not 5 related to environmental or occupational factors based on the 6 current state of the science. 7 Q. So it's your opinion that no acute myelogenous 8 leukemias of the M3 variety can be related to benzene 9 exposures. Correct? 10 A. No. I'm speaking specifically to the photogenetic 11 profile of Mr. Boren. 12 Q. 15:17 translocations? 13 A. Only. 14 Q. And you have earlier in the deposition told us the 15 studies that you're relying upon, and we've marked those as 16 exhibits for that proposition. Correct? 17 A. I believe so. 18 Q. The Otto Wong study dated 1995, "Risk of acute 19 myeloid leukemia and multiple myeloma in workers exposed to 20 benzene," are you relying on that for your opinions in this 21 case? 22 A. Yes. 23 Q. In which regard? 24 A. Discussing the lower threshold of what AML risk -25 when AML risk increases. 130 1 Q. And what -- how were -- how was the exposure 2 information collected for this Otto Wong study? 3 A. It was provided by NIOSH. 4 Q. What was he studying? 5 A. Pliofilm cohort. 6 Q. And has the government accepted his article as 7 authoritative on the issue of risk assessment? 8 A. I don't know what that means. What do you mean? 9 Q. For instance, with EPA, when you see them discuss 10 risk assessment in relationship to the Pliofilm cohorts, you 11 see them talking primarily about Rinsky's data. 12 A. Well, that is Rinsky's data. 13 Q. But I'm talking about Rinsky's articles, and you'll 14 see them be very critical of long stuff and kind of exclude his 15 summary of it. Have you seen that? 16 A. That's an incorrect characterization. The -- the 17 difference between approaches is that the EPA still uses total 18 leukemia for their risk assessments, and Dr. Wong and I and 19 others believe that only AML is the relevant cell type that 20 should be used in the calculation. 21 Q. All right. What assumptions did Wong make in this 22 article about the exposure levels? 23 A. He used Rinsky's exposure levels in one calculation, 24 and he used Paustenbach's in another calculation. 25 Q. Well, if he used Rinsky's exposure levels in one 131 1 calculation, shouldn't his conclusions have been the same as 2 Rinsky's? 3 A. They are applied to acute myelogenous leukemia. 4 Rinsky's are applied to... 5 Q. And that would be in table one? 6 A. At least, yes. Yes. 7 (RAABE Exhibit No. 23 was marked.) 8 Q. (By Mr. Lubel) And we've marked that as Exhibit 23? 9 A. Fine. 10 Q. Next article we'll mark as Exhibit 24. 11 (RAABE Exhibit No. 24 was marked.) 12 Q. (By Mr. Lubel) What are you using that for? 13 A. This and Rinsky's -- these are two letters to the 14 editor that discuss that exposures much beyond 15 to 20 years; 15 in other words, only the most recent 15 to 20 years of exposure 16 are relevant to risk assessment. 17 Q. Do you agree with that? 18 A. Yes. 19 Q. Why is that? 20 A. Well, because -- let me just say the -- right now we 21 have observational data from epidemiology studies and both 22 Rinsky and Glass and others that -- that -- that when they lag 23 the exposures, only the most recent exposures are relevant. 24 And we -- and there -- biologically there's lots of speculation 25 what that might be, but it suggests that the earlier exposures, 132 1 if they did -- if they occurred, the body recovers from it. 2 Q. Is there a consensus that exposures longer than 15 3 years prior to diagnosis are not significant disease-forming 4 process? 5 A. Not in the absolute sense that you said it. I think 6 there is a consensus that earlier exposures is relevant, but 7 the specific cut periods may be dose -- dose rate dependent. 8 So... 9 Q. Could depend on whether they're peak exposures or 10 chronic exposures that are more important? 11 A. Only speculation. 12 Q. Nobody knows? 13 A. We just know that the early exposures -- we know that 14 just the most recent exposures seem to be the ones that afford 15 the risk, even in the Pliofilm. 16 Q. You're aware of the health watch study at Australia. 17 Correct? 18 A. Yes. 19 Q. And I take it that you agree with the findings that 20 they made 2001? 21 A. No. Their case control study? Like what? 22 Q. The Australian Institute of Petroleum. 23 A. The cohort study? Which study? 24 Q. The health watch study that Exxon-Mobil sponsored. 25 They sponsored multiple studies. 133 1 A. There are multiple papers. 2 Q. Do you have them here? 3 A. I have the two most recent. 4 You want me to pull them out to save time? 5 Q. Yes. Thanks. 6 MR. SHOEBOTHAM: Take about a three-minute 7 break. 8 MR. LUBEL: Sure. 9 (Recess from 2:59 p.m. to 3:06 p.m.) 10 (RAABE Exhibit No. 25 was marked.) 11 Q. (By Mr. Lubel) Can you identify Exhibit 25 from your 12 files? 13 A. Yes. It's a paper by Deborah Glass. It's case 14 control study of -- conducted in Australia. 15 Q. Was it a study of benzene-exposed workers? 16 A. Yes. 17 Q. And does the study address what benzene exposures 18 caused leukemias and their cohort in their study group? 19 A. Can you restate that? 20 Q. Does the Glass study that we marked as Exhibit 25 21 address specific benzene exposures leading to certain outcomes 22 like leukemia? 23 A. Yes. 24 Q. And what do they say about AML? 25 A. They find an association between acute nonlymphocytic 134 1 leukemia and benzene exposure. 2 Q. At any particular levels? 3 A. For AML? 4 Q. AML. 5 A. Significant findings above 8 ppm years. 6 Q. How many years? 7 A. Eight ppm years. 8 Q. See that real quick. In the abstract, the conclusion 9 section, the last sentence, it reads, "No evidence was found of 10 a threshold cumulative exposure below which there was no risk." 11 Did I read that correctly? 12 A. That's a modeling result. You read it correctly. 13 Q. Do you agree with that statement? 14 A. No. 15 (RAABE Exhibit No. 26 was marked.) 16 Q. (By Mr. Lubel) Exhibit 26 from your files, if you 17 can identify that for us? 18 A. This is a paper, first author is Gun. It's an update 19 of the cohort mortality and cancer incidence study in the 20 Australian petroleum industry. 21 Q. Same cohort that Glass wrote about? 22 A. Glass is case control study from that cohort. 23 Q. So it's a different type of study? 24 A. Yes. 25 Q. Do they reach different conclusions? 135 1 A. Yes. 2 Q. In what respect with regard to acute myelogenous 3 leukemias? 4 A. Gun doesn't find much of an excess of leukemia in the 5 study. 6 Q. So he didn't quibble with the exposures. He just 7 doesn't think there's more leukemias than -- or an excess? 8 A. They -- the case control study has different numbers 9 than the cohort study, and Gun has difficulty trying to 10 reconcile that. They're actually part of the same research 11 team. 12 Q. Well, who put Gun up to this? Exxon? 13 MR. SHOEBOTHAM: Objection, form. 14 Q. (By Mr. Lubel) Do you know? 15 A. Put what? Put up? 16 Q. What caused Gun to look into a study that was done by 17 Glass in 2003, caused Gun to write -- to do a different study 18 in 2004? We know some industry member put him up to it. Who 19 was it? 20 MR. SHOEBOTHAM: Objection, form. 21 A. That's not correct. 22 Q. (By Mr. Lubel) Who put him up to it? 23 MR. SHOEBOTHAM: Objection, form. 24 Q. (By Mr. Lubel) Do you know? 25 A. Gun is part of the same university group doing the 136 1 health watch studies. 2 Q. I understand that but the original study that I have 3 here -- let me see it. The 2001 version, it's about two inches 4 thick. I'm sure you've seen. Right? 5 A. Yes, but you -- but there is also -- there's also a 6 cohort paper that I think is also on the website that Gun is 7 responsible for. That's the case control study. 8 Q. Were you aware that for the case control study that 9 the project advisory group were people from Shell and Exxon? 10 A. I don't recall Shell, but I knew that there was one 11 Exxon member. 12 Q. Well, can you explain how the 2001 version referenced 13 a -- an excess of CLLs and how the version that we see here by 14 Glass in 2003 doesn't make a reference to CLLs being in excess? 15 What changed, if you know? 16 A. I don't know specifically. 17 Q. And then we've got Gun in 2004 saying almost exactly 18 the opposite from what Glass said in 2003. Correct? 19 A. Not the opposite. Gun points out that there are 20 inconsistencies between what they find in the cancer incident 21 study and the cancer mortality study and the conclusions that 22 one would reach from the case control study. That -- that's 23 the level of criticism. 24 Q. And which one is right? 25 A. Don't know. 137 1 (RAABE Exhibit No. 27 was marked.) 2 Q. (By Mr. Lubel) And Exhibit 27? 3 A. Exhibit 27 is -- is three letters: One from 4 Dr. Schnatter to Dr. Glass, one from Bernie Goldstein to 5 Dr. Glass, both criticizing the case control study, and 6 Dr. Glass's reply. 7 Q. Who does Schnatter work for? 8 A. Schnatter works for Exxon Biomedical Sciences. 9 Q. Did you know him when you worked in epidemiology? 10 A. Yes. 11 Q. Was he part of the CMA? 12 A. No. What -- I don't think -- I don't know. He would 13 have been very young in his career, so I don't recall. 14 Q. His employer is part of the CMA? Exxon. 15 A. Exxon, yes. 16 Q. Do you know who paid Bernie Goldstein for his 17 critique? 18 A. Dr. Goldstein is Dean of the School of Public Health, 19 University of Pittsburgh, and I think he did it on his own. 20 Q. He's written a lot of about benzene? 21 A. He has lots of opinions about benzene. Correct. 22 Q. It goes back many years. 23 A. Yes. 24 Q. He actually had a book that he authored about 25 benzene. Correct? 138 1 A. Sort of before my time. 2 Q. Mine, too. 3 All right. The remaining materials that you've 4 brought with you that we have not otherwise marked as an 5 exhibit I'm going to mark as 28 and ask you if you would just 6 go through and tell us how you're using them for your opinions 7 in the case. 8 (RAABE Exhibit No. 28 was marked.) 9 Q. (By Mr. Lubel) Just let you flip through at your 10 leisure? 11 A. The first paper is a paper by -- actually it's a 12 letter -- letter to the -- Dr. Hayes and an exchange. It's 13 followed by several other papers, essentially varying 14 criticisms of the Chinese studies. 15 There is a paper not included here that I did 16 not bring with me by a gentleman by the name of Badinski 17 (phonetic) in the same vein. But it actually discusses the 18 problems with the Chinese studies. 19 Q. Which all relate to exposure assessments as I recall. 20 Is that true? 21 A. Cohort -- well, a little bit more than that. Some is 22 case ascertainment, but probably the bulk of it is 23 exposure-related problems. 24 The next two documents are excerpt papers from 25 the tox profiles of gasoline and benzene prepared by the Agency 139 1 for Toxic Substances and Disease Registry, ATSDR, in case I 2 rely on them as part of my discussion on odor threshold. 3 Q. That is the odor threshold for benzene? 4 A. Fairly low. In a range around 1. -- 1.2 to 2.5. 5 Q. For all people? 6 A. No. Reception of odor is very subjective and that's 7 -- and it would be used in the discussion, if the discussion 8 ensues, about perceptions of odor. 9 Q. And are you relying upon the study that you just 10 referenced on the odor threshold for benzene? 11 A. Yes. I would consider -- I mean, there are many 12 others. There's a whole list of different studies, but the US 13 ATSDR seems to think that range represents some of the better 14 studies. So, yes, I am relying on it. 15 Q. And you're talking about the toxicological profile 16 for gasoline? 17 A. And that odor threshold discussion is for gasoline. 18 This one is for benzene. 19 Q. Okay. Thank you. 20 A. More for historical purposes I brought the ACGIH, the 21 most recent ACGIH documentation on benzene, from which I may 22 extract specific information about TLVs or vapor pressure, you 23 know, things like that. 24 Also for historical perspective I brought the 25 NIOSH 1976 criteria document as it relates to when -- when a 140 1 consensus of science believed that leukemia is potentially 2 related to benzene. 3 Q. What year? 4 A. '74 they raised the question; '76 they felt that they 5 -- that it was getting close. 6 Q. And when did the API suspect that there was a 7 relationship between benzene and leukemia? 8 A. I don't know. 9 Q. Would 1948 surprise you? 10 A. Yes, as it relates to leukemia it would. 11 Q. It would? But if I could show you the 1948 12 toxicological review on benzene where the American Petroleum 13 Institute acknowledges that there -- they suspect that benzene 14 causes leukemia, that would -- would that change your opinion? 15 MR. SHOEBOTHAM: Objection, form. 16 A. No. 17 Q. (By Mr. Lubel) Why not? 18 A. Because there were no epidemiologic investigations in 19 that time period that could have come to those conclusions. 20 So, however those conclusions, if you're correctly summarizing 21 them, came about, it would not be based on scientific evidence. 22 Q. Well, do you know who Phillip Drinker is? 23 A. I think he was a Harvard professor. 24 Q. Was he an epidemiologist? 25 A. I don't think so. 141 1 Q. Was Selocough (phonetic) an epidemiologist? 2 A. No. 3 Q. What was going on with the field of epidemiology in 4 1948? Was it a robust field? 5 A. I wasn't there. 6 Q. What's your hunch from, you know, going to school to 7 become an epidemiologist, what was going on back in the '40s 8 with that field? 9 A. Occupational and environmental epidemiology were just 10 beginning in this country. They were more active in Europe but 11 just beginning in this country. 12 Q. Are there any diseases that you're aware of that were 13 related to exposures before there was epidemiology? 14 A. Yes. 15 Q. Like vinyl chloride? 16 A. I -- my mind was not where you were. I don't recall 17 the vinyl chloride science issues, so I can't answer that. I 18 was going to speak to the plastic anemia in benzene-exposed 19 groups. There -- there was sufficient robust clinical 20 information that some causation conclusions could be drawn in 21 the absence of formal epidemiologic investigation. That would 22 have been my -- my example in this context. 23 Q. Okay. Continue on. 24 A. Next document is the IRIS -- Integrated Risk -- US 25 EPA benzene IRIS documentation. It's relevance would be that 142 1 it's a 2003 document where the US EPA concluded for a second 2 time that the Chinese studies were unsuitable for doing dose 3 response and risk assessment. 4 Q. Well, what's the difference between risk assessment 5 and whether or not a chemical can cause a particular outcome? 6 A. One is an intrinsic characteristic of the material 7 that at some dose, at some duration, it could cause a disease, 8 a specific disease. For risk assessment purposes -- and when I 9 use the term "dose response," they're similar issues you are 10 attempting to characterize when that risk occurs and how large 11 that risk is. We've know for sometime now that benzene can 12 cause AML. It's ultimately important for public health and 13 occupational health to know accurately the shape of that dose 14 response, and not just at the high level but at the low level. 15 Q. And that's what you believe the industry-funded 16 studies in China regarding benzene are out to finally assess 17 once and for all? 18 A. Well, there's no finally in science ever. Hopefully 19 the studies will be well conducted and can contribute new 20 information to that, yes. 21 The next document is a 2004 -- only a few pages 22 of a report of a US surgeon general entitled "The Health 23 Consequences of Smoking." In this surgeon general report using 24 the Hill criteria they conclude that acute leukemias, 25 specifically acute myelogenous leukemias, are causally related 143 1 to cigarette smoking. 2 Q. At any dose? 3 A. That's why I want to read the underlying papers. The 4 surgeon general does not remark on that. 5 Q. But what's your hunch? I'm not holding you to it 6 because I understand that you want to go look at that paper. 7 A. Multiple pack years. 8 Q. Like more than 10? 9 A. More than 20 probably. 10 Q. More than 20 pack? 11 A. Hunch. 12 Q. That's a hunch. Got ya. 13 A. Just so we all agree. 14 Next paper is the -- is a paper by Robert 15 Rinsky, et al, 1987, here for historic purposes in case we -16 anyone discusses some of that. 17 The next paper is 1994 Paxton, there for the 18 same reason, historical context. 19 The next paper is Bob Rinsky's 2002 update which 20 he provides the most recent dose response information and the 21 most recent cases for the Pliofilm cohort that he originally 22 did. 23 Q. You can continue. Thank you. 24 A. The next paper is a paper by Robert Schnatter, et al. 25 It's an analysis of the Pliofilm cohort, specifically looking 144 1 at concentration levels, not just ppm years, not just 2 cumulative exposure. So it supports what I think a number of 3 us believe. It's not just -- not just ppm years but some 4 thresholds of concentration that you have to have besides just 5 cumulative. 6 Q. What plant did he state? 7 A. He used the Pliofilm data using both Rinsky estimates 8 and Paustenbach estimates and Crump estimates. Like I said, 9 these are now some of the publically available data sets. 10 The next paper is in case it becomes a discussion, a 11 broad discussion on petroleum exposed workers. I just brought 12 along a paper that I did on -- the 2000 paper on what is 13 essentially solid tumors. 14 Q. Is it relevant to Mr. Boren's case? 15 A. I don't think so. 16 Q. But just in case I bring it up? 17 A. You got it. 18 Q. You're ready? 19 A. Also brought the TLV documentation, ACGIH TLV 20 documentation for gasoline. 21 Q. How is that relevant? 22 A. Probably not but I had it. 23 Q. What is the NIOSH recommended exposure level for 24 benzene today? 25 A. I don't know. 145 1 Q. Would it surprise you if it's half of what the OSHA 2 level? 3 A. No, it would not surprise me. 4 Q. Has NIOSH historically been out in front of OSHA as 5 far as recommending reduced levels of exposure? 6 A. NIOSH's charge is to provide technical support for 7 OSHA. That's all I know. I don't know what "out in front" 8 means. 9 Q. Are they the investigative arm for OSHA? 10 A. Yes, I would think that's a fair characterization. 11 The next paper -- and actually the next two 12 papers are by Otto Wong. They both relate to gasoline 13 mortality study, essentially the same -- same study, two 14 different variations in publication in case the issue of what 15 are the effects of gasoline exposures are. Probably not 16 related to Boren. 17 Q. Have you from anyone, including Dow's lawyer 18 Mr. Shoebotham, been told that somehow gasoline exposures may 19 become pertinent to this lawsuit? 20 A. No, not at all. 21 Q. I just want to make sure that -- something not out 22 there I'm not aware of. 23 A. It's material I brought since, you know, it was 24 unclear where some of the exposure discussions may drift to. 25 The next document is a US EPA 2002 document 146 1 looking at the Toxicological Review of Benzene (Noncancer 2 Effects) which contains assessments of toxicity of benzene for 3 other things including noncancer such as thrombocyte cytopenia 4 (phonetic) or something like that. 5 And the last paper is well put together. It is 6 actually three papers of various durations of Dante Picciano's 7 work on circulating lymphocytes, and the cover page of that is 8 a critique of that body of work. 9 Q. Was it a published critique? 10 A. No. It's a letter from Jandl who is a very famous 11 Harvard professor in hematology as to what he thinks about it. 12 Q. Was Dr. Picciano's work published? 13 A. Yes. 14 Q. Do you remember which publication? 15 A. I believe I had it clipped here. Yes. It was 16 published in Environmental Research. Those are all the papers 17 I have brought with me. 18 Q. And how do you intend to use the cytogenetic studies 19 that you brought, including the critique? 20 A. The early one? Oh, these, what we were just talking 21 about here? 22 Q. Right. 23 A. I was -- I brought them really to -- you know, I 24 think it's probably more appropriate to deal with the other 25 experts, but this -- the approach of looking for circulating 147 1 markers of toxicity in benzene-exposed workers was -- was 2 fairly active in the late '70s through the mid '80s, including 3 several attempts -- neologic attempts to interpret those, see 4 how they correlate with the pin points. And only if asked I 5 would revolve around the discussion that it's no -6 surveillance using circulating lymphocytes turned out to be not 7 predictive of any adverse health outcomes and therefore has 8 essentially been discontinued. 9 Q. When? 10 A. Probably, except for research purposes, a lot of it 11 was stopped, because I don't think -- I don't even think OSHA 12 endorsed it when OSHA came out with their standard. 13 Q. Do you have any articles that you believe are 14 authoritative on when it stopped? 15 A. No, I don't. 16 Q. Did Mobil, when you were the Director of 17 Epidemiology, run cytogenetic testing on their benzene-exposed 18 workers? 19 A. No. After -- after Picciano and there are several 20 other papers in literature, we had conversations with our 21 toxicologists and felt that at this stage it was such a 22 researchy technique that we weren't going to get into it. 23 Q. Before the Picciano paper came out in 1978, had Mobil 24 done any cytogenetic testing of any of their chemical-exposed 25 workers? 148 1 A. I don't believe so. 2 Q. Do you know if Dow studied any of their 3 chemically-exposed workers cytogenetically? 4 A. Only what I recall the population that we looked at 5 in Freeport. 6 Q. Do you know if they studied their -- the chromosomes 7 of the Midland people? 8 A. I don't know. 9 Q. Do you know if they studied the chromosomes of their 10 people exposed to vinyl chloride? 11 A. I don't know. 12 Q. Any other chemical? 13 A. Don't know. 14 THE REPORTER: What chemical did you say? 15 MR. LUBEL: Any other chemical. 16 THE REPORTER: Before that. 17 MR. LUBEL: Vinyl chloride. 18 Q. (By Mr. Lubel) Have you given us all the opinions 19 that you intend to express at the trial of this case regarding 20 Mr. Boren? 21 A. I think going through these papers we covered it. 22 Q. In other words, you're not a neurologist. Correct? 23 A. No, I'm not a neurologist. 24 Q. You're not addressing any neurological issues 25 concerning them, are you? 149 1 A. I am not. 2 Q. And if I've understood you correctly today, where you 3 have drawn the line on Mr. Boren and his AML, his particular 4 type of AML, and why you do not believe that his benzene 5 exposures contributed whatsoever to it is primarily based upon 6 what you believe is new literature that suggests that 7 translocations of 15 and 17 could not be related to benzene 8 exposures. True? 9 A. I think that oversimplifies the testimony a bit. I 10 -- it's certainly correct in that the epidemiology which is 11 fairly recent work on -- for myocytic leukemia does not draw 12 any -- all the papers published to date can't find occupational 13 or environmental relationships. So yes, I'm relying on that. 14 And -- but even besides that, everything I have seen from 15 exposure profiles suggests that he did not have exposures 16 sufficient to increase his risk materially. 17 Q. And that's where I wanted to make sure we were, 18 because even if you and I could reach an agreement on his 19 benzene exposures causing his particular type of AML with his 20 chromosome abnormalities, what I'm hearing you say is that 21 based upon the information you have regarding the alleged 22 exposures to benzene of Mr. Boren, you don't think they're 23 sufficient enough to have contributed to cause AML? 24 A. Correct. 25 Q. In any person? 150 1 A. As a general proposition they are probably too low. 2 Q. Okay. And so even if you agreed that Mr. Boren's AML 3 could be related to benzene exposures if the exposures were 4 high enough, you would come down and say, "Look, I've looked at 5 the exposure information that both sides' lawyers have given 6 me, and with that I can exclude with a certainty that 7 Mr. Boren's benzene exposures were not a contributing factor to 8 his AML." Is that your point? 9 A. I would -- if it were a 5-7, if his AML was 5-7, 10 okay, and I had this information, I would on that specific case 11 drill down much further to make -- to make sure that we had the 12 exposure profiles correct and the work histories understood. 13 Q. How? What would you do? 14 A. Speculation. I don't know. 15 Q. But here's my point: Let's just assume that both 16 sides agree that a particular individual's exposures are less 17 than 200 parts per million of benzene, cumulative exposures, 18 and let's say that you and I agree that the disease can be 19 caused by a sufficient amount of benzene. But where you and I 20 disagree is you say there's got to be at least 200 parts per 21 million exposures, and your only evidence is a hundred parts 22 per million. Are you always going to draw that line and say no 23 way, no how did benzene contribute to causing that man's AML 24 because he didn't have a threshold of 200 parts per million 25 exposure? 151 1 A. Certainly at a hundred which is half of what the 2 observed excess risk is, I would probably always say that based 3 on the current state of the science. 4 Q. So you don't see AML being caused even in part for 5 any individual if the benzene exposures don't exceed a hundred 6 parts per million. True? 7 A. We're now starting to speculate all over the lot 8 because I said the observed level is 200, and I'm not backing 9 off of the 200. 10 Q. But you gave 200 -- I mean a hundred a minute ago. 11 A. Well, I gave you a hundred where you were trying to 12 pin me down where I always say. And now you're trying to make 13 it sound like I have -- I -- you know, I don't speculate 14 because there are so many variables in play. I don't do 15 hypotheticals like that. I just don't. 16 Q. So if I were to ask you if a person was exposed to 17 175 part per million years of benzene and they had an AML of 18 the right subtype that you could agree could be a 19 benzene-induced AML, would you say as a general rule that that 20 person's 25 parts per million years short of me ever connecting 21 up as a contributing factor their benzene exposure to their 22 leukemia, or do you have to look at other stuff? 23 A. I would want to look at other stuff, but clearly the 24 closer we are to 200, the less comfortable we'll be saying it's 25 not. 152 1 Q. But you would agree that it may be four or five years 2 before we have the China studies back, assuming that they're 3 properly designed and done properly and all that stuff that you 4 told us previously, to see if there's a threshold for benzene 5 exposure? 6 MR. SHOEBOTHAM: Objection, form. 7 A. That's incorrect. We have a lot of science now. It 8 would be nice to have more studies that are well done to help 9 bolster that -- that body of science. That's what science is. 10 Q. (By Mr. Lubel) What study are you talking about? 11 What studies are you saying establishes that there is no effect 12 for benzene exposures less than 200 parts per million? 13 A. For AML we have the varying analyses done by 14 Schnatter and Wong on the Pliofilm cohort. They come out of 15 the Pliofilm cohort. 16 Q. Do we have anything else other than people's 17 interpretation of the data from the Pliofilm cohort? 18 A. Well, we have some data in UK and we have some data, 19 but they're very small cohorts. One of the recommendations was 20 that you need to be merged together. We need bigger data sets 21 to get more robust to those responses. 22 Q. Well, how big is the Pliofilm cohort? 23 A. Pretty small. 24 Q. Like 1200 people? 25 A. 1218, depending if you include St. Mary. 153 1 Q. We've got bigger cohorts that have been studied on 2 benzene, do we not? 3 A. Yes. But big does -- big is not intrinsically 4 better. It's got to be better. 5 Q. It's got to be big and better? 6 A. Correct. 7 Q. And although the China study done by Hayes and Yin, 8 the National Institute of Health and the Chinese equivalent, 9 has looked at a bigger set of people, the population exposed to 10 benzene, you don't think that fits the better part of it? 11 A. Absolutely no. 12 Q. And although the Australian study by Glass, the case 13 control version, reflects excesses of AMLs at what you would 14 consider -- most people consider low level benzene exposures, 15 that doesn't do it for you either. Correct? 16 A. That's also a very small study. 17 Q. What size? 18 A. The cohort from which those cases are extracted is 19 smaller than Dow's Freeport chemical complex. And that's one 20 single facility of Dow versus the entire country of Australia. 21 So it's not a large study. We have refinery studies that are 22 bigger than the whole petroleum study. But they're -- without 23 extending this further, we -- we have discussed some other 24 limitations, and I went into the papers. 25 Q. Well, you understand that I asked to take your 154 1 deposition in case you show up to trial, I -- if I'm doing a 2 good job for my client, I need to have a pretty good 3 understanding of what you're going to testify to. You 4 understand generally that's what lawyers are hired to do? 5 A. Yes. 6 Q. Okay. I'm getting ready to leave here, shut this 7 thing down. You're going to go back to work -- Pennsylvania, 8 where you live, and I'm going to go see my little kid. Do you 9 feel as though we together have communicated about the general 10 substance of your major opinions concerning Mr. Boren's case? 11 A. Yes, I believe we have. 12 Q. Can you think of anything that's been missed? 13 A. Not -- not as I sit here, no. 14 Q. And the information that you're relying upon for the 15 bases of your opinions as you sit here today, you've brought 16 with you and we've marked as exhibits. Correct? 17 A. All -- all the key pieces. There are some historical 18 and supporting documents around this, but yes, the gist of it 19 is all there. 20 MR. LUBEL: Thank you for your time. 21 THE WITNESS: Thank you. 22 MR. SHOEBOTHAM: Is there a CV in there? Was 23 there a CV? 24 MR. LUBEL: Yes. 25 MR. SHOEBOTHAM: What exhibit number is 155 1 that? 2 THE WITNESS: I don't -3 MR. SHOEBOTHAM: It's hard to keep up. 4 THE REPORTER: Are we on or off? 5 MR. SHOEBOTHAM: We're on. I have a few 6 questions. 7 THE WITNESS: I don't know. This is a list of 8 that. 9 MS. RHYNE: Exhibit 15. 10 MR. SHOEBOTHAM: 15? 11 THE WITNESS: 15 would be the other way. 12 MR. SHOEBOTHAM: There it is. 13 (Time: 3:43 p.m.) 14 EXAMINATION 15 QUESTIONS BY MR. SHOEBOTHAM: 16 Q. Dr. Raabe, I just have a few follow-up questions for 17 you. And I want to ask you first about Exhibit 15. Would you 18 please identify that for the record? 19 A. It's my most current curriculum vitae. 20 Q. Okay. And what is a curriculum vitae? 21 A. Scientific version of a resume. 22 Q. Would you please describe your educational 23 background? 24 A. I have a Bachelor of Arts in biology from Hofstra 25 University and a Master of Science in computational science and 156 1 computer science from Pratt Institute, Doctor of Public Health 2 from Columbia University specializing in epidemiology. 3 Q. Are you an epidemiologist? 4 A. Yes, sir. 5 Q. Do you have any affiliation with the American College 6 of Epidemiology? 7 A. I'm a Fellow of the American College. 8 Q. And what does it mean to be a Fellow of the American 9 College of Epidemiology? 10 A. It's the most senior recognition you can get from the 11 college. The Board examines your publications and your 12 contributions to the field of epidemiology and invites you to 13 become a Fellow. It's like a Board certification. 14 Q. You received a PhD from Columbia University; is that 15 correct? 16 A. Doctor of Public Health. 17 Q. When did you -- when did you receive your Doctor of 18 Public Health from Columbia University? 19 A. '87. 20 Q. And what specializations did you have when you 21 received your Doctor of Public Health from Columbia University? 22 A. Epidemiology, statistics, research methods, and a 23 discipline called sociomedical science. 24 Q. Would you please describe your work in the field of 25 epidemiology? 157 1 A. From 1970 through 1977, I was a senior research 2 scientist in the State of New York, attached to Columbia 3 University, conducting epidemiologic research, infant 4 mortality, and disease patterns in New York City. 5 Beginning the end of October '87 and through a 6 number of positions, I worked for Mobil Corporation in the 7 Corporate Medical Department and various functions related to 8 epidemiology and medical surveillance. 9 Q. Have you conducted any research concerning the 10 chemical benzene? 11 A. I've conducted a number of studies relating to 12 petroleum refinery, workers who were exposed to benzene. 13 Q. Are those studies listed on your curriculum vitae? 14 A. Yes, sir. 15 Q. Are they listed under "Publications"? 16 A. Yes. 17 Q. Would you please describe for the jury your 18 publications that have involved the chemical benzene? 19 A. The activities that resulted in publications that 20 have some discussion of benzene or are benzene relevant 21 would -- would include the study of Paulsboro laboratory 22 workers, the cancer epidemiologies of petroleum workers with 23 meta-analysis in 1989, participation in the IARC monograph on 24 cancer risks in petroleum refining, work on a potentially 25 relevant scheme for classifying carcinogens with John Ashby, 158 1 working with the work group on the environmental health 2 criteria for benzene with the World Health Organization, review 3 of carcinogenic potential of gasoline, some benzene 4 discussions, cell type specific leukemia in petroleum-exposed 5 workers. 6 And then there are just a number of other 7 refineries that are listed. And there's another paper on acute 8 myla -- myeloid and mono -- mono -- getting late, I'm sorry -9 AML and benzene exposure in petroleum distribution workers in 10 the United Kingdom, paper relating -- with Dr. Bergsagel, 11 B-E-R-G-S-A-G-E-L, regarding benzene and multiple myeloma, 12 paper by Dr. Wong and myself on non-Hodgkins lymphoma in 13 benzene-exposed workers, a paper by myself and Dr. Wong on 14 leukemia on benzene, and one on multiple myeloma on benzene, 15 and one on non-Hodgkins lymphoma on benzene. 16 Q. All right. Thank you. So you have a number of 17 publications listed on your curriculum vitae that you have 18 published in the scientific literature concerning benzene? 19 A. In some form or fashion or another, yes. 20 Q. Let me hand you Exhibit 3 to your deposition. 21 MR. LUBEL: Oh, I'm sorry, John. I thought you 22 were telling me it was 3. 23 Q. (By Mr. Shoebotham) Dr. Raabe, Mr. Lubel asked you 24 about Exhibit 3 earlier in the deposition. What is that 25 grouping of scientific articles in Exhibit 3? 159 1 A. They're a number of papers that look at the -- the 2 risk factors in epidemiology associated with acute 3 promyelocytic leukemia or AML 3 -- in 3 that Mr. Boren has. 4 Q. What opinions do you hold concerning the causation of 5 acute promyelocytic leukemia specifically with a 15:17 6 translocation like Mr. Boren had? 7 A. All the data I've reviewed specific to both APL and 8 specific to benzene-exposed cytogenetic abnormalities indicate 9 to me that there's no occupational -- no known occupational 10 associations with acute promyelocytic leukemia, and any 11 environmental are occupational exposure. 12 Q. The paper that's at the top of the stack marked 13 Exhibit 3, when was that published? 14 A. That's the most recent paper I could find in 2003. 15 Q. And this paper contains in the abstract a 16 statement -- and let me read it to you: "So far no 17 environmental and/or occupational risk factors have been found 18 for APL." Do you see that sentence? 19 A. Yes. 20 Q. Is this one of the papers you rely upon to support 21 your opinion? 22 A. Yes. 23 Q. Do the papers that you marked as Exhibit 3 contain 24 any information about the distribution of APL or promyelocytic 25 leukemia between the sexes? 160 1 A. Yes. 2 Q. What do they -- what do they demonstrate? 3 A. Unlike other forms of AML which are heavily weighted 4 in the male population, the promyelocytic leukemia is equally 5 distributed amongst males and females. 6 Q. Does that have any significance to your opinions? 7 A. Yes. It supports the -- the notion described 8 elsewhere in epidemiology that one sometimes considers 9 occupational factors with an exposure having some influence 10 on -- on differentially -- differential rates between men and 11 women. 12 So the fact that APL is equally distributed at 13 least supports the notion that whatever risk factors there are 14 apply to both men and women equally. 15 Q. Do these papers provide any information about the 16 distribution of promyelocytic leukemias by age? 17 A. Yes. It's a somewhat younger form of AML. It's not 18 uncommon to see in the 30 to 50 range of the cases. It does go 19 up with age, but not as more -- there is more cases at the 20 younger ages than I've seen typically in the other forms. 21 Q. And do these papers that you brought with you and 22 that have been marked as Exhibit 3 provide any information with 23 regard to the latency period that one would see for a 24 promyelocytic leukemia if it's induced by chemotherapy that 25 someone might be taking at a doctor's office or hospital? 161 1 A. Yes, they do. 2 Q. What -- what is the latency period for a 3 promyelocytic leukemia if it's induced by chemotherapy that a 4 doctor might give? 5 A. They -- the vast majority of them appear within two 6 to three years from -- from treatment. 7 MR. SHOEBOTHAM: I'll reserve further questions 8 until time of trial. Thank you. 9 MR. LUBEL: I've got a few more for you. 10 What -- what number did we end with? 11 THE REPORTER: 28. 12 (Time: 3:53 p.m.) 13 (RAABE Exhibit No. 29 was marked.) 14 EXAMINATION 15 QUESTIONS BY MR. LUBEL: 16 Q. Can you identify Exhibit 29? 17 A. It's a 2001 paper by Hayes, et al. 18 Q. Had you seen that before? 19 A. Yes. I probably would have brought it with me had I 20 thought about it. 21 Q. Is it authoritative in the field? 22 A. It's one of many published scientific papers. 23 Q. I'm not saying it's the only one, but it's one of 24 many? 25 A. It's not authoritative. It's just a paper. 162 1 Q. Why would you have brought it with you? 2 A. Because I expected you'd want to have some discussion 3 about the Chinese epidemiology. Not because it formed any 4 basis of my opinion. 5 Q. Well, let me ask you: Do you agree that a scientific 6 consensus concludes that benzene can be etiology approved 7 related to the development of acute nonlymphocytic leukemia 8 based upon epidemiologic studies? 9 A. Yes, if the exposures are of sufficient duration and 10 in high enough dose. 11 Q. Do you agree that studies have confirmed that benzene 12 causes leukemia? 13 A. Only -- I would agree only in benzene has been 14 established to cause acute myelomas. 15 Q. You're saying there's no studies that have 16 established benzene causes leukemia? 17 A. There are -- a number of the epi studies only 18 classify leukemia. So if acute myelogenous leukemia is 19 elevated, the whole category is elevated. 20 Q. Are there studies that relate benzene exposures to 21 leukemia in general? 22 A. Yes. 23 Q. Would you agree that the data from the Pliofilm 24 cohort are essentially uninformative at doses below 200 part 25 per million years? 163 1 A. No. 2 Q. Would you agree that -- that Rinsky's most recent 3 article reflects that there's an increase incidence of AML's 4 exposures less than a hundred parts per million? 5 A. Not statistically significant. 6 Q. Would you agree that he writes that -- that there is 7 an increase? 8 A. The SMR is elevated so that is an increase, but it is 9 not statistically significant. So you don't know if it's a 10 real increase or not. 11 Q. So when you look at the Pliofilm cohort as evidenced 12 by the 95 percent confidence interval on the risk estimates, 13 you wouldn't agree that exposures below 200 part per million 14 years are consistent with increases in a risk for AML as great 15 as six to 14 fold? 16 A. I would disagree. And I -- I don't know where that 17 statement comes from. 18 Q. Would you agree that the National Cancer Institute 19 and the Chinese Academy of Preventative Medicine study provides 20 evidence that cumulative benzene exposures of less than 200 21 part per million years is associated with increased risk for 22 acute nonlymphocytic leukemia such as AML? 23 A. I don't dispute that the Chinese study makes that 24 statement, but the reliability and interpretability of that 25 statement I think are very questionable. 164 1 Q. Do you agree that the study states that significant 2 excesses of acute nonlymphocytic leukemias and MDSs were 3 observed at average exposures of less than 25 part per million? 4 A. Not statistically significant. There were cases. 5 You don't know if they're related to exposure or not. 6 Q. And would you agree that the article states that 7 there's evidence of a doubled risk for acute nonlymphocytic 8 leukemia and MDS at average exposure levels under 10 part per 9 million for benzene? 10 A. I don't recall that statement, so I'd have to go back 11 and spend some time looking at it. 12 Q. Would you agree that there's evidence that suggests 13 that in -- induction of chromosomal ab -- alterations by 14 benzene is likely to play an important role in leukemogenic -15 leukemogenesis or other genotoxic effects? 16 A. That's what we've been talking about to some extent 17 right here, yes. 18 Q. So you agree with that? 19 A. Generally, yes. 20 Q. Now, the study done in China by the National Cancer 21 Institute from the United States and the Chinese equivalent was 22 not funded by the chemical refinery industry, was it? 23 A. I don't believe it was. 24 Q. Would you agree that benzene is a known human 25 carcinogen by all routes of exposure? 165 1 A. Subject -- now, I know what you're reading from. I 2 would agree subject to dose and intensity. I mean, it's a -3 it's a generic statement of its intrinsic potential. 4 Q. Would you agree that this statement that benzene is a 5 known human carcinogen by all routes of exposure has been 6 supported by evidence from human epidemiologic studies, animal 7 data, and an improvement and understanding of mechanisms of 8 action? 9 A. I would generally agree with that. 10 Q. Has it been clearly established and accepted that 11 exposure to benzene causes acute nonlymphocytic leukemia and a 12 variety of other blood-related disorders in humans? 13 A. Yes, at varying doses. 14 Q. Is it true that the findings from the National Cancer 15 Institute's study in China would suggest that workers exposed 16 to benzene at average levels of less than 10 parts per million 17 are subject to a higher risk of hematologic neoplasms? 18 A. I don't think you can make -- draw any statements or 19 inference from a study that you can't interpret, because you 20 don't know what the exposure profiles are accurately. 21 Q. So you disagree with that statement -- what the 22 statement suggests? 23 A. I -- I think that that's what the individual study 24 may -- may state, but I disagree with the -- that suggestion 25 can be validly interpreted at this time. 166 1 Q. Would you agree that with respect to the Pliofilm 2 studies that the absence of earlier definitive ambient air 3 measurements for benzene has led to many quantitative risk 4 estimates by numerous investigators over the past several years 5 that have differed from each other partially on the basis of 6 differences and the assumptions made about what those earlier 7 exposures to benzene were? 8 A. Yes, I agree with that. 9 Q. Do you agree that the second Rinsky study in 1987 10 included individual estimates of personal exposure that were 11 not included in his previous study of 1981? 12 A. I don't recall, but my recollection is everybody has 13 been using the estimates generated post '87. But... 14 Q. Would you agree that there's been some recent limited 15 epidemiologic evidence that supports certain alternative dose 16 measures as perhaps better than the measurement of cumulative 17 dose? 18 A. That's the Schnatter paper that I gave you. I'm not 19 sure if I agree that it's -- demonstrates that it's better, but 20 it certainly -21 Q. Suggested? 22 A. -- suggests that the importance of concentration. 23 Concentration is important, which I do agree with. 24 Q. Would you agree that for AMML, a significantly 25 increased risk tended to be associated with peaked -- peaked 167 1 exposures to benzene but not with cumulative exposure? 2 A. Let's go back to those papers. 3 Q. Rushton? 4 A. I don't recall. 5 Q. This analysis suggests that a person exposed to 40 6 part per million of benzene for one year might be at a greater 7 risk of leukemia than a person exposed to one part per million 8 for 40 years. What are your thoughts on that? 9 A. Without sticking to those specific numbers, that's 10 essentially what we're talking about, con -- a threshold 11 concentration as having some importance relative to cumulative 12 dose. So that's not any different from what we've just been 13 talking about. 14 Q. Were you aware that nine -- there were nine leukemia 15 victims in the Pliofilm cohort that's been studied by these 16 various authors? 17 A. There is more now in the update. 18 Q. Pre2002 update? 19 A. I don't disagree with the statement. 20 Q. Were you aware that out of those nine, seven had 21 experienced latent periods of 15 years or longer? 22 A. I don't recall that. 23 Q. Would that surprise you? 24 A. It wouldn't surprise me or not surprise me, because 25 you don't know which are the actual benzene-induced cases. So 168 1 you -- you can't easily make decisions on -- on -- on latency. 2 Q. Can a person be exposed to benzene and have a latency 3 period of 20 or more years for which if the exposures were 4 right and the disease was right, you could connect the two or 5 call it a benzene-induced leukemia? 6 A. I don't think -- let's put it this way: All -- I 7 would find that unusual based on what we know about 8 secondary -- secondary AMLs, either from chemotherapeutic or 9 even from case series where there is strong evidence that they 10 probably are benzene-related AMLs. Those are much shorter 11 periods of time, so I would question that. 12 Q. So what's the latency period for benzene-induced 13 leukemia? 14 A. Well, as I just described: In general, you don't 15 know which are which, but the two published estimates that I'm 16 aware for benzene-induced leukemias are both around ten years. 17 Q. So if Dr. Irons says 15 years, he'd be wrong. Right? 18 A. No. I would just ask him what the source of that 19 information was. 20 Q. And how do you calculate it? Is it ten years from 21 the first exposure or ten years from the last exposure? 22 A. Well, ideally it would be ten years from the most 23 meaningful where the exposure starts to become biologically 24 relevant. So it would be closer to the early years, not to the 25 last year. 169 1 Q. Do you agree that the Paustenbach exposure estimates 2 for the Pliofilm cohort were based on worst-case assumptions 3 concerning actual exposure levels? 4 A. I would not agree or disagree. 5 Q. Just don't have an opinion? 6 A. I don't have an opinion. 7 THE WITNESS: I do need to take a restroom break 8 if you're going to be much -9 MR. LUBEL: I'm almost done. Do you want to 10 give 30 seconds? Or you can take a break. 11 THE WITNESS: I can go a minute or two. 12 MR. LUBEL: Okay. 13 Q. (By Mr. Lubel) Do you agree that elevations in 14 exposure to benzene tend to suppress blood counts? 15 A. Read that again. 16 Q. Elevations in exposures to benzene tend to suppress 17 blood counts? 18 A. Yes. As a general proposition that would be true if 19 the doses were high enough. 20 Q. Did the Schnatter, S-C-H-N-A -21 A. Schnatter. 22 Q. -- T-T-E-R, 1996 article and that analysis indicate 23 that the critical concentration of benzene exposures for risk 24 of acute myelogenous leukemia or AML is in the 20 to 25 part 25 per million range? 170 1 A. Now, he presents three different estimates. The 2 lowest estimate is in that range. The highest estimate, I 3 think, is in the 50-plus range. And I think the median is 4 around -5 Q. 35 to 40. 6 A. Okay. 7 Q. Does that sound right? 8 A. Yeah, it could be. That's -- that's concentration, 9 not ppm. 10 Q. Did we -- did I ask you what the exposures were in 11 the Dow Chemical Ott study back in '86? 12 A. I don't recall, but you didn't ask. 13 Q. Do you know? 14 A. I don't recall. 15 MR. SHOEBOTHAM: You need to take a break? 16 MR. LUBEL: Go ahead. I think I'm almost -17 MR. SHOEBOTHAM: Go ahead and take a break. 18 (RAABE Exhibit No. 13 was marked.) 19 (Recess from 4:09 p.m. to 4:12 p.m.) 20 MR. LUBEL: We're done. 21 MR. SHOEBOTHAM: We'll reserve further questions 22 until time of trial. 23 (Signature required.) 24 25 171 1 CHANGES AND SIGNATURE 2 PAGE/LINE CHANGE FROM/CHANGE TO REASON 3 ________________________________________________________ 4 ________________________________________________________ 5 ________________________________________________________ 6 ________________________________________________________ 7 ________________________________________________________ 8 ________________________________________________________ 9 ________________________________________________________ 10 ________________________________________________________ 11 ________________________________________________________ 12 ________________________________________________________ 13 ________________________________________________________ 14 ________________________________________________________ 15 ________________________________________________________ 16 ________________________________________________________ 17 ________________________________________________________ 18 ________________________________________________________ 19 ________________________________________________________ 20 ________________________________________________________ 21 ________________________________________________________ 22 ________________________________________________________ 23 ________________________________________________________ 24 ________________________________________________________ 25 ________________________________________________________ 172 1 I, GERHARD K. RAABE, MD, have read the foregoing deposition and 2 hereby affix my signature that same is true and correct, except 3 as noted above. 4 5 ___________________________ GERHARD K. RAABE, MD 6 7 8 9 THE STATE OF TEXAS ) 10 COUNTY OF HARRIS ) 11 12 Before me, ________________, on this day personally appeared 13 GERHARD K. RAABE, MD, known to me (or proved to me under oath 14 or through __________________) (description of identity card or 15 other document) to be the person whose name is subscribed to 16 the foregoing instrument and acknowledged to me that they 17 executed the same for the purposes and consideration therein 18 expressed. 19 20 Given under my hand and seal of office this _____ day of 21 _______________, 2004. 22 23 ___________________________ 24 NOTARY PUBLIC IN AND FOR 25 THE STATE OF TEXAS 173 1 CAUSE NO. 17958-JG01 2 3 JAMES BOREN AND GINGER ) IN THE DISTRICT COURT OF BOREN ) 4) VS. ) BRAZORIA COUNTY, TEXAS 5) THE DOW CHEMICAL ) 6 COMPANY, ET AL. ) 239TH JUDICIAL DISTRICT 7 ********************************************************** 8 REPORTER'S CERTIFICATION DEPOSITION OF GERHARD K. RAABE, MD 9 OCTOBER 6, 2004 10 I, Valerie B. Corrales, Certified Shorthand Reporter in and for the State of Texas, hereby certify to the following: 11 That the witness, GERHARD K. RAABE, MD, was duly sworn by the 12 officer and that the transcript of the oral deposition is a true record of the testimony given by the witness; 13 That the deposition transcript was submitted on 14 _________________ to the witness or to the attorney for the witness for examination, signature, and return to me by 15 __________________; 16 That the amount of time used by each party at the deposition is as follows: 17 Mr. Lance Lubel - 4 hours, 20 minutes 18 Mr. J. Robert Black - 0 hours, 0 minutes Mr. Jonathan Shoebotham - 0 hours, 10 minutes 19 Ms. Katherine L. Rhyne - 0 hours, 0 minutes 20 That pursuant to information given to the deposition officer at the time said testimony was taken, the following includes 21 counsel for all parties of record: 22 FOR THE PLAINTIFFS: Mr. Lance H. Lubel 23 Mr. J. Robert Black HEARD, ROBINS, CLOUD, LUBEL & GREENWOOD, LLP 24 500 Dallas, Suite 3100 Houston, Texas 77002 25 Tel 713-650-1200 174 1 FOR THE DEFENDANT THE DOW CHEMICAL COMPANY: Mr. Jonathan Shoebotham 2 THOMPSON & KNIGHT, LLP 333 Clay Street, Suite 3300 3 Houston, Texas 77002 Tel 713-654-8111 4 Ms. Katherine L. Rhyne 5 KING & SPALDING, LLP 1730 Pennsylvania Avenue, NW 6 Washington, DC 20006-4706 Tel 202-626-3743 7 I further certify that I am neither counsel for, related to, 8 for employed by any of the parties or attorneys in the action in which this proceeding was taken, and further that I am not 9 financially or otherwise interested in the outcome of the action. 10 Further certification requirements pursuant to Rule 203 of TRCP 11 will be certified to after they've occurred. 12 Certified to by me this the 8th day of October, 2004. 13 14 _____________________________ Valerie B. Corrales, CSR 15 Texas CSR No. 6113 Expiration Date: 12-31-2005 16 Word for Word Reporting Firm Registration No. 222 17 7015 Gulf Freeway, Suite 110 Houston, Texas 77087 18 (713) 847-8984 19 20 21 22 23 24 25 175 1 FURTHER CERTIFICATION UNDER RULE 203 TRCP 2 The original deposition was/was not returned to the deposition 3 officer on ____________________; 4 If returned, the attached Changes and Signature page contains any changes and the reasons therefor; 5 If returned, the original deposition was delivered to 6 ______________________, Custodial Attorney; 7 That $_____________ is the deposition officer's charges to the Plaintiffs, for preparing the original deposition transcript 8 and any copies of exhibits; 9 That the deposition was delivered in accordance with Rule 203.3, and that a copy of this certificate was served on all 10 parties shown herein and filed with the Clerk. 11 Certified to by me this ______ day of ______________, 2004. 12 13 _____________________________ Valerie B. Corrales, CSR 14 Texas CSR No. 6113 Expiration Date: 12-31-2005 15 Word for Word Reporting Firm Registration No. 222 16 7015 Gulf Freeway, Suite 110 Houston, Texas 77087 17 (713) 847-8984 18 19 20 21 22 23 24 25 176