Document kDKxRrgrvdvNXZbxZQB2agZdy

1 CAUSE NO. A-167,693 2 JAMES COWEY AND RUTH ) IN THE DISTRICT COURT COWEY ) 3) PLAINTIFFS, ) 4 VS. 5 ) ) JEFFERSON COUNTY, TEXAS ) RADIATOR SPECIALTY 6 COMPANY, ET AL ) ) ) 7 DEFENDANTS. ) ) 58TH JUDICIAL DISTRICT 8 9 ******************************************************** 10 ORAL DEPOSITION OF 11 GERHARD K. RAABE, Dr.P.H., F.A.C.E. 12 DECEMBER 2, 2003 13 ******************************************************** 14 15 ORAL DEPOSITION OF GERHARD K. RAABE, Dr.P.H., 16 F.A.C.E., produced as a witness at the instance of the 17 PLAINTIFFS, and duly sworn, was taken in the 18 above-styled and numbered cause on the 2nd of December, 19 2003, from 8:57 a.m. to 2:19 p.m., before Kathy Miller, 20 CSR in and for the State of Texas, reported by machine 21 shorthand, at the law offices of Fulbright & Jaworski, 22 1301 McKinney, Suite 4400, Houston, Texas, pursuant to 23 the Texas Rules of Civil Procedure and the provisions 24 stated on the record or attached hereto. 25 1 1 APPEARANCES 2 3 FOR THE PLAINTIFFS: MR. LANCE LUBEL 4 MR. DENMAN H. HEARD MR. J. ROBERT BLACK 5 HEARD, ROBINS, CLOUD, LUBEL & GREENWOOD 910 TRAVIS STREET, SUITE 2020 6 HOUSTON, TEXAS 77002 7 FOR THE DEFENDANTS UNITED STATES STEEL CORPORATION, 8 ARISTECH CHEMICAL CORPORATION AND USX CORPORATION: MR. JEFFREY W. KEMP 9 FULBRIGHT & JAWORSKI 2200 ROSS AVENUE, SUITE 2800 10 DALLAS, TEXAS 75201 11 FOR THE DEFENDANT RADIATOR SPECIALTY COMPANY: 12 MR. JAMES M. RILEY COATS ROSE 13 1001 FANNIN, SUITE 800 HOUSTON, TEXAS 77002-6707 14 15 16 17 18 19 20 21 22 23 24 25 2 1 INDEX 2 PAGE 3 Appearances.................................... 2 4 5 GERHARD K. RAABE, Dr.P.H., F.A.C.E. 6 Examination by Mr. Lubel................ 4 7 8 Signature and Changes.......................... 174 9 Reporter's Certificate......................... 176 10 11 12 NO.DESCRIPTION EXHIBITS PAGE 13 1 Article titled "A Critique of the Exposure Assessment in the Epidemiologic 14 Study of Benzene Exposed Workers in China Conducted by the Chinese 15 Academy of Preventive Medicine and the US National Cancer Institute"............ 36 16 2 "References for Dr. Raabe's Affidavit in Cowey" with attached articles......... 36 17 3 Photocopy of documents in Dr. Raabe's Redweld containing deposition 18 transcripts, correspondence,etc.......... 114 4 Article titled "The Myelodysplastic 19 Syndrome(s): A Perspective and Review Highlighting Current Controversies"...... 119 20 5 John W. Spencer's Summary Report 23 October 2003.......................... 121 21 6 Photocopy of Dr. Raabe's file containing billing information...................... 161 22 23 24 25 3 1 GERHARD K. RAABE, Dr.P.H., F.A.C.E., 2 having been first duly sworn, testified as follows: 3 EXAMINATION 4 BY MR. LUBEL: 5 Q. Please state your full name. 6 A. Gerhard Karl Raabe. 7 Q. Where do you live? 8 A. 2215 Aquetong Road, New Hope, Pennsylvania, 9 18938. 10 Q. What is your profession? 11 A. I am an epidemiologist. 12 Q. Are you a medical doctor? 13 A. No, I'm not. 14 Q. Are you a toxicologist? 15 A. I have training in toxicology, but I don't 16 hold myself out as an expert. 17 Q. All right. Are you an industrial hygienist? 18 A. Once again, I have training in industrial 19 hygiene but don't hold myself out as an expert. 20 Q. Have you -- have you been retained in this 21 case to offer opinions on either toxicology or 22 industrial hygiene? 23 A. No. 24 Q. I take it that you understand I have had the 25 chance recently to review the report that you issued, or 4 1 the affidavit, in this case, correct? 2 A. Yes. 3 Q. And as I appreciate it, what you have been 4 asked to do in the Cowey case is to serve as an 5 epidemiologist and to discuss causation with the jury; 6 is that correct? 7 A. Yes. 8 Q. Do you agree with the diagnosis of Mr. Cowey 9 of myelodysplastic syndrome? 10 A. I have no objective reason not to disagree. 11 Q. Okay. But as we sit here today, for the 12 purposes of the opinions that you offer in this case, 13 between now and trial, can we assume that you're going 14 to take the position that, in fact, Mr. Cowey does have 15 myelodysplastic syndrome? 16 A. Well, specifically, he has refractory 17 cytopenia with multilineage dysplasia, which is a -18 which is a myelodysplastic syndrome. One of many. 19 MR. HEARD: Lance, you need to clarify 20 the question. He accidentally said he has no reason not 21 to disagree. 22 MR. LUBEL: Okay. 23 THE WITNESS: I accept the diagnosis 24 that -- that has been presented. 25 Q. (BY MR. LUBEL) All right. By his treating 5 1 physician? 2 A. Correct. 3 Q. So, today, when we talk about Mr. Cowey and 4 myelodysplastic syndrome, is it -- is it okay that we 5 refer to that as MDS? 6 A. I will at times qualify my answer based on 7 specific forms of MDS. 8 Q. But -- but you do appreciate that he does have 9 a form of MDS? 10 A. Yes. 11 Q. All right. 12 A. No question. 13 Q. What caused Mr. Cowey's MDS? 14 A. As far as I can view it at this stage, based 15 on what I have seen, it's idiopathic. We don't know 16 what caused it. 17 Q. What are the accepted causes of MDS? 18 A. Well, depending on specific forms, but 19 generally speaking, would -- would be high, continuous 20 exposure to benzene, elec -- ionizing radiation, and a 21 variety of cytotropic drugs used in the treatment of 22 various cancers. 23 Q. Are there any other causes, or at least 24 recognized causes, of MDS other than the exposures to 25 benzene, ionizing radiation, or drugs in the treatment 6 1 of cancer? 2 A. Well, this -- I'd say those are probably 3 the -- the best established causes. Association with 4 farming, pesticides, nonionizing radiation, all appear 5 in literature with -- with varying degrees. MDS has 6 only recently been categorized in a way that you'll 7 start to see more studies coming forward. So, there's 8 not a lot out there. 9 Q. Is it your position as an expert in this case 10 that farming causes MDS? 11 A. No. 12 Q. Is it your position as an expert in this case 13 that pesticide exposure causes MDS? 14 A. The data isn't sufficient to establish 15 causation at this time. 16 Q. So, what you're saying is that one day in the 17 future, pesticide exposures may in fact cause MDS or be 18 recognized to cause MDS? 19 A. Well, there are not enough systematic studies 20 on MDS, particularly subtypes of MDS, out there; so, you 21 don't have a body of literature for which you can say 22 this is showing up consistently. 23 Case series of MDS that have been used in some 24 of these studies are not all defined in terms of their 25 subtypes or their genotoxicity; and as a result, you're 7 1 going to get varying results depending on the mix of 2 cases in the series that are on the study. So, more 3 refined study is going to be needed before we're going 4 to be able to pin down -- pin down to the causes -5 potential environmental causes, as there are. 6 Q. But as you sit here today, you agree with 7 Dr. Irons and Dr. Natelson that benzene exposures can 8 cause MDS; is that true? 9 A. Certain forms, yes. 10 Q. What forms? 11 A. Well, I'm not sure if we understand that 12 completely; but it's -- certainly -- the signature 13 chromosomal aberrations of 5 and 7 are demonstrably 14 there in -- in pretty much all forms of what we would 15 consider secondary MDS, those -- in other words, MDS 16 caused by some external factor. 17 Q. Can you tell us as you sit here what forms of 18 MDS are caused by benzene exposures? 19 A. I don't think we know that very well. 20 Certainly, if there are blasts -- blasts -- blasts 21 present in the early stages, it's much more likely to 22 progress to AML, which would suggest a closer 23 association. And as I indicated, chromosomal 24 aberrations in 5 and 7 -- in other sites as well but 5 25 and 7 most reproducibly. 8 1 Q. Can you write down for us on a piece of paper 2 the forms of MDS that are not caused by benzene 3 exposure? 4 A. No, I cannot. 5 Q. Can you write down for us on a piece of paper 6 the forms of MDS that are caused by benzene exposure? 7 A. Well, I don't think we know enough about the 8 various subtypes of MDS, other than what I described to 9 you earlier, that provide a clear guidepost; so, the 10 answer is no. 11 Q. And as you sit here today, you can't tell us 12 what caused Mr. Cowey's MDS, correct? 13 A. Based on the data available, I don't see any 14 known cause. 15 Q. As you sit here today, can you tell us the 16 most likely causes of Mr. Cowey's MDS? 17 A. No. 18 Q. Do you understand the distinction I am 19 drawing? I understand what you're saying is you can't 20 tell us to a certainty what caused it. And I am trying 21 to lower that threshold and say: Can you tell us, more 22 likely than not, what you believe caused his MDS? 23 A. Well, I -- no, I can't, because it's -- the 24 chromosomal aberrations are not suggestive of the 25 secondary forms that are -- that are induced by the 9 1 known causes we discussed. The vast majority of MDS's 2 are idiopathic. 3 Q. That's true with all cancer, isn't it? 4 A. Some more than others. I mean, some we have, 5 you know, a lot -- lot more information on -- on 6 causation. 7 Q. But there is a number of cancers for which we 8 know of certain causes of it; but, by and large, most of 9 what we know about it is idiopathic? 10 A. I think you would have to be very specific in 11 which forms of cancer we're talking about. 12 Q. Well, like lung -13 A. You don't -14 Q. Talking about lung cancer. 15 A. You, you know, very rarely see a lung cancer 16 in a nonsmoker or someone without enormous -- well, a 17 nonsmoker for sure. Radionuclide exposures. I mean, 18 it -- you don't see lung cancers frequently without some 19 suggestion of an environmental cause out there 20 somewhere. And by environmental, I mean life-style 21 factor as well as occupational or ambient environmental. 22 Q. Can smoking cause lung cancer? 23 A. Yes. 24 Q. What type of cigarettes can cause lung cancer? 25 A. Pretty much any type of inhaled tobacco smoke 10 1 can cause lung cancer. 2 Q. What -- what is it about tobacco that causes 3 lung cancer? What is in the tobacco? 4 A. Well, a number of materials that act as 5 initiators, such as benzopyrene; polonium-210, which is 6 an alpha emitter. There's a whole bunch of variety of 7 tars. I mean, it's a -- you know, it's a list of, I 8 don't know, 500,000 different materials, a significant 9 number of which have been known to be initiators and a 10 significant number of which have been known to be 11 promoters. 12 Q. Now, does every cigarette have the same 13 components? 14 A. No. 15 Q. And does it -- there's different makers of 16 cigarettes. Different companies make them. You 17 understand that? 18 A. I understand that. 19 Q. And my question is: Do each of those 20 companies have the same components in their cigarettes? 21 A. I have no way of knowing. I mean, the answer 22 is, they share a significant overlap on common 23 components. Some cigarettes have additive materials, as 24 well, that I am not really that familiar with. 25 Q. Do you believe that there is sufficient 11 1 evidence that all forms of cigarettes, made by whichever 2 company, cause lung cancer? 3 A. Well, it's not as simple as that. I mean, 4 there -- there is a significant element of dose in 5 the -- in the mixture. I mean, you would theoretically, 6 at least, if not practically, have to smoke way -- many 7 more low tar cigarettes than -- than the older, 8 unfiltered, high tar cigarettes. So, there is an 9 element of dose in all of this. But intrinsically, the 10 -- the intrinsic hazard components are probably there in 11 all cigarette smoke. 12 Q. When you look at studies that -- that stand 13 for the proposition that smoking can cause lung cancer, 14 do the studies tell us which cigarette company's 15 cigarettes they're studying? 16 A. I haven't looked at all the studies. Probably 17 not. Most of the -- most of the time you see pack 18 years, and that's it. 19 I don't know what you're looking for. 20 Q. Well, what I am trying to figure out is how 21 scientists such as yourself make the leap that cigarette 22 smoking for all brands, for all manufacturing brands, 23 can cause lung cancer if the scientists don't know the 24 differences between the brands, what -- what the 25 components of the cigarettes are. 12 1 A. But cigarette smoke -- I mean, I -- I have not 2 looked at this literature in a very long time; but 3 cigarette smoke from a variety of different sources, 4 filtered, unfiltered, different tobacco sources, which 5 is generally known, all share intrin -- intrinsic 6 carcinogenic materials of the same -- in the same class. 7 Some more than others. Some less than others. 8 So -- and then, of course, when we're looking 9 at long latency cancers like cigarette smoking, what 10 you're talking about has not been as big of an issue as 11 it might be going forward because the differences 12 between the cigarettes was not that great in terms of 13 trying to market ultra low and ultra lights. I mean, 14 those are relatively recent events. 15 So, basically -- I mean, this -- what you're 16 saying is not in -- what I think you're getting at, so I 17 might as well just go into it for you, is when you have 18 mixtures where you don't have a clear understanding of 19 all the components, in an epidemiologic study sometimes 20 you will get results that are unexpected, in the sense 21 that you might -- and that does happen from time to 22 time. You will see cigarette studies that don't show a 23 clear dose response except for maybe at the very highest 24 smoking edge. That could be for a number of reasons, 25 but one of the reasons could be that the mix of pack -- 13 1 individuals that make up that cohort and the pack years 2 that are being calculated for each individual vary 3 because some people smoked a particular brand of 4 cigarette that may have been lower in tar than another 5 brand. 6 So, studies -- that's why when -- when you 7 study something called "organic solvents," you really 8 can't establish any form of meaningful causation because 9 all organic means, it's got a carbon atom in it. So, 10 it's not very useful for specific causation. It's 11 useful in establishing hypotheses for more refined 12 studies. 13 Q. But is it a -- only a hypothesis that 14 cigarette smoking causes lung cancer, or is it past 15 that? 16 A. No, because -- way past that. I mean, we -17 we -- there have been so many different studies done, 18 all types of different ways, in different populations. 19 So, you've got -- going back to what we use to -- to 20 assess causation, Bradford Hill criteria: We have 21 strong associations, statistical associations. We have 22 many studies that show dose response, even though they 23 were done in different fashions and different cohorts 24 and different designs. We have consistency. We have 25 pretty good specificity. I mean, cigarette smoking does 14 1 contribute to several other cancer sites, but it is very 2 prominent in smoke -- in lung cancer. 3 So, you have a body of literature, 4 well-established, demonstrating consistent 5 relationships; and that's how you eventually come to a 6 causation. And if you read the preamble to either the 7 '64 Surgeon General report or the later one, which at 8 the moment I'm blocking on the date, probably in the 9 '80s somewhere, both of them sort of walk you through 10 the literature in a sense of, "Here are all the -- array 11 of all the studies here. There are statistical 12 findings. Here are the dose-response relationships. 13 Here is the level of consistency. Here is the level of 14 specificity. Temporally, they all have, you know, 15 latencies varying depending on dose but -- but 16 reasonably consistent latency periods." 17 So, that's how you establish causation. 18 Q. You have to get to those criteria? 19 A. Yeah. 20 Q. And once you've met the Bradford Hill criteria 21 in more than one competent, well-done study, then do you 22 have causation? 23 A. Well, we're talking general causation, right? 24 Q. Right. 25 A. We -- yes, you would -- and when you say more 15 1 than one, that doesn't necessarily imply two; but some 2 body of literature -- and, remember, that you also 3 have -- and the Bradford Hill tends to be glossed over 4 when we're talking about epidemiology, but consistent 5 understanding of underlying biologic mechanism, 6 concordance with studies done in animals. So, you have 7 a body of literature where you have at least some notion 8 of mode of action as well as the statistical and 9 epidemiologic evidence to work from. 10 So, when you have gone through all -- all that 11 and -- and the answer is still yes, this all hangs 12 together, it makes sense, you have established general 13 causation that this can, indeed, cause cancer in humans; 14 but you're still on -- when you get to an individual, 15 now you still have to talk about issues of dose and 16 exposure. 17 Q. But the Bradford Hill criteria -- and I guess 18 that's the point I am driving at -- they address general 19 causation, not specific causation, correct? 20 A. Well, they were designed to assess a body of 21 literature, yes. 22 Q. And a body of literature, by its very nature, 23 includes more than one person? 24 A. Oh, yeah. 25 Q. It includes groups of people? 16 1 A. Sure. 2 Q. And that's your focus, is groups of people, as 3 an epidemiologist? 4 A. Yeah. But, I mean, I'm also trained in risk 5 assessment. I mean, my firm does risk assessments, as 6 well; so, the body of epidem -- if you spoke in purely 7 epidemiologic criteria, they're generally in groups; so, 8 when you're looking at a specific causation, the issue 9 becomes how well does this person line up against what 10 you've learned from -- from -- from group -- from groups 11 of similar people -- people with similar 12 characteristics. 13 Q. But would you agree, Dr. Raabe, that the 14 Bradford Hill criteria were designed to look at groups 15 of people to determine whether an agent or substance was 16 capable of causing a given outcome or disease? 17 A. Yes. 18 Q. And I take it that since you, like Dr. Irons 19 and Dr. Natelson, do, in fact, believe that benzene 20 exposures -- at least certain benzene exposures can 21 cause MDS, that you-all do believe that, in fact, they 22 have met the Bradford Hill criteria. Would that be an 23 accurate statement, at least from your perspective? 24 A. Well, now you're talking generally MDS -25 Q. Correct. 17 1 A. -- okay, not specific forms or specific -2 Q. That's right. 3 A. -- chromosomal aberration groups? 4 Yes. Yeah. It's weak, though. 5 Well, actually, let me -- let me step back 6 from that. 7 The -- we don't have -- I mean, we're really 8 looking at causation, benzene and MDS, from an 9 extrapolation of what we know about AML. There are no 10 studies out there that demonstrate a dose response from 11 benzene to MDS in any particular form. 12 Q. What about the Hayes and Yin 2000 study? 13 A. I discount trying to use the -- the Chinese 14 studies in their -- in their current form because there 15 are so many confounding issues on the way they -- the 16 way they did the case identification. It's been heavily 17 criticized. The cohort itself is really enormously 18 heterogeneous in terms of industrial makeup. There is 19 very little information on confounding. A lot of the 20 leukemia cases in the earlier studies, in later studies 21 become MDS cases. 22 I, and a bunch of others, including the U.S. 23 E.P.A., both in -- in their large risk assessment update 24 and in their most recent, I guess, 2000-2001 update in 25 IRIS, say you can't use that study for dose response. 18 1 So, while it's sitting there, I don't -- and 2 there is no question in -- because of the enormously 3 high exposures to benzene in China that some of those 4 MDS cases are related to benzene. I am not trying to 5 discount what have already been found, but you can't use 6 it for dose response. And that being the case, you 7 know, I go back to my original statement. You don't -8 you don't have dose response information for MDS. 9 So, in -- in the traditional sense -- I mean, 10 I think -- when we say we believe that benzene can cause 11 MDS, or at least certain -- under certain conditions, 12 we're talking about more what we've learned from very 13 large case series and what we know from -- from AML. 14 So, in the purest sense, it hasn't met the Bradford Hill 15 criteria. 16 Q. Why is it acceptable for scientists such as 17 yourself to rely on the information that you have on AML 18 to make the leap, if you will, that, in fact, benzene 19 can cause MDS? 20 A. Well, there have been a number of -- let's put 21 it this way -- enough case series -- you know, normally 22 case series would not be acceptable to us as 23 epidemiologists, but we -- we do have a large body of 24 literature on AML, and we do have enough knowledge from 25 case series that generally, for -- across all forms of 19 1 MDS, about 30 percent might progress to AML; and 2 specifically, the -- the form that Mr. Cowey has, some 3 percentage lower, 15, 16, 17 -- pick a number -- may 4 progress to AML. 5 So, with -- with knowledge of the form and 6 knowledge of the chromosomal aberrations that are also 7 seen in AML, and the underlying biology, I think, you 8 know, we're in a comfort zone where we don't have to 9 have every piece of Bradford Hill checked off purely for 10 MDS because, clearly, some MDS is on the road to AML. 11 And if you go back in time, you know -- we all -- it's 12 also consistent with what we know about AML in general, 13 in that -- benzene-related AML in that in most cases for 14 there to be increased risk for AML, you need a high 15 enough exposure to induce some observable toxicity. We 16 don't always observe it because you're not looking, but 17 some type of bone marrow toxicity that -- that is a 18 precondition. 19 So, I mean, if you just sort of make -20 stretch the timelines out, some people, maybe, go 21 right -- right through early bone marrow toxicity into 22 AML; some go into an MDS phase, or preleukemic phase. 23 You know, pick your historical jargon. I mean, that's 24 been the problem with MDS, it just has not been 25 well-defined as a disease up until, you know, into the 20 1 middle, late '90s, really. 2 So, you don't have a rich body of it by 3 itself; but I think I am giving you a rationalization of 4 why we're comfortable in -- on moving into the AML 5 literature as the -- as the baseline. 6 Q. Do you remember the conclusion in the Hayes 7 and Yin article of 2000 where they state that the -- the 8 relative risk for people exposed at levels less than 10 9 parts per million was 3.1? 10 A. I remember that's -- that's one of -- one of 11 the statements in the report, yes; but I -- as I 12 mentioned earlier, I -- I and many others, including our 13 U.S. Government, believe you can't rely on their dose -14 on their dose-response information. 15 Q. Now, do you have with you today documentation 16 that sets forth the criticisms of that article? 17 A. I didn't bring that because I actually keep 18 that in a separate file; but if you have everything that 19 was attached to my affidavit there, you will have -- you 20 will have a paper by Travis, you'll have a paper -- I 21 mean, I didn't cite all of that literature; but I cited 22 some of it. You have got a paper by Wu. You have got a 23 paper by Wong. 24 Q. Can we -- can I interrupt you real quick? 25 A. Sure. 21 1 Q. You -- your attorney handed me a stack of 2 articles. 3 A. Yeah, I can -4 Q. Can I just -- will you just pull out the ones 5 that say that? 6 A. Sure. Certainly. 7 I did not cite in this report, and therefore 8 wouldn't -- I didn't bring it with me, the E.P.A. 9 documents; but here are three -- three references that 10 deal with at least some of that criticism. 11 Q. What -- what is the E.P.A. document you're 12 talking about? What's the title of them? 13 A. Okay. The title of them are -- actually, I 14 might have the IRIS with me. We were talking about that 15 with something else yesterday. 16 Q. Take your time. 17 A. Well, actually, if you go to the IRIS -- the 18 cancer information retrieval system, it's the U.S. 19 E.P.A. -- well, just look up IRIS, E.P.A. and IRIS, 20 I-R-I-S. You will get their calculation -- you'll be 21 sent to a web site that has their environmental risk 22 assessments for ambient exposures out in the community 23 for benzene. That -- the documentation of -- of -- in 24 their -- the documentation of that number speaks to 25 criticism about the Chinese studies. 22 1 The other document, I believe, is 1997; and it 2 is the -- it's a rather thick document. I am sure it's 3 on the web site for E.P.A. -- the Carcinogenic Risk 4 Assessment Guideline document. It looks at multiple 5 myeloma, leukemia, non-Hodgkin's lymphoma, and all the 6 studies on benzene, and concludes, essentially, that 7 leukemia is the site that we've got to look at, and 8 makes conscious mention about all the Chinese studies 9 and why they're currently unsuitable for -- for 10 quantitative risk assessment. 11 Q. But I take it, since this 1997 E.P.A. document 12 is dated before the -- the Hayes and Yin 2000 article, 13 that it couldn't be -14 A. No. 15 Q. -- be referring to that article in particular? 16 A. Well, that article was rereviewed in the 2001 17 IRIS document. 18 Q. So, specifically, when you talk about the -- a 19 government agency, you're saying I need to go to the 20 IRIS document? 21 A. Well, you're trying to pick out one specific 22 study. 23 Q. Correct. 24 A. I mean, there's a whole long list of Chinese 25 studies, starting with Yin in the late '80s, moving into 23 1 Hayes or Dosemeci. I mean, there is quite a long list 2 of -- their -- coming out of that cohort. And the most 3 recent -- if you're looking for something that 4 criticizes them, the most recent one is after the -- the 5 most recent Hayes paper, and that's in the IRIS. 6 But the -- the fundamental problem has been 7 that there is not -- despite all these criticisms, and 8 at sometime some attempt for rebuttal from some of the 9 investigators, the underlying issues have never really 10 been addressed. That's why there's a 11 multimillion-dollar consortium in Shanghai now doing 12 studies of benzene -- MDS, aplastic anemia, leukemia, 13 and non-Hodgkin's lymphoma. 14 Q. I didn't -- I need to talk to you about that. 15 Tell me about this -- the Shanghai consortium. 16 A. There's a consortium of researchers associated 17 with the Fudan University, the National Cancer Institute 18 of China, the Regional -- I might not have all these 19 terms -- names correct -- the Regional Cancer Registry 20 for Shanghai, which is a huge population of some 23, 24 21 million; and they have set up a large laboratory, and 22 they're identifying very early cases of 23 myeloproliferative diseases, including MDS. They have 24 got an extensive biology program and an extensive 25 industrial hygiene and epidemiology program appended to 24 1 that that will follow a bunch of cases for the next five 2 to ten years; and I think its current price tag is 3 somewhere in the 25, 27 million, not counting the 4 Chinese contributions. 5 Q. The current -6 A. Budget. 7 Q. -- consortium? 8 A. Uh-huh. 9 Q. And you think that consortium was, in part, 10 put together to look at low-level benzene exposure? 11 A. I -- that consortium was, in part, put 12 together for two reasons: China is one of the few 13 places where you will have a range of benzene exposures 14 going from moderate levels, probably in the 10 ppm 15 range, all the way up to still 50 and 100 ppm daily 16 time-weighted averages, unfortunately. So, it's one of 17 the last places you can really study benzene 18 systematically. It's a place that has a -- a very 19 rigorous catchment process, but there is -- in other 20 words, they can identify cases over a large population 21 very effectively in a relatively short time; so, you can 22 get good samples, good -- you know, good, fresh bone 23 marrow, all the things that the biologists want to look 24 at. 25 The workplaces are still in existence, so you 25 1 can get direct measurements. You'll be able to study 2 the course of these diseases much better than has ever 3 been done; and since the -- since the study is 4 essentially prospective in -- the exposure assessments 5 are going to be much more reliable than they had been in 6 the original Chinese cohort. 7 Q. Are you involved in that study at all? 8 A. I helped try and get funding for it while I 9 was still working for Mobil Oil when I was still -- when 10 I was chairing a large A.P.I. committee. I'm not 11 involved with it currently. 12 Q. And were you successful in getting funding? 13 A. Yeah, but -- although the price tag has grown 14 radically from -15 Q. Who did you get funding from? 16 A. A number of major U.S. petrochemical 17 companies. I believe there's some government funding in 18 the mix. I mean, it's a -19 Q. I am talking about you in particular. Who did 20 you go to and get funding for that study? 21 A. Oh, at the time I was chairman of the Health 22 and Products Stewardship Committee of the American 23 Petroleum Institute; so, I was the senior committee 24 chair on the health side, so I gave several 25 presentations to what would be either vice presidents or 26 1 directors of health, environment and safety for member 2 companies. 3 Q. To oil companies? 4 A. Yeah, that was my audience. There were other 5 folks who got -- trying to get money from other groups. 6 Q. And did you do a PowerPoint presentation, or 7 how did you present it? 8 A. Yeah, it was a PowerPoint presentation. 9 Q. Do you still have it? 10 A. Yeah, I think so. 11 Q. Do you have any problem giving us a copy of 12 that? 13 MR. KEMP: I prefer you direct your 14 request to me, Lance; and I'll get back to you on that. 15 MR. LUBEL: I'm just asking him if he has 16 a problem. I understand that you can make objections. 17 Q. (BY MR. LUBEL) I'm just asking you if you 18 have a problem letting us see it. 19 A. As far as I understand, I'm under no 20 confidentiality restriction on the presentation. 21 Q. And as I understand -- and correct me if I am 22 wrong -- you were making presentations to members of the 23 American Petroleum Institute, such as major oil 24 companies, concerning why you -- the group needed to 25 fund -- or help fund the studies over in China? 27 1 A. Right. 2 Q. And this is work that Dr. Irons is currently 3 working on, I take it? 4 A. Yes, he manages the -- the diagnostic 5 laboratory for them, and obviously is an active 6 researcher in molecular biology of myeloproliferative 7 diseases. 8 Q. That's the hardest words to say in this area. 9 What was Dr. Irons' involvement, if any, in 10 the fundraising? 11 A. Well, it was a very long process. I don't 12 think he had any direct -- well, he was -- he was 13 asked -- there was advisory committees put together, and 14 I don't remember who all was on them, but he was 15 certainly one of -- one of the people asked to come up 16 with research proposals. At that time they were 17 skeleton proposals of the types of research questions 18 that could be answered by such -- such an exercise. 19 And I don't know -- you would have to ask 20 Dr. Irons whether, you know, he was filing grant 21 applications simultaneously with that. I don't know. 22 But -- but he wasn't part of the fundraising group. He 23 was -- he was more one of the potential investigators. 24 Q. Would you take information from Dr. Irons and 25 put it into your presentation? 28 1 A. No, I don't think I did that. 2 Q. Were there -3 A. I mean, maybe in a general sense, the type -4 you know... 5 Q. And what was your primary pitch, if you will, 6 or presentation, as to why the major oil companies 7 should participate in the studies in a funding sense? 8 A. Well, we -- I don't know what my major pitch 9 was -- I mean, we're talking -- we're going back to '97, 10 '98, and '99; so, I -- I don't even remember what's all 11 in the PowerPoint presentation. 12 I mean, clearly, we were concerned that the 13 investigations all based on the original Yin cohort 14 would forever be tainted. In other words, there was -15 because they lost most of the cohort. I mean, there's a 16 very complex history on that -- on that cohort. The 17 National Cancer Institute, Hayes, and the rest of them 18 really don't know who the people are in that cohort 19 because they were assembled in a very ad hoc way. Some 20 of the materials they have well laid out, and some of 21 the materials they have very -- very poor documentation 22 for. 23 So, recognizing that over time we needed -- we 24 needed a -- more study specifically focused on 25 non-Hodgkin's lymphoma, which was one of my concerns, 29 1 personal concerns, I wanted to see more data, because I 2 didn't feel comfortable that what was coming out of the 3 China studies made sense in the rest of the body of 4 literature. Folks like you and others seem to still 5 periodically think multiple myeloma is related to 6 benzene, despite all the evidence; and that the only 7 thing we really had that's really good for dose-response 8 analysis is the Pliofilm cohort, and even there we have 9 three different, if you will, proposals -- published 10 versions of what their exposures were. So, even there 11 you get a range of dose response. They're all quite 12 high. 13 So, there seemed, to me, to be value in -- in 14 doing additional epidemiology and molecular biology 15 using more current techniques than we had available in 16 the '60s and '70s and '80s to help better specify 17 dose-response issues, general causation issues. So, I 18 mean, I think that's -- that was sort of my motivation. 19 Q. But I don't understand what the benefit to the 20 oil companies would be. How did you convince them to 21 help fund the studies? 22 A. Well, you may have noticed, but indirectly 23 there are subparties in -- in litigation. There are 24 parties in regulation. Every time somebody regulates 25 benzene, it has an impact on gasoline production. It 30 1 has an impact on -- on a whole range of their 2 activities. So, it's in their interest to get it right. 3 In other words, if you -- you know, if -- you 4 know, in a very hypothetical sense, you know, does it 5 make sense to keep benzene -- benzene levels in gasoline 6 at 1 percent, which is where they are now in this 7 country? They're not that everywhere around the world. 8 It costs money to control the benzene content to those 9 levels. You know, is that money well spent? Are there 10 better things to do with the -- with the resources? 11 So, I mean, you know, there is a whole bunch 12 of business reasons that getting a good scientific 13 answer as to what -- what are the risks at low levels, 14 what are the specific -- you know -- I mean, while we're 15 convinced that AML is -- is the primary or only real 16 hazard associated with high levels of benzene exposure, 17 other than aplastic anemia, of course, that doesn't mean 18 everybody else is. So, walking away from the science 19 doesn't make a lot of sense. 20 Q. But what was it about the Chinese studies that 21 kind of initiated the need, if you will, to go push for 22 additional studies, get funding from oil companies and 23 other parties? What conclusions, if you will, out of 24 the Chinese studies generated the -- the energy for 25 people to say, "Hey, we need to go fund some other 31 1 studies and find" -2 A. Well, the one that bothered me was the 3 suggestion that benzene had -- was related to 4 non-Hodgkin's lymphoma. I mean, if there was a single 5 driving force, that had never shown a -- you know, been 6 demonstrated anywhere else. So, is there something 7 about the Chinese genetics? Is there something about -8 remember, part of the problem in the Chinese cohort, 9 which I alluded to earlier, is the fact that, you know, 10 we're not talking urban dwellers. 11 We're talking about a significant part of that 12 cohort cooks their food with -- with brown coal in 13 closed environments. They have subsistence farming and 14 agriculture. Their pesticide exposures are dramatically 15 different than ours. Their -- none of -- their benzene 16 exposures are normally different from what -- probably 17 what we ever had in this country, unless you go before 18 1950 when benzene wasn't really presumed to be all that 19 toxic. 20 So, there are many, many factors in that -21 that are not part of the Chinese cohort. The Chinese 22 cohort was essentially, "Let's look at benzene." 23 Dr. Yin, who I have worked with and been on committees 24 with over the years, was trying desperately to convince 25 the government that 50 ppm, which wasn't even a -- like 32 1 an OSHA regulation, it was the recommended guideline, so 2 you didn't even have to actually follow it that well, 3 was trying to convince the federal government that 50 4 was too high. 5 He would have been enormously comfortable with 6 10. But what ended up happening is as he was losing 7 funding, N.C.I. was looking for more international 8 partners; so, they took his original cohort, with its 9 many, many limitations, and, you know, frankly ran with 10 it. So, that's problematic to the body of science that 11 we have around the world from other places. So, we need 12 to understand it better. 13 Q. What was driving Dr. Yin, in your opinion? 14 A. Well, I think I just told you. I mean, you 15 know, he and I were on an international program panel 16 for -- international program for chemical safety panel. 17 We wrote a monograph on benzene. And, you know, we're 18 discussing in the monograph meeting, you know, 19 recognizing that it's a worldwide recommendation, so you 20 weren't, you know, trying to push the lowest technical 21 levels but what was -- what did the science say seemed 22 to be safe. So, we were sitting there debating, you 23 know, is 1 too low? Is 5 okay? Should it be 3? Should 24 it be 10? 25 But, you know, as you got down to the last 33 1 chapter in the monograph, and -- and poor Dr. Yin is 2 trying to say, you know -- "You know, we have got folks 3 well exposed over 50s." I mean, his motivation was, we 4 knew 50 was wrong. We -- that you shouldn't be exposing 5 people at those levels. I mean, your aplastic 6 anemias -- they have a lot of cases of aplastic anemia 7 in China. 8 Q. But, I mean, was there an external source, if 9 you will, that you felt as though was driving Dr. Yin 10 to -- to try and reach these conclusions, or did you 11 feel like he honestly and genuinely thought this is 12 where things ought to be? 13 A. Well, he was, you know, a 14 physician/epidemiologist in China that had seen lots of 15 aplastic anemia, looked at where these guys worked, 16 recognized that they were almost -- you know, that it 17 almost certainly was benzene related, initiated a very 18 large cohort with internal funding, doing the best job 19 you could in the period for him, which was way below our 20 standards of quality control, to help demonstrate that. 21 So, I mean, you have to -- you know, his English is not 22 very good. So, you know -- but -23 Q. What I -24 A. -- but I think that's what his motivation -25 Q. Was he biased, in your opinion? 34 1 I am not talking about from a scientific 2 standpoint. 3 A. No, I -- well, I mean, biased only in the 4 sense that going into the study he knew that they were 5 exposed too high. Okay? But I -- I -- there is nothing 6 that I -- there is nothing in his studies or demeanor 7 that strikes me that, you know, the data was manipulated 8 to show responses where there weren't any. I think it 9 was just sort of by our standards, you know, moderate, 10 inadequate quality work. He relied on the diagnoses 11 that were coming out of these little regional clinics. 12 Many of the diagnoses were wrong. 13 Q. Didn't the 2000 study that he and Dr. Hayes 14 and others did, didn't they go back and look at that 15 data again? 16 A. Well, they -- they redid a big chunk of the 17 hematology that they could. They couldn't do it all. 18 So, yeah, I mean, I am not saying improvements haven't 19 been made where they can be made; but the -- but 20 remember -- I remind you, again, they had no 21 identification on these individuals. So, they could not 22 go back and -- and really do good audits on exposure. 23 They couldn't go get additional materials. I mean, if 24 they had the materials -- they didn't -- if Yin had the 25 materials, they had it. If he didn't have the 35 1 materials, they didn't. And that was sort of the end of 2 it. 3 And that's why the numbers changed so 4 dramatically too, you know, which that's not -- you 5 know, if a study was done by me and -- and every time I 6 reported out, the numbers changed dramatically, I'd be 7 sitting in very long depositions when people wanted to 8 use my study in their case. 9 So, you know, there's lots of problems that I 10 don't think were, you know, intentional that are just -11 you know, say that you need another Chinese series of 12 studies using more modern techniques to help define, you 13 know, what -- what was really going on. 14 MR. LUBEL: Do you mind if we take a 15 short break? 16 THE WITNESS: Fine with me. 17 MR. LUBEL: Is that okay with you guys? 18 MR. KEMP: Yes. 19 MR. LUBEL: Thank you. 20 (A break was taken, 9:43 to 9:49 a.m.) 21 (Exhibits 1 and 2 marked.) 22 Q. (BY MR. LUBEL) Can you identify Exhibit 23 Number 1? 24 A. Exhibit Number 1 is a paper authored by 25 Dr. Otto Wong, published in 1999, titled "A critique of 36 1 exposure assessment in the epidemiologic study of 2 benzene-exposed workers in China conducted by the 3 Chinese Academy of Preventive Medicine and the US 4 National Cancer Institute." 5 The second paper is also a paper by Dr. Wong, 6 titled "Benzene and Dose-related Incidence of 7 Hematopoietic [sic] Neoplasms in China." 8 And the third paper is by Weiai Wu, W-U, 9 "Occupational Cancer Epidemiology in the People's 10 Republic of China." 11 And these are just a sampling of -- from me. 12 MR. KEMP: Are these all Exhibit 1? 13 MR. LUBEL: Yes. 14 MR. KEMP: All three papers? 15 MR. LUBEL: Yeah. 16 Q. (BY MR. LUBEL) And what I asked you to do was 17 to take out, out of the articles that your lawyer handed 18 me, the ones that you felt criticized the Chinese 19 studies that we have been talking about today, correct, 20 and that's what you did? 21 A. Yeah, of the set -- I mean, I have additional 22 ones; but of the ones I brought with me, that's -- those 23 are the ones that I think relate to your question. 24 Q. And then you told us about an E.P.A. document 25 that you said we could get on IRIS, I R I S? Is that 37 1 correct? 2 A. Yes. 3 Q. Can you put your hands on that and fax that to 4 your attorneys? 5 A. Yes. 6 MR. LUBEL: Jeff, will you provide that 7 to me? 8 MR. KEMP: Absolutely. 9 Q. (BY MR. LUBEL) I don't know that I'm computer 10 intelligent enough to find it. 11 A. Would you like the earlier one, as well? 12 Q. Yes, sir, please. 13 And then, Exhibit Number 2 is a list of the -14 is actually the articles that are referenced in your 15 affidavit in this case, except for the three articles 16 that you pulled out and marked as Exhibit Number 1; is 17 that correct? 18 A. Umm -19 Q. Sir? 20 A. -- this really should be part of Exhibit 1. 21 Q. Okay. What is it? And we will attach it. 22 A. It's an article titled "Hematopoietic 23 Malignancies and Related Disorders Among Benzene-exposed 24 Workers in China" by Lois Travis; and that really -- we 25 are placing that in with Exhibit 1. 38 1 But the remainder are -- are the studies I 2 attached to and used specifically for my affidavit. 3 Q. One of the authors in these studies is a 4 Dr. Wong. Do you know him? 5 A. Yes, I do. 6 Q. And how do you know Dr. Wong? 7 A. We've worked together over the years and 8 co-authored papers together over the years. 9 Q. Are you generally familiar with his 10 involvement with the American Petroleum Institute and 11 Chemical Manufacturers Association? 12 A. Yes. 13 Q. What do you know about it? 14 A. Well, it was -- he was contracted to conduct 15 an epidemiologic study by the then-called Chemical 16 Manufacturers Association. Actually, I believe he was 17 working with -- started out working with Dr. Irving 18 Kaybashore in that process. That's where I first met 19 him. Mobil contributed data to those studies. 20 Over the years, he has conducted several very 21 large cohort mortality studies at the behest of the 22 American Petroleum Institute. Over the years, he and I 23 have independently worked on projects together that I 24 had an interest in, or specifically I and Mobil had an 25 interest in; and we co-authored several papers together. 39 1 Q. And were you aware that oil companies, 2 including Mobil, have hired Dr. Wong to testify in 3 benzene exposure cases just like Mr. Cowey's? 4 A. I don't know that -- I mean, I know he's been 5 hired to give testimony. I don't know specifics or 6 whether any of them were anything like Mr. Cowey. 7 Q. Were you aware that Dr. Wong had been hired by 8 Mobil, and other oil companies like Mobil, on benzene 9 exposure cases? 10 A. I don't understand the question. 11 Q. Were you aware that Mr. Wong had been hired as 12 an expert by Mobil in benzene exposure cases? 13 A. You mean toxic tort cases? 14 Q. Correct. 15 A. I think I am -- well, I am not aware that he 16 was specifically hired by Mobil, but I am aware that he 17 has testified for oil companies in such cases. I -- I 18 never -- I never hired him; and so, I don't -- I don't 19 know whether he was ever used -- retained specifically 20 by Mobil in any of these litigation cases. I don't know 21 that. 22 Q. Now, who did you hire when you were at Mobil 23 to do this expert witness work? 24 A. I didn't. That was -- that would have been 25 the law department. My -- my group is only scientific 40 1 in the medical department. 2 Q. Did you participate in helping the law 3 department find experts to work on these cases? 4 A. No, I don't believe so. I don't recall doing 5 that. 6 Q. Nobody ever asked you, as a scientist with 7 Mobil Oil Company, what experts they should hire to 8 defend these toxic tort cases? 9 A. I honestly don't recall participating in those 10 types of discussions. I mean, certainly they knew of 11 Dr. Wong and my association with Dr. Wrong; so, I am not 12 saying that we hadn't discussed Dr. Wong. But I don't 13 recall sitting down with the -- any of our environmental 14 counsel and giving them a list of -- a list of potential 15 witnesses. I -- I know I probably sat down with them in 16 the course of various settings and listed 17 epidemiologists that we had worked with that I felt 18 were, you know, professionally very good; but I don't 19 think it was in the context specific to the kind of 20 question you're asking. 21 Q. Well, what context would it have been in? 22 A. Well, if -- if we were proposing -- well, 23 environmental counsel would have probably sat in on 24 large decision points where I was going to go ahead and 25 do a study or contract a study, one or the other, and 41 1 either wanted -- was letting them know who we would bid 2 it to or letting them know who we were considering for 3 putting on an advisory panel, a reviewer panel; so, they 4 would have heard those discussions. 5 Q. Why would the lawyers be involved in that? 6 A. Well, I don't know if it -- there was only one 7 lawyer involved in that. He was environmental lawyer 8 for the corporation, and he sat in on all executive 9 briefings; so... 10 Q. Was he a scientist? 11 A. Yeah. I am trying to get money from 12 management; so, I have got to explain to management. I 13 mean, it wasn't a scientific meeting. By the time I -14 you know, we -- we decided in the medical department 15 what we wanted to do. Now -- now I would go to -- to 16 the level of the organization that would free up a 17 couple hundred thousand dollars so I could go ahead and 18 do it; so, that would be general managers or vice 19 presidents, depending on how -- how many hundred 20 thousand dollars I needed. 21 Q. What I am trying to figure out is what role a 22 lawyer would play in this whole process of you trying to 23 hire people to perform studies. 24 A. I don't think -- I don't know if he played any 25 role other than part of the information -- I mean, he 42 1 was not part of the decision process, if that's what 2 you're getting at. 3 Q. Now, what studies have you worked at Mobil 4 that you participated in? 5 A. Oh, many. 6 Q. Well, let's talk about benzene. What studies 7 on benzene? 8 A. Benzene or benzene related? 9 Q. Benzene related. 10 A. Okay. I contracted initially in the early -11 late '70s, early '80s for -- to reconstruct the 12 employment cohort for -- and subsequently conducted 13 mortality analysis for the Beaumont refinery, the 14 Torrance refinery, the Paulsboro refinery, which were 15 owned by Mobil at the time. 16 Q. Who asked you to do that? 17 A. I -- it was my recommendation that we do that 18 because we had a P.M.R. study from Terry Thomas that 19 suggested that there might be some excesses and that the 20 best way to understand that was not with a P.M.R. study 21 but with a cohort study. 22 Q. Who is Terry Thomas? 23 A. Terry Thomas was a -- at the time a master's 24 level epidemiologist working for the National Cancer 25 Institute that was working with partial union data. So, 43 1 we initiated those studies. 2 A few years later, after those studies were 3 completed, we began -- initiated the process. By that 4 time I'd built an in-house resource so we could update 5 those studies internally; so, we went through a process 6 and updated those studies. 7 As we gained more knowledge about the 8 specificity of -- in the early days, it wasn't clear 9 whether we were just -- most of the epi studies tended 10 to just look at the large category of leukemia. As 11 biologies got better understood, it became more 12 important to look at cell types; so, we further updated 13 those studies and specifically looked at cell type. 14 It was -- I determined that we didn't have 15 enough cases inside Mobil and that it would be useful to 16 try and pull results from a number of different cohorts, 17 and I'd say Otto Wong and I worked together on it and 18 published a paper on cell type specific leukemia in the 19 petroleum industry. 20 Q. What did you call the -- how do we refer to 21 the late '70s, early '80s study where you included the 22 Beaumont refinery and others? What's -- what phrase can 23 we use to refer to that? 24 A. Initial cohort mortality study. 25 Q. And who did you hire to work on that study 44 1 outside of Mobil? 2 A. Robert Morgan, Phil Enterline, Otto Wong. The 3 Stanford Research Institute did a lot of the data 4 collect -- assembled a lot of the data for us in 5 Beaumont. 6 Q. But you weren't just looking at the Beaumont 7 refinery, correct, you were looking at the other Mobil 8 refineries? 9 A. The three largest. 10 Q. And how did you select those, other than size? 11 A. Well, the Joliet refinery was recently built; 12 and I -- it was designed to be a cross-crafting 13 refinery, so it would not have been -- well -- so, all 14 the work population was relatively young, hired in the 15 midwest, and were all cross-crafted in the sense that 16 maintenance workers did not just single-job things. And 17 at that period we were trying to get a sense of if there 18 are any specific crafts or specific work groups that -19 which might show an excess of disease. 20 So -- so, we went to the ones that were the 21 oldest, had -- and we had done site visits and 22 established that had record -- paper records that were 23 adequate to reconstruct into the late '40s, starting 24 with post-war years '46 and '47. Torrance, we could 25 only go back to the -- to '60. So, it was really a -- 45 1 part feasibility, part size. 2 Q. But there were other Mobil plants at the time 3 that you decided to run these studies that had benzene 4 in them, correct? 5 A. Well, we had a very small refinery in the 6 State of Washington, and we had the refinery in Joliet; 7 and I think we still had but were in the process of -- I 8 don't remember if we commissioned it or sold it or what, 9 a refinery in Augusta -- it wasn't Georgia -- Augusta -10 what -- I forgot what state it's in, but it's not -11 it's not Georgia. It was another Augusta. 12 And that was it. We -- those were the 13 total -- sum and substance of refineries in the United 14 States. 15 Q. Did they have benzene at those other 16 refineries? 17 A. No. The -- the only refinery that 18 manufactured -- well, yes. I mean, obviously you have 19 benzene in a lot of refinery streams everywhere; but 20 only -- in that time period, the only refinery that had 21 a petrochemical operation specific to benzene was in 22 Beaumont. In other words, manufactured benzene was in 23 Beaumont. 24 Q. Are you familiar with the -- the stream 25 dripolene? You ever heard of dripolene? 46 1 A. I have heard it. I honestly don't remember 2 what it means -- what it stands for right now. 3 Q. I mean, you understand in some of these 4 refineries and chemical plants that there are products 5 that are not -- that have -- that have benzene as a 6 component of them? 7 A. Oh, certainly. Sure. 8 Q. And wouldn't those be relevant to study if you 9 have got plants that have benzene as a component of a 10 product? 11 A. See, you asked me what studies had benzene 12 relationships. We didn't study those plants because of 13 benzene. 14 I mean, we -- we're in an era where our 15 concern was what -- it was basic descriptive 16 epidemiology. This is the plant. These are the -17 what -- what they manufacture, and these are the 18 populations. Are there any unusual patterns of disease? 19 I mean, we've had a medical department since 20 the '50s; but, you know, there -- there was nothing 21 coming out of clinical observations to suggest that 22 there was any specific problems. So, this was a more 23 traditional cohort mortality study looking for patterns 24 of disease that we would then subsequently study in more 25 detail, as warranted. So, benzene was not, you know, 47 1 particularly -2 Q. Wasn't the focus? 3 A. No. It was recognized that it was at these 4 plants, but it -- it wasn't -- it wasn't a benzene 5 study. 6 Q. And Mr. Morgan, Mr. Wong, Mr. Enterline, and 7 the Stanford research group are the people that were 8 involved in the study that were not employed by Mobil? 9 A. Well, they had staffs -- additional staffs. I 10 mean Bob -- Bob Morgan actually brought Otto Wong in. 11 Bob was principal investigator at Beaumont. Phillip 12 Enterline was principal investigator in Torrance. 13 And -- and Morgan was also principal investigator in 14 Paulsboro. 15 Q. Now, did you know these men before you hired 16 them to conduct the study? 17 A. I had met Bob Morgan. He was brought in as an 18 epidemiologic consultant at some meeting or another of 19 the American Petroleum Institute. That's where I first 20 met him. 21 Q. The A.P.I.? 22 A. Uh-huh. 23 Q. Is that a yes? 24 A. Yes. I'm sorry. 25 Q. And Mr. Morgan brought Wong into these 48 1 studies, correct? 2 A. Yes. 3 Q. And how did Mr. Enterline get involved in 4 them? 5 A. Phil Enterline is a -- an internationally 6 known epidemiologist, as well. He was at University of 7 Pittsburgh. I knew him. He had familiarity with the 8 petroleum industry. And I don't actually remember where 9 I first met him. 10 And so -- I mean... 11 Q. Why do you say he had familiarity with the 12 petroleum industry? 13 A. Phil had done -- by that time, published a 14 number of studies already on some petroleum-related 15 exposures and had done some work on epichlorohydrin and 16 a few other chemicals. I mean, he was an occupational 17 epidemiologist of -- of high regard. 18 Q. Had he done work with the A.P.I. or the 19 Chemical Manufacturing Association in the past? 20 A. I think he may have done some work for Shell, 21 specifically; but I -- but to my knowledge, at that time 22 he had not done any work for A.P.I. 23 Q. Now, did you -- did you enter into a contract 24 with these men to perform this study? 25 A. Yeah, that's one of the reasons why the lawyer 49 1 sits in -2 Q. All right. 3 A. -- because at the end of the day, I have got 4 to write a conclusion -- write a contract. 5 Q. So, you and the lawyer for Mobil wrote the 6 contract? 7 A. Well, they gave me the boilerplate version. I 8 added a section on -- the boilerplate contracts didn't 9 address publications and things like that; and so, I 10 made some modifications to them and -- and sent them in 11 to the contractor. 12 Q. And was there more than one contract for these 13 men for this study? 14 A. Separate contracts for each refinery. 15 Q. Why is that? 16 A. Well, under different profit centers, the 17 accounting is done that way. 18 Q. But was the form of the contract itself the 19 same? 20 A. I think so. Yes. 21 Q. And did -- did Mobil retain editorial rights 22 over the study? 23 A. No. We had a three-month window of review, 24 and we could offer -- offer comments. And then the -25 the investigator, I think, had one month to issue a 50 1 final report; and then he could do anything he wanted 2 with it. 3 Q. Who was the investigator? 4 A. Well, Dr. Morgan for -- the ones we just 5 discussed, the principal investigators. 6 Q. Was there a confidentiality clause or 7 agreement regarding this study? 8 A. Well, there's -- there was a medical -- a 9 medical confidentiality clause. They couldn't just -10 could not disclose identity of any of the individuals in 11 the study. I mean, medical -- it's sort of a standard 12 medical confidentiality. And they could not discuss 13 results of the study outside -- outside their 14 organization or with -- until such time as the time 15 report was issued; so -16 Q. In other words -17 A. -- no. 18 Q. -- what would happen if -- if Mobil didn't 19 agree with the final report? 20 A. That's happened in other settings. Nothing 21 happens. I mean, we offer our comments. They take 22 them; they don't take them. The report is the report. 23 And -24 Q. Were the investigators free to issue a report 25 at their discretion, irrespective of Mobil comments? 51 1 A. Yes. Oh, absolutely. 2 Q. And that would be contained in the agreement, 3 correct? 4 A. Yes. It was very explicitly contained in the 5 agreement. 6 Q. And I take it that you're -- the comments that 7 Mobil had were put in writing? 8 A. You know, I don't remember. They may not have 9 been. We may have -- may have been just invited to come 10 in, and we sat down and sort of walked through -- walked 11 through it. 12 Q. Now, did you have anybody look at the draft 13 report done by the investigator before you met with the 14 investigators to discuss your comments? 15 A. Well, it would have been myself; I think by 16 that time I had a master's level person I had hired; and 17 the -- probably the domestic medical director and the 18 medical director probably would have read it. I don't 19 recall at the -- at the draft stage whether any counsel 20 had read it. They may have, but I don't remember. I'm 21 not sure if they would have been normally in the loop. 22 Q. Did -- did you know from the outset that the 23 results of the study would be published? 24 A. I assumed so. We weren't paying the 25 contractors extra money to write a publication version 52 1 of the report. They were only being paid -- compensated 2 to write the -- you know, the thicker internal -- if 3 you're familiar with epidemi -- epidemiology, there is a 4 tendency to have, in an unpublished version, more 5 tables, more information than you could ever get 6 published in a scientific journal. So, our contracts 7 only asked for the -- and those early contracts -- a -8 a report. 9 Q. What do you call that? What's the difference 10 between the short, published report, and the -- the 11 report that's got all the tables and raw data referenced 12 in it? 13 A. I -- I don't think we have any jargon for 14 that. I will say, in later years, when Otto and I 15 worked together, we started going directly to a 16 publication version of the report because it just added 17 a lot of unnecessary time to, you know, have a -- one 18 report and then another report. 19 But I think the term was report -- well, the 20 jargon would be issue a written report versus issue a 21 written report suitable for publication. 22 Q. All right. Now, I take it that in your field 23 of epidemiology, you prefer to see the long report 24 that's got all the tables and data, as opposed to the -25 the published report that's got less information? 53 1 A. Well, certainly in that era where -- where to 2 a large extent you're just trying to look for patterns; 3 so, you would have more tables in some of the 4 unpublished reports than you would see in -- in... 5 After we've updated the cohort several times, 6 there was even -- not even a reason to rerun some of 7 those tables over and over again because, you know, you 8 knew they weren't going to provide any additional 9 information; so... 10 Q. Now, did the workers at the plant sign 11 anything to be a part of the study? 12 A. In that time frame, we notified the union 13 that -- that we were doing the exercise; but since no -14 anything coming out of the medical records, they would 15 have already signed such a release. The Mobil release 16 in that time period in the medical department said that 17 you -- the results of the -- the examinations could be 18 used for statistical reasons, statistical purposes. But 19 in those studies there wasn't any -- I think we looked 20 for Death Certificates in the medical records, but at 21 that time there was no medical data being used in those 22 records. So, the basic answer is no, they were not 23 asked. 24 Q. How did you notify the Mobil workers that they 25 were being studied at the various plants? 54 1 A. You said plaintiffs? 2 Q. Plants. 3 A. Oh. 4 Q. Sorry. 5 A. I -- how did we do that? I think there was -6 there's a -- back then there was a bulletin board. I 7 mean, the -- only the active workers would have known 8 that -- that we were doing a study. The -- there 9 wasn't -- I don't think there was any separate 10 correspondence going out to retirees, and there 11 certainly would not be to terminees because we wouldn't 12 have -- we wouldn't have -13 Q. Were you studying the retirees or the current 14 workers? 15 A. We were studying anyone who worked a year or 16 more from essentially 1946 to -- I forget the cutoff 17 date right now, '80-something -- no, '70-something -18 '79, probably, worked a year or more at the Beaumont 19 refinery. So, that would include active workers, 20 terminated workers, and retirees. 21 Q. What motivated the study? What initiated it? 22 A. Well, we were looking -- as I said, we were 23 looking for patterns -- specifically cancer mortality, 24 looking for patterns of potential for excess cancer 25 mortality of the various cancer sites. 55 1 Q. Right. But, I mean, what -2 A. You needed -- you needed the terminees and you 3 needed the retirees because you -- cancer is a long-term 4 process. So, to get a large population, you would want 5 a large -- as large a population as you could establish; 6 and you would want to have long -- you know, be able to 7 look at duration of employment, and that included 8 long-term workers. 9 Q. I guess my question is: Why in the late '70s 10 did Mobil become interested in studying cancer and 11 whether there was any pattern of cancer in the Beaumont 12 refinery? 13 A. Well, let me just -- Mobil did a -- a study -14 the medical department did an epi study on -- on their 15 own in 1964 across the entire population of -- of Mobil. 16 Now, that tended to be just active and retirees because 17 it was -- everything was administered through one 18 insurance plan. 19 Mobil's had a medical department since 1950. 20 They've always been very interested in -- in the 21 patterns of disease in the population, making sure that 22 workers weren't harming themselves. 23 Q. Was the '64 Mobil study published? 24 A. No. That was in an era where, you know, 25 public -- publication of things wasn't on any of these 56 1 radar. 2 Q. Have you seen the '64 study? 3 A. Yeah, it's been surrendered in some cases over 4 the years. Actually, fairly recently only. I actually 5 did not come across that report until I was cleaning out 6 files in the Mobil-to-Exxon transition. So, I probably 7 saw it when I first was hired and forgot about it 8 because, I mean, by the -- by the standards of -- it 9 doesn't show specific groups except in very broad 10 classes; so, you know, office personnel, executive 11 personnel, distribution personnel. So, it wasn't as 12 informative as -13 Q. And when was that surrendered in litigation, 14 to your knowledge? 15 A. Oh, probably sometime this year somewhere. 16 Q. Do you remember who that was surrendered to? 17 Was that Provost and Umphrey or Herschel Hobson or -- do 18 you know these names I'm talking about? 19 A. Yeah, I know the names. I knew Herschel when 20 he was a real -- a real professional. 21 Q. I'll tell him you said that. 22 A. You certainly can. Herschel knows me well. 23 It -- it may have been a Provost and Umphrey 24 case. It wasn't a Herschel case, I'm pretty sure; but I 25 don't remember. 57 1 Q. But did you have that data from the 1964 Mobil 2 study to review, as you were, you know, an 3 epidemiologist for Mobil? 4 A. Well, as I say, I'm pretty -- pretty sure -5 when I found it, I recognized that I had seen it. Okay? 6 But -- and -- and, of course, realized that -- you know, 7 that it had some important import in today's -- today's 8 world; but when I -- rereading it over again, I -- it 9 reminded me why I probably forgot that I -- that it ever 10 existed, because it -- it doesn't inform on any of the 11 issues that -- I mean, it talks -- it -- it talks about 12 the issues of cardiovascular disease and encourages 13 Mobil to -- the medical department to continue its 14 efforts for early diagnosis and treatment of those kinds 15 of things. It talks about cancer, loosely talks about 16 smoking, but didn't find any unusual distributions or 17 patterns; so -- and it didn't look -- it didn't -- other 18 than, I think, lung cancer, there was no other 19 site-specific cancers. I mean, it was either all 20 cancer, lung cancer, cardiovascular disease, accidents. 21 I think that was the -- sort of the -- the focus. 22 Q. Do you know if Dr. Morgan and the group that 23 performed the -- this initial cohort mortality study, 24 whether they had access to the 1964 Mobil study? 25 A. No, they probably never saw it. They probably 58 1 never saw it. 2 Q. Where is the raw data from the '64 Mobil 3 study? 4 A. I -5 Q. The long report, as you call it, that's got 6 the tables and all of that stuff. 7 A. Well, I mean, I have the whole report. Okay? 8 I mean, that's what we're talking about. When you say 9 the data, I don't -- I mean, I -- that's an era of mag 10 tapes and IBM cards. I am sure it doesn't exist. 11 Q. Other than the -- this late '70s, the early 12 '80s Beaumont refinery study that I think you have 13 called the initial cohort mortality study, and this 1964 14 study that you just said was surrendered recently, what 15 other benzene-related studies has Mobil either conducted 16 or asked others to conduct on their behalf? 17 A. Well, after some toxicologic information on 18 unleaded gasoline, there was a concern about kidney 19 cancer specifically and exposure to gasoline; and -- and 20 we conducted -- no individual company had enough 21 distribution workers to do it, and -- on their own; so 22 we, through A.P.I., conducted a very large study of the 23 distribution of gasoline in the United States and the 24 marine component of the distribution of gasoline. So, 25 it's terminals, tankers, and -- and marine barging. 59 1 That study was conducted in the late '80s. 2 Q. Who conducted that for Mobil? 3 A. A number of investigators. Tom Smith, who is 4 now at Harvard, handled the exposure component. 5 Environmental Health Associates and Dr. Wong handled 6 the -- the statistical and the report, the basic 7 epidemiology reporting. We had Phil Enterline, Wegman, 8 and -- and -- and -- I am blocking out his name -- a 9 very famous industrial hygienist, I think from 10 Harvard -- on a very active oversight panel that met 11 several times a year. 12 And I guess that's the key players. 13 Q. Was that study published? 14 A. Yes. 15 Q. What's it called? 16 A. It's public -- there is quite a few 17 publications out on it. There's an Environmental Health 18 Perspectives monograph. I can actually tell you the 19 publication date because I have a paper in it. It's 20 peer-reviewed, but it's one whole issue. The 1996 21 Environmental Health Perspectives monograph, Volume 104, 22 Supplement 6. It is entirely devoted to gasoline. 23 And then there are two subsequent publications 24 by Dr. Wong in later years. I don't remember the dates. 25 But if you do a search on unleaded gasoline and 60 1 epidemiology, you'll find them. 2 Q. Did -3 A. And then -4 Q. Oh, I'm sorry, go ahead. I didn't mean to 5 interrupt you. 6 A. Well, you -- I'm back to your original 7 question. 8 Additionally, in the late '90s -- well, in the 9 '80s, I had been tagged to represent the U.S. at a World 10 Health Organization IARC monograph on exposures in 11 petroleum refining and gasoline; and, with Otto's 12 assistance, we conducted a pooled analysis, sometimes 13 called a meta analysis, of the major cancer sites coming 14 out of not just our studies but the whole published 15 literature. That was -- we published that. 16 And then in the '90s, Otto and I published a 17 series of papers on multiple myeloma, non-Hodgkin's 18 lymphoma, and solid tumors in petroleum-exposed groups. 19 Q. Were you doing that on Mobil's behalf? 20 A. Mobil let me use my time, and -- and I raised 21 some money from A.P.I. to pay -- to pay Otto for his 22 time. 23 Q. But I take it that you were still an employee 24 of Mobil at the time those studies were -25 A. Yeah. 61 1 Q. -- done? 2 A. Yes, that's correct. 3 And then we also updated the refineries one 4 more time and published all of those. 5 So, all of this -- at least all the ones that 6 my names are on is on the back of my C.V.; so... 7 Q. At any time have you published a study that 8 relates to benzene where you were not employed in some 9 capacity by a refinery or chemical company? 10 A. No, I didn't -- when I was with the State of 11 New York, I didn't -- we didn't to that much 12 occupational, since we were focused on New York City. 13 No. 14 Q. Do you know John Spencer? 15 A. Yes. 16 Q. Did he do any work for you when he was at -17 when you were at Mobil? 18 A. You know, I actually don't know. He did not 19 for me specifically, and my group was epidemiology and 20 health risk assessment. 21 Whether he did any contract work for other 22 parts of Mobil, I don't know. 23 Q. As you sit here today, you don't ever recall 24 hiring John Spencer to do work on behalf of Mobil. Is 25 that true? 62 1 A. Well, I know I never -- I know I never did. 2 Q. Do you know if John Spencer has ever been 3 hired on any of the studies that you have done on -4 related to benzene? 5 A. I -- I don't think so, but I -- but, you know, 6 I -- I wouldn't know all the subcontractors that may 7 have been used by some of these other investigators. 8 So, I honestly -- I guess my better -- the best answer 9 is I don't know, but I don't think so. 10 Q. How did you first meet? 11 A. I think when I first met John Spencer was when 12 I had been asked to look at -- conduct some health risk 13 assessment work for a silica-exposed foundry plant. 14 That's where I first met John. 15 Q. For silica exposures? 16 A. Silica, and I think they had -- also had some 17 asbestos found. 18 Q. Do you remember which plant? 19 A. Yeah. 20 Q. Was it Tyler Pipe? 21 A. Yes. 22 Q. It's a real shocker, isn't it? 23 A. It's interesting. 24 Q. Were you hired on behalf of Tyler Pipe or some 25 product manufacturer? 63 1 A. Some product manufacturer. 2 Q. And were you -- was your role having something 3 to do with cancer? 4 A. Yes. 5 Q. And did you understand Mr. -- Mr. Spencer's 6 role to have something to do with exposure? 7 A. Yes. I had seen his name previously on -8 on -- on exposure or assessment reports. I sort of knew 9 him, but when -- you asked me when I first met him. 10 Q. Do you recall who you were working for in the 11 Tyler Pipe case, the foundry case? 12 A. No, I don't remember the law firm or the -- or 13 who they were specifically retained for. 14 Q. Was that just one case that you worked on? 15 A. Yeah, I worked on a gastrointestinal cancer 16 case. 17 Q. What other cases or involvement have you had 18 with Mr. Spencer in his role as an industrial hygienist, 19 other than that one litigation case we have talked 20 about? 21 A. I mean, he -- I read his reports in some other 22 litigation cases; and I have spoken with him on his 23 exposure reconstruction and the exposure monitoring he 24 did on Liquid Wrench. 25 Q. You talked to him? 64 1 A. Yes. 2 Q. What -- go ahead. 3 A. But I don't -- I mean, I -- I have a local 4 industrial hygienist that I use when I -- when I need 5 somebody to help me out in -- you know, on a project. 6 Q. Who is that? 7 A. Wayne Skopypec. 8 Q. When did you talk to Mr. Spencer about this 9 particular case? 10 A. Saturday? Saturday, I think. 11 Q. Which Saturday? 12 A. This -13 Q. Any Saturday? 14 A. Any Saturday. Last Saturday. 15 Q. And who set that call up? 16 A. I think it was Saturday. It may have been 17 Sunday, but I think it's Saturday. 18 I did. I initiated the call. 19 Q. So, it's been a couple of days ago, 20 essentially? 21 A. Yeah. 22 Q. And why did you call Mr. Spencer? 23 A. Well, two reasons: one is, after reading 24 Vernon Rose's report, I thought he made a misstatement, 25 flat out incorrect, on the issue of what would happen if 65 1 you spiked benzene into an over-the-counter product like 2 a current version of Liquid Wrench; and so, I wanted to 3 review that with him. As I said, I'm trained; but I -4 I always like to check my opinions. 5 And, also, I have been aware previously, 6 although never seen the work product, that he had been 7 doing some exposure reconstruction work on Liquid 8 Wrench. And in this case I did see a work product and 9 wanted to review with him, make sure I understood what 10 Table 1 was versus Table 2 and 3 and, you know, how we 11 did the analysis, how the monitoring was done, how long 12 the samples were taken for, that kind of stuff. 13 Q. And do you have notes of that conversation? 14 A. I don't have notes, but I have a very clear 15 recollection of it because it's only a couple of days 16 ago. 17 Q. Now, had you visited with Mr. Spencer about 18 these two issues before you issued your sworn affidavit 19 in this case? 20 A. If I understand the question, no. 21 Q. Let me be more specific. 22 You issued an affidavit on approximately 23 October 30th of the year 2003 specifically about 24 Mr. Cowey's case, correct? 25 A. Correct. 66 1 Q. Had you talked to Mr. Spencer about any 2 matters related to Mr. Cowey's case before you issued 3 that particular affidavit? 4 A. Not specific to Mr. Cowey. I mean, I -- from 5 previous discussions going back, I don't know, six, 6 eight months ago, I -- I knew he had done Liquid Wrench 7 reconstruction work; and I had a vague recollection of 8 what it was. And so, I assumed that what I was seeing 9 in this case was a product from that exercise. I don't 10 remember actually when he did it, but -- but I knew it 11 was done; and I knew -- knew vaguely what the results 12 were. 13 Q. Well, I take it that you would not have spoken 14 to Mr. Spencer this past Saturday about his exposure 15 reconstruction work in this particular case if you had 16 felt like the work you had seen six to eight months ago 17 was adequate for your needs. Is that true? 18 A. No. I felt it was adequate -- well, I mean, 19 it wasn't -- I didn't need it for my opinion to begin 20 with; but -- but as long as I wanted to check -- knowing 21 that I was going to be asked questions today, as long as 22 I was going to call him, I -- you know, re -- you know, 23 rather than -- I guess what you would say is I 24 reconfirmed, you know, that this was sampling that they 25 had done in -- in the generic sense and not specific for 67 1 Mr. Cowey and that Table 1 was actually monitored 2 results and they were essentially two-hour -- two hours 3 extrapolated data out of time-weighted average 4 concentrations. What I knew previously, it reconfirmed 5 that, you know, it was standard NIOSH-OSHA protocol, 6 that they did it in a -- I guess the -- I got a few more 7 specifics than I had previously described. 8 Q. Like what? 9 A. Well, it described that they had a closed-in 10 like -- I guess mini room with sheeting -- he mentioned 11 that there is actually videotape on that. I have not 12 seen those. And described how they used two different 13 concentrations. 14 I asked him why -- why the concen -- the 15 level -- why they used so much Liquid Wrench because, 16 from my own personal experience, you don't need that 17 much. 18 But, you know, basically just reconfirmed what 19 I -- what I think -- what I -- my impressions of, of 20 what the whole exercise was; and I figured getting it 21 firsthand wouldn't hurt. 22 But I called him -- I mean, I wanted to know 23 about the -- the spiking issue. I mean, Levy 24 suggested -- not Levy -- Dr. Rose suggested that you'd 25 end up with -- with variable results, actually implying 68 1 that you would end up with lower numbers; and based on 2 what I knew about -- about the chemistry of mixtures, 3 that, if anything, the number -- the benzene -4 evaporative emissions off of the current raffinate would 5 be higher and faster than they would have been -- not 6 off the raffinate, excuse me -- the emissions -- the 7 vapor emissions of benzene would actually be potentially 8 higher when mixing it in with the current version of 9 Liquid Wrench as opposed to a raffinate mixture of 10 Liquid Wrench. 11 So, that's really what I, you know, started 12 going in to get clarification on. 13 Q. Have you seen the videotape? 14 A. No, I have not. 15 Q. Did he talk to you about that? 16 A. He described the room and said that they taped 17 it, but I have not had an opportunity to see it. I 18 don't know if I need to see it. 19 Q. You don't know? 20 A. Well, I mean, it -- it would be nice to see; 21 but it is not going to change anything in my -- in my 22 view. I mean, it's just... 23 Q. The product that Mr. Spencer tested, was it 24 the product that Mr. Cowey used back in the 1950s, '60s, 25 and '70s? 69 1 A. No, it was a -- it was a current version of 2 Liquid Wrench with the benzene content adjusted to two 3 different levels -4 Q. What was -5 A. -- or three different. It might have been 6 three different levels. 7 Q. What was the difference between the version of 8 Liquid Wrench that Mr. Spencer tested and the version of 9 Liquid Wrench that Mr. Cowey used back in the '50s, '60s 10 and '70s? 11 A. Well, first off -12 MR. KEMP: Objection, form. 13 A. -- first off, it's unclear from any of the 14 testimony of Mr. Cowey which version of Liquid Wrench he 15 used; but presuming that some -- you know, if we accept 16 that in some time period he may have used a raffinate 17 version, it would have been a -- a version that 18 contained an unknown quantity of benzene in a mix with 19 a -- with a waste oil or some -- a drip oil of some ilk 20 in this raffinate mix. Its composition would have been 21 different from what is currently used today because, 22 after 1978, benzene was no longer a component of the 23 material. 24 So, Mr. Spencer spiked the -- what is probably 25 a lighter molecular weight material -- total molecular 70 1 weight material than the earlier raffinate containing 2 Liquid Wrench and then simulated, with no air flow, some 3 exposure scenarios, directly measuring some and 4 calculating using near -- Near Field model, calculating 5 some others. 6 Q. All -- my question simply is: Can you tell us 7 the -- the make-up difference, the component -- the raw 8 ingredient difference between the Liquid Wrench version 9 that Mr. Spencer tested, which you've called the current 10 Liquid Wrench version, and the Liquid Wrench version 11 that Mr. Cowey used back in the '50s, '60s, and '70s? 12 MR. KEMP: Objection, form. 13 A. I -- I am not sure if I have a -- a material 14 specification for exactly what John Spencer used, but I 15 do have material specifications provided as part of 16 disclosure on raffinate-containing and 17 nonraffinate-containing mixtures. So, I think I can, 18 although it's not my area of expertise to start playing 19 that exercise. 20 Q. (BY MR. LUBEL) In other words, was cat -- was 21 kerosene in either version? 22 A. I don't recall. 23 Q. Does the mixture of the Liquid Wrench 24 version -- in other words, what's in it -- does it have 25 any effect on how much a person's benzene exposure is 71 1 going to be? 2 A. Yeah. I mean, benzene in a higher 3 molecular -- higher molecular weight set of materials 4 would have a different -- would evaporate differently 5 than benzene in a lighter molecular weight set of 6 materials. But, as I say, the -- the -- I mean, that's 7 my knowledge base of the exercise; and that's why when 8 Dr. Rose suggested -- and I think I knew -- well, I'm 9 pretty sure that I knew that the current version would 10 have been a lighter version. 11 So, it struck me that, if anything, what Dr. 12 Spencer did was likely to result in a conservatively 13 high number, not a number that would -- in other words, 14 if it -- it would not only probably be as accurate as 15 using, if you could ever find a sample of 7 percent or 16 -- or if -- or, if it ever existed, a 30 percent version 17 of raffinate, that what Mr. Spencer did would give you 18 numbers that would be potentially higher, but certainly 19 adequate to give you a ballpark estimate of what kind of 20 exposure you were looking at. 21 Q. Well, you said that Mr. Spencer spiked the 22 current version of Liquid Wrench, correct? 23 A. Yeah, I think that's correct. 24 Q. Is this what he told you? 25 A. Well, I think that's what his report states as 72 1 well. I didn't -- I didn't ask him again on that. 2 Q. And what were the other components of the 3 current Liquid Wrench version that Mr. Spencer spiked? 4 A. You should ask him this evening. I did not -5 Q. I am asking you what you think -- what you 6 know about that. 7 A. Well, I think it was probably -- I don't know 8 what the 19 -- well, I guess the 2000-plus component 9 mixture of Liquid Wrench is. I presume it's, you know, 10 a lighter cut. It's either a kerosene or a stoddard 11 solvent type material or a naphtha kind of cut, but it 12 would be a low aromatic -- probably lower aromatic 13 content than the raffinate was; so, I mean, that's 14 generally what I -- what I would expect it to be, based 15 on what -- what looked to be where they were heading on 16 a formulation basis. 17 Q. But as you sit here today, you're not familiar 18 with what the components were of the current version of 19 Liquid Wrench that Mr. Spencer tested, correct? 20 A. Other than the benzene content. 21 Q. That he spiked? 22 A. Yes. But you asked me... 23 Q. But take aside the benzene that he -- that he 24 added to it. Do you know any of the other components? 25 A. I have not seen any material chemistry on it; 73 1 so, I don't know. 2 THE REPORTER: I need to change paper. 3 MR. KEMP: Take a quick break, Lance? 4 MR. LUBEL: Yes, you sure can. 5 MR. KEMP: Thanks. 6 (A break was taken, 10:43 to 10:48 a.m.) 7 Q. (BY MR. LUBEL) You and I, before we took a 8 break, were talking about John Spencer and your 9 conversation with him, correct? 10 A. Right. 11 Q. And you told us that on this last Saturday, 12 you talked to him about two particular issues: one, 13 Dr. Rose's comment with regard to spiking the benzene; 14 and Number 2, the exposure reconstruction work and, in 15 particular, the tables? 16 A. Correct. 17 Q. Is there anything else that you talked to him 18 about? 19 A. Yeah. He -- he referred me to a paper that he 20 knew that I probably had to support -- to support the 21 statement that spike -- you know, that what he did 22 would -- would actually be -- yield predictable results. 23 Q. Do you have that with you? 24 A. No, I don't. 25 Q. What's the report? 74 1 A. It's the Elkins, Pagnato report. 2 Q. The 1963 study? 3 A. Uh-huh. 4 Q. Is that a yes? 5 A. Yes. I'm sorry. 6 Q. And, in fact, I take it that you have looked 7 at that study? 8 A. I don't have it here. 9 Q. In the past? 10 A. Yes. 11 Q. At some point, you have looked at it? 12 A. Yeah. 13 Q. Did you recognize from looking at the 1963 14 Elkins study that the content of benzene -15 A. I -- I did take notes. 16 Q. Okay. Great. 17 A. Up -18 Q. We will come back to that. 19 A. That's all I have. 20 Q. In looking at the Elkins study of 1963, did 21 you appreciate that the content of benzene in the 22 petroleum naphtha that they were studying was less than 23 2 percent? 24 A. You know, it's -- I don't recall that level of 25 detail. 75 1 Q. Well, tell me what Spencer told you about 2 that -- the Elkins study. 3 A. Well, he told me that the -- Vernon Rose 4 actually misread that study and -- and I probably should 5 have been taking notes, but I figured I would not be 6 expert enough to redo the calculation; but he referred 7 me to a section of that report where he says, you 8 know -- he said that, you know, if -- if you read it and 9 understood it, you would see what I did was, you know, 10 perfectly reasonable. 11 Q. Is the Elkins study applicable to Mr. Cowey's 12 case? 13 A. I think it's -- no. I think it -- it -- only 14 in the sense that -- that I believe Vernon Rose has used 15 that as a reference -- as a criticism of what 16 Mr. Spencer did. I mean, I wouldn't... 17 Q. Do you think that's the reason he used the 18 Elkins' study? 19 A. Well, that and the fact that you can get, 20 under some conditions, exposures of -- you know, 21 moderately high exposures from mixtures containing 22 benzene; but, I mean, that's not a -- a world-renown 23 secret, either. So... 24 Q. So, I take it that you don't disagree with 25 the -- the proposition that even low content benzene 76 1 mixtures, such as the naphtha that was studied in the 2 1963 Elkins study, can give off pretty high exposures in 3 the 30 part per million range? 4 A. I -- I am not -- I've not reviewed the Elkins; 5 so, I'm not going to agree with that piece of your 6 statement. What I will agree with is that 7 benzene-containing mixtures, under the right conditions 8 of use, can give you exposures above the current -9 current accepted T.L.V.s. 10 Q. And what information do you need to know with 11 your experience in industrial hygiene to determine 12 whether the mixtures itself that contained benzene, 13 under the right conditions, can get you levels in excess 14 of the permissible exposure limits? 15 A. Well, a big piece -- big piece of this is a 16 quantity issue and conditions of use. I mean, we're 17 talking -- we're talking Liquid Wrench exposures; and 18 I -- I suspect, if you're at all a handyman, which I was 19 in my first life when I was poor and had to do 20 everything myself, you know, I have used Liquid Wrench 21 on numerous occasions. I know that you don't need 22 copious quantities of the material. Use -- you know, 23 not even -- I mean, the levels of material that 24 Mr. Spencer uses are, in my judgment, much higher than 25 you would typically use; so, I considered what he is 77 1 doing sort of the worst case scenario type stuff. 2 Mr. Cowey, in his testimony, said he'd put 3 it -- he'd put it on the -- on the piece and go away. 4 And, in fact, I think he specifically said he'd go away 5 for 24 hours, which is probably unusual in my mind, you 6 know, to wait that long for it to work; and that 7 Mr. Cowey tended to use it in ventilated areas. 8 But you're still talking, you know, half 9 ounce, ounce kinds of quantities of a material that 10 contained, you know, 1 to 14 percent, depending on -- on 11 time period. You know, we don't know precisely what the 12 exposure was. 13 But even in Mr. Spencer's simulation of -- of 14 30 percent -- and I say simulation. Not that he made it 15 up. I mean, he directly applied that quantity to -- to 16 a -- to a fitting and then measured evaporative 17 emissions over a two-hour period. I mean, that -- that 18 is not what Mr. Cowey says he routinely did; but it 19 certainly gives you an estimated ballpark that confirms 20 my own belief that the exposures were -- were relatively 21 minor. 22 And remember, you know, I have done a lot of 23 studies of acute myelogenous leukemia. You need 24 dramatically high, repeated exposures to -- to initiate 25 that disease process. So, they just aren't there in 78 1 Mr. Cowey's case. 2 MR. LUBEL: Will you read back my 3 question? 4 (Requested Question read back.) 5 Q. (BY MR. LUBEL) I am not asking you about 6 Mr. Cowey's case. I am talking about generally -7 A. Okay. Generally? 8 Q. -- what you need. 9 A. Well, first I'd want to know what permissible 10 exposure limits are you talking about? Are we talking 11 about permissible exposure limit in the 1960, 1970, 1980 12 or 1990? So, that goes a long way in -- in the amount 13 of detail and historical information I would need, I 14 would -- if we have a material that has the intrinsic 15 hazard to cause a disease. So, we have benzene and we 16 have leukemia, acute myelogenous leukemia -- I generally 17 would like to know as much about the quantitative nature 18 of the exposure as I can get. 19 As an epidemiologist, I would not routinely be 20 the one to generate that information; but if there isn't 21 quantitative information specific to reconstruct it for 22 the individual, I rely on what I know from petroleum 23 refinery workers. We've studied them extensively. 24 They -- we know that benzene is in 1 to 30 percent -- 1 25 percent to 30 percent in the streams all over the 79 1 refinery; so, it's not unusual to have refinery workers 2 exposed to lows levels. I know that we have not seen 3 excesses of leukemias in refinery workers hired after 4 the 1950s when the T.L.V. went to 25. 5 So, I sort of would work through the logic of 6 how likely is this individual to be exposed to 7 concentration levels or time-weighted averages 8 substantially above 25 ppm, how long that would have 9 occurred, and when that occurred relative to when his 10 disease was diagnosed. 11 So, that's the mental process I would go 12 through. 13 Q. But how would you, with your experience in 14 industrial hygiene, look at a mixture and determine what 15 the exposures to benzene were from that mixture? 16 Generally speaking. 17 A. I wouldn't. I mean -- I mean, while I may 18 have had the academic training to do it, unless you do 19 those things regularly and with precision, you know, I 20 am not qualified to do that. So, I mean, I -- I would 21 go back to whoever has asked me to do a risk assessment 22 on an individual and say tell -- you know, "Do we have 23 a -- an estimate of his exposure that's quantifiable?" 24 Q. You would hire somebody else to do it, is what 25 you're saying? 80 1 A. Yeah. Well -- but not in all cases do you get 2 one. So -- but, you know -- yeah, I mean, I -- I'd 3 recommend that you go get one if you can. But you need 4 a certain amount of information to -- to get -- to get 5 a -- let me restart. 6 For purposes of a specific risk assessment, 7 depending on the disease, you need varying levels of 8 precision on the exposure estimate, if there was any 9 reason to believe that the exposures were high during 10 certain periods of time, that would suggest that you 11 would be approaching cumulative time-weighted averages 12 of 200 ppm, where the risk for AML goes up dramatically. 13 So, you -- I would look for more precision in 14 the estimates when there are higher exposures. If the 15 exposures are essentially trivial or diminimus, I need 16 less precision in the estimate because I can see very 17 simply that if -- if its concentration of exposures or 18 time-weighted average s are, you know, under a ppm or 19 under a few ppm, he's just not going to get a dose 20 suitable. So, I can work from an exclusionary place, 21 not -- not necessarily an inclusionary place. 22 Q. Let me ask you this: Does the content, the 23 amount of benzene, in a mixture influence or have any 24 impact on the person's exposure to it? 25 A. No, because that's intrinsic -- that's an 81 1 intrinsic property of the material. You have to look at 2 conditions of use before it starts to make any sense. 3 Q. Conditions of use affect the exposures, 4 correct? 5 A. Correct. 6 Q. But as a general proposition, the more benzene 7 in the product, does that mean more likely than not 8 there is going to be more exposure, if it's a mixture? 9 A. Only if exposure -- if the material is being 10 used in -- in a condition that results in exposure. I 11 can have 100 percent benzene sitting on my shelf for 30 12 years and come down with MDS, and that benzene did not 13 cause -- cause it -14 Q. Well -15 A. -- because I don't have exposure to it. 16 Q. -- let's put it this way -17 A. I am just trying to get you to separate -18 Q. Yeah, but -19 A. -- in my mind, a very -20 Q. -- but you're talking about causation. I'm 21 not talking about causation. 22 A. Yeah, but I'm talking very specifically about 23 intrinsic hazard of a material versus the -- what the 24 risk could be from that material. 25 Q. But I am not asking you about risk. 82 1 A. Okay. Then I misunderstood. 2 Q. I'm asking you about industrial hygiene. 3 A. The question. 4 Q. Let me ask it again. 5 If a person is working with a mixture, a 6 product that contains benzene, would you agree with the 7 general statement that the more benzene that is in the 8 product would mean that exposures would be higher, 9 assuming that the use condition -- or the conditions of 10 use, there's going to be some exposure? 11 A. Yes. I mean -- I mean, that's kind of, in one 12 sense, obvious. I mean, the -- even -- you get very 13 dramatic differences, looking at the -14 Q. I am not asking you about this case. I am 15 just asking you in general. 16 A. No, but I'm saying, obviously, I mean, if you 17 have the same amount of -- if you're exposed to the same 18 quantity of the material and conditions of use, the 19 higher the benzene content of that material is going to 20 affect the total benzene exposure. I mean -21 Q. Now, from an industrial hygiene standpoint, in 22 order to estimate what the benzene exposures are from 23 the mixture, assuming you know how much benzene is in 24 the mixture, do you also need to know what the raw 25 ingredients or components are of the rest of the 83 1 mixture, other than benzene? 2 A. We're rapidly getting to the edge of where I 3 am comfortable offering opinion on industrial hygiene 4 matters, but I will -- will go so far as to say it 5 depends on the importance of the precision of the result 6 that you're looking for. If -- if you are looking for 7 high levels of precision and you're not testing the 8 material directly, yeah, the more -- you will need more 9 information. 10 Q. Okay. So, would it be appropriate for you, as 11 an epidemiologist, assuming you didn't have any 12 quantitative data, for instance, to rely on the Elkins' 13 study if that study stands for the proposition that 14 under different use conditions a mixture that contains 15 as little as 1.6 to 2 percent benzene can result in some 16 pretty high part-per-million exposures? 17 A. You're misunderstanding, and I think now you 18 are going back to the Elkins' report. I think you are 19 misunderstanding an intrin -- a key element of -- of 20 this whole exercise, and that key element is it is 21 substantially -- the volume of material that is being 22 evaporated, it plays a big role in what the total ppm 23 content in a -- in a relative space is going to be. 24 And you're -- you're trying to oversimplify 25 the issue of the quantity of material that is -- that is 84 1 evaporating. And here we're talking half ounce, ounce 2 of materials. We're not talking an industrial exposure 3 where, you know, there's 2 gallons of -- of 3 percent 4 material spilled in a confined space. Different beasts. 5 Q. Are you -- is it your understanding that the 6 Elkins' exposure data came from confined spaces? 7 A. No. I am just giving you my -- trying to give 8 you my -- my analogy as it -- as it applies generally to 9 this case. 10 Q. But tell me how the Elkins' -11 A. I don't remember the Elkins' report. 12 Q. -- data -- okay. 13 A. We've covered that already. 14 Q. All right. 15 A. If you want to get into that, I will sit here 16 and read it and go over it; but I think it was a pretty 17 detailed industrial hygiene report. 18 Q. Can you point to me or -- what were 19 Mr. Cowey's exposures? 20 A. To -21 MR. KEMP: Objection, form. 22 A. -- what? 23 Q. (BY MR. LUBEL) To benzene. How often did he 24 use Liquid Wrench? 25 A. Oh, potentially -- well, we -- 85 1 MR. KEMP: Objection, form. 2 A. From my recollection of reading his 3 deposition, we don't have specific information on how 4 frequently he used it. Based on the fact that during 5 the period of time when Liquid Wrench contained benzene, 6 he worked on approximately eight or nine houses -- I 7 mean, most of the houses he worked on were in later 8 years -- and his description of using it to free up 9 pipes, that -- that doesn't -- I don't believe from any 10 of the testimony that he gave that he was replacing 11 every pipe in the bloody house. So, you know, if he 12 used it periodically when -- when he was doing the 13 plumbing piece of his fixing -- house fixing up, he'd 14 have intermittent, periodic exposure to whatever level 15 of benzene it contained; but he also describes that he 16 would just apply it and then leave the area and come -17 come back 24 hours later. 18 So, unless you're postulating instantaneous 19 exposure, he may -- even if it did contain benzene -20 have trivial exposure. 21 Q. (BY MR. LUBEL) How often -22 A. He would have had other exposures to a variety 23 of materials going back into those time periods for 24 which I have not seen data on, but presumptively other 25 materials, paints, or -- I don't know if he did 86 1 furniture stripping. It wasn't quite clear what all he 2 was doing in some of these houses. You would have had 3 other solvent material -- containing materials that -4 that may have had benzene levels. 5 Q. How often did Mr. Cowey use Liquid Wrench, or 6 do you know? 7 A. I -- I don't think -- my reading doesn't 8 permit me to offer a quantitative estimate. 9 Q. Do you recall there being a specific question 10 asked that detailed to Mr. Cowey? 11 A. I remember questions on how much Liquid Wrench 12 he may have used in the course of a year, and that 13 seemed -- struck me as quite a large volume; but I think 14 it was -- he did offer a volume. I don't recall how 15 frequently he said he used it on a daily -- I don't 16 know -- I don't recall anything that says daily or 17 weekly or... 18 Q. You don't remember that line of questioning -19 A. No. 20 Q. -- correct? 21 How do you recall the testimony where there is 22 an indication that he used approximately 6 gallons a 23 year? 24 MR. KEMP: Objection, form. 25 A. I recall that -- that his original statement 87 1 was like three to five, maybe six, kind of range of -2 so, I don't know exactly whether it was six or three or 3 something less than that; but that's a lot of Liquid 4 Wrench, if you've ever used Liquid Wrench. 5 Q. (BY MR. LUBEL) And it's in particular a lot 6 of Liquid Wrench over 26 years with benzene in it, is it 7 not? 8 A. Well, we don't -9 MR. RILEY: Objection, form. 10 MR. KEMP: Objection, form. 11 A. I don't recall any statement saying that "I 12 used 6 gallons a year up until '78"; so, we -- we 13 really -- we don't know two things: we don't know which 14 Liquid Wrench he used, and we don't know the -- the time 15 period you're laying out. It did not contain benzene 16 the whole time period. 17 Q. (BY MR. LUBEL) Really? 18 A. Well, which -- maybe I misheard your -- the 19 time period. 20 Q. Let me ask you this: If Mr. Cowey used 21 approximately 6 gallons of Liquid Wrench that contained 22 benzene between 1952 and 1979, would you agree that 23 that's a lot of Liquid Wrench containing benzene? 24 MR. KEMP: Objection, form. 25 A. It's -- I -- I don't know if it contained any 88 1 benzene -2 Q. (BY MR. LUBEL) I am saying assuming. 3 A. -- what he bought. 4 Q. I said assuming. 5 MR. KEMP: Same objection. 6 A. I have already said it's a lot of Liquid 7 Wrench to use annually; so, I mean -- I don't know. I 8 mean what -- what... 9 Q. (BY MR. LUBEL) That's a lot of -10 A. We all -- but we already know that he -- that 11 he also used -- states he uses it when -- wherever 12 possible, in well-ventilated areas. He used a fan. And 13 he put it on and would leave the area. So, I don't know 14 if it's a lot of benzene exposure. It's a lot of Liquid 15 Wrench. That's all I can tell you. 16 Q. You don't have enough information to assess 17 his benzene exposure, do you? 18 A. Quantitatively? 19 Q. Correct. 20 A. No. 21 Q. Have you seen Dr. Samimi's report? 22 A. Yes. 23 Q. Okay. When were you furnished that? 24 A. I read it briefly yesterday. 25 Q. And did you talk to Dr. Spencer about 89 1 Dr. Samimi's conclusions? 2 A. No, I didn't. 3 Q. Do you have any criticisms of his report? 4 A. Dr. Samimi's? 5 Q. Yes. 6 A. It's ridiculous. I mean, it's... 7 Q. What are the criticisms? 8 A. Well, I -- I didn't go over it -- I didn't go 9 over any of the calculations, per se; but it is 10 ridiculous to presume that -- one of the scenarios is 4 11 ounces per application. And then the next scenario is 12 using it twice a day, eight -- five days a week, 50 13 weeks a year. I did do a quick calculation that that's 14 roughly 14 gallons of the material a year. 15 I -- I don't think refineries use that much 16 material. It just -- it is just so improbable and so 17 out of -- inconsistent with both the -- the testimony of 18 Cowey. It doesn't even give me a -- an intelligent 19 ballpark. I just found the whole thing sort of silly. 20 And that's -- I stopped reading it, and I threw it back 21 across the table. 22 Q. Well, how much is -- is a teacup? 23 A. Well, it depends what kind of teacup you have; 24 but I will tell you the teacups that -- that my mother 25 used to have were, I believe, 6 ounces. 90 1 Q. So, a half a teacup would be approximately 3 2 ounces? 3 A. Yes. But I don't know of people who go around 4 putting Liquid Wrench in teacups and then applying it to 5 pipes; so, the -- the speculation, what was that, from 6 Mrs. Cowey, that -- that he used teacup -- half a teacup 7 quantities, you can't -- you can't use that as a basis 8 to try and quantitatively estimate how many ounces would 9 be used. It would be way more logical to -- to look 10 realistically at the -- at the material. I mean, I've 11 done cast iron pipes. I've done nuts and bolts with it. 12 You -- you apply, you know, enough material to, you 13 know, saturate the joint that you're trying to loosen; 14 and -15 Q. How much is it? 16 A. I -- well, in my personal experience, it's 17 probably somewhere between a few drops and a -- and a 18 half ounce, because I know my can -- my 8-ounce can, or 19 whatever can size it is, lasts for years. Now, I grant 20 you, I'm not, you know, doing -- running bolts every 21 time; but it's not a material you need copious 22 quantities of. It would drip right off and make quite a 23 mess. 24 It's just -- it's just -- and -- and 25 nowhere -- I mean, using it twice a day, he had the 91 1 individual exposed, I think, for an entire hour period 2 in his calculation, maybe longer, or maybe -- no, I 3 recall, the 70 percent of the total volume -- sufficient 4 to evaporate; so, there was no actual time calculation 5 in there. 6 It just -- in my judgment, it was just too 7 artificial to be of any utility for -- for anything. 8 Q. Have you covered all of the criticisms 9 regarding Dr. Samimi's report? 10 A. Well, I said I have not attempted -- it's not 11 an easy report to read, and I think I spent 15 minutes 12 on it. So, I did not attempt to actually check to see 13 whether his calculations are correct or other elements 14 of his estimates made any sense. 15 Q. Would you agree that if Dr. Samimi -- any of 16 the scenarios that he gave are reliable exposure levels 17 for Mr. Cowey, that, in fact, he would have had enough 18 exposure to benzene over a 26-year period to develop 19 MDS? If his information is accurate. 20 A. I didn't actually follow it all the way 21 through. It just struck me as so ludicrous on the 22 volumes and the frequency that I didn't -- I don't even 23 remember what -- what final numbers he came up with. 24 They were all STELs; so, there was no -- I believe they 25 were STELs. So, it's -- one would need to reconvert 92 1 them back to time-weighted averages for me to understand 2 it better. 3 I mean, yes, I saw some numbers that would 4 have been over the -- today's STEL, but a number of the 5 numbers would have been under the time-weighted averages 6 of the '60s -- of 1950 and -- well, certainly 1950 and 7 1940s, the numbers would have been acceptable T.L.V.s. 8 So, I didn't attempt to go through the report at that 9 level of detail. I leave that to others. 10 Q. What is the safe level of benzene exposure? 11 A. Safe is a political statement. A scientific 12 statement is that there is no evidence of increased risk 13 of disease until you accumulate 200 parts per million 14 person years, and typically the concentrations would 15 have to be over -- at least some of the concentrations 16 would have to be over 50 ppm concentration levels. So, 17 it's not just purely person years. 18 Q. So, if a person is exposed to less than 19 200-part-per-million years of benzene, they're at no 20 risk of developing a benzene-related disorder or 21 disease, correct? 22 A. They would be at no measurable risk. 23 Q. What do you mean by measurable? 24 A. Well, only that there is no evidence to say 25 that they're at increased risk. I mean -- 93 1 Q. So, they would be safe? 2 A. Yeah. It would be safer if they were exposed 3 to substantially less than that, as well. I mean, 4 any -- any number -- substantial -- you know, that's the 5 level where we've got evidence that it's bad. So, you 6 pick a safe level below that. 7 Q. So, I take it that you disagree with the 8 statement that the American Petroleum Institute made in 9 1948 that there is absolutely no safe level of benzene 10 exposure? 11 A. But that's a generic toxicity statement. I 12 mean, no exposure to a toxic material cannot -- is the 13 safest level you can achieve. I mean, at -- it's a 14 semantic statement. It's not a -- a statement of -- of 15 reality. Zero will be the safest exposure on any toxic 16 material. 17 Q. Do you know what the A.C.G.I.H., the American 18 Conference of Governmental Industrial Hygienists, 19 recommended exposure level is to benzene right now? 20 A. Yeah. I believe it's .5 -- .5 MTLV. 21 Q. A half of a part per million? 22 A. Uh-huh. 23 Q. Over a working career? 24 A. Well, they presume a 40-year working career. 25 Q. That would be about 20-part-per-million years, 94 1 correct? Forty years at 25 -2 A. Right. 3 Q. -- would be 20-part-per-million years, true? 4 A. Correct. 5 Q. That's a lot less than 200-part-per-million 6 years? 7 A. That's correct. 8 Q. So, I take it that you disagree with the 9 American Conference of Governmental Industrial 10 Hygienists that exposure levels in excess of 20 part per 11 million years are unacceptable? 12 MR. KEMP: Objection, form. 13 A. No. They -- they have chosen a wide margin of 14 safety in their calculation. I mean, you're -- and 15 you're talking something that they came up with in '92 16 or so. Up until that point it was 10 for many years. 17 Actually, maybe -- it may have gone down to 1 before 18 they went there. 19 But, as I say, setting of safe limits -- and I 20 don't want to use political -- I mean social -- social 21 politics is a -- is an -- is a different proposition 22 than estimating where -- what -- what the risk levels 23 are for demonstrable disease. So, I have no problem 24 with the level. I did comment to them in that process 25 that it was unnecessarily low. 95 1 Q. (BY MR. LUBEL) Do you have with you the 2 studies that -- that show us that people that are 3 exposed to -- or that conclude, actually -- do you have 4 studies with you that conclude that workers exposed to 5 less than 200-part-per-million years are safe from 6 benzene? 7 A. Yeah, we have lots of -- I mean, the way you 8 have just stated it, it would be any study that didn't 9 show an excess of leukemia; and there -- are you 10 interested in reports that demonstrate the 200 ppm as 11 the point of departure where the risk goes up? 12 Q. I am interested in a study -13 A. Or are you interested in studies that show 14 that there is no risk in workers exposed to levels below 15 that? 16 Q. I am interested in a study that concludes that 17 workers exposed to less than 200-part-per-million of 18 benzene are safe. Can you find that study or those 19 studies that conclude that specifically? 20 A. Well, you don't write studies that way; but if 21 you look at the petroleum refinery workers studies that 22 are summarized in one of the papers that I have attached 23 there, that demonstrates that since 1950 -- do you want 24 me to -25 Q. If you can just pull the studies -- 96 1 A. Okay. 2 Q. -- because I am going to ask you to find the 3 conclusion that says this. 4 A. Well, the conclusions don't -- you don't write 5 conclusions that way. 6 Q. Well, get me the closest conclusion that says 7 it. 8 A. I mean, what the study will say is that there 9 was some evidence of increased risk in workers hired 10 before 1950. There isn't in workers hired after 1950. 11 Here's the array of acute myelogenous leukemia across 12 all the studies. There will be discussion of what the 13 exposure -- the published exposure numbers that have 14 been described in various literature for benzene in 15 petroleum refinery workers, and there will be a 16 conclusion that there does not appear to be a risk at 17 these levels. That's it. You don't work off of a 18 threshold. 19 Q. Can you find the study that you believe is 20 closest to stating the conclusion that workers at 21 exposure levels to benzene below 200 parts per million 22 are safe, or are not at risk of getting disease? 23 A. It appeared -- there are two references in the 24 pile that you've got here. One is the -- the -- one is 25 the -- is the short letter by Dr. Wong, 19 -- 1998, in 97 1 the Journal of National Cancer Institute. The other is 2 the discussion of acute myelogenous leukemia in the 3 paper -- and there are a couple of versions of the 4 published paper. The ones -- the one that is included 5 here is a paper by Raabe and Wong entitled "Leukemia 6 Mortality by Cell Type in Petroleum Workers with 7 Potential Exposure to Benzene." 8 Q. That's by who? 9 A. Raabe and Wong. Me, myself, and Dr. Wong. 10 Q. Okay. Now, let's go -- let's first talk about 11 your study. 12 A. Okay. 13 Q. Can you find for me the conclusion -- or the 14 closest thing you can find to a conclusion that people 15 that are exposed to less than 200-part-per-million are 16 not at risk of some type of benzene-related disorder? 17 A. Yeah, it's -- under the word, "Conclusion," 18 there is a paragraph that resummarizes what I just said 19 to you before. And if you go into the "Result" section 20 and the "Discussion," section you will see more 21 background on -- on that. 22 Q. Can you just -- will you highlight for us 23 the -- the sentence that says it? 24 A. It's not a sentence. It's a paragraph. 25 Q. Can you highlight the paragraph? Or circle 98 1 the paragraph. 2 A. I mean, you're asking me for a conclusionary 3 statement. That's the closest to -- to that. There is 4 more discussion on -- about benzene exposures under the 5 section called "acute myelogenous leukemia," which goes 6 on for several pages. 7 Q. How do you deal with the -- the Australian 8 Petroleum Institute study that ExxonMobil sponsored that 9 says that lower levels than what you're suggesting 10 causing benzene-related disorders can, in fact, cause 11 benzene disease? 12 A. Well, you're talking about the Health Watch 13 studies, most -- the first -- the first partial of that 14 was published just this year. There is a whole -15 excuse me. Are we -- are we done with this? 16 Q. Right now I'm talking about the A.P.I. 17 A. Okay. 18 Q. I mean, not the A -- the Australian Petroleum 19 Institute? 20 A. The Australian? 21 That study has just come out. The unpublished 22 version of the report clearly demonstrates that however 23 they reconstructed the exposures, they came out with 24 exposures substantially lower than either the U.K. 25 study, the Canadian study, or any of the studies that 99 1 we've seen so far. 2 That suggests to me there's something wrong 3 because it's hard for me to believe that the Australian 4 Petroleum Institute was so different from the rest 5 during that period. So, while they may -- you do 6 understand enough statistics that a dose-response curve 7 can slide anywhere on an axis. If I multiply all 8 exposures by 10, I'll get the exact same shape of the 9 curve. I have just moved the -- where -- where it falls 10 in the various levels on a -- on the risk exposure 11 profile. 12 So, I think they've got it wrong. It's -- and 13 it only speaks to AML. I mean, they found no 14 relationship to multiple myeloma and non-Hodgkin's 15 lymphoma; so, it suggests to me that they may have the 16 right shape, they just have the dosimetry wrong. 17 Q. Well, they did say there was a statistically 18 significant excess of CLLs. You read the same study I 19 did. 20 A. Well, I'm not sure if it's still significant 21 in the published study. 22 Q. What happened from the unpublished to the 23 published study? 24 A. Well, the numbers are different from the 25 unpublished to the published, which is one of the things 100 1 that is going to have to get resolved in the scientific 2 community over the next couple months or years. 3 Q. Well, why would the -4 A. The numbers are different. 5 Q. Why would it be different? 6 MR. KEMP: Objection, form. 7 A. I'd just -- I'd be speculating. I can tell 8 you what happens in studies that could account for that, 9 but I wouldn't know why they're different. The numbers 10 are different, though, between the published and the 11 unpublished. And not all the tables. Some of the 12 tables. 13 Q. (BY MR. LUBEL) Have you talked to anybody 14 from ExxonMobil about the study? 15 A. I spoke with Rob Schnatter when the 16 unpublished version came out. 17 Q. What did you say to him? 18 A. That this thing is a bear to read, and it 19 looks like they got -- you know, why -- I mean, they 20 were just a sponsor; so, I mean, they're sort of stuck 21 with the same report that I am. They had difficulty 22 understanding what's going on because a lot of the 23 analyses you would like to see at cell type levels are 24 not done at cell type levels. So, as you move through 25 the unpublished version of the report, there's some 101 1 interesting stuff in one analysis, but they never do 2 that analysis again when they're looking at other parts. 3 Are you familiar with -- this is a 300-and-something 4 page report with lots and lots of tables. 5 Q. So, they just missed it -6 A. Well, I don't know what -- I mean, I -- I 7 think there is reason to believe that there are errors 8 in -- errors in either the exposure assessment or the 9 way they calculated the dose response. 10 We already know from reading the unpublished 11 one that the tumor registry from which they're 12 generating their expecteds did not identify all the 13 cases in their own cohort. So, you do have a potential 14 problem where they used best evidence to get the cases; 15 and -- and in the actual cohort piece of the study, the 16 expecteds are coming from a somewhat different set. 17 So, there are a number of technical 18 methodologic problems. The study's just recently out. 19 Clearly has a different exposure profile for the 20 industry than we have seen elsewhere. So, I -- you 21 know, I think it's too early to tell whether it's -- you 22 know, has any utility or not. I mean, I talk about it 23 in my report briefly. 24 Q. And the -- the conclusion reached by Hayes and 25 Yin and others in the 2000 Chinese study article, if you 102 1 will, that talks about excess risk of MDS at exposure 2 levels below 10 parts per million, you disagree with 3 that, too, correct? 4 A. I don't know if it's right or wrong. I am 5 telling -- I am telling you that the -- the analyses of 6 the -- of that series of cohort studies that come out of 7 it are presumed to have what are potentially fatal flaws 8 in exposure reconstruction, and that's -- I mean, I am 9 not going to try and adopt a -- a result that even 10 E.P.A. says can't be used. 11 Q. All right. The second article that you 12 referenced as evidence that exposure levels to benzene 13 in excess of 200 parts per million were necessary to 14 cause benzene-related disorders was another Wong 15 article, correct? 16 A. Yeah. 17 Q. Is it Exhibit -- in Exhibit Number 1? 18 A. Yeah. 19 Q. Is it the first article? 20 A. No. Well, I don't think he discusses that. 21 No, it's -- it is this one. 22 Q. Can you highlight the section -23 A. Sure. 24 Q. -- or circle it? 25 A. (Witness complies.) Well, this -- this -- 103 1 there's -- there is another paper that I thought I also 2 included in here, but I didn't. This -- this one you 3 would have to pretty much read the -- I mean, it's only 4 two typed columns. You would have to read the whole 5 shebang to get the -- the essence of what I have -- what 6 we were just discussing out of it because it tends to 7 focus more on -- it just briefly focuses on leukemia. 8 There is one additional paper that I didn't 9 cite here -- that is not cited, but it's also published 10 by Wong, and I think it's probably 1996; but it's not in 11 the -- the material is rereviewed in a number of 12 different papers, but the -- the first paper in that 13 series is not -- the first Wong paper in that series is 14 not here. 15 Q. What other authors, in addition to Wong, of 16 which you have articles, have reached this conclusion in 17 the published paper? 18 Let me restate. Do you have an article here 19 before you, or one that's referenced in your affidavit, 20 that states or concludes the same thing that we have 21 been talking about but was authored by somebody other 22 than Wong or yourself? 23 A. There's a paper by Kenny Crump that does an 24 analysis specifically looking at AMLs and nonAML 25 leukemias. 104 1 Q. Do you have that with you? 2 A. No, I don't. But -- but Kenny Crump used 3 different cut points. His interest was more a 4 regulatory modeling interest; so, his cut points were 45 5 ppm years versus -- I don't know what the next higher 6 category was. But you get -- it's the same -- exact 7 same data set; it's just cut differently. And you get 8 the same interpretations with just cut points that don't 9 quite come up to the 200. I mean, what -- what Otto and 10 I have done in various papers is essentially go back it 11 up. 12 The other paper that you would want to look 13 at, if you're interested in that subject, is a paper by 14 Robert Schnatter -- not Robert -- Rob is -- that first 15 name is Rob, R O B, Schnatter did using the -- the 16 same -17 Q. Is it Schnatter or Schattner? 18 A. Schnatter. 19 Schnatter took a different approach than Otto 20 and I. He actually -- because our paper was already 21 out, he's of the opinion that concentration is perhaps a 22 more -- a more important metric than the actual 23 cumulative exposure. 24 Q. What do you mean by that? 25 A. It's not -- and I don't disagree -- disagree 105 1 with him. 2 There are two ways to look at exposure 3 metrics, or dose: dose rate -- in other words, how 4 much -- they both have elements of time, but one is how 5 much dose -- how much exposure is actually delivered in 6 the period of time, as opposed to cumulative dose, which 7 is how much exposure is accrued over time. 8 Q. Is he the fellow that thinks that the STELs, 9 the short-term exposure limits, are more important than 10 the long-term exposures? 11 A. Well, there are -- no. That's a different set 12 of folks. Rob -- Rob is an epidemiologist. Rob -- what 13 he thinks about the STELs, I have never discussed it 14 with him. 15 But Rob -- Rob's analysis suggests that -16 which is not inconsistent with -- with everything 17 else -- that you really need exposures substantially 18 above 25, probably over 60, ppm concentration over some 19 period of time. 20 Q. What period of time? 21 A. He shows in excess at 60, AML, excess at 60 22 for six years. I think I am quoting it correctly. 23 Q. Sixty over what duration? 24 A. Six years. 25 Q. Every day? 106 1 A. Yeah. Well, time-weighted averages, the -- he 2 did several analyses with different exposure metrics. 3 One analysis says they have to be over 25 -- 20, 25 for 4 six years; the other says 60 for six years, which is not 5 inconsistent with what -- with what I have in my report. 6 Once -- once the T.L.V.s went down below 50 -7 in other words, once we went down 25 ppm time-weighted 8 averages -- we no longer saw AML excesses in any of 9 these populations. I mean, that's an indirect way of 10 saying the same thing. 11 What -- what -- what Rob was doing in his 12 analysis was looking at -- he cut the concentration -13 remember from the Pliofilm cohort, we have T -- we have 14 time-weighted averages annually for these workers. So, 15 he'd look at all the workers who never had time-weighted 16 averages above X, and then another cut above X plus 10; 17 so, in essence, you end up with a dose-response curve 18 that is really focusing only on concentration. And you 19 don't see any increased risk for AML until you get a 20 long-term exposure at concentrations above 60, which was 21 the average metric. 22 Q. So what he found was if you have high enough 23 exposure levels, which you say is above 60 parts per 24 million -25 A. Well, I didn't say. I mean, it's -- 107 1 Q. You said that's what the study says? 2 A. Right. 3 Q. -- for six years, then you can have an excess 4 risk of leukemia? 5 A. Right. 6 Q. You disagree with that? 7 A. But that gives you -- you know, in the same -8 you're in the same person years -- you're in relatively 9 high person year levels at that point; so... 10 Q. I am just asking you if you disagree with his 11 conclusions. 12 A. No, I don't disagree with it. It's just a 13 different way of looking at it. I mean, what it all 14 says is that we go back to the underlying biology. You 15 need a certain threshold of dose that is going to 16 initiate toxicity in the bone marrow that's going to -17 and you need to sustain that over some period of time 18 before you're going to increase the risk of -- of AML. 19 And that's, in essence, why the T.L.V. is dropped -- I 20 mean -- and why they left it at 25 for such a long time, 21 because they were trying to reduce toxicity; and once 22 you reduce toxicity to very low levels, the AML risk 23 goes away. 24 Q. And does that risk vary depending on 25 individual susceptibility? 108 1 A. Oh, sure. I mean, individual susceptibility, 2 which is something we can't measure, is -- is -- I mean, 3 otherwise everybody exposed, you know, would be -- would 4 come down with the disease. 5 Q. In other words, not everybody that smokes a 6 pack of cigarettes a day for 30 years gets lung cancer, 7 correct? 8 A. Correct. 9 Q. There is variation, not only in groups but in 10 individuals, correct? 11 A. Yes. But we just -- I mean, we don't -- I 12 mean, that's why we're doing more and more molecular 13 biology and molecular epidemiology where you're not only 14 spitting -- splitting people by their external exposures 15 but you're -- you're looking at whether there is 16 different dose-response curves in people with different 17 genetic phenotypes. 18 Q. Right. 19 Now we're getting ready to take a lunch break 20 we agreed to, but I want to ask you just a few questions 21 on the area before we take a break. And that is, you 22 made reference to Mr. Cowey being exposed to other 23 products other than Liquid Wrench. Do you recall that? 24 A. Yes. He states that he used a variety of 25 different -- 109 1 Q. Paints, thinners, et cetera? 2 A. Yeah. 3 Q. Are you of the opinion that any of those 4 products or any components in those products have caused 5 or contributed -- contributed to cause his MDS? 6 A. I don't have enough compositional information 7 to -- to render -- to draw an opinion on that. I -- I 8 am just stating that he had a number of other materials 9 that if we had more information about -- I mean, unlike 10 Liquid Wrench, there is not even a large discussion 11 of -- about those other materials. The detailed 12 discussion seems to be a little confined to Liquid 13 Wrench. So, I just say that -- state that in the time 14 periods that he was at those exposures, some of those 15 materials would have contained some levels of benzene. 16 Q. But as you sit here today, are you of the 17 opinion that any of those other products contributed to 18 cause his MDS, given the information you have? 19 A. His chromosomal analysis is not of a pattern 20 that's -- that is consistent with a benzene or secondary 21 exposure MDS. I mean, he does have a trisomy 8, but he 22 doesn't have the 8 that is -- is very frequently 23 associated, and that's 5, 7 deletion. 24 Q. But as you sit here today, yes or no, did the 25 other products that he used over his career cause or 110 1 contribute to cause his MDS? 2 MR. KEMP: Objection, form. 3 A. I don't know. 4 Q. (BY MR. LUBEL) But do you have an opinion 5 that it did? 6 MR. KEMP: Objection to form. 7 A. My opinion is I don't know. 8 Q. (BY MR. LUBEL) What information do you need? 9 A. That means I have no opinion. 10 Q. Okay. What information do you need? 11 A. Com -- at least some composition -- well, I'll 12 give you an illustration. Can we do that? If -- if 13 we're talking about the paints, if we had compositional 14 information on those paints, the -- the nature of use of 15 painting an interior room and the time it takes to do 16 that would have afforded him a much greater opportunity 17 for an exposure to benzene if benzene was in those 18 paints. I have no knowledge that benzene was in those 19 paints; so, I can't offer an opinion whether paint 20 contributed to his -- to anything. 21 Q. But you do know that benzene was a component 22 of paints before the 1980s, correct? 23 A. I mean, I've seen the statements. I have not 24 seen any analytic quantification as to what kinds of 25 paints contained what levels of benzene. 111 1 Q. You can't say that the other products caused 2 his disease, correct? 3 A. I don't have enough information to make that 4 statement. 5 Q. Have you asked the lawyers that hired you to 6 go assemble that information? 7 A. I asked the lawyers if they had more 8 information on where -- were there -- was there another 9 deposition that dealt with specifics on some of the 10 other materials that he used at the same level of detail 11 and did we know anything about -- with any level of 12 detail the paints that he used, and the answer I 13 received is no, they did not. So, I don't know if they 14 looked, didn't look; but my question is was there more 15 detail, and the answer was no. 16 Q. Based upon scientific probabilities, you can't 17 relate any of the other products that Mr. Cowey used to 18 his disease, correct, with the information you have? 19 A. No. I can just list them as potential sources 20 of exposures that could be related to MDS generally, and 21 I don't think they may have had the role with his MDS 22 specifically because I think his karyotype is not the 23 typical profile of a secondary MDS. 24 Q. And if I hear you correctly, what you're 25 saying is that if you had a list of the products that he 112 1 used, including paints, as your example, and you knew 2 the components of those products, then you would be in a 3 better position to render an opinion as to whether any 4 of those other products may have contributed to cause 5 his disease. 6 MR. RILEY: Objection, form. 7 Q. (BY MR. LUBEL) Is that true? 8 A. That's true, Part A, yes. 9 Q. What's part B? 10 A. Part B is I would like to have had -- had the 11 same types of questioning as to how frequently he used 12 them, where he used them, and -- and what time periods. 13 Q. And other than that, what else, if anything, 14 would you need? 15 A. Well, I mean, if we had that kind of 16 information, then I -- then I would have gone back and 17 said, you know, "It strikes me that a significant -18 that this man was getting a significant benzene exposure 19 from painting, and is there any way that someone could, 20 you know, give me some ballpark quantitative estimates?" 21 That would have been my next question. But -22 Q. And then from there you would render an 23 opinion? 24 A. Well, I probably could have rendered -- I 25 mean, it depends on how much benzene was in the paints 113 1 and what I knew about its application. I probably could 2 have rendered an opinion without the quantitative 3 material, certainly a differential opinion. 4 Q. What do you mean by that? I've got to stop 5 you there. What do you mean a differential opinion? 6 A. Well, for example, even if we could confirm 7 that he actually used a benzene-containing Liquid 8 Wrench, okay, I -- I'd be able to say that the painting 9 was so dramatically -- I am making this all up. We are 10 all understanding that, right? 11 Differential opinion could be that the nature 12 of the exposure from this source is so dramatic that, 13 you know, the fact that he occasionally smoked and that 14 he occasionally used Liquid Wrench and that he 15 occasionally went to self-service gas stations, none of 16 those contributed materially to his -- to any benzene 17 exposure risk because it was swamped by this class of 18 exposure. That's what I mean, a differential. 19 MR. LUBEL: Okay. Let's take our lunch 20 break, and then we will come back. 21 (Lunch recess, 11:45 a.m. to 12:42 p.m.) 22 (Exhibit 3 marked.) 23 Q. (BY MR. LUBEL) What is Exhibit Number 3 that 24 I have marked? 25 A. Exhibit Number 3 are the materials that I 114 1 received, less two depositions from Fulbright & Jaworski 2 concerning Mr. Cowey. 3 Q. And do Exhibits Number 1, 2, and 3 constitute 4 your file materials in this case? 5 A. Materials that I used in direct preparation 6 for this. I have more -- more on myelofibrosis and a 7 lot more on benzene and AML. 8 Q. But as far as materials that you used 9 specifically for this case, does it constitute those 10 materials? 11 A. Yes. 12 Q. Can you pull out the study that you brought 13 with you that stands for the proposition that to have a 14 ben -- benzene-induced disease, you need the chromosome 15 defects 5 and 7? 16 A. I may not have brought all the -- cited 17 directly all the cytogenetic articles, but I think 18 that's discussed in at least one of these. Well, 19 actually, you just overstated what I stated earlier. 20 What I stated was secondary MDSs most frequently have, 21 as the key representation, a 5, 7, plus other issues. 22 Q. Well, can a person that has a benzene -23 benzene-induced MDS not have chromosome defects of 5 and 24 7? 25 A. I don't know. I am not an expert in that 115 1 area. I am just recounting you my recollection of the 2 literature. I wasn't asked to specifically opine in 3 that area. 4 Well, some of that is discussed in Ciccone. I 5 think it's discussed in Rodella, "Cytogenetics and 6 Occupational Exposures in Acute Nonlymphocytic Leukemia 7 and Myelodysplastic Syndrome." 8 Q. Can you just -- as you're going through them, 9 if you can just highlight those pages and the sections 10 that deal with that. 11 A. All right. That will take a little longer. 12 The second paper is Rodella, 1993; and -- the 13 whole Rodella paper is, frankly, related to that subject 14 matter; but there is a specific table that speaks to the 15 chromosomal aberrations that perhaps summarizes some of 16 it, and that's in Table 2 of Rodella. 17 Q. Are there any of these studies that stand for 18 the proposition that chromosome defects 5 and 7 need to 19 be present in a person for their MDS disease to be 20 related to benzene exposures? 21 A. I've not reviewed the literature from that 22 perspective exclusively. There have been several 23 studies specific to AML looking at long -- large numbers 24 of cases -- I didn't bring those papers. I am not even 25 sure if I have them all -- and they speak to the issue 116 1 more that -- that it is a frequent, very high percentage 2 marker in cases that are either treatment therapeutic or 3 benzene-related; and that's sort of where the 4 proposition comes from. 5 I think the two I mentioned are the only two 6 that I -- that I have with me here that specifically 7 speak to the frequencies of cytogenic abnormality. 8 Q. Right. Do you mind handing me those? 9 A. Yeah. 10 Q. Oh, I just wanted to focus in on those two 11 studies. 12 A. Well, as I say, it's not the complete 13 literature by any regard, because I wasn't specifically 14 rendering an opinion in that area. 15 I am pulling these out from my set -- from 16 your set. 17 Q. Yes, sir. 18 So, the three studies that you've pulled are 19 "The Myelodysplastic Syndromes" by David P. Steensma, et 20 al? 21 A. Uh-huh. 22 Q. Is that true? 23 A. Yeah. 24 Q. And myelo -- "Myeloid Leukemias and 25 Myelodysplastic Syndromes" by -- how do you pronounce 117 1 the first name? Ciccone? 2 A. Well, that's how I pronounce it. 3 Q. Okay. And then the third study is by Rodella, 4 and it's "Cytogenetics and Occupational Exposures in 5 Acute Nonlymphocytic Leukemia and MDS" -6 A. Right. 7 Q. -- correct? 8 And have you highlighted for us those sections 9 that deal with the chromosome abnormalities? 10 A. Yeah. As I say, this is not the best 11 literature set for -- for those statements; but, yes, I 12 did. 13 Q. Okay. 14 A. At least -- I probably didn't in Steensma. I 15 did not highlight anything in Steensma. I mean -16 Q. All right. 17 A. -- those are sections I found. There may be 18 other sections in those papers. 19 Q. We are going to mark those three studies -20 A. Can I mark them on your papers? 21 Q. Well, I have got mine as a whole group. I 22 will make sure that the court reporter, or Jeff, copies 23 them and gives them back to you before you take off. Is 24 that fair? 25 A. Yeah. I -- just annoying because I made a 118 1 whole set for you just to prevent this from taking 2 place. 3 Q. Well, I've had you highlight the set you 4 brought with you. 5 A. Well, on three papers. I can do that in two 6 seconds on those. 7 Q. Would you prefer to do that? 8 A. Yes. 9 Q. Okay. No problem. 10 A. They don't come back as fast -11 Q. No, I know. 12 A. You imply they do. 13 Q. Of course, we've got the world's greatest 14 court reporter here today. That's the only thing 15 Dillard and I agree on. 16 A. Now I'm getting confused. All right. We will 17 go along with your exercise, only because I don't see 18 one of them in here. So, we will mark these three as -19 separately, and please return them as expeditiously as 20 possible. 21 Q. Yes, sir. 22 MR. LUBEL: So, we have marked these as 23 Exhibit Number 4; and I am going to go ahead and put a 24 clip on them. 25 (Exhibit 4 marked.) 119 1 Q. (BY MR. LUBEL) And Exhibit Number 4 are the 2 three studies that you have currently in your possession 3 at this deposition that address the chromosome defect 4 issue; and you have highlighted the most significant 5 areas, correct? 6 A. Yes. I think -- I think they were the most 7 significant areas. 8 Q. The presentation/PowerPoint that we talked 9 about earlier that you did to fundraise -10 A. Uh-huh. 11 Q. -- how long will it take you to find that? 12 A. Probably by -- by the weekend, end of the 13 week. 14 Q. In your materials -15 A. And there were two other items that you 16 requested as well, the two E.P.A. documents -17 Q. Correct. 18 A. -- but I will send those to Mr. Kemp. 19 Q. Great. 20 Now, will you do your best to locate the John 21 Spencer report that you have in your file materials? 22 A. I have got it here. 23 Q. You have got it in front of you? 24 A. Right. Well, you pulled it out. 25 Q. Great. 120 1 A. Do you want to mark it? This was sent to me 2 from e-mail; so, I know I have a copy. 3 Q. I'll go ahead and mark it as Exhibit Number 5. 4 Is that okay? 5 A. Fine. 6 (Exhibit 5 marked.) 7 Q. (BY MR. LUBEL) Where in his report are the -8 the monitoring results he did from the spiked, new 9 version of Liquid Wrench? 10 A. The actual results that were measured are in 11 Table 1; and from table -- from the underlying data, 12 there are near-field models of different ventilation 13 rates in Tables 2 and 3. This is monitored results. 14 This is model extrapolation. 15 Q. Now, during the monitoring test that was done, 16 what was the worker doing? 17 A. As I understand it, I don't remember 18 specifically what piece of equipment they -- they had, 19 but they had a piece of equipment sitting on a -- on 20 a -- on a counter that he applied different quantities 21 of Liquid Wrench to; and they -- he had standard monitor 22 near his breathing zone, and they took 15-minute and 23 2-hour samples for benzene analysis. 24 Q. Okay. Where in Mr. Spencer's report, if you 25 can find the -- the sentence that -- that talks about 121 1 there was a piece of equipment on a counter when they 2 ran the test? 3 A. That's just my recollection from earlier 4 conversations with him, that they had something that 5 they applied -- I don't recall what it was, whether it 6 was a pipe joint or -- or -- it was a piece of metal. 7 It was some -- something metallic that they put the 8 various quantities on and then measured the airborne 9 concentrations. 10 Q. Does the piece of equipment on the counter, is 11 that referenced in the report? 12 A. No. I know that from prior discussions with 13 Mr. Spencer. 14 Q. Now, who was the person that they used to 15 test? 16 A. I don't know the individual's name. I believe 17 it was one of -- I am presuming it was one of his 18 employees or technicians. 19 Q. Does it say in that report? 20 A. No. 21 Q. Now, how close was the person to this piece of 22 equipment on the counter when the Liquid Wrench in the 23 current version was being applied? 24 A. I don't know. I presume that's contained in 25 the videotape. It's specifics that I am -- I'm not 122 1 aware of. I mean -2 Q. What does the report tell us about that? 3 A. It doesn't provide specifics about the 4 methodology. At least, this one doesn't. I don't know. 5 Q. What was the breathing rate of the person that 6 they tested? 7 A. I don't presume that they had him running in 8 place; so, I presume it was a sedentary breathing rate, 9 which is probably 18 per minute or something. 10 Q. Does the report tell you that? 11 A. No. 12 Q. What type of monitor were they using? 13 A. Total -- I actually don't know if they used 14 the passive dosimeter or charcoal pump; but it was an 15 approved NIOSH-OSHA procedure that he indicated to me 16 was used. 17 Q. What does the report tell us about that? 18 A. It doesn't speak to the specifics of the -- of 19 the methodology. 20 Q. Does the report tell you the -- where the test 21 was run? 22 A. Where the analysis was run or where the sample 23 was taken? 24 Q. Where the sample was taken. 25 A. No, it does not. 123 1 Q. Does the report tell you the -- the city that 2 the test was done in? 3 A. No, it does not. 4 Q. Does it tell you who was present when the test 5 was run? 6 A. No, it does not. 7 Q. Does it tell you when the test was done? 8 A. No, it does not. 9 Q. Do you know the answers to any of those 10 questions? 11 MR. KEMP: Objection, form. 12 A. I have already answered the -- the questions 13 individually, so... 14 Q. (BY MR. LUBEL) But from your discussions with 15 Mr. Spencer, do you know the answers to those questions? 16 MR. KEMP: Objection, form. 17 A. Some of them. 18 Q. (BY MR. LUBEL) Which ones? 19 A. These -- I didn't ask him what city it was in, 20 because I didn't think it relevant; but I -- I know it 21 was done in a corner of a -- a warehouse that they had 22 erected a plastic enclosure around. I don't recall the 23 specific dimensions of that enclosure. And I know it 24 had a work space like a table or platform in it for 25 which the -- the material was applied to something that 124 1 was sitting on that work -- or table. That's the extent 2 of the questions that you asked me that I have specific 3 answers to. 4 Q. And that was information that you got from 5 Mr. Spencer approximately six to eight months ago from a 6 telephone discussion with him, correct? 7 A. I don't -- I said six to eight months. It 8 could have been three months. It could have been eight 9 months. I -- it was some time ago, totally unrelated to 10 Mr. Cowey. 11 Q. What was the temperature in this warehouse 12 when this test was being done? 13 A. I think at one time he told me, but -- but I 14 don't -- I don't recall it now. 15 Q. What does the report tell you about 16 temperature? 17 A. It -- the report just summarizes some previous 18 work that Mr. Spencer did. It's -- it's not the 19 analytical report that would back up the numbers that 20 you're talking about. 21 Q. But does the report tell you what the 22 temperature was when the test was run? 23 A. No, it doesn't. 24 Q. What difference does -25 A. Well, I don't think it does. I didn't see it. 125 1 Q. What difference can temperature have on the 2 results? 3 A. Well, the higher the temperature, the faster 4 the -- the material would evaporate. 5 Q. And what difference does that make in a 6 worker's exposures? 7 A. Only wrote -- most relevant to a short-term 8 exposure. I mean, it's -- most industrial hygiene 9 samples are -- you know, are calculated at the ambient 10 temperature of where -- when the sample was -- was 11 taken. So, I mean, this was obviously an indoor, no air 12 movement; so, you know, it was probably 65- to 75-degree 13 range. But that's all the information it tells you, or 14 can surmise from it. 15 Q. What happens if the temperature is 92? 16 A. If the temperature were 92, the 15-minute 17 STEL, which is not reported in this -- in this report, 18 might be higher. 19 Q. Why is that? 20 A. Because you -- you'd get a -- materials don't 21 evaporate instantaneously. They evaporate on -- on a 22 curve. And don't ask me what that curve is or looks 23 like; but, you know, the hotter it would be, the faster 24 evaporation would take place. So, in a short-term 25 measurement, you would tend to get a higher number. 126 1 Q. So, the hotter it is, you'd expect the 2 exposures to be higher, at least on a short-term basis, 3 correct? 4 A. Well, this -- this is a very specific 5 scenario. I mean, you have no way of predicting what 6 would happen, you know, standing outside doing this or 7 in a -- or in a garage or workroom with a fan blowing. 8 I mean, there is lots of variables that -- that have 9 potential impact. I mean, what I liked about the 10 Table 1 was the fact that it was essentially no air 11 movement in a -- what you would consider a confined 12 space. 13 So, by definition, it would be -- you know, at 14 least at the -- and as I say, the numbers in the table 15 are from the 2-hour sample, which probably would not 16 have changed whether it was 90 degrees or 60 degrees; 17 so... 18 Q. But would you agree on a short-term basis, 19 like a 15-minute interval, that the hotter it is, the 20 higher the exposures would be? 21 A. If the exposure was on a surface that was the 22 same temperature as the air, I am not an expert, but I 23 would believe that to be the case. 24 Q. And you -25 A. It seems logical to me. 127 1 Q. -- you said that this test, to your knowledge, 2 was done in a confined space. Does the report tell you 3 that? 4 A. I don't see in this report where it 5 specifically states that, although it does speak to the 6 issue of no air movement, which implies some 7 containment, because there's substantially more air 8 movement here than just in this room than what would 9 have been reflected in these numbers. 10 Q. And what did you say the containment was? 11 A. They created a structure out of, you know, 12 some -- some contained room out of plastic sheeted -13 sheeting. 14 Q. Did it have a roof on that structure? 15 A. I don't remember. I mean, I want to say yes; 16 but I actually don't remember. 17 Q. Does the report tell you? 18 A. No, it doesn't. 19 Q. And we don't know how big that -- that room 20 is, correct, from the report? 21 A. No, not from the report. 22 Q. Does the report provide any data on what 23 Mr. Cowey would have been exposed to over two hours in a 24 crawl space underneath the house using Liquid Wrench? 25 A. Well, as I said, I don't -- I don't recall 128 1 that was his common usage; but, no, it doesn't speak to 2 that, in and of itself. But if he's in the crawl space 3 putting on this ounce of material and then leaves and 4 comes back the next day, these numbers are still going 5 to be higher than what he would have been exposed to. 6 Q. I noticed in your report that you had reports 7 from Dr. Irons and Dr. Natelson; is that true? 8 A. Yes. 9 Q. Do your opinions differ from theirs? 10 MR. KEMP: Objection, form. 11 A. I don't believe they do substantively. 12 Q. (BY MR. LUBEL) In general, would it be fair 13 to say that you agree with the opinions given by 14 Dr. Irons and Dr. Natelson, at least as they're 15 contained in their reports? 16 A. I have one question on one of Dr. Irons' 17 numbers that I think he may -- I don't know where he got 18 it from. It's not -- it doesn't match up with the 19 reference he gave for it -- where he speaks about 60 ppm 20 years; but the rest of the material, at least in my 21 reading -- cursory reading of those two reports, I have 22 no argument with their conclusions. 23 Q. In general, would it be fair to say that the 24 conclusions that you've reached in this case are the 25 same as theirs? 129 1 MR. KEMP: Objection, form. 2 A. I didn't see their -- I didn't see their 3 reports until quite recently; but -- yeah, I think we 4 probably come at it in very different ways, but I think 5 the bottom line is there's -- they're consistent with 6 each other. 7 Q. (BY MR. LUBEL) How do you come at it 8 different ways? 9 A. Well, Dr. Irons is, you know, a molecular 10 biologist with a great deal of both diagnostic and study 11 experience on this specific disease; so, his -- his 12 focus tends to come at more of the various case series 13 that he sees. So, you know, in the molecular genetic 14 level and areas like that, he's much more of an expert 15 than I. 16 I think from the epidemiologic perspective, 17 we're both looking at the same set of literature and, 18 therefore, are consistent; and the same with 19 Dr. Natelson. 20 Dr. Natelson is a, you know, clinical 21 toxicologist; so, you know, his perspective is also 22 slightly different. But, you know, there's only one 23 body of scientific literature that we're all working 24 from. It's just a matter of which pieces you emphasize 25 relative to your disciplinary expertise. 130 1 Q. Irrespective of what your different 2 perspectives and the pieces that you emphasize, would it 3 be fair to say that you-all's conclusions, in general, 4 are the same, with regard to Mr. Cowey? 5 A. Yeah. I don't think any of us see the 6 possibility of any exposure that would be high enough 7 over sustained periods of time to increase his risk. If 8 that's the basic conclusion, yeah, we -- we agree on 9 that. 10 Q. Can you pull out for us the studies that 11 you've brought with you that reflect that the Bradford 12 Hill criteria require -- requires a relative risk of 13 greater than 2.0 for a study to be statistically 14 significant? 15 A. Well, both those statements are -- one -16 you're misinterpreting two pieces. The Bradford Hill 17 criteria do not require 2.0. The -- the relative -- the 18 relative risk of standardized mortality ratio of greater 19 than 2.0 is not inherent in the Bradford Hill criteria. 20 Bradford Hill criterion is more generic in that it 21 speaks to strong statistical associations. It does 22 imply that statistical significance of those 23 associations is -- is important. 24 And the issue of what -- whether the relative 25 risk is 2.0, 3.0, 1.5, deals more with the issue of 131 1 relative risks above 2.0 are less likely, or unlikely, 2 to be impacted by simply -- simple confounded exposures. 3 And most of the 2.0 tends to come from academic 4 textbooks and in litigation-related issues, Superior 5 Court opinions; but 2.0, itself, is not a magic number 6 in either epidemiology or in Bradford Hill. 7 Q. It doesn't come from science, does it? 8 A. Well, it comes from science to the extent that 9 if you read classic textbooks like Monson's Occupational 10 Epidemiology, you'll see a discussion -- in fact, Monson 11 says 3.0 -- that once -- if you have consistent, 12 relative risks of 2.0 or 3.0 or greater that are 13 statistically significant across studies, even if the 14 studies themselves had not -- for example, if you're 15 looking at lung cancer and there isn't a special 16 handling of the smoking issue, it's unlikely that 17 difference in smoking rates, unless they're enormous, 18 are going to impact that relative risk as a confounder. 19 In other words, on a variable that you have not 20 measured. 21 So, there is a large body of epidemiologic 22 methodologic report -- reports and textbooks that -23 that speak to high relative risks. But that's strength 24 of association. That's just one element in the Bradford 25 Hill criterion. 132 1 Q. Have you brought with you any authority that 2 stands for the proposition that you need a 2.0 or 3 greater relative risk for SMR? 4 A. No. I just told you that's not, in and of 5 itself, a condition of Bradford Hill. There are -6 Q. The reason -7 A. I have such literature, but it's irrelevant to 8 my report, as far as I'm concerned. 9 Q. But you don't have it with you today? 10 A. No. 11 Q. Is it cited in your report at all, that 12 literature? 13 A. No. I think I said I -- the Bradford -- one 14 of Bradford Hill's speeches -- and I believe that -15 well, that my not be included because it's such a 16 standard piece that you guys all have copies of; so, I 17 tend not to carry all of it around with me -- that talks 18 about strength of association and may give examples, but 19 it doesn't say 2.0 is a -- it doesn't say 2.0 is a magic 20 number. At least, I don't recall it saying that. 21 Q. In your report you say, "Cancer induction is a 22 multistep process whose clinical onset is typically 23 measured in years, if not decades, from the first time 24 of exposure." 25 A. As a general statement, yes. 133 1 Q. What do you mean by that? 2 A. Well, traditional thinking -- and I think it's 3 still current thinking -- is that you -- it's a 4 multistep process. You need -- if we're -- if we're 5 talking about -- well, it doesn't matter if we're 6 talking about occupational or nonoccupational cancer. 7 You need a step that is an initiating step, some sets of 8 repeated -- the initiating step is typically thought to 9 be a stochastic process. 10 That means repeated -- the body is constantly 11 being bombarded with things that will interact with DNA, 12 through diet, everywhere, constantly. The body normally 13 repairs those, and everything's fine. If you have 14 material that is constantly bombarded -- bombarding a 15 target tissue and causing DNA disruption, at some point 16 in time you could -- you would not get the appropriate 17 level of repair and you have an initiating, potentially 18 carcinogenic effect. 19 What you then need to have happen is -20 fortunately the body is a redundant system. Many times 21 those would just -- just be cleaned up by other parts of 22 the organ system. But in -- sometimes they don't; and, 23 as a result, you start to get what might be considered 24 clonal expansion. It starts replicating. This defected 25 cell starts making copies of itself that continue to 134 1 survive. 2 And then you have -- and along the way, there 3 are, depending on which cancer you're talking about, 4 lots of different chemical interactions that are either 5 attempting to control that or promoting that; so, you 6 have an initiation and promotion. And that process 7 takes, depending on the cancer, a fair amount of time; 8 but it's very cancer specific. 9 Q. You're talking about years? 10 A. Yeah, typically. Yeah. I mean, I don't think 11 we're seeing -- certainly for environmental cancers, you 12 know, it's very -- other than cancers that are induced 13 through the use of chemotherapeutic agents, you're 14 typically looking at, you know, a minimum of seven to 15 ten years; and then depending on the cancer, 15 or 20. 16 Q. It's usually decades, is what your report 17 says? 18 A. Yeah, as a general rule; but that's -19 that's -- that's a motherhood and apple pie statement, 20 not a -- not a -- an AML-specific statement. 21 Q. How -- how does benzene exposure cause MDS? 22 A. I don't think anybody knows exactly how it 23 causes MDS. I mean, benzene is metabolized first in the 24 liver, and then the various metabolites are further 25 metabolized in -- in the -- in the bone marrow by a 135 1 variety of processes. There are several hypothesized 2 metabolites of benzene that are thought to be key 3 components. 4 The presumption is, is that there is a toxic 5 event, a disruption of the homeostatic process in the 6 bone marrow; and if that process is not abated, you have 7 a -- that cell line is clonally expanded, and you end up 8 with some type of myeloproliferative or 9 lymphoproliferative disorder. 10 For AML, you -- it's a -- and you really 11 should speak to Rich Irons on this subject. He's 12 published a lot more than anyone else. There are a 13 whole bunch of proteins that are in -- in mol -- and 14 very complex molecular chemistry that support that 15 clonal expansion. But you're looking at -- you know, a 16 decade, and not much more over a decade for the whole 17 process to cycle through once you have bone marrow 18 toxicity going on to AML. I mean, you're looking at 11 19 years, outside 15 years, based on what we've seen in 20 defined benzene exposed populations where you can 21 actually make those types of calculations. 22 Q. And is MDS a deadly disease? 23 A. Depending on which specific form you have, it 24 doesn't have a great prognosis. 25 Q. What about the form Mr. Cowey has? 136 1 A. Yeah, it's -- it typically has survivorship 2 that doesn't go much past five years. I mean -3 Q. But how does it kill? 4 A. -- I don't -5 Well, most myelodysplastic or 6 myeloproliferative diseases essentially don't kill you 7 outright. You die of the fact that your body can't 8 defend off other types of infections or disease. So, it 9 kills in a variety of ways because the hematopoietic 10 system isn't operating correctly; and depending on -- on 11 the specifics of that, there is a whole cast -- range of 12 cascading events that can be associated with it. 13 Q. Do you believe that Mr. Cowey's MDS will 14 ultimately kill him? 15 A. You know, I don't -- I've not had enough 16 clinical reports available to me to -- it's not 17 something I would normally do anyway; but -- but I don't 18 even have enough material to -- to know what -- what his 19 recent blood counts look like or what his health status 20 currently is. 21 Q. If his treating doctor, Dr. Youman, says that 22 his life expectancy from his MDS is about six months to 23 18 months, would you agree or disagree with that? 24 A. From his current status? 25 Q. Correct. 137 1 A. Because, I mean, he's obviously lived longer 2 than that since his diagnosis. 3 No, I would have no reason to dispute that. I 4 have no data to dispute it with. 5 Q. Now, the Bradford Hill criteria require -- or 6 one of the criteria of Bradford Hill is dose response 7 between the agent and the disease; is that true? 8 A. Yes. That's why I said MDS in particular 9 really doesn't, in the formal sense, satisfy the 10 Bradford Hill criteria. We don't have studies that 11 really deal with MDS or any of the subtypes in that 12 regard. 13 Q. But you agree that benzene exposure can lead 14 to MDS? 15 A. Yes. 16 Q. Can you tell us why it is that your affidavit 17 that you gave says that benzene exposure does not cause 18 MDS? 19 MR. KEMP: Objection, form. 20 A. It doesn't say that; so, that's -- I don't 21 know where it is. That's a missreading. It doesn't say 22 that. 23 What I say when I am discussing causality is 24 that -- has been repeated AML -- a causal association 25 between benzene and MDS has not -- has not -- and I use 138 1 Cole as the reference, what I'm -- what I'm specifically 2 speaking to is general causation under the Bradford Hill 3 I don't dispute, nor -- nor meant to imply, that -- that 4 -- that benzene doesn't cause. 5 Q. (BY MR. LUBEL) But what does the affidavit 6 say in that regard, if you can read that sentence for 7 us? 8 A. Well, it -- essentially literally 9 paraphrasing, I might even be quoting, Phil Cole's 1993 10 formal review of the Hill criteria as they apply to -11 to a causal association between benzene and MDS has not 12 -- has not, and then I cite Cole. 13 Q. Has not what? Just read that sentence for us. 14 A. (Reading) While a causal relationship has 15 been established between repeated high doses of benzene 16 and AML, a causal association between benzene and MDS 17 has not, in the general sense of the Bradford Hill 18 criteria. 19 And we talked about that earlier. I don't -20 you -- you don't -- you can't show me a study where we 21 have dose-response data specific for MDS in a group 22 of -- in a set of -- in a study that we would all agree 23 is suitable for risk assessment. That's what that says. 24 Q. That's what you mean? I mean, it doesn't say 25 that. 139 1 A. Well, that's what it -- that's what it means. 2 I mean, it then goes on to discuss if -- if 3 benzene, indeed, does cause MDS, this is how we have to 4 look at it, by looking at the leukemia literature. 5 Q. You make a statement that "Scientific thinking 6 today believes that bone marrow toxicity is a precursor 7 event necessary for initiation of the AML process." 8 A. Yes. That's -- I do. That -- I think you 9 just read the statement. 10 Q. Do you have a study with you that states that? 11 A. No, but I -- I didn't -- I didn't put a 12 reference on it because I think there's a -- a fairly 13 general consensus that you need some hematotoxicity as 14 part of the initiating process. There are references 15 out there. I don't -- I have not gone back and dragged 16 that material out because most people generally accept 17 that there is some truth to it. 18 Actually, what you would want to look at is 19 some of Snyder's work, Bob Snyder from Rutgers, and 20 probably -- well, I know for sure, although I don't 21 remember the papers per se, I believe Rich Irons has 22 also published in that area. 23 But most -- most of the folks that are doing 24 molecular biology of -- of -- of aplastic anemia and 25 leukemia recognize that there is a high probability, if 140 1 not a demonstrated requirement, for some toxicity. If 2 there wasn't, there would be no point in doing medical 3 surveillance for benzene-exposed workers. 4 Q. When was there published information available 5 to companies that were interested in learning about the 6 potential health hazards of benzene exposures concerning 7 potential adverse health effects from it? 8 A. Well, you can go quite far back in time. I 9 mean, it's -- the -- you know, the companies would tend 10 to look at National Safety Council records and the 11 American Conference of Governmental Industrial 12 Hygienists, both of which have been reporting on benzene 13 toxicity since the late '40s; and there's literature 14 earlier than that, but when you talk about what 15 companies would have reason to be knowledgeable about, 16 the A.C.G.H. [sic] has a -- you know, put out a T.L.V., 17 in '46 or so. 18 Q. 1946? 19 A. Sometime in that time range. 20 Q. And by benzene toxicity, are you referring to 21 damage to the blood or blood-forming organs? 22 A. Well, the big concern up until the '70s was 23 aplastic anemia. All the focus of toxicity concern was 24 related to -- to bone marrow suppression and overt 25 aplastic anemia, which is a -- a very serious, 141 1 frequently fatal, disease. 2 You'll also find -- I mean, at one point in 3 the -- in the late '20s and early '30s, benzene was used 4 to treat leukemia, because if you gave somebody -5 injected them with a high -- a high dose of benzene, you 6 killed the bone marrow. So, the thought was that if we 7 could induce an aplastic state, we -- we would kill -8 we'd reset the clock, so to speak. I mean, obviously 9 they died -- many died of aplastic anemia as a 10 consequence of the treatment; but... 11 But, no, the -- the toxicity has been known 12 for a very long time; and that's what -- and if you look 13 at the history of how the T.L.V.s have changed, like -14 and I believe it was -- it was '40 -- it might have been 15 '49, but '40 -- in that time range -- it was 100, then 16 they lowered it to 50, then they lowered it to 35, and 17 then sat with it at 25 for a very long time. 18 Q. My question is: When you referred to bone 19 marrow toxicity, were you including damage to the 20 blood-forming organs? 21 A. Well, it was mostly -- I mean, that's what 22 aplastic anemia is, damage to the blood-forming organs. 23 I mean, in its most severe state. So -- so, the -24 so -- so that the -- that early literature was always 25 looking at what -- what are levels that don't induce 142 1 hematotoxicity, however you want to measure that. 2 But the cancer issue, you know, the leukemia 3 issue, didn't -- didn't really surface until -- I mean, 4 you started seeing -- seeing dribs and drabs in the 5 early '70s. I don't think anyone accepted general 6 causation -- I mean, the general causation that benzene 7 could cause leukemia probably didn't really arise 8 until -- or get broad acceptance until the mid '70s or a 9 little later. 10 Q. Were you aware that the American Petroleum 11 Institute study that was authored in 1948 referenced 12 leukemia? 13 A. The A.P.I. never did a study in 1948. 14 Q. You weren't aware of Dr. Drinker's study that 15 the A.P.I. sponsored? 16 A. Are you talking about his -- his -- his 1948 17 summary of -- of the toxicity of Benzene? That's not a 18 study. That's a review article. 19 Q. Are you familiar with that article? 20 A. Sure. 21 Q. Were you aware that that article discussed 22 leukemia and benzene? 23 A. I am -- I mean, there have been case reports 24 out there; but no -- no one accepted benzene as a cause 25 of leukemia. I mean, if you go to the NIOSH 1974 143 1 document, it states quite clearly that while the -2 there have been reports in the literature, the 3 possibility of benzene causing leukemia needs to be 4 further studied. 5 So, I mean, you will find reports in 6 literature of people who had insights, based on either 7 clinical experience or case -- case experience; but I 8 know it wasn't -- I know that was not a generally 9 accepted scientific assessment. 10 Q. Well, my question simply was: Were you aware 11 that the A.P.I. 1948 article referenced benzene and 12 leukemia? 13 A. I know it made some mention of leukemia, but 14 I -- but I believe the primary discussion in the 15 later -- I mean, the document also says 50 ppm of 16 benzene is acceptable. And then I think there is 17 probably a 1960 document of a very similar writing style 18 that says if you take an A.P.I. document that says if 19 you -- written by another outside expert that says if 20 you take 60 milligrams of vitamin C daily, you will 21 protect from benzene toxicity. I mean these are 22 state-of-the-art documents that are not, by our thinking 23 today, correct. So... 24 Q. Well, was it firmly established in the late 25 1940s that benzene exposures could cause blood-forming 144 1 disorders? 2 A. Toxicity. Always toxicity. 3 Q. They don't refer to the blood? 4 A. Yeah. I said hematotoxicity. Tox -- benzene 5 killed stem cells and bone marrow cells, resulting in 6 disruption of the blood-forming organs. But -- but the 7 disease leukemia was not presumed to be directly caused 8 by benzene. It just wasn't the case. I mean, yes, 9 there were case reports. I am not saying that there 10 weren't individual reports in the literature of 11 individuals with leukemia who had benzene exposure; but 12 there were lots of reports -- case reports of different 13 things that never panned out, ever, either. 14 So, what I am speaking to are, you know, 15 things like the National Safety Council reports of '50 16 and others that are speaking to hematotoxicity; and 17 that's -- and if you read the A.C.G.I.H. documentation, 18 which is probably a pretty good historical account of 19 what a group of folks dedicated to looking at safe 20 exposure limits, if you look at that over time -- and I 21 think that I -- did I include that in this report or 22 not? But that speaks quite clearly to the issue that 23 leukemia is not -- is not even on the radar screen until 24 you're well into the '70s. 25 Q. I am not asking you about leukemia. I am just 145 1 asking you if in the late '40s it was firmly established 2 that benzene exposures could damage the blood-forming 3 organs? 4 MR. KEMP: Objection, form. 5 A. I've said yes to that several times. That's 6 what aplastic anemia is, and that's what anemia is -7 toxic anemia is, damage to the blood-forming organs and 8 the results therefrom. 9 Q. (BY MR. LUBEL) Do you have an opinion as to 10 whether Mr. Cowey's smoking caused his MDS? 11 A. Based on my -- what he says in his deposition, 12 his implication is that he did not smoke very much at 13 all; and while smoking is strongly associated with acute 14 myelogenous leukemia, it tends to be in heavy smokers. 15 So, I don't see it as a risk factor for Mr. Cowey. 16 Q. So, smoking didn't cause his MDS? 17 A. If he -- if he's accurately reporting his 18 smoking history, I don't believe so. 19 Q. Did ionizing radiation cause his MDS? 20 A. I attempted to get as much detail on his early 21 treatment of -- for his prostate cancer. Best as I can 22 judge, he did not have any either radionuclide or 23 radiographic or radiation treatments. So, my conclusion 24 is he did not have any exposures that could be 25 associated with it, based on the data I have seen. 146 1 Q. Did any drugs cause Mr. Cowey's MDS, to your 2 knowledge? 3 A. Well, that's a good question. But I don't 4 have any drug history for Mr. Cowey; so, I can't make 5 this -- I can't draw any opinion on that. 6 Q. Did any chemotherapy treatments cause his MDS? 7 A. Similar to the radiation issue, I could not 8 locate any objective evidence that said he had 9 chemotherapy for treatment of his cancer; so, I can't 10 offer any opinion one way or the other. 11 Q. Did hair dyes cause his MDS? 12 A. I don't think hair dyes are -- have been 13 established causally uniformly, but there is no evidence 14 in the -- in the record to suggest that he dyed his hair 15 regularly; so, I -- I mean, in my discussion of what -16 what's been thrown out there, I list some of those 17 things; but certainly I don't -- in my conclusionary 18 remarks, I don't reiterate that I think they have any 19 role. 20 Q. Did -- did pesticides cause Mr. Cowey's MDS? 21 A. That's an interesting possibility, because 22 although we have no specific information on what 23 pesticides were being used, I do recall at least in a 24 couple of places that he was present during what would 25 be very heavy exposures through air distribution of 147 1 pesticides; but I don't have any objective information 2 that would permit me to draw even a partial inference on 3 that, but it's certainly a possibility. 4 Q. As you sit here today, you can't say that 5 pesticides played any role in his MDS? 6 A. No. I don't have enough information. 7 Q. Did farming cause his MDS? 8 A. Once again, similar to the pesticide story. 9 It's -- it's an actively -- it's a research objective 10 that's actively being researched. Right now there is 11 not sufficient information to point to a specific form 12 of farming or specific exposures within farmers; so, I 13 can't, based on current evidence, derive a conclusion 14 there. 15 Q. Will you agree that Mr. Cowey used 16 benzene-containing Liquid Wrench over 26 years? 17 A. No, I would not agree with that. I don't see 18 that in the record being established. 19 Q. If that is established, could that change your 20 opinions one way or the other? 21 A. No, because, actually, my -- my opinion 22 probably goes to the -- goes to the -- even if that were 23 a true scenario, using an ounce of it periodically, 24 particularly under the conditions that Mr. Cowey did, 25 because it sounded like he actually was a responsible 148 1 user of the products he used, there would be no way he 2 could get -- get an exposure high enough. 3 Q. But you're basing that on John Spencer's 4 exposure data, correct? 5 A. No. No, not at all. I mean, I know enough 6 about Liquid Wrench -- I mean, John Spencer's stuff is 7 sort of like icing on the cake. It's nice to have 8 because it sort of confirms what I already believed. 9 But, you know, we've -- I am very familiar with the 10 material he's using; and I am very familiar on how it 11 was used. It's been used widely in -- you know, inside 12 the petroleum industry for decades. We've -- you know, 13 maintenance workers have been measured for benzene 14 routinely; and Liquid Wrench, although, you know, it's 15 an exposure that we would have, you know, reduced, and 16 did reduce as soon as we were aware of it, there is no 17 evidence that you could get exposures high enough to 18 warrant -- to induce a disease from it. 19 Q. So, you don't need quantitative data on 20 Mr. Cowey's benzene exposures to reach your conclusions, 21 correct? 22 A. I'd very much like to have it. And as we 23 discussed at some length earlier, I can render an 24 opinion on an exclusionary argument that there's just no 25 reasonable expectation that you could reach an exposure 149 1 threshold. I am not saying that he wasn't exposed to 2 benzene. I am just saying that I can't see any scenario 3 that would have given him, from Liquid Wrench, a high 4 enough exposure. 5 Q. But you didn't need quantitative data to reach 6 that conclusion? 7 A. Well, I'm very familiar with benzene and 8 benzene literature and what types of workers are 9 exposed; and, I mean, I -- I am not a novice about 10 petroleum -- you know, petroleum refinery workers and 11 the opportunities for benzene exposure. I -- I can see 12 in this particular case that this infrequent and, in my 13 estimation, still probably relatively trivial household 14 use just doesn't get there. So, I mean, I don't need a 15 number to -- to confirm it. 16 As I said, if we were closer to the 200 p -17 if I could envision a scenario that gave -- you know, 18 gave me higher concentrations regularly, then I would 19 probably, you know, be more adamant about wanting a 20 quantitative exposure assessment. 21 Q. How regularly? 22 A. Well, I mean, he's not even -- you know, he's 23 not doing this daily. That's for sure. He's not. 24 There's just no possibility in my mind that -- that this 25 man has been daily undoing rusted -- rusted pipes and 150 1 bolts. I mean, it just doesn't have prime fascia face 2 validity of any truth to it. I mean, this was not his 3 occupation. He was not a mechanic in a petrochemical 4 plant. And even there, I am not at all convinced that 5 there is even any daily use. So, I mean, it just -6 just doesn't cut it for me. 7 And, as I say, I mean -- you know, it is nice 8 to have Spencer's stuff because it sort of confirms what 9 I already believed. 10 Q. Have the lawyers for United States Steel 11 Corporation provided you with the Mobil documents where 12 they tested Liquid Wrench and the benzene content of it? 13 A. Oh, yes. As a former Mobil employee, they 14 really made sure I saw those. 15 Q. Did you know the employees that were in those 16 documents? 17 A. Yes. 18 Q. Were they good hands? 19 A. Well, one -- one said -- came from a refinery. 20 I mean, there was the refinery environmental or safety 21 manager -- I don't exactly recall his title -- that 22 did -- that did the original -- or at least sponsored 23 the original analysis somewhere in the refinery. I 24 don't know where it was done. And -- and I know he was 25 a well-meaning guy. He was doing exactly what he was 151 1 supposed to be doing. 2 The -- the replication of the work, as you see 3 in the other Mobil document, which unfortunately is not 4 an exact replication -- well, the same sample wasn't 5 tested in both labs. One sample was tested down in 6 Beaumont, and then another sample acquired and tested in 7 Princeton -- I think it was Princeton, New Jersey; and 8 that one only showed 7 percent. So, I mean, there -9 there's still, in my mind, some reasonable belief that 10 there may have been some error in the 30. 11 But fundamentally, even at the 7 percent, you 12 know, if we had suitable alternative, you know, 13 products, that those documents outline very clearly what 14 we were doing in that time period. 15 Q. Do you have any question of the results 16 reached by the Mobil employees that apparently you knew 17 that authored these documents on Liquid Wrench? 18 MR. KEMP: Objection, form. 19 A. Well, they did not -- just to clarify, those 20 gentlemen were manager -- you know, business managers. 21 They did not do the analysis. They were just reporting 22 analysis. So, I don't -- I don't know anything about 23 who did the analysis. I know that we had -- Mobil 24 technical services in Paulsboro and Princeton had superb 25 analytic capability to measure benzene in a mixture. 152 1 So, the confirmatory -- what I would call confirmatory 2 results are ones that I believe quite strongly. I mean, 3 obviously the sample they had at 7 percent. 4 And the 30, I have no way of knowing if that's 5 an accurate analysis or not. I mean, it doesn't comport 6 with any of the internal documents that -- that either 7 U.S. Steel in what they were sending out in their 8 raffinates would suggest. So, I have no way of knowing 9 if that 30 is correct. I am suspicious that it's not. 10 Q. (BY MR. LUBEL) And have you considered this 11 Mobil -12 A. But let me also go further -13 Q. -- data -14 A. -- and say that if it contained 30, it would 15 have fallen into a whole different labeling requirement. 16 I mean, it would have had probably a skull and 17 crossbones, or something else, on it as well. And I -18 I just don't think it had 30. 19 MR. KEMP: Objection, nonresponsive. 20 Q. (BY MR. LUBEL) Have you considered the Mobil 21 data in your analysis in this case? 22 A. Well, clearly, I -- in trying to come up with 23 my worst case scenarios, I was willing to accept that 30 24 could be a possibility. I mean, I have no reason -25 THE REPORTER: Could you excuse me for 153 1 just a second? 2 (Brief Pause.) 3 (Requested testimony read back.) 4 A. I mean, I have no objective reason to throw 5 the 30 away, only the extent that it -- the analytic 6 chemistry coming out of the -- the raw material going in 7 never seemed to show a number that high. So -- so, I 8 used, in my mind, the 30 as the worst case scenario. 9 And still, you know, even if it were pure benzene, you 10 know, what I would consider what you would use, the, 11 quite honestly, few drops, not ounces, that you use when 12 you apply Liquid Wrench, I mean, that's why they sold it 13 in, what, 4- or 8-ounce containers typically. So, I 14 mean... 15 Q. (BY MR. LUBEL) Did you -16 A. I think I answered your question. 17 Q. Did you, based upon considering the Mobil 18 data, assume that the most likely benzene content of the 19 Liquid Wrench was 7 percent as opposed to 30 percent? 20 A. Well, remember, the approach I was taking was 21 an exclusionary approach. So, it -- if I couldn't come 22 up with a high exposure scenario at 30, obviously it was 23 going to be lower at 7; and obviously, you know -- so -24 I mean, the -- the raffinate documents say 1 to 14, 25 average 3. Some other documents said 7. The Mobil 154 1 documents said 7. I mean, you have quite a range of 2 potentially -- of benzene in the raffinate. That gets 3 cut back in the actual formulation a little bit because 4 there are other oils added in the final product; but in 5 my mind, if I couldn't come up with a scenario that made 6 it particularly hazardous at 30, it didn't matter to me 7 whether it was 7, 6, 5, 29, 28, 24. 8 Q. But you took the Mobil information into 9 account when you assessed your opinions? 10 A. Absolutely, because I would have never 11 considered 30 as a possibility. I mean, I would have 12 gone by the analytic chemistry coming from the supplier. 13 Q. Who were the companies that funded the 14 approximately 26 million-dollar Shanghai consortium 15 studies? 16 A. I don't know who all are in there. I know 17 probably the top five petroleum companies are part of 18 the group -- Mobil, Exxon, Chevron, Shell, BP -- if I 19 had to guess. I don't know exactly. But I don't know 20 what share -- you know, how much of that total comes 21 from them. Well, it -- first of all, it doesn't all 22 come in -- I mean, that's over the whole -- I think 23 they're anticipating it to be an eight- to ten-year 24 study -- set of studies. So, it's not a single check 25 being written today. 155 1 Q. When you went and made your PowerPoint 2 presentation to the companies, which companies do you 3 remember talking to? 4 A. Well, when I was trying to go ahead -- go -5 the budget estimates were way more -- were much more 6 modest. I mean, I think we were looking at, you know, 7 outside numbers of 6 to 8 million; and at the time I was 8 trying to get the American Petroleum Institute to put it 9 as a budget line item, in which case every petroleum 10 company in the United States would have paid their 11 dues -- proportional dues share. So, in my era, it -12 it was really to try -- try to sell it to get a vote at 13 A.P.I. to -- to budget the project. 14 As I understand it, that didn't -- they were 15 unwilling -- I mean, some of this happened after I 16 departed; so, it's hearsay -- A.P.I. elected not to put 17 it as a budget line item, and individual companies were 18 -- I think it became a subscription type of activity. 19 Q. What were you doing for Mobil back during the 20 time period in 1977 when they were looking at the 21 benzene content of Liquid Wrench? 22 A. October -- I came on board October, '77. I 23 was -- which is right when the emergency temporary 24 standard came out. I was part of the medical 25 department. I was the medical department representative 156 1 to all of the various committees trying to figure out 2 what do we do with this emergency temporary standard. 3 So, I sat in on lots of meetings. My role then was 4 advisory, as -- as an adviser, not as a -- not as a 5 decision maker. 6 Q. Did you participate in Mobil's decision to 7 take Liquid Wrench out of their complexes? 8 A. No, not directly. I mean, I -- I -- I 9 actually don't remember the dates. I am pretty sure I 10 was aware of -- I mean, looking at those documents, I 11 have awareness of the -- of those kinds of issues. So, 12 I probably sat in on some of the discussion around that; 13 but -14 Q. Do you recall offering any opinions or 15 providing any input in the -- Mobil's decision to not 16 let their workers use Liquid Wrench? 17 A. Well, as I recall, it was a recommendation. I 18 don't actually -- I don't actually recall seeing any 19 formal directives. We have a tendency to put things in 20 directives when -- when it's a "thou shalt" issue. But 21 it was normal practice for us to -- if we became aware 22 of toxicity -- of a toxicity issue, that at -- that we 23 didn't have firsthand knowledge of or could directly do 24 a risk assessment on, if we had substitute materials 25 readily available, they'd swap those out and then sort 157 1 it out over time. In other words, if it turned out 2 that, you know, this is much ado about nothing, then, 3 you know, sort of back off of the early procedures. 4 Q. Did Mobil continue to use Liquid Wrench after 5 1977 when they were looking at the benzene content of 6 Liquid Wrench? 7 A. I don't know. I don't know operational 8 details at that level routinely. I was at headquarters. 9 Q. You said you sat in on some meetings on it, 10 though. 11 A. Yeah. They would have -- they would have been 12 -- the environmental toxicology and medical department 13 met quite regularly to keep each other informed of 14 what's surfacing on each other's plate; so, we would 15 have been aware of it and -- and would have not weighed 16 in heavily, for -- I mean, you know, sitting in the 17 medical department in New York, if the substance was 18 Liquid Wrench, I'd use it. It's not exactly rocket 19 science from a decision point of view. 20 Q. What did Mobil ultimately decide to do about 21 Liquid Wrench that contained benzene? 22 A. I don't know. I think I already answered that 23 question. At the operational level, I don't know what 24 the -- what the final resolution was. 25 Q. When you refer to "alkylating agents," are you 158 1 referring to chemotherapy treatments? 2 A. Generally, yeah, in the context we were 3 discussing here. 4 Q. And you're not saying that any alkylating -5 A. No. 6 Q. -- agents caused his MDS, are you? 7 A. No. No. 8 Q. And then there is another word that you use in 9 your report, and I can't pronounce it. It's 10 epipodophyllotoxins, or something like that. 11 A. Yeah, I found that quite interesting. That -12 I did not spend much time trying to go to primary 13 references, but that comes out of Cancer Society 14 summaries of the literature. It was something that -15 it's on my list of interesting things to find out more 16 about, but -17 Q. What are they? 18 A. I don't know. That's why I wanted to spend 19 more time and find out. 20 Q. How do you pronounce it? 21 A. Oh, I don't know. 22 Q. Nobody knows? 23 A. Nobody knows. Nobody knows. 24 Q. Well, you're not taking the position that that 25 caused Mr. Cowey's MDS, are you? 159 1 A. No. I mean, I routinely, in my reports, 2 list -- list materials of that type that -- that are 3 recognized by others as having strong, if not causally, 4 associations; and the reason I do that is sometimes 5 subs -- as much to inform other parties because, as 6 they're going through additional materials or new 7 discovery, you know, if you never mentioned it, nobody 8 will know that it's important; so... 9 If I thought it was important specific to 10 Mr. Cowey, it would be -- my report style would be that 11 it would be rediscussed in my conclusionary remarks as 12 being potentially associated. 13 Q. Have you -- have you told us about all of your 14 opinions regarding Mr. Cowey's case? 15 A. Yes, I believe. 16 MR. KEMP: Objection, form. 17 Q. (BY MR. LUBEL) Does your report -- between 18 your report and what you've told us today cover your 19 opinions in this case? 20 A. Unless I am given additional information, I 21 think it summarizes, certainly, the current status of my 22 thinking. 23 MR. LUBEL: Can we take a short break? 24 And I think I am getting close. 25 MR. KEMP: Yes, sir. 160 1 (A break was taken, 1:54 to 2:00 p.m.) 2 (Exhibit 6 marked.) 3 Q. (BY MR. LUBEL) Can you identify Exhibit 6 for 4 us? 5 A. Exhibit 6 is correspondence between 6 Fulbright & Jaworski and myself, and it is -- it's 7 complete except for, I guess, one bill that I sent in 8 that doesn't seem to be here; but that's -9 Q. What was that bill for? 10 A. For writing the report. 11 Q. How much did that cost? 12 A. I actually don't remember. I don't know, 8, 13 $10,000, something like that. 14 Q. Can you go ahead and provide to Mr. Kemp all 15 of your invoices? 16 A. Well, he has the invoice. He hasn't paid it. 17 MR. KEMP: We paid the retainer, and we 18 take some time to pay the invoice. 19 Q. (BY MR. LUBEL) Who hired you in this case? 20 MR. KEMP: We're good for it. 21 A. Mr. Kemp. Mr. Kemp, I believe, made the 22 initial contact. 23 Q. (BY MR. LUBEL) On behalf of United States 24 Steel Corporation? 25 A. Yes, I believe that's correct. I normally 161 1 don't pay attention to those kind of things. 2 Q. In this case, have you talked to anybody other 3 than Mr. Kemp? 4 A. Yes. I -- I had a few conversations with 5 Mr. Dillard. 6 Q. Anybody else? 7 A. Mr. Epps. Carl Epps. 8 Q. What does Mr. Epps have to do with it? 9 A. I believe he is associated with either 10 Radiator or U.S. Steel. I mean, I am -- I actually am 11 not 100 percent sure at times. 12 Q. When did you learn that you were also hired as 13 an expert for Radiator Specialty Company? 14 A. I don't -- I get hired by a law firm; and, 15 quite frankly, I am not -- I don't pay a whole heck of a 16 lot of attention to who all else -- who all is paying 17 the tab, because I am looking at risk assessments and 18 evaluation of the epidemiology on a particular case. 19 So, when you ask me a date like that, it makes it sound 20 like that was sometime after Mr. Kemp retained me. 21 Q. Were you aware that Radiator Specialty Company 22 is paying half your bill in this case? 23 A. Now that you say it, I think I probably am; 24 but I don't recall if I got two checks on the retainer 25 or not. 162 1 Q. Well, irrespective of who sent you the first 2 check, as you sit here today, do you understand that 3 you're an expert for both United States Steel 4 Corporation and Radiator Specialty Company? 5 A. As it applies to the epidemiology we're 6 talking about here? Yes, I guess so. 7 Q. Well, the reason I ask you this is because in 8 the correspondence between you and United States Steel 9 Corporation's attorneys, there's a reference to half of 10 your bill will be paid by counsel for Defendant Radiator 11 Specialty. 12 A. Then, I don't -- I just don't remember that. 13 But -- I mean, I don't know -- to me, all that means is 14 that they're paying half the bill; so... 15 Q. Well, have you talked to Mr. Riley at all? 16 A. No. I mean, spoken with Mr. Riley regarding 17 this case? 18 Q. Right. 19 A. This is the first time I met Mr. Riley. 20 Today. 21 Q. Was that unusual for you to receive half your 22 payment from a company when you hadn't met their lawyer 23 or talked to them? 24 A. No, not at all. I mean, there are -- I don't 25 need, nor do I particularly want to know, how you guys 163 1 run your business. But there have been occasions where 2 there's either been, quote/unquote, joint defense funds, 3 and there have been cases -- in which case I get a check 4 written from some artificially created fund; and there 5 are times when I send in a bill and I get six -- you 6 know, one-sixth checks coming back and in no particular 7 logical time sequence to cover that invoice. 8 So, while it might be important to you, it's 9 not an important issue to me. I mean, I am retained by 10 a law firm to evaluate a case. How they pay me is an 11 issue for them, not for me. 12 Q. So, nobody from Radiator Specialty Company, to 13 your knowledge, has contacted you to discuss this case 14 as it applies to them? 15 A. Well, in the course of conversations with 16 Mr. Epps, I mean, I think, you know, we have covered a 17 lot of Radiator documents; but -- and, you know, that -18 this is not the first, quote/unquote, Liquid 19 Wrench-related case I have ever worked on. But I don't 20 make a big -- I don't distinguish -- no, I -- to my 21 knowledge, I have not spoken with anybody specifically 22 from -- from Radiator. 23 Q. But you have got a written contract with Jeff 24 Kemp at Fulbright & Jaworski, the attorney for United 25 States Steel Corporation, specifically for the Cowey 164 1 case, correct? 2 A. Well, you -- I mean, I now know that it is 3 for -- for United States Steel Company; but if you will 4 notice, my agreement is between me and Fulbright & 5 Jaworski. 6 Q. Right. 7 Why don't you have an agreement with Radiator 8 Specialty Company? 9 A. Because they've agreed to -- they -- they've 10 retained me to look at this case, and how they get their 11 money back is not a concern to me. 12 Q. But they don't say they're going to get their 13 money back from Radiator. They say that half the money 14 is going to -15 A. Well, that's what he's telling me; but the 16 agreement that they signed says that they're going to 17 pay me. Okay? 18 Q. Who is "they"? 19 A. Well -20 Q. Fulbright? 21 A. -- Fulbright & Jaworski is going to see that I 22 get paid at this rate for my work on this case. I don't 23 care if they solicit on the corner for people who want 24 to contribute to the payment fund. 25 Q. Well, where is the -- your check -- 165 1 A. You're making me want to know a lot more about 2 this than I historically ever wanted to know, but -3 Q. Where is your -- the correspondence that 4 reflects checks you've received for the other half of 5 the monies from counsel for Radiator Specialty Company? 6 A. I don't even recall if I got two checks. I 7 don't know that for a fact. Oh, I guess -- I guess I 8 must have, if that's what he said. So, I must have 9 received a half check... 10 I didn't bring any of this material -- I mean, 11 other than a couple e-mails that I actually had in my 12 possession, I did not bring my billing records for this 13 case. So, I -- my set of records is not here; so, I 14 must have something back in the office that has -- I 15 mean, I don't even know whether there was correspondence 16 attached to it. I do recall that the retainer has been 17 paid; so, I presume that I have received two checks for 18 $1400. But that's sort of the extent of my interest in 19 the -- in the matter. 20 Q. Well, as you sit here today, do you know 21 whether or not you have received any money from Radiator 22 Specialty Company or their lawyers for this case? 23 A. I know the retainer has been paid; so, I have 24 obviously received two checks for $1400. I don't recall 25 whether -- I mean, very often I get a check that just 166 1 hasn't -- has a -- a name on it, has no correspondence; 2 so I am -- I am not trying to be evasive. I just -- I 3 just don't spend any time on that subject matter. 4 Q. Well, who owns Health Risk Services, 5 Incorporated? 6 A. Health Risk Sciences. 7 Q. Who owns that? 8 A. I do. 9 Q. How long have you owned it? 10 A. Since its -- since it was created in 1999. 11 Q. Are there any co-owners? 12 A. No. Well, I don't know if my wife -- I don't 13 remember how -14 Q. Other than your spouse? 15 A. I don't know how that works, but -16 Q. Other than your spouse? 17 A. No. 18 Q. And what is the business of that company? 19 A. Health Risk Sciences is a -- a -- specializes 20 in the conduct of epidemiology and integrating 21 epidemiology with industrial hygiene toxicology in 22 conducting health risk assessments; so, we do a -- a 23 variety of things. I mean, some litigation-related 24 work, some cluster investigation, some epidemiology, 25 some general consulting. 167 1 Q. And what percentage of your work is done on 2 behalf of plaintiffs? 3 A. That varies dramatically year to year. This 4 year -- oh, plaintiff -- you said plaintiffs? 5 Q. I did. 6 A. Good catch. I have not been retained by a 7 plaintiff. For some reason, they don't knock on my 8 door. 9 Q. So, would it be fair to say that 100 percent 10 of your income, at least in the litigation context, 11 is -- comes from defendants? 12 A. In the litigation context, to date, that's 13 correct. 14 Q. And what percentage of the total income that 15 your company makes comes from oil companies, chemical 16 companies, industry of that sort? 17 A. That's what I was starting to answer. I mean, 18 it varies dramatically year to year. Probably 80 to 90 19 percent comes from the petrochemical industry; and then 20 there's a -- a mix of trade associations. I have 21 occasionally done some work for health departments. I 22 mean, it's a -- the rest is a mix of different -23 different groups. 24 Q. Which trade associations? 25 A. The only trade association I am currently 168 1 working for is the asphalt industry. As -- as -2 Asphalt Institute, I guess it's called. 3 Q. Have you done any work for the American 4 Petroleum Institute? 5 A. Not since I retired. 6 Q. How about the Chemical Manufacturers 7 Association? 8 A. Not since I retired. 9 Q. What are you doing for the Asphalt Institute 10 or organization? 11 A. They're interested in conducting a large U.S. 12 epidemiology study, and they have -- and it will be done 13 in conjunction with the American Pavers Association, 14 which is another association of the Pavers, as opposed 15 to the manufacturer; and they've asked me to sit on -16 in on all their planning meetings to help guide them to 17 make sure that whatever they do turns out to be a good 18 piece of science. 19 Q. What are they trying to learn from this study? 20 A. There was a -- some preliminary reports coming 21 out of Europe where coal-tar pitch is -- is -- was a -22 a high component of asphalt for many years, suggesting 23 that there may be a lung cancer excess in pavers in 24 Europe. 25 And so, they have spent a fair amount of time 169 1 on toxicity and on related chemistry of the U.S. paving 2 industry and are looking now to reconstruct historical 3 chemistry and formulation information. We're working 4 with some folks from Harvard and a few other groups to 5 look at the feasibility of could we do a -- in this 6 country could you do a good paving study -- a study of 7 asphalt pavers. 8 Q. Why isn't the study from Europe valid for the 9 United States? 10 A. Because the formulation history, at least it's 11 commonly viewed in the U.S., used much less coal-tar; 12 and there is common agreement that the coal-tar pitch is 13 the car -- the high carcinogenic component in asphalt. 14 So, if -- if the U.S. chemistry history is correct, 15 which you could confirm in an epidemiology study, you 16 would not expect to see even a hint of lung -- I mean, 17 there is still ongoing studies in Europe; so, I mean 18 it's not that it's been established yet, but -19 Q. What about bladder and kidney cancers? 20 A. No, not really. The -- World Health 21 Organization/IARC just released a five-country cohort 22 study, and the only questionable cancer site is -- is 23 lung. Kidney and bladder are fine. The -- you don't 24 get enough -- the PNA exposures just aren't high enough. 25 I mean, it's not like coal -- you know, it's not like 170 1 coke oven workers or any of those areas where you might 2 expect to see those high exposures. 3 Q. And would benzene -- benzo(a)pyrene be the 4 component of concern in the coal-tar pitch? 5 A. It's probably a leading component. I mean, 6 there is a whole range of PAHs and a few nitroso-PA 7 compounds that have similar action. Coal-tar pitch is a 8 pretty dirty dimish. They typically use benzo(a)pyrene 9 as an indicator marker for it. But, yeah, it certainly 10 is at the top of the list; but it's not the only PAH. 11 Q. Where did you retire from? 12 A. I retired from Mobil when Exxon acquired Mobil 13 Corporation. 14 Q. And why is that? 15 A. Well, Mobil had a -- a retirement plan that 16 you could actually retire at age 50. At the time I was 17 52. Because Exxon was taking over Mobil, Mobil had 18 adopted a poison pill for its executives; and I was -- I 19 was director of health risk assessment at that point, 20 and I was high enough to be able to get a several -21 several-year severance on top of an early retirement, on 22 top of all the options being fully -- fully vested. So, 23 when you sat down and ran the numbers out, unless I 24 really wanted to work for Exxon, there was no good 25 reason to stay. 171 1 Q. Was that in 1999 that you retired? 2 A. I actually stayed on into the early part of 3 2000 to do what we call "transition" work. We have a 4 lot of confidential epidemiology medical records that 5 had to be transitioned legally -- you know, I had to -6 I had signed confidential documents for various state 7 and health departments; so, we had to transition all 8 that stuff so that I could transfer those documents, 9 because I sure as heck didn't want to take them home. 10 Q. So, you started your company, Health -- Health 11 Risk Sciences, Incorporated, before you left Mobil? 12 A. Yeah, because I had -- actually didn't know 13 how long they -- how long the transition was going to 14 go. I mean, it didn't -- it didn't -- when we say 15 created the company, I mean, it was a set of legal 16 activities. It was not the -- that there was a shingle 17 hung on the door. 18 Q. And have you had a stable group of 19 petrochemical companies that have been clients of yours 20 since you started? 21 A. Well, I mean, you can see from my C.V., I'm 22 widely published in certain areas of petroleum-related 23 exposures; so, companies come to me when they have -24 think they might have a problem. I mean, I have 25 published on how to look at cluster investigations, a 172 1 variety -- wide variety of stuff. So, if they think 2 there might be a problem, they will come to me and ask 3 for advice. 4 I have done some work in Kazakhstan in 2000 5 through 2002, looking at environmental epidemiology 6 where there -- they had set aside a large amount of 7 money to build infrastructure in some of these rural 8 Kazak villages and needed help to try to figure out 9 how -- what was the best place to put the money kind of 10 thing. So, it's quite a variety. 11 They tend to be petrochemical companies, but 12 they're not -- it's not like -- I am not on a retainer 13 for any company. They come to me on not as -- on an ad 14 hoc basis when they have a problem. 15 MR. LUBEL: That's all I have. Thank you 16 for your time. 17 THE WITNESS: Thank you. 18 MR. KEMP: I'll reserve my questions 19 until the time of trial. 20 MR. RILEY: Same. 21 22 23 24 25 173 1 CHANGES AND SIGNATURE 2 PAGELINE CHANGE REASON 3 _______________________________________________________ 4 _______________________________________________________ 5 _______________________________________________________ 6 _______________________________________________________ 7 _______________________________________________________ 8 _______________________________________________________ 9 _______________________________________________________ 10 _______________________________________________________ 11 _______________________________________________________ 12 _______________________________________________________ 13 _______________________________________________________ 14 _______________________________________________________ 15 _______________________________________________________ 16 _______________________________________________________ 17 _______________________________________________________ 18 _______________________________________________________ 19 _______________________________________________________ 20 _______________________________________________________ 21 _______________________________________________________ 22 _______________________________________________________ 23 _______________________________________________________ 24 _______________________________________________________ 25 _______________________________________________________ 174 1 I, GERHARD K. RAABE, Dr.P.H., F.A.C.E., have read the foregoing deposition and hereby affix my 2 signature that same is true and correct, except as noted above. 3 4 5 ___________________________________ GERHARD K. RAABE, Dr.P.H., F.A.C.E. 6 7 THE STATE OF __________) 8 COUNTY OF _____________) 9 Before me, ___________________________, on this day personally appeared GERHARD K. RAABE, Dr.P.H., 10 F.A.C.E., known to me (or proved to me under oath or through ___________________________) (description of 11 identity card or other document) to be the person whose name is subscribed to the foregoing instrument and 12 acknowledged to me that they executed the same for the purposes and consideration therein expressed. 13 Given under my hand and seal of office this __________ day of ________________________, __________. 14 15 16 ___________________________________ NOTARY PUBLIC IN AND FOR 17 THE STATE OF ______________________ COMMISSION EXPIRES: _______________ 18 19 20 21 22 23 24 25 175 1 CAUSE NO. A-167,693 2 JAMES COWEY AND RUTH ) IN THE DISTRICT COURT COWEY ) 3) PLAINTIFFS, ) 4) VS. ) JEFFERSON COUNTY, TEXAS 5) RADIATOR SPECIALTY ) 6 COMPANY, ET AL ) ) 7 DEFENDANTS. ) ) 58TH JUDICIAL DISTRICT 8 9 REPORTER'S CERTIFICATION DEPOSITION OF GERHARD K. RAABE, Dr.P.H., F.A.C.E. 10 DECEMBER 2, 2003 11 12 I, Kathy Miller, Certified Shorthand Reporter in 13 and for the State of Texas, hereby certify to the 14 following: 15 That the witness, GERHARD K. RAABE, Dr.P.H., 16 F.A.C.E., was duly sworn by the officer and that the 17 transcript of the oral deposition is a true record of 18 the testimony given by the witness; 19 That the deposition transcript was submitted on 20 ____________________ to the witness or to the attorney 21 for the witness for examination, signature and return to 22 me by ____________________; 23 That the amount of time used by each party at the 24 deposition is as follows: 25 MR. LANCE LUBEL.....04 HOURS:17 MINUTE(S) 176 1 That pursuant to information given to the 2 deposition officer at the time said testimony was taken, 3 the following includes counsel for all parties of 4 record: 5 FOR THE PLAINTIFFS: 6 MR. LANCE LUBEL HEARD, ROBINS, CLOUD, LUBEL & GREENWOOD 7 910 TRAVIS STREET, SUITE 2020 HOUSTON, TEXAS 77002 8 9 FOR THE DEFENDANTS UNITED STATES STEEL CORPORATION, ARISTECH CHEMICAL CORPORATION AND USX CORPORATION: 10 MR. JEFFREY W. KEMP FULBRIGHT & JAWORSKI 11 2200 ROSS AVENUE, SUITE 2800 DALLAS, TEXAS 75201 12 13 FOR THE DEFENDANT RADIATOR SPECIALTY COMPANY: MR. JAMES M. RILEY 14 COATS ROSE 1001 FANNIN, SUITE 800 15 HOUSTON, TEXAS 77002-6707 16 I further certify that I am neither counsel for, 17 related to, nor employed by any of the parties or 18 attorneys in the action in which this proceeding was 19 taken, and further that I am not financially or 20 otherwise interested in the outcome of the action. 21 22 23 24 25 177 1 Further certification requirements pursuant to Rule 2 203 of TRCP will be certified to after they have 3 occurred. 4 Certified to by me this 5th of December, 2003. 5 6 7 ___________________________________ Kathy Miller 8 Texas CSR No. 739 Expiration Date: 12/31/04 9 Nell McCallum & Associates 10 Firm Registration No. 243 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 178 1 FURTHER CERTIFICATION UNDER RULE 203 TRCP 2 The original deposition was/was not returned to the 3 deposition officer on _________________________; 4 If returned, the attached Changes and Signature 5 page contains any changes and the reasons therefor; 6 If returned, the original deposition was delivered 7 to _________________________, Custodial Attorney; 8 That $__________ is the deposition officer's 9 charges to the Plaintiff for preparing the original 10 deposition transcript and any copies of exhibits; 11 That the deposition was delivered in accordance 12 with Rule 203.3, and that a copy of this certificate was 13 served on all parties shown herein on and filed with the 14 Clerk. 15 Certified to by me this __________ day of 16 ____________________, 2003. 17 18 19 ___________________________________ Kathy Miller 20 Texas CSR No. 739 Expiration Date: 12/31/04 21 Nell McCallum & Associates 22 Firm Registration No. 243 23 24 25 179