Document nNrnj3dY5e0z7bXNxz4Vd65j2

1 IN THE GENERAL COURT OF JUSTICE SUPERIOR COURT DIVISION 2 STATE OF NORTH CAROLINA, COUNTY OF FORSYTH 3 Civil Action No. 07-CVS-3770 _______________________________________________________ 4 VIDEOTAPE DEPOSITION OF: DAVID W. PYATT, Ph.D. 5 September 23, 2009 _______________________________________________________ 6 ANDREW WOLFE and DENISE WOLFE, 7 Plaintiffs, 8 v. 9 E.I. DUPONT DE NEMOURS AND COMPANY, et al., 10 Defendants. 11 _______________________________________________________ 12 PURSUANT TO NOTICE the videotape 13 deposition of DAVID W. PYATT, Ph.D., was taken on behalf of the Defendants at the St. Julien Hotel, 14 900 Walnut Street, Boulder, Colorado 80302, on September 23, 2009, at 9:37 a.m., before Teresa 15 Coogle, Registered Professional Reporter, Certified Realtime Reporter, and Notary Public within Colorado. 16 17 18 19 20 21 22 23 24 25 1 1 APPEARANCES 2 For the Plaintiffs: TED N. GIANARIS, ESQ. SimmonsCooper, LLC 3 100 N. Sepulveda Boulevard Suite 1350 4 El Segundo, California 90245 5 For the Defendants: JAMES R. MILLER, ESQ. PPG Industries, Inc. Dickie, McCamey & Chilcote, P.C 6 2115 Rexford Road, Suite 210 Charlotte, North Carolina 28211 7 For the Defendant: ANDREW C. SCHIRRMEISTER, ESQ. 8 E.I. DuPont Schirrmeister, Diaz-Arrastia, De Nemours Brem, LLP 9 and Company 700 Milam, 10th Floor Houston, Texas 77002 10 Also present: Stacey Manela 11 Jerry DeBoer, Videographer 12 13 14 15 16 17 18 19 20 21 22 23 24 25 2 1 INDEX 2 EXAMINATION OF DAVID W. PYATT, Ph.D.: PAGE September 23, 2009 3 By Mr. Schirrmeister 8, 142 4 By Mr. Gianaris 140, 143, 145 5 INITIAL 6 PLAINTIFFS' DEPOSITION EXHIBITS: REFERENCE 7 1 API Toxicological Review, Benzene, 18 September 1943 8 DEFENDANTS' DEPOSITION EXHIBITS: 9 1 David W. Pyatt, Curriculum Vitae 19 10 2 Slide, Summary of Opinions 19 11 3 Declaration, David W. Pyatt 21 12 4 Slide, DuPont and PPG paint solvents 21 13 have been extensively evaluated and studied 14 5 Slide, 11th Report on Carcinogens, 33 Table of Contents 15 6 Slide, Hematopoietic Cell 35 16 Differentiation 17 6A Slide, Hematopoietic Cell 38 Differentiation, Hematopoietic and 18 Stromal Cell Differentiation 19 7 Slide, Chromosomes and the 44 15;17 translocation 20 8B Slide, Hematopoiesis 49 21 9 Slide, Epidemiology, Douer, 2003, "The 58 22 epidemiology of acute promyelocytic leukaemia" 23 10 "The epidemiology of acute promyelocytic 58 24 leukaemia," Douer, Best Practice & Research Clinical Haematology, 25 Vol. 16, No. 3, pp. 357 - 367, 2003 3 1 11 Slide, Epidemiology, Avvisati, et al., 1991, "Epidemiology of acute 2 promyelocytic leukemia in Italy" 3 12 "Epidemiology of acute promyelocytic leukemia in Italy", G. Avvisati, et al. 4 Annuals of Oncology, pp. 405-408, 1991 5 13 Slide, Scientific literature does not support link between benzene 58 58 65 6 and APL, Mitelman, et al., 1981, "Chromosome pattern, occupation, and 7 clinical features in patients with acute nonlymphocytic leukemia" 8 14 "Chromosome Pattern, Occupation, and 9 Clinical Features in Patients with Acute Nonlymphocytic Leukemia", 65 10 F. Mitelman, et al., Cancer Genetics and Cytogenetics 4, 197-214, 1981 11 15 Slide, Scientific literature 12 does not support link between benzene 65 and APL, Glumb, et al., 1982, "Correlation 13 of occupation and karyotype in adults with acute nonlymphocytic leukemia" 14 16 "Correlation of Occupation and Karyotype 65 15 in Adults With Acute Nonlymphocytic Leukemia", by Harvey M. Golomb, et al. 16 17 Slide, Scientific literature 67 17 does not support link between benzene and APL, Crane, et al., 1989, 18 "Environmental exposures in cytogenitically defined subsets of acute nonlymphocytic 19 leukemia" 20 18 "Environmental Exposures in Cytogenetically 67 Defined Subsets of Acute Nonlymphocytic 21 Leukemia", Martin M. Crane, Ph.D., et al., JAMA, August 4, 1989, Vol 262. 22 No. 5 23 24 25 4 1 19 Slide, Scientific literature does not support link between benzene 2 and APL, Fagioli, et al., 1991, "Distinct cytogenic and clinicopathologic 3 features in acute myeloid leukemia after occupational exposure to pesticides and 4 organic solvents" 5 20 "Distinct cytogenic and clinicopathologic features in acute myeloid leukemia after 6 occupational exposure to pesticides and organic solvents", Franca Fagioli, M.D., 7 et al. 8 21 Slide, Scientific literature does not support link between benzene 9 and APL, 1992, "Countrywide Analysis of Risk Factors for Leukemia and Aplastic 10 Anemia" 11 22 "Countrywide Analysis of Risk Factors for Leukemia and Aplastic Anemia", 12 National Investigative Group for the Survey of Leukemia and Aplastic Amenia 13 23 Slide, 1996 Estimated County 14 Median Exposure Concentration Benzene - North Carolina Counties 15 24 Slide, Benzene content in 16 everyday foods 17 25 Slide, Dose Response 18 26 Slide, Dose Response Chart 19 27 Slide, Doses of Common Substances 20 28 Slide, Dose response curve for aspirin 21 29 Slide, Dose response curve for alcohol 22 30 Slide, Benzene exposure measurements 23 31 Slide, Benzene and AML: Dose 24 response Quantitative studies of benzene and leukemia 25 68 68 72 72 73 75 76 77 78 80 81 82 87 5 1 32 Slide, Mr. Wolfe's exposure 2 33 Slide, epidemiology 3 34 Slide, Cohort Studies 95 97 99 4 35 Slide, Case-Control Studies 109 5 36 Slide, Relative Risk 111 6 37 Slide, Evaluating the role of chance 7 38 Slide, Confidence Interval 8 39 Slide, 95% Confidence Interval 112 114 114 9 40 Slide, Studies show painters 117 do not have an elevated risk of AML 10 or leukemia 11 41 Slide, NIOSH study of 57,000 119 painters 12 42 "Cohort mortality study of 57,000 13 painters and other union members: a 15 year update," Steenland and Palu 119 14 43 Slide, Study of 49,000 painters, 123 15 Brown, et al., 2002, "Exposures in the Painting Trades and Paint Manufacturing 16 Industry and Risk of Cancer Among Men and Women in Sweden" 17 44 "Exposures in the Painting Trades and 18 Paint Manufacturing Industry and Risk of Cancer Among Men and Women in Sweden", 123 19 Linda Morris Brown, Dr.Ph., et al. 20 45 Slide, Study of 58,000 painters, 124 Bouchardy, et al., 2002, "Cancer risk 21 by occupation and socioeconomic group among man - a study by the Association of Swiss 22 Cancer Registries" 23 46 "Cancer risk by occupation and socioeconomic 124 group among man - a study by the Association 24 of Swiss Cancer Registries", Christine Bouchardy, M.D., et al. 25 6 1 47 Letter to Salveson from Pyatt, 7/9/09, Subject: Andre Wolfe and Denise Wolfe 2 v. E.I. DuPont de Nemours and Co., et al. In the General Court of Justice, Superior 3 Court Division, No. 07-CVS-3770 4 48 Slide, Formaldehyde, Pinkerton, et al., 2003, "Mortality among a cohort 126 129 5 of garment workers exposed to formaldehyde: an update" 6 49 "Mortality among a cohort of garment workers 129 7 exposed to formaldehyde: an update", L.E. Pinkerton, et al., Occup Environ Med 8 2004; 61, 193-200 9 50 Slide, Formaldehyde, Coggon, et al., 130 2003, "Extended Follow-Up of a Cohort of 10 British Chemical Workers Exposed to Formaldehyde" 11 51 "Extended Follow-Up of a Cohort of 130 12 British Chemical Workers Exposed to Formaldehyde", David Coggon, et al., 13 Journal of the National Cancer Institute, Vol. 95, No. 21, November 5, 2009 14 52 Slide, Formaldehyde, Beane Freeman, 15 et al., 2009, "Mortality From Lymphohematopoietic Malignancies Among 132 16 Workers in Formaldehyde Industries: The National Cancer Institute Cohort" 17 53 "Mortality From Lymphohematopoietic 132 18 Malignancies Among Workers in Formaldehyde Industries: The National 19 Cancer Institute Cohort", Laura E. Beane, et al., JNCI, Vol. 101, Issue 10, 20 May 20, 2009 21 EXHIBIT DISPOSITION: 22 Original Exhibits: With transcript 23 24 25 7 1 THE VIDEOGRAPHER: We are on the record 2 at 9:37 on September 23, 2009, at 900 Walnut Street, 3 Boulder, Colorado. We are here for the videotape 4 deposition of David W. Pyatt, Ph.D., in the matter of 5 Andrew Wolfe and Denise Wolfe versus E.I. Du Pont de 6 Nemours and Company, et al., in the General Court of 7 Justice, Superior Court Division, State of North 8 Carolina, County of Forsythe, Case No. 07-CVS-3770. 9 The videographer is Jerry DeBoer. The 10 court reporter is the Teresa Coogle from Hunter + 11 Geist, Inc. Will counsel please state their 12 appearances beginning with the plaintiffs' counsel. 13 MR. GIANARIS: Ted Gianaris, Simmons 14 firm, by way of pro hoc vice. 15 MR. SCHIRRMEISTER: Andrew Schirrmeister 16 for DuPont. 17 MR. MILLER: James R. Miller for PPG 18 Industries. 19 DAVID W. PYATT, Ph.D., 20 having been first duly sworn to state the whole truth, 21 testified as follows: 22 DIRECT EXAMINATION 23 BY MR. SCHIRRMEISTER: 24 Q. Would you into yourself -- introduce 25 yourself to the court and to the ladies and gentlemen 8 1 of the jury? 2 A. Sure. My name is David Pyatt. 3 Q. Okay. And, David, you're appearing here 4 by videotape rather than in person. Would you explain 5 to the court and the jury why you're appearing by 6 videotape. 7 A. I'm appearing by videotape because I will 8 not be in the country when this goes to trial in 9 October. 10 Q. Okay. What are you going to be doing? 11 A. I'm going to be -- I'm going to be on a 12 climbing trip in Nepal. 13 Q. And how is it that you came to be on a 14 climbing trip in Nepal during this period? 15 A. Well, my -- I've been trying to get to 16 Nepal and climb this peak for three or four years. 17 And finally, we got the permit. And I got the people 18 together that I felt comfortable enough doing this 19 climb with. And that all happened before this case 20 got started. So that's why that took priority over -21 over what we're doing here. 22 Q. Okay. Where are you originally from? 23 A. I was born in Pensacola, Florida, but I 24 spent most of my childhood and early adulthood in 25 North Carolina. 9 1 Q. Okay. Tell us where you grew up, where 2 you went to high school, where you worked at -- up 3 through your high school years? 4 A. I -- most of the time, we spent -- I 5 lived in Raleigh, North Carolina, for a little while, 6 and then we moved to the mountains. So I grew up and 7 went to high school in a place called Marion, North 8 Carolina. It's about an hour and a half further west 9 from Winston Salem. That's where I went to school. 10 And then when I -- after high school, which was 11 McDowell High School, I moved back to Raleigh and went 12 to North Carolina State University for my 13 undergraduate. Both my parents still live in Western 14 North Carolina. My mom is a retired nurse and she 15 lives in Asheville, and my dad is a retired 16 construction developer, and he lives in -- still lives 17 in Marion. 18 Q. Okay. What year did you graduate from 19 high school? 20 A. 1976. 21 Q. Okay. And tell the jury a little about 22 yourself personally? Are you married? Do you have a 23 family? 24 A. I am married. I've been married for 22 25 years. And I have two daughters. One is a junior in 10 1 college, and she's here at Boulder at CU. And the 2 youngest one is a junior in high school, and she's, 3 obviously, still living at home with us. 4 Q. Okay. I'm going to put up -5 A. Go ahead. I can move. 6 Q. -- the first slide. So tell us about 7 where you went to college and what you graduate -8 A. I'm going to have to slide over. Is this 9 okay with every one? This way. Just so that's not -10 okay. Everybody all right with that? 11 Q. Yes, sir. 12 A. Okay. 13 Q. So just tell us where you went to college 14 and what you studied there. 15 A. Thanks. My undergraduate at North 16 Carolina State University was biological sciences. I 17 think that was the name of the college. I also took a 18 lot of chemistry classes, so I probably could have 19 gotten a double major; but anyway, biological 20 sciences, agricultural sciences, I think was the name 21 of the school. And then I went back and got an 22 additional B.S. degree in science education, because I 23 wanted to -- I wanted to teach. And then my graduate 24 degree was at the University of Colorado. And that 25 was in toxicology. 11 1 Q. Okay. Explain to the jury what 2 toxicology is, David. 3 A. Well, the -- the word means the study of 4 poisons. So you are looking at why things are toxic, 5 amounts that it takes to be toxic, potential remedies 6 for that toxicity. So that's what toxicologists do. 7 We study chemicals and other things that have the 8 potential to be toxic and try to understand why that 9 happens. 10 Q. Okay. And presently, do you have faculty 11 appointments and teach students at the University of 12 Colorado? 13 A. I do. 14 Q. Okay. And which -- which faculty 15 appointments do you have? 16 A. I'm still with the same group that I got 17 my Ph.D. with, and that's the University of Colorado, 18 School Of Pharmacy, where I teach a toxicology course, 19 I teach a risk assessment course. I have an 20 appointment with the newly formed school of public 21 health where I also help them teach their toxicology 22 course. And I'm developing a risk assessment course 23 for them. 24 I teach a toxicology course for the 25 University of Colorado, the Denver campus, and also 12 1 teach an environmental epidemiology class for those. 2 So I guess technically I have three different 3 appointments, but it's all part of the University of 4 Colorado. 5 Q. Okay. Now, you have a Ph.D., correct? 6 A. I do. 7 Q. And so it would be appropriate to address 8 you as Dr. Pyatt? 9 A. I -- I think in a formal setting, yes. 10 Q. But I'm -- if it's all right with you, 11 I'll just call you David. 12 A. That's perfectly fine. 13 Q. Okay. Are you currently or since your -14 receiving your Ph.D., what type of work have you done 15 and what research have you conducted? 16 A. When I first graduated with my Ph.D., I 17 did what is typically called a post-doctoral 18 fellowship. So this is when you -- you work with 19 someone. They are the ones that got the grant, so 20 they are paying you a salary out of their grants. And 21 you're doing research that they have an interest in in 22 their lab. And I did that with Dr. Richard Irons, and 23 we were looking at benzene metabolites and the 24 toxicity associated with the benzene metabolites in 25 bone marrow cells in the immune system. And then 13 1 typically the way an academic profession goes is you 2 start -- as you develop scientifically, you start 3 writing your own grants and submitting your own 4 grants. They were getting funded. My grants were 5 getting funded. 6 So at that point, I kind of separated, 7 and I was doing my own basic research in the lab. I 8 had lab space, I had technicians that I was directing. 9 And then my appointment at that -- was assistant 10 research professor. And I did that until about 2003. 11 Q. Okay. Now, if you would go to the second 12 page of the slides. The first bullet point says over 13 80 abstracts, peer-reviewed publications and book 14 chapters primarily on bone marrow and immunological 15 toxicity and/or benzene. 16 What are abstracts pier reviewed 17 publications, David? In other words, what -- what are 18 the nature of your publications? 19 A. The -- I've combined them together for 20 this point. But sciences gets out into the scientific 21 community several different ways. And you can write 22 book chapters. I've written one book chapter 23 specifically on benzene. Peer-reviewed publications, 24 those are primarily literature where you're describing 25 your research. You submit it to a journal. They -- 14 1 they send it out for external reviewers. And then 2 they publish it in the literature. Abstracts were 3 typically smaller pieces of your science that you have 4 submitted to various scientific organizations, and you 5 usually present those at -- at national or 6 international meetings. 7 Q. Okay. 8 A. Not all of those -- not -- not every 9 abstract is peer-reviewed, but the -- the meetings 10 that I attend, they do have a peer review process for 11 their abstracts. 12 Q. Okay. And, David, if you could just 13 scoot a little bit over. The light is -14 A. Yeah, sorry. 15 Q. -- is on the side of your head there. 16 THE VIDEOGRAPHER: Counsel, may we 17 briefly go off the record. 18 MR. SCHIRRMEISTER: Yes. 19 THE VIDEOGRAPHER: Going off the record. 20 The time is 9:46. 21 (Recess taken, 9:46 a.m. to 9:47 a.m.) 22 THE VIDEOGRAPHER: We are back on the 23 record. The time is 9:47. 24 Q. (BY MR. SCHIRRMEISTER) Okay. David, the 25 second bullet point describes some of your clients and 15 1 the government agencies you work for. Briefly 2 describe those for the jury. 3 A. Since about 2003 when I officially left 4 the university in a -- a research capacity and I 5 worked for a couple of consulting companies, and then 6 in 2000 -- the end of 2004, I started my own, which is 7 called Summit Toxicology. And within those 8 organizations, I've done a variety of projects for 9 lots of different kinds of clients. Those include 10 private sector, various industries, various law firms, 11 but also a wide variety of regulatory agencies that -12 some of which are listed here. I've done work for the 13 USEPA. I worked for USEPA as a full-time employee for 14 a while. Department of Health and Services, the CDC. 15 I've done work for -- or we've done work for Health 16 Canada, various state organizations: California, 17 Texas, Colorado. So there -- it's been a long -18 pretty long list of clients that we've had through the 19 years. 20 Q. Okay. What type of work have you done 21 for the centers for disease control? 22 A. Mostly just reviewed scientific 23 literature. 24 Q. Okay. How about for the Environmental 25 Protection Agency? 16 1 A. The Environmental Protection Agency, what 2 I did for them -- well, I used to work for them. And 3 then we were evaluating a specific hazardous waste 4 site here in the Denver region called the Rocky 5 Mountain Arsenal. So I was kind of an amateur 6 toxicologist, because I was working with -- this is 7 before I got my Ph.D., and I was working with a 8 toxicologist on that site. I really liked him, really 9 respected him. And, in fact, that was part of the 10 motivation for me taking the vow of poverty, if you 11 will, and going back to graduate school and getting my 12 own Ph.D. in toxicology. 13 Q. Okay. Now, the-second-to-the-last bullet 14 point is, "Organizer presenter, Benzene 2009, Health 15 Effects and Mechanism of Bone Marrow Toxicity. What 16 is that, David? 17 A. About every four or five years, all of 18 the researchers across the country, really, across the 19 -- the globe are -- who have an active research 20 program or an active interest in benzene, they get 21 together and put these symposiums together where 22 people can discuss and -- and present all of the new 23 things that have come out in the world of benzene 24 toxicology. And the first one I attended was in 2004, 25 and it was in Munich, Germany. 17 1 This one, 2009, I was on the planning 2 committee, so I designed a web site for the meeting 3 and was part of the review process for some of the 4 abstracts for the posters. But anyway, it was a big 5 meeting that was held two weeks ago in Munich, 6 Germany. It was about four days' worth of 7 presentation; so, you know, anyone really that had 8 anything to say about benzene research and toxicology, 9 most everyone was there. 10 Q. Okay. David, I'm going to hand you what 11 has been marked as Defendants' Deposition Exhibit 12 No. 1. Would you identify that, please. 13 A. This is my CV or resume. 14 Q. Okay. Is that a true-and-correct copy of 15 the most recent CV that you have? 16 A. Yes. This looks to be very recent. 17 Q. Okay. 18 MR. SCHIRRMEISTER: I'll offer 19 Defendants' Exhibit No. 1. 20 THE DEPONENT: What -- what do I do with 21 it? 22 MR. SCHIRRMEISTER: Just put it down 23 there. That's fine. Thank you. 24 Q. (BY MR. SCHIRRMEISTER) Okay. David, I'm 25 going to also hand you what has been marked as 18 1 Defendants' No. 2, which is slide page No. 4. And 2 would you identify that first for the jury, please. 3 A. What you've handed me is what's on the 4 projector there, the slide. This is a list of -- kind 5 of a summary of my opinions in this case. 6 Q. Okay. Did you prepare that? 7 A. Yes. 8 Q. Okay. And that has been marked as 9 Defendants' Exhibit 2? 10 A. Okay. 11 Q. Would you just confirm that, that's -12 A. Oh, yes. 13 Q. Okay. 14 A. Yes. 15 MR. SCHIRRMEISTER: Okay. I'll offer 16 Exhibit 2. 17 MR. GIANARIS: Over my objection. 18 Q. (BY MR. SCHIRRMEISTER) Okay. Now, 19 David, from this point forward, when I ask you to 20 express your opinions, would you agree to do that for 21 me that the standard is based upon reasonable and 22 medical scientific probability? 23 A. Sure. 24 Q. And if there's any -- any opinion that 25 you have on any other standard other than reasonable 19 1 medical and scientific probability, please tell us 2 that. 3 A. Okay. 4 Q. Otherwise, we will assume that all your 5 opinions are based upon reasonable and medical and 6 scientific probability. 7 A. Sure. 8 Q. Are you agreeable to that? 9 A. Yes. 10 Q. Okay. Now, what is the first opinion? 11 A. That the paint solvents in Dupont or PPG, 12 or really any paint product in these solvents are not 13 established carcinogenic agents. They don't cause 14 cancer generally or leukemia specifically. 15 MR. GIANARIS: Object to form. 16 Q. (BY MR. SCHIRRMEISTER) Okay. I'm going 17 to offer -- offer you -- offer as well Defendants' 18 No. 3. Would you identify that, please. 19 A. This is my report that I wrote and 20 submitted in this case. 21 Q. Okay. And is that a true-and-correct 22 copy of the report that you prepared and submitted in 23 this case? 24 A. It doesn't appear to have been changed, 25 so, yes. 20 1 Q. Okay. 2 A. I would say it is. 3 Q. Okay. And along with the supplemental 4 report, which we will tender later, is a summary of 5 your opinions that's been marked as Exhibit No. 2 a 6 summary of the report that's been marked as 7 Exhibit No. 3? 8 A. Yes. Yeah, it may not be exactly in this 9 order; but, sure, all of these things are definitely 10 covered in my report, this declaration. 11 Q. Okay. And when you say all of these 12 things, are you referring to the summary of 13 opinions -14 A. Sorry. 15 Q. -- that's been marked as Exhibit 2? 16 A. Yeah, sorry. Yes. 17 Q. Okay. Okay. Now, let's -- okay. Would 18 you read that to the jury, please. 19 A. The first opinion was "Dupont and PPG 20 paint solvents do not cause cancer or leukemia." 21 Q. Okay. Now, let's look at the next slide, 22 please. And I'm going to hand you what has been 23 marked as Defendants' Exhibit 4. Okay. David, what 24 solvents are in Dupont and PPG paints? 25 MR. GIANARIS: Object to the form. 21 1 A. The predominant ones which you're going 2 to find are going to be toluene, which I think is in 3 the highest concentrations. Xylene. It depends on 4 the product so that the -- the composition can change 5 somewhat. And then a variety of things that would 6 fall under the category of petroleum distillates. So 7 that would be mineral spirits, Stoddard solvent, 8 various naphthas, things of that nature, which, from a 9 toxicological point of view, are all very -- are all 10 very similar. And typically in these regulatory 11 groups, they -- they -- they combine all of those 12 together. 13 Q. Okay. And what do you understand the 14 plaintiffs' claims to be in this lawsuit? 15 A. My understanding is that the -- the trace 16 levels of naturally occurring benzene that are likely 17 found in these various solvents were of sufficient 18 magnitude to cause Mr. Wolfe's acute promyelocytic 19 leukemia. 20 Q. Okay. You understand Mr. Wolfe never 21 worked with benzene, correct? 22 A. I've never seen any evidence -23 MR. GIANARIS: Object to form. 24 A. -- that that's true, yes. 25 Q. (BY MR. SCHIRRMEISTER) Okay. Now, on 22 1 the bottom of the slide, there are a number of 2 different agencies. And then there are those color 3 circles above in the graph. What -- are you familiar 4 with organizations -- or are there organizations that 5 study and evaluate chemicals as to whether they are 6 capable of causing cancer or leukemia? 7 A. Yes. 8 Q. Okay. The first one on there is the 9 IARC, I-A-R-C. What is IARC? 10 A. IARC is -- the -- the acronym stands for 11 the International Agency for Research on Cancer. And 12 it is an international grouping of preeminent 13 scientists, toxicologists, physicians, epidemiologists 14 that look at -- collectively look at the sum total of 15 the published literature. 16 So for them, they have a bright line that 17 it has to be published before it will be evaluated 18 under the IARC kind of in their panel. But then they 19 evaluate various chemicals, drugs, viruses, anything 20 that is a potential cause of human cancer. 21 Q. Okay. David, the next one is N-I-O-S-H, 22 NIOSH. What is NIOSH? 23 A. NIOSH stands for the National Institute 24 of Occupational Safety and Health. And that's the 25 research arm of OSHA. So they conduct research on 23 1 behalf of OSHA in support of OSHA's regulations that 2 -- that they have. 3 Q. Okay. ACGIH, what is that, David? 4 A. That's the American Conference of 5 Governmental Industrial Hygienists. And this is a -6 I think it's actually voluntary, but this is a large 7 group of industrial hygienists that, from all 8 different occupations across the country, some 9 academic, some in -- actually out in the workplace, 10 but they get together and discuss what they call a 11 TLV, which is a threshold limit value. And it's 12 essentially what they consider to be a safe working 13 level of these various chemicals. 14 Q. Okay. Next one is NTP. What is that? 15 A. That's the National Cancer -- sorry. NTP 16 stands for the National Toxicology Program, so that's 17 a -- a branch of the federal government that also has 18 a lot of collaborators within university and academic 19 institutions. And they are the ones -- and it's 20 usually dictated by the Environmental Protection 21 Agency, but they are the ones that conduct or oversee 22 or interpret the data that comes out of long-term 23 animal studies. 24 So if anyone wants to know, does my 25 chemical cause cancer in one or more experimental 24 1 animals, then they submit that to the National 2 Toxicology Program, they rank them based on their 3 priorities, and then they actually go out and conduct 4 the study, and then report back whether there was 5 evidence of carcinogenicity in that -- in those 6 species. 7 Q. Okay. EPA? 8 A. That's the Environmental Protection 9 Agency. 10 Q. Okay. And what do they -- what is their 11 role with regard to determining whether toluene, 12 xylene, or petroleum distillates are capable of 13 causing cancer or APL? 14 A. Well, EPA is a -- their -- their role is 15 to protect the environment and people that are exposed 16 to chemicals from the environment, as well as animals 17 and ecosystems. But they, for various chemicals -18 excuse me -- publish -- put out what's called an IRIS 19 database. And within that, they classify chemicals 20 according to their toxigenicity. 21 Q. Okay. And, finally, the State of North 22 Carolina. How does the State of North Carolina 23 regulate or interpret the potential carcinogenicity of 24 toluene, xylene, or petroleum distillates? 25 MR. GIANARIS: Object to the form. 25 1 A. My understanding is -- well, lots of 2 states have environmental departments. My 3 understanding of the State of North Carolina is they 4 rely on these national organizations like OSHA, NIOSH. 5 They -- they -- they base their decisions on what 6 these other groups -- I don't think they do any 7 independent evaluation. 8 Q. (BY MR. SCHIRRMEISTER) Okay. Now, 9 let's -10 A. And we skipped one, the AT -- ATSDR. 11 Q. Oh, I'm sorry. What is the ATSDR? 12 A. Just because there's a dot on there. 13 That's the Agency for Toxic Substances and Disease 14 Registry. So it is a specific branch of the CDC. The 15 CDC is the Center for Disease Control. And they are 16 tasked with and their -- their sole job is to go out 17 and look at environmental exposures typically from 18 hazardous waste sites, from Superfund sites, and 19 conduct studies to see if the people living in 20 proximity to these hazardous waste sites -- if there's 21 any evidence of toxicity associated with those 22 exposures. 23 Q. Okay. Now, I'm going to ask you 24 questions about the classification by these agencies 25 for these three chemicals. Okay? 26 1 Now, has the IARC ever classified toluene 2 with naturally occurring trace benzene as a che -- as 3 a chemical that causes cancer? 4 A. Say that again. I'm sorry. 5 Q. Yes. Has IARC ever classified toluene 6 with naturally occurring trace benzene as a chemical 7 that causes cancer? 8 A. No. 9 Q. Has IARC ever classified toluene with 10 naturally occurring trace benzene as a chemical that 11 causes APL? 12 A. No. 13 Q. Okay. Same question with regard to 14 toluene and NIOSH. Has NIOSH ever classified toluene 15 with naturally occurring trace benzene as a chemical 16 that causes cancer or APL? 17 A. No. NIOSH puts out a report where they 18 make a -- a comprehensive listing of all of the 19 chemicals that they believe there is some evidence of 20 carcinogenicity. And toluene is not included on that 21 list. 22 Q. Okay. The ACGIH, David, has the ACGIH 23 ever classified toluene with naturally occurring trace 24 benzene as a chemical of causing cancer or APL? 25 A. No. The ACGIH publish what I consider to 27 1 be really helpful, relatively short summaries of the 2 toxicity have these various chemicals. And it's their 3 documentation or their support for what they think the 4 TLV would be, the threshold limit value. And within 5 that, for toluene, they specifically say that there is 6 not enough evidence to support that this is a human 7 carcinogen. 8 Q. Okay. The NTP, the National Toxicology 9 Program. Has the NTP ever classified toluene with 10 naturally occurring trace benzene as a chemical that 11 causes cancer or APL? 12 A. Again, like NIOSH, the NTP puts out these 13 reports periodically. And the most recent was the 14 eleventh report on carcinogenicity is what they call 15 it. And they list very comprehensively any chemical 16 for which there is evidence in their animal studies 17 that there was evidence of carcinogenicity. And 18 toluene is not listed on that. 19 Q. Okay. The next one is the ATSDR of the 20 Centers for Disease Control. Has that agency ever 21 classified toluene with naturally occurring trace 22 benzene as a chemical that can cause cancer or APL? 23 A. It has not. The ATSDR publishes these 24 exhaustive -- basically they are books that are called 25 toxicological profiles on these various chemicals. 28 1 And within those toxicological profiles, they have all 2 of the animal data, all of the epidemiology, all of 3 the metabolism, all of the toxicity data associated 4 with that chemical that they could find in the 5 literature. And, no, the ATSDR does not believe that 6 toluene is a carcinogen. 7 Q. Okay. The EPA, David. Does the 8 Environmental Protection Agency -- has it ever 9 classified toluene with naturally occurring trace 10 benzene as either a chemical that causes cancer or 11 APL? 12 MR. GIANARIS: Object to the form, 13 foundation. 14 A. The USEPA publishes what's called the 15 IRIS, Integrate Risk Information System. And in IRIS, 16 it is a more condensed form than the AT -- ATSDR tox 17 profiles, but it still goes through a relatively 18 comprehensive review of the literature. And they have 19 a various gradation of whether they think it's a known 20 human carcinogen or whether it might be a human 21 carcinogen. And toluene is neither of those in their 22 opinion. 23 Q. (BY MR. SCHIRRMEISTER) Okay. And then, 24 finally, the State of North Carolina. How does the 25 State of North Carolina classify these -- classify 29 1 toluene as to whether it's capable of causing either 2 cancer or APL? 3 MR. GIANARIS: Object to the form, 4 foundation. 5 A. My understanding is that they are going 6 to base their classification system on these other 7 organizations. So there is nothing any different that 8 they would say that hasn't been already said in these 9 other groups by these other groups. 10 Q. (BY MR. SCHIRRMEISTER) Okay. Now, let 11 me ask you about xylene next, David. Has the IARC, 12 NIOSH, ACGIH, the NTP, the ATSDR, or the EPA ever 13 classified xylene with naturally occurring trace 14 benzene as a chemical capable of causing cancer? 15 MR. GIANARIS: Hold for one second before 16 he answers. Did you put -- was North Carolina in that 17 question? I didn't catch it. 18 MR. SCHIRRMEISTER: No. 19 MR. GIANARIS: So I don't interrupt you, 20 may I just have a continuing objection to foundation 21 as to questions regarding North Carolina? 22 MR. SCHIRRMEISTER: Yes, sir. 23 MR. GIANARIS: And you all can proceed. 24 Thank you very much. 25 MR. SCHIRRMEISTER: Repeat the question? 30 1 A. Are we on? Am I going? I heard the 2 question. 3 Q. (BY MR. SCHIRRMEISTER) Okay. 4 A. The answer is, no. I mean, xylene is not 5 a thing. It's a -- it's -- actually, there's three 6 different kinds of xylene, but none of them have been 7 classified by any regulatory agency that I am aware 8 of, including the ones listed here, as a human -- as a 9 human carcinogen. 10 Q. Has the IARC, the International Agency 11 for the Research of Cancer, the NIOSH, National 12 Institute Occupational Safety and Health, the ACGIH, 13 the American Conference of Governmental and Industrial 14 Hygienists, the NTP, the National Toxicology Program, 15 the ATSDR, the Agency For Toxic Substances and Disease 16 Research, or the EPA, the Environmental Protection 17 Agency -- has any of those agencies ever classified 18 xylene with naturally occurring trace benzene as a 19 chemical capable of causing APL? 20 A. No. 21 Q. Okay. Finally, to the petroleum 22 distillates, same two questions, David. Has IARC, 23 NIOSH, ASGIH, NTP, ATSDR, or the EPA ever classified 24 petroleum distillates with naturally occurring trace 25 benzene as capable of causing cancer? 31 1 A. Not that I've ever seen. And they -2 there are -- depending on which group you're looking 3 at, IARC or ASGIH or the ATSDR, they -- some of them 4 have data on naphthas, some of them have data on 5 mineral spirits, some of them have data on Stoddard 6 solvents; but all of those things are chemically 7 similar enough to where, from a toxicological point of 8 view, it is fair to put them all into this group 9 called petroleum distillates, which is what we did. 10 And the answer is, no, none of those groups consider 11 any of those various things that we would call a 12 petroleum distillate as a -- a human carcinogen. 13 Q. Okay. And then, finally, do any of those 14 agencies: The IARC, NIOSH, ACGIH, NTP, ATSDR, or EPA 15 ever classify this group of chemicals under the name 16 petroleum distillates as ones capable with naturally 17 trace benzene as ones capable of causing APL? 18 A. No. 19 Q. Okay. Now, with regard to the 20 classification by toluene -- of toluene, xylene, and 21 petroleum distillates by the State of North Carolina, 22 how do you understand the nate of -- State of North 23 Carolina classifies and regulates these three 24 chemicals? 25 A. My understanding is that -- and I've 32 1 never done any work for the State of North Carolina, 2 so I'm not exactly sure what their inner workings are, 3 but that they rely on OSHA and IARC. And these are 4 their international and national agencies, and they 5 base their decisions on what these other national 6 groups say. 7 Q. Okay. 8 MR. GIANARIS: Same objection. 9 Q. (BY MR. SCHIRRMEISTER) David, does 10 Exhibit No. 4 -- does this accurately portray the 11 regulatory classifications of toluene, xylene, and 12 petroleum distillates with naturally occurring trace 13 benzene with regard to their classification as capable 14 of causing cancer or APL? 15 A. Certainly my interpretation of -- of 16 their various regulatory documents, yes. 17 MR. SCHIRRMEISTER: Okay. I'll offer 18 Defendants' Exhibit 4. 19 MR. GIANARIS: Over my objection. 20 MR. SCHIRRMEISTER: We'll leave that 21 there. Thank you, sir. 22 Q. (BY MR. SCHIRRMEISTER) David, would you 23 turn -- I'm going to now hand you what has been marked 24 as Exhibit 5. 25 A. Okay. 33 1 Q. And it is three pages long. And would 2 you identify Exhibit 5 for us, please. 3 A. Yeah, this is what I was talking about 4 with the NTP. They periodically publish these reports 5 on carcinogens. And they are pretty -- pretty 6 conservative with the listings. And by that I mean, 7 if there's any evidence in their animal studies that 8 there is an increased risk of tumor genesis in any of 9 these species or that there's evidence of 10 carcinogenicity in these species, then it makes it 11 onto this list. 12 Q. Okay. So -- and is this the most recent 13 list issued by the -- the National Toxicology Program? 14 A. The eleventh report is the most recent 15 one that I've seen. When this one comes out, then 16 they are automatically working on the next one. So 17 internally, there's probably a twelfth; but this is 18 the only one that I think is publically available. 19 Q. Okay. And anywhere on this eleventh 20 report, that lists all of these different chemicals 21 that cause cancer, do toluene, xylene, or petroleum 22 distillates appear? 23 A. No. 24 MR. SCHIRRMEISTER: I offer Defendants' 25 Exhibit 5. Would you like to take a break? Let's 34 1 take a five-minute break. 2 THE VIDEOGRAPHER: Going off the record. 3 The time is 10:09. 4 (Recess taken, 10:09 a.m. to 10:19 a.m.) 5 THE VIDEOGRAPHER: We are back on the 6 record. The time is 10:19. 7 Q. (BY MR. SCHIRRMEISTER) David, would you 8 read the slide, which is page 11, please. 9 A. Oh. The APL, which stands for Acute 10 Promyelocytic Leukemia, is a distinct clinical disease 11 and is different than other subtypes of AML, which is 12 acute myeloid or myelogenous leukemia. 13 Q. Okay. David, I'm going to hand you what 14 has been marked as Exhibit 6. 15 A. Okay. 16 Q. And this is called "Why APL is a unique 17 clinical disease," correct? 18 A. Yes. 19 Q. And just take us -- and I'm going to go 20 back in detail, but -- what is No. 1, morphology? 21 What does that mean? 22 A. Morphology is the shape of the cell. So 23 that would be a way to describe how the cells would 24 look microscopically. So if you took them out, looked 25 at them under a microscope, a hematologist might do 35 1 that, they -- they have a very distinctive morphologic 2 presentation. You would be able to recognize them. 3 Q. And are you talking about an APL cell? 4 A. Correct, APL. 5 Q. Okay. 6 A. Well, they all do. All of the different 7 subtypes of AML have unique -- well, not all of the 8 them, but what -- morphologic presentations, but APL 9 is quite different than the other ones. 10 Q. And are -- is morphological a fancy way 11 of saying it looks different under the microscope than 12 other cells? 13 A. That's exactly what that means. 14 Q. Cell of origin, what does that do? 15 A. Cell of origin is we're -- we believe 16 that the malignant transformation or the thing that 17 causes the cell to become leukemia where that happens 18 within the hematopoietic progression, which I think we 19 have a slide or two to discuss. 20 Q. Okay. Psychogenetics, what is that data? 21 A. Sorry. Cytogenetics, that is a branch of 22 medicine, science where you're looking at the shape of 23 the chromosomes. So basically how many chromosomes 24 are there, whether some are missing, some or broken, 25 whether they are combining with each inappropriately. 36 1 So that's just a way to describe what the chromosomes 2 look like. And that is critically important in the 3 diagnosis and the prognosis for -- for all forms of 4 leukemia. 5 Q. Okay. Treatment? 6 A. The treatment for A -- APL is 7 categorically different than the treatment for -- for 8 any other -- any other type of leukemia that I'm aware 9 of. 10 Q. Okay. And lastly, epidemiology, what is 11 that? 12 A. Epidemiology is the science where you're 13 looking at what causes diseases in the human 14 population. And because APL is unique enough, there 15 have been epidemiological studies looking at it as -16 not as a subtype of AML, but as its own unique entity. 17 Q. Okay. And are these five factors ones 18 that you've identified to explain why APL is a unique 19 disease? 20 MR. GIANARIS: Object to the form. 21 Leading. 22 Q. (BY MR. SCHIRRMEISTER) Okay. What are 23 these five factors? Why have you chosen these five 24 factors? 25 A. These -- these categories are ways in 37 1 which there is clear -- there are clear differences 2 between APL and the other forms of acute myelogenous 3 leukemia. 4 Q. Okay. 5 A. So it is different -- distinctly 6 different in each one of these categories. 7 Q. Okay. 8 MR. SCHIRRMEISTER: I'll offer 9 Defendants' Exhibit 6. 10 MR. GIANARIS: Over my objection. 11 Q. (BY MR. SCHIRRMEISTER) Okay. David, now 12 I'm going to put up what I will hand you and mark -13 it's previously been marked as Exhibit 6A. And why 14 don't you stand up, if you would, so you can explain 15 to the jury -16 A. Okay. I'll try not to trip. 17 Q. -- what this is. 18 A. This is going to work? Yeah. Okay. 19 This is a slide that I actually made for a talk that I 20 gave at SOT. And at that -- the Society of 21 Toxicology. And what I was doing in that presentation 22 was describing the role that the bone marrow 23 microenvironment plays in various hemopoietic 24 diseases. Why I have it in this presentation or today 25 is it just gives a very simplistic view of the process 38 1 of hematopoiesis. 2 Q. Okay. Now -- okay. Okay. I'm going to 3 interrupt you, David. 4 A. Okay. 5 Q. Have you spent -- how much of your career 6 have you spent on this issue? 7 A. On hematopoiesis? 8 Q. Yes, sir. 9 A. That's -- that's really all that I've 10 done from a research point of view as well as a 11 consultant. It's either been hematopoietic 12 development or toxicity in the bone marrow that 13 impacts on hematopoietic development. That's -14 that's what I do. 15 Q. Okay. Now, let's start with the 16 left-hand side where it says, "bone." What are we 17 looking at there and what is happening? What happens 18 in your bone marrow? 19 A. Yeah, this is just a depiction of a bone. 20 And this we don't really need to talk about. It's 21 just kind of a blow-up of this region right on the 22 inside of the -- the -- the trabecular bone. But it's 23 demonstrating -- these cells here: Killer cells, 24 lymphocytes, basophils, platelets, red blood cells, 25 all of these things, these are cells that you would 39 1 recognize in the peripheral circulation. 2 So if I took blood out of anyone here and 3 looked at it under a microscope, I would see these 4 various cell types. So everyone knows what they are 5 probably and what they do. But what is beautiful 6 about the hematopoietic system is that all of these 7 various cell types all are thought to be derived from 8 an ancestral cell that resides in the bone marrow. 9 Q. Okay. Now, as a beginning definition, 10 hematopoietic, what is that -- what's that a big word 11 for? 12 A. Hematopoietic is blood. It's -- so 13 hematopoietic pieces is blood formation. So that's 14 what's going on in the bone marrow that is producing 15 the billions of red blood cells that we have and all 16 of the other cell types that are -- that are found in 17 the peripheral circulation. 18 Q. Okay. Now, you mentioned stem cell. 19 What is the stem cell? 20 A. Well, this is a word that's given to -21 you know, I mean, you'll get hematologists together, 22 and they will argue passionately about the definition 23 of a stem cell. It's pretty irrelevant. But what the 24 stem cell is is a cell that retains the ability to 25 turn into all of these different things. 40 1 So a cell at this level, it can turn into 2 lymphocytes, it can turn into a red blood cell. But 3 as it progresses through its maturation, eventually, 4 it starts becoming what we consider to be lineage 5 committed. And that point, it is only going to turn 6 into one cell type. 7 Q. Okay. 8 A. And once it lineage commits and says, 9 okay, I'm going to be a red blood cell, then it won't 10 have the ability -- it will not have the ability to 11 turn into these other cell types. 12 Q. Okay. Now, how -- generally, how many 13 different blood cell types are there for our purposes? 14 A. I -- that's a hard question to answer. 15 Q. Okay. Well -16 A. Six, seven. 17 Q. Well, I've heard of red blood cells. 18 What is the function of a red blood cell? 19 A. The -- they -- have hemoglobin in them, 20 so their primary function is to carry oxygen. 21 Q. Okay. 22 A. Or to carry carbon dioxide away from the 23 tissues. 24 Q. Okay. White blood cells? 25 A. White blood cells, there's a lot of 41 1 different kinds of white blood cells, which is why I 2 paused on your question. There probably are five or 3 six different things that a hematologist would be 4 interested in knowing if they were looking at your 5 blood, all of which would be considered a white blood 6 cell. 7 In general, the white blood cells, all of 8 them collectively, their primary role is to fight 9 infection. 10 Q. Okay. And then how about a platelet? 11 What is the function of a platelet? 12 A. A platelet comes from a megakaryocyte, 13 which is this thing, and its primary role is in blood 14 clotting or wound healing. 15 Q. And how does a stem cell become all of 16 these different types of blood cells? Just walk us 17 through that process, David. 18 A. I don't -- that's a really hard question. 19 Q. Okay. 20 A. I mean, basically, you've got a very 21 elaborate system of growth factors and feedback loops. 22 And it's a very complicated process; but, essentially, 23 this cell becomes more and more committed, more and 24 more mature, more and more differentiated as it's 25 moving through this pathway. 42 1 Q. Okay. 2 A. And it's also proliferating, so you're 3 getting more and more of them. But that's not -- I 4 can't answer that question in two minutes. 5 Q. Okay. How about -- well -- how about 6 this, the different types of cell lines. How many 7 different types of cell lines are there in the blood? 8 And if you would show where those are on Exhibit 6. 9 A. You know, from a hematopoietic -- I mean, 10 all of these are different cell lines. But typically, 11 hematologists will consider three -- there are 12 platelets, red blood cells, and white blood cells; so 13 those are considered to be the three main cell lines. 14 Q. Okay. And I've heard of the term 15 lymphoid lines and myelocytic or myeloid lines. 16 A. Right. Well, that's a whole different 17 classification system. It doesn't fit in with what I 18 just said. So you don't really consider those cell 19 lineages based -- it depends on how you're defining 20 those terms. But you do have lymphoid cells -- and 21 this isn't a very good picture to depict that, but you 22 do have lymphoid cells and you have myeloid cells, and 23 that is a pretty major break in the differentiation of 24 these cells. 25 Q. Okay. And where -- where is the cell 43 1 here that is the APL cell? 2 A. You -3 Q. Or should we look at it in a different 4 slide? 5 A. You can't see it on this slide. 6 Q. Okay. 7 MR. SCHIRRMEISTER: I want to -- I'd like 8 to offer Exhibit 6A. 9 MR. GIANARIS: Over my objection. 10 Q. (BY MR. SCHIRRMEISTER) Okay. David, I'm 11 going to hand you what has been marked as Exhibit 7, 12 please. 13 A. Okay. Um-hum. 14 Q. Now, would you explain -- first of all, 15 explain what chromosomes are. 16 A. Chromosomes are the structures within the 17 nucleus of a cell that -- that are within a cell that 18 -- that contain all of the genetic information. 19 So the genetic information, hair color 20 and weight and height, and all of the other things 21 that make a person a person, all of that is contained 22 in the DNA. And that DNA is really long, and so you 23 can't just have these really long strands -- you know, 24 hundreds of yards, this DNA is, and you can't have 25 these strands of DNA just flopping around. So they 44 1 are condensed. They are wrapped up around certain 2 structures into very nice, neat, little tight 3 packages. And those little, neat, tight packages, you 4 can see under a microscope, they look like this, and 5 we call those chromosomes. But really all that is is 6 a tight collection of DNA that can be unwound when 7 you're expressing certain proteins. So those are your 8 chromosomes. 9 Q. Okay. And how many chromosomes do -- do 10 we all have in each cell? 11 A. 46. 12 Q. Okay. And do the pairs of chromosomes 13 have different functions in the body? 14 A. Each chromosome has different roles, 15 correct. 16 Q. Okay. Now, give us an example that the 17 jury may be familiar with of a chromosomal problem 18 that leads to a disease or leads to a condition. 19 A. Really, for as long as we've been able to 20 identify chromosomes -- and that hasn't been that long 21 ago. I mean, probably in the '50s was the first time 22 that we were able to clearly identify -- reproducibly 23 identify chromosomes. We've known that if you see 24 alterations in the karyotype or you see alterations in 25 the number of chromosomes that it can have important 45 1 pathologic manifestations or diseases that can arise 2 from that. 3 Probably the most common, I think the one 4 that most everyone has heard of is a disease called 5 Down's Syndrome. And Down's Syndrome means you have 6 an extra copy of chromosome 21. So you have three 7 copies of chromosome 21. 8 Q. Okay. 9 A. Now, we don't know exactly how that extra 10 copy manifests itself in Down's Syndrome, but it's 11 clear that that is the basis for that -- that 12 syndrome. 13 Q. Okay. Now, you have here chromosomes in 14 the 15;17 translocation. How is the -- how does a 15 chromosomal condition in APL, the disease that 16 Mr. Wolfe had -- how do they relate to one another? 17 A. The -- the cytogenetics, however, are 18 extremely important in defining any type of leukemia. 19 And, in fact, of the New World Health Organization in 20 2008 for diagnosing and identifying leukemias, they 21 are relying more and more and more heavily 22 cytogenetics. 23 So different forms of leukemia have 24 specific cytogenetic problems associated with those. 25 And hematologists are keenly interested in that 46 1 because it allows them to accurately diagnose it, it 2 allows them to give a good prognosis or an accurate 3 prognosis to the family or the patient as well as more 4 appropriately treating it. 5 Acute promyelocytic leukemia or APL has a 6 very distinctive cytogenetic abnormality associated 7 with it, and that is a translocation between 8 chromosomes 15 and 17. 9 Q. Okay. So explain to us what is happening 10 here that leads to APL. 11 A. This 15;17 translocation, it is a 12 hallmark of APL. So in the United States, anyway, you 13 -- they will not diagnosis a patient with APL unless 14 they see this 15;17 translocation. And the 15 translocation means that a little piece of chromosome 16 15 is going over here. And this is chromosome 17. 17 And a little piece of chromosome 17 is moving over 18 here. So some of 15 is now part of 17 and some of 17 19 is now part of 15. And you can't see it on these 20 slides, but chromosomes are banded. So there is a 21 unique set of bands that allow people, under a 22 microscope, to identify which piece of which 23 chromosome belongs where. 24 So you can see this under -- under an 25 appropriate microscope. 47 1 Q. Okay. And does Mr. Wolfe have a 15;17 2 translocation? 3 A. Correct, he does. And when you get this 4 15;17 translocation -- and this is a little 5 complicated, but the result of that translocation is 6 what's called a fusion protein. And it is because you 7 have these pieces that are combining with each other 8 inappropriately. And that's what this is down here. 9 And we don't know exactly how it works, but this 10 fusion protein is thought to be the -- is thought to 11 underlie why someone gets APL. 12 Q. Okay. Very simplistically, would it be 13 correct that some of the information that should be on 14 chromosome 15 ends up on chromosome 17 and some of the 15 information that should be on chromosome 17 ends up on 16 chromosome 15? 17 MR. GIANARIS: Object to the form. 18 A. That's exactly what happens. 19 Q. (BY MR. SCHIRRMEISTER) And does that 20 lead to APL? 21 A. It certainly leads to something that you 22 can always see in APL. 23 Q. Okay. 24 A. You know, we're not at a point where we 25 can absolutely draw out a path and say here's exactly 48 1 where the transformation occurs, but this is always in 2 APL. So clearly, it has something to do with the 3 disease. 4 Q. Okay. 5 MR. SCHIRRMEISTER: Offer Defendants' 6 Exhibit 7. 7 MR. GIANARIS: Over objection. 8 Q. (BY MR. SCHIRRMEISTER) Okay. I'm now 9 going to offer what has been marked as 8B. 10 MR. GIANARIS: You're offering it into 11 evidence or just showing it to him. 12 MR. SCHIRRMEISTER: I'm going to show it 13 to him first. 14 MR. GIANARIS: So you haven't offered it 15 yet? 16 MR. SCHIRRMEISTER: I will in a moment. 17 MR. GIANARIS: Okay. 18 MR. SCHIRRMEISTER: I will -- I will, 8B. 19 MR. GIANARIS: I'll make my objection now 20 and we'll be all right. Mr. Schirrmeister, just so I 21 don't interrupt you so you don't have to edit this as 22 much if you play it, may I just have a standing 23 objection to offering the exhibits that you guys have 24 created into evidence so I don't have to make an 25 objection every time? 49 1 MR. SCHIRRMEISTER: Sure. 2 MR. GIANARIS: Okay. Thank you. 3 Q. (BY MR. SCHIRRMEISTER) Okay, David. 4 Now, this is called hematopoiesis, correct? 5 A. Yes. 6 Q. And tell us -- and I -- we -- we prepared 7 this slide in connection with the treatment, 8 understanding the disease and the treatment, correct? 9 A. Yes. I think that's why we put it in. 10 It actually provides a clearer picture of what you 11 were asking me earlier about the different lineages, 12 because they are all listed here -13 Q. Okay. 14 A. -- pretty clearly. And it also depicts 15 how these -- this differentiation occurs. As the 16 cells are marching through this pathway, they are 17 picking up characteristics of these various cell 18 types. So they start picking up the functionality. 19 Like for the red blood cell, somewhere around in here, 20 they start expressing hemoglobin. Okay. This cell 21 doesn't express hemoglobin, so it -- it has said, I'm 22 going to be a red blood cell, and it has started in 23 that process to allow it to be an erythrocyte. So 24 that's -- that is depicted very nicely on this slide. 25 Q. Okay. Now, show us where on this slide 50 1 you believe the APL disease develops. 2 A. This is called a granulocyte. And 3 there's actually lots of different kinds of 4 granulocytes, so this is a mature cell that you can 5 find in the periphery. And some of the precursor 6 cells or the cells that are more immature but are 7 leading to the formation of a granulocyte have 8 different names. This one is known as a myelocyte. 9 This one is called a promyelocyte. Pro means it's a 10 little earlier than that. And so promyelocytic 11 leukemia is happening at this level. 12 Q. Okay. And the -- what -- what -- the 13 myelocyte, what type of cell is that? Is it a red 14 blood cell, a white blood cell, a platelet? What type 15 of cell is it? 16 A. Yeah, all of these are going to be -- all 17 of these are going to be white blood cells. This is 18 the only red blood cell. This is the only platelet. 19 Even lymphocytes would be considered white blood 20 cells. So that determination doesn't really fit with 21 this categorization, but these are -- are going to be 22 granulocytes. They are white blood cells. They are 23 important in fighting infections. 24 Q. Okay. So the -- a cell that is affected 25 in APL, what is its function in the blood? 51 1 A. The cell that is affected in APL, its 2 function is just to continue to mature and 3 differentiate and ultimately produce a granulocyte, 4 whose role is to fight infections. 5 Q. Okay. Now, tell us what the disease of 6 APL is vis-a-vis what is happening on Exhibit 8B. 7 A. Yeah. What happens is -- which is why 8 the treatment is -- is so beautiful, really, is that 9 we know that in this process in patients that have 10 acute promyelocytic leukemia, the process stops right 11 here or, perhaps, right here; but it is not allowed to 12 take the final differentiation step. 13 So it stops at a promyelocyte stage. So 14 you get an increase in promyelocytes. Those do not 15 take the next step and produce functioning 16 granulocytes. 17 So the individuals don't -- they are not 18 as capable in fighting infection, they don't have 19 enough granulocytes, and they have too many of these 20 cells that are -- that are present in the bone marrow 21 or the periphery. 22 Q. Okay. And is that the APL disease? 23 A. That is the APL disease. You have -- the 24 leukemia is that you have a huge collection of these 25 promyelocytes that are not fully functional, so they 52 1 are not really doing anything; but they are blocked in 2 their differentiation probably by that fusion protein 3 that I showed you on the 15;17. That blocks it in its 4 differentiation and -- and prevents it from turning 5 into a granulocyte. 6 Q. Okay. And how -- what -- what is the 7 standard treatment and how does it work? 8 A. The standard treatment, the first -- the 9 first stage treatment is a drug called altransretnoic 10 acid. And altransretonoic acid, it really is kind of 11 magical, because what it does is it allows that block 12 and differentiation to be overcome. 13 So it allows this promyelocyte to take 14 these additional steps and differentiate and mature 15 into a granulocyte. Now, why that's important in 16 treating leukemia is that granulocytes only live about 17 eight hours. So they have a relatively short half 18 life. So when you -- this one can live for a long 19 time. But when you allow a promyelocyte to convert 20 itself to a granulocyte, it dies on its own. So the 21 drug, altransretnoic acid, doesn't have to kill 22 proliferating cells, like most other chemotherapeutic 23 agents do. It is a differentiation agent, and it 24 allows this cell, basically, to kill itself by 25 converting itself to a granulocyte. 53 1 Q. Okay. How -- and what is the name of 2 that treatment? 3 A. The drug is called altransretonoic acid, 4 ATRA. 5 Q. Okay. And that is the treatment that 6 Mr. Wolfe received? 7 A. Yes. 8 Q. Okay. And is -- and how is the altrans 9 -- this treatment, altransretonoic acid treatment, 10 different than other chemotherapy drugs such that it 11 is unique? 12 A. There's no -- there's really nothing like 13 it. Any -- in any treatment of any disease that I've 14 seen, altransretonoic acid induces differentiation 15 like I just described. So it's causing these cells to 16 turn into granulocytes; they die on their own. 17 Every other form of treatment for various 18 types of leukemia -- now, there is a new one for CML. 19 But for AML, all of the different subtypes of AML, 20 they are treated with anti-proliferating agents. So 21 these are alkylating agents, or somehow these are 22 drugs that kill cells that are dividing. Since the 23 leukemia cells are dividing, the thought is, well, we 24 can kill the leukemia cells, and that's going to help 25 the patient. So all of these drugs -- and there's, 54 1 you know, too many to list, but they all act basically 2 the same way, and that is they are killing 3 proliferating cells. 4 Q. Okay. 5 A. Because proliferating dividing cells are 6 not just leukemia cells, and you've got dividing cells 7 all over the place, then that causes a lot of the side 8 effects that people know and appreciate with these 9 chemotherapeutic agents, like hair falling out, 10 because the hair follicles have a lot of proliferating 11 cells in them. And some of the nausea that's 12 associated with these chemotherapeutic agents, because 13 it's killing these proliferating cells in the GI 14 tract. So -- I mean, altransretonoic acid has some 15 side effects, too, but it's a different -- totally 16 different process than what are treating the other 17 AML types. 18 Q. Okay. And then the next -19 MR. SCHIRRMEISTER: I'm going to offer 20 Exhibit 8B. Okay. 21 Q. (BY MR. SCHIRRMEISTER) David, the next 22 reason you mention was epidemiology. And what is this 23 article? 24 A. This is a study by Dr. Douer. It's in 25 California. And he's not the only one, but this is 55 1 where he went out and, recognizing these distinct 2 clinical characteristics of APL, he published a paper 3 on the epidemiology of this specific subtype. 4 Q. Okay. Now, some experts on behalf of the 5 plaintiffs, a Dr. Milman, I believe, has testified 6 that it is not possible to conduct epidemiology 7 studies on APL. Do you agree with that? 8 A. I -- I don't understand the basis for 9 that comment, because we're -- we're going to talk 10 about lots, and there are many that we aren't going to 11 put in this presentation. So APL -- either APL or the 12 15;17, which they are synonymous, they are the same 13 thing, people look for those all of the time and have 14 done studies on those all the time. 15 Q. Okay. Are any other forms or subtypes of 16 AML studied uniquely in epidemiology? 17 A. To my knowledge, there are no more FAB 18 subtypes, but people are starting to think -19 epidemiologists today are starting -- they recognize 20 that the cytogenetic changes, let's say, an 8;21 21 translocation, every one that has an 8;21 22 translocation, their leukemias are very similar to one 23 another. So they are starting to conduct 24 epidemiological studies based on these cytogenetic 25 profiles. 56 1 So people are recognizing that that is a 2 more appropriate way of grouping these diseases, so 3 the 15;17 or 8;21 or inversion 16 or any of the other 4 ones, that is where the field of epidemiology is 5 going. Up to this point, the answer to your question 6 is no. 7 Q. No. Okay. Now, tell us why you've 8 selected this study and what the significance is. 9 A. Well, I selected this study because it 10 specifically addressed the question at hand, and it 11 illustrates pretty clearly that Dr. Douer, based on 12 his research, concluded that APL is very different 13 from the other subtypes of -- of AML. In fact, I'll 14 just read it. "Descriptive epidem" -15 Q. Why don't -- just -- if you would -- well 16 go ahead read the top and the bottom, too. I'm going 17 to ask you about the bottom. 18 A. Do you want me to read the top? 19 Q. Why don't you read the bottom. 20 A. Okay. "It is, therefore, likely that 21 etiological factors for APL are different from those 22 of other AML subtypes. So far, no environmental 23 and/or occupational risk factors have been found for 24 APL." 25 Q. Okay. And -- and that is based on an 57 1 epidemiology study? 2 A. Yes. And his review of the literature 3 and his understanding of the disease and all of the 4 things that we've been talking about. 5 Q. Okay. 6 MR. SCHIRRMEISTER: I'm going to offer 7 Exhibits 9 and 10. 8 Q. (BY MR. SCHIRRMEISTER) Okay. David, I'm 9 now going to hand you what has been marked as Exhibits 10 11 and 12. Would you identify those, please. 11 THE REPORTER: Can we go off the record 12 for a second, please? 13 MR. SCHIRRMEISTER: Yeah. 14 THE VIDEOGRAPHER: Going off the record. 15 The time is 10:45. 16 (Discussion off the record.) 17 THE VIDEOGRAPHER: We are back on the 18 record. The time is 10:45. 19 Q. (BY MR. SCHIRRMEISTER) Okay. David, 20 I've handed you what has been marked as Exhibits 11 21 and 12. Would you identify these for us, please. 22 A. Oh, right. This is another study that 23 really did the same thing. The epidemiology of acute 24 promyelocytic leukemia in Italy. Recognizing that 25 it's a distinct disease, they went out and conducted 58 1 an epidemiological study and looked for occupational 2 risk factors associated with this specific disease, 3 APL. And as you can see -- and I think it might be on 4 the second page, but they concluded, "The results 5 obtained in our study confirm that epidemiologically, 6 as well as clinically and hematologically, that APL 7 behaves differently from other subtypes of" -- this is 8 acute non-lymphocytic leukemia, which is just another 9 way of saying AML basically. 10 Q. Okay. Now, David, I'm going to go back 11 to your five factors that you identified. Would you, 12 again, describe the significance of these five factors 13 with regard to how APL is a different disease than 14 AML? 15 A. Sure. We didn't show any pictures; but 16 morphologically, you can identify APL, and it is 17 different than the other subtypes. That's probably 18 less important, because there can be variability in 19 the way the cells look. 20 The cell of origin we discussed. And 21 that the cell of origin for APL is thought to arise at 22 a different place than the other subtypes of AML 23 subject to some -- you know, some discussion in the 24 literature about, you know, really where that happens. 25 We don't know definitively where it occurs, but it 59 1 seems to be happening where I pointed out. 2 The cytogenetics -- this is totally 3 distinct. There is nothing else like APL that has the 4 15;17. If it's a leukemia and it has 15;17, it's 5 called APL. If it's APL, it has the 15;17. The 6 treatment -- I only talked about altransretonoic acid, 7 because that is the front-line therapy. If that 8 fails, there are other things. And eventually, if 9 everything fails, they will fall back on 10 anti-proliferation agents and, you know, just try to 11 kill dividing cells. But most people have pretty good 12 response to altransretonoic acid. And because it is a 13 differentiation agent and not just killing dividing 14 cells, it's -- it's unique. There's really nothing 15 else like it in the treatment of leukemia. And then 16 as we just discussed, there are two nice examples of 17 epidemiological studies where they concluded, they 18 agreed that APL is different. It is not just another 19 subtype of AML. 20 Q. Okay. And if the plaintiff -- if a 21 plaintiff's expert were to testify that there is no 22 difference between an APL and an AML, would you 23 disagree with that? 24 A. I -- I would hope that everyone would 25 disagree with that. But, yes, I would, for sure. 60 1 Q. Okay. 2 MR. SCHIRRMEISTER: I'm going to move and 3 I would like to offer into evidence Exhibits 11 and 4 12. 5 THE DEPONENT: I'm not keeping these in a 6 very nice order over here. 7 MR. SCHIRRMEISTER: That's all right. 8 Q. (BY MR. SCHIRRMEISTER) Okay. David, why 9 don't you sit now. And I'm going to ask you about -10 MR. GIANARIS: Sit. 11 Q. (BY MR. SCHIRRMEISTER) -- ask you about 12 a few other things. The next opinion that you have, 13 would you read this opinion, please. 14 MR. GIANARIS: Object to the form, 15 leading. 16 A. I'm going to get to where we are, so -17 Q. (BY MR. SCHIRRMEISTER) Yes, I'm sorry. 18 A. That's fine. I got it. 19 Q. It's page 18 on the slides. 20 A. That the best available scientific 21 literature does not support a link between benzene and 22 acute promyelocytic leukemia or APL. 23 Q. Okay. And, again, I asked you earlier 24 what you understood the plaintiffs' allegations in 25 this case to be. How is that statement relevant to 61 1 what you understand the plaintiffs' allegations in 2 this case to be? 3 A. Well, I think this is completely germane 4 to this question. I mean, I think what they want to 5 say is that there was enough benzene in these solvents 6 to cause leukemia, not segregate out and discuss APL 7 as a distinct entity, and not back away and talk about 8 toluene and xylene, but try to make this about, you 9 know, a really, really minor component in those 10 solvents. So I think that this question here has been 11 asked, and it is directly relevant to what they are 12 alleging. 13 Q. Okay. So is the -14 MR. GIANARIS: Object -- object to the 15 form. Nonresponsive. Move to strike. 16 Q. (BY MR. SCHIRRMEISTER) Is the al -- is 17 the -- is -- the next slides that we'll be seeing, 18 have you examined the literature in order to identify 19 studies that question whether there is a link or an 20 association between benzene and Mr. Wolfe's disease, 21 APL? 22 MR. GIANARIS: Object to form. 23 A. As far as I know, I have looked at all of 24 the scientific evidence that could be used to discuss 25 a link between benzene or organic solvents or 62 1 occupational exposures and the development of acute 2 promyelocytic leukemia. 3 Q. (BY MR. SCHIRRMEISTER) Okay. David, 4 would you scoot a little over. You're in the -5 A. Yeah. 6 Q. Sorry about that. Okay. Now, I'm going 7 to hand you what's been marked as Exhibits 13 and 14. 8 A. Okay. 9 Q. Now, tell us what type of studies have 10 you looked for? What type of question were you 11 attempting to answer as you examined the literature 12 here? 13 A. Well, I mean, I -- I cast the net as wide 14 as I possibly could, and I looked for what anyone -15 what anyone has said about the epidemiology associated 16 with APL. And I've looked at what anyone said with 17 regard to what benzenes can do and the various 18 subtypes of AML. So I've -- I've looked at all of the 19 literature that I can think of that is -- that has 20 some angle of relevance to this question. 21 Q. Okay. Now, would you identify this 22 article, please, and tell us the author and what it 23 was about. 24 A. This was a study published by 25 Dr. Mitelman. And chromosomal pattern -- the title 63 1 is, "Chromosome pattern, occupational, and clinical 2 features in patients with acute non-lymphocytic 3 leukemia," which is another word for AML. And they -4 they really did exactly what we're talking about. 5 What he wanted to do was to understand whether there 6 was a specific chromosomal pattern or a specific 7 pattern of various types of AML associated with 8 occupation. And one of the diseases that he 9 segregated out was acute promyelocytic leukemia. And 10 as you can see in the exposed group, they were exposed 11 to solvents, insecticides -- I mean, there were 12 different categories -- or petroleum solvents. There 13 was only one case of APL in that group. There were 14 five cases in the nonexposed. So this -- I mean, he 15 clearly did not see an increase in APL with regard to 16 these exposures. 17 Q. Okay. So does this graph, then, show 18 that people who were not exposed to solvents, 19 insecticides, or petroleum products were -- there were 20 five people who developed APL, whereas the people who 21 were exposed only developed -- there was only one? 22 MR. GIANARIS: Form objection. 23 A. That's correct. That's correct. In 24 that, you know, the overriding conclusion was that 25 that red box that there's more APL cases in the 64 1 unexposed individuals. 2 Q. (BY MR. SCHIRRMEISTER) Okay. And what 3 does that tell you with regard to Mr. Wolfe's claims 4 in this case? 5 A. Well, this study would not support that 6 anything that he was exposed to, as far as solvents go 7 or petroleum products, or anything that he was doing, 8 played a role in the development of his disease. 9 Q. Okay. 10 MR. SCHIRRMEISTER: Offer Exhibit -11 Defendants' Exhibits 13 and 14. 12 Q. (BY MR. SCHIRRMEISTER) Okay. David, 13 would you look at -- I'm going to hand you what is 14 marked as Exhibit 15 and 16. And is this another 15 article? 16 A. Yes. Yes. This was by Dr. Golomb at the 17 University of Chicago. And James Vardiman -- I just 18 noticed that. And James Vardiman was an author as 19 well, basically doing the same thing. They were 20 looking for a correlation with occupation. Here were 21 the groups of solvents that they looked at and whether 22 or not they saw a difference in karyotypes, whether 23 they saw any change in -- in this case, they were 24 looking for 15;17, but that really is the same 25 epidemiological question, is trying to understand 65 1 whether people are getting APL. So those -- because 2 those go hand in hand. 3 Q. Okay. And how -- how many people were 4 exposed and developed APL versus how many people who 5 were never exposed and developed APL? 6 A. There was one case of APL out of the 7 exposed group, and there were four cases of APL in the 8 control group. So -9 Q. Okay. 10 A. -- clearly this cannot be used to support 11 the position that exposure to insecticides, solvents, 12 or petroleum products increased the risk of developing 13 the 15;17 translocation, which is APL. 14 Q. Okay. And how -- what is the relevance 15 of this to Mr. Wolfe's claim that exposure to toluene, 16 xylene, and petroleum distillates which naturally 17 occur in trace benzene caused him to develop APL? 18 A. Well, I think those would either fall 19 into the solvent category or these petroleum products 20 would have just as much benzene in them or perhaps 21 more than what toluene and xylene is going to have in 22 it. And there is just not -- based on this study, 23 there is not a relationship between exposure to those 24 solvents and this specific disease. 25 MR. SCHIRRMEISTER: Okay. Offer 66 1 Defendants' 15 and 16. 2 Q. (BY MR. SCHIRRMEISTER) David, I'd like 3 -- I'm going to hand you what has been marked as 4 Exhibit 17 and 18. 5 A. Okay. 6 Q. And is this another study? 7 A. Yes. 8 Q. Okay. And tell us what the -- who the 9 author is and the name of the study. 10 A. Dr. Crane. I -- I don't know him. But 11 this is a Journal of the American Medical Association. 12 But it was really the same thing, environmental 13 exposures, although they actually look at occupation, 14 in cytogenetically defined subsets. 15 So they were using cytogenetics to define 16 the types of AML that they were interested in. Here's 17 the 15;17. So this is specifically relevant to APL. 18 And in their study, they didn't find any cases in 19 their exposed group. 20 Q. Okay. 21 A. Now, it's a small study -- all of these 22 are very small studies, but it certainly does not 23 support that there was an increase based on their 24 occupational exposures. And that was very wide. As I 25 recall, there were solvents, but there were lots of 67 1 other things that they were potentially exposed to as 2 well. 3 Q. And what is this rel -- what is the 4 relevance to this study to Mr. Wolfe's claim that 5 toluene, xylene, and petroleum distillates with 6 naturally occurring trace benzene caused him to 7 develop APL? 8 A. That there were no cases of people that 9 had any kind of occupational exposure to APL. So this 10 does not support that APL was a disease that was 11 associated with occupational exposures. 12 Q. Okay. 13 MR. SCHIRRMEISTER: Offer Exhibits 18 -14 let's see, was that 18 and 19? What were the last two 15 that I handed you? 16 THE DEPONENT: 18 and 9 -- 17. 17 MR. SCHIRRMEISTER: 17. 18 THE DEPONENT: 17 and 18. 19 MR. SCHIRRMEISTER: Offer 17 and 18. 20 Q. (BY MR. SCHIRRMEISTER) Okay. David, I'm 21 going to hand you what's been marked as Exhibits 19 22 and 20, Fagioli, 1991 articles. If you would take a 23 look at those, sir. 24 A. Thanks. 25 Q. Okay. What is the title of this article 68 1 and what were the authors attempting to do? 2 A. The title is "Distinct cytogenetic and 3 Clinicopathologic Features in Acute Myeloid Leukemia 4 After Occupational Exposures to Pesticides and Organic 5 Solvents." 6 So this is directly relevant to the 7 question that we are asking, whether or not exposure 8 to organic solvents causes AML or a specific subtype 9 of AML, in this case, APL. And what they concluded 10 and was in their abstract is, whereas the classic 11 AML-specific translocations -- those are the ones that 12 you classically see in de novo or new leukemias that 13 have no occupation, i.e., the 15;17. So this is the 14 APL. They were detected only in unexposed subjects. 15 So they did not see any people with the 15;17 in the 16 exposed -- people exposed to pesticides or organic 17 solvents. There weren't any. So they couldn't do any 18 statistical analysis of them. 19 Q. Okay. And what is the relevance of these 20 authors' conclusions with regard to Mr. Wolfe's claims 21 in this case? 22 A. The -- this -- these conclusions in this 23 study does not support that occupational exposure to 24 organic solvents increases the risk or increases the 25 number of people that have acute promyelocytic 69 1 leukemia and express this 15;17 translocation. 2 MR. SCHIRRMEISTER: I'll offer 3 Defendants' 19 and 20. 4 Q. (BY MR. SCHIRRMEISTER) David, I'm going 5 to hand you what's been marked as Exhibits 21 and 22, 6 sir. 7 A. Okay. 8 Q. Would you identify this particular study 9 for the jury and explain its significance. 10 A. This study came out of China. And this 11 is a certified translation from the National 12 Investigative Group for the Survey of Leukemia and 13 Aplastic Anemia. And what they did was a countrywide 14 analysis of various types of AML, various sub -15 various types of leukemia as well as some subtype 16 analysis of AML and aplastic anemia. They looked at a 17 variety of agents. And this was -- the data that they 18 presented, the little asterisk here means that it 19 achieved statistical significance. We'll discuss that 20 in a minute; but that means that it, you know, is 21 likely a real association. 22 They found an association between benzene 23 and M2. They did not find an association between 24 benzene and M3. So this study -- and it's a really 25 large study. They looked at over -- it was over a 70 1 million people. They looked at a 1,200 cases of 2 leukemia. So it was way bigger than all of these 3 others combined. But they did not find a 4 statistically significant excess of M3s, acute 5 promyelocytic leukemia, in these Chinese populations 6 associated with benzene exposure. 7 Q. Okay. And M3 is APL? 8 A. M3 is APL. That is the same -- that's 9 the FAB classification system for it. So this stands 10 really in direct contradiction to the allegations in 11 this case, that benzene can cause APL. 12 Q. Okay. To your knowledge, is this the 13 only study anywhere that has specifically examined 14 benzene and increased risk of APL? 15 A. It's the only one that I know of that has 16 -- has done it to this level of specificity. I mean, 17 all of those other studies with organic solvents and 18 this, that, and the other, they are going to have some 19 benzene in there. But this one specified benzene as a 20 chemical -- a specific chemical and looked at the 21 relationship between benzene and APL. 22 Q. Okay. 23 A. There has -- there's not another one that 24 I am aware of. 25 Q. Okay. And what is the significance of 71 1 the results of this study for Mr. Wolfe's claims in 2 this case? 3 A. It -- it does not support the position 4 that exposure to benzene is a risk factor for the 5 development of this particular subtype of APL. And it 6 did have the statistical power. It was a strong 7 enough study to see statistical changes. So it did 8 find a risk with M2s, but it did not find one with M3. 9 So you can't really look at this and argue that this 10 study isn't big enough and it didn't have the power to 11 -- to measure that association. 12 Q. Okay. 13 MR. SCHIRRMEISTER: We're going to offer 14 Exhibit -- Defendants' Exhibits 21 and 22. And I 15 think this would be a good time to take a break. 16 MR. GIANARIS: Okay. 17 MR. SCHIRRMEISTER: Thank you, sir. 18 THE VIDEOGRAPHER: Going off the record. 19 The time is 11:02. 20 (Recess taken, 11:02 a.m. to 11:18 a.m.) 21 THE VIDEOGRAPHER: We're back on the 22 record. The time is 11:18. 23 Q. (BY MR. SCHIRRMEISTER) Okay. David, 24 would you read your next opinion and briefly explain 25 to the jury what you will be discussing -- 72 1 MR. GIANARIS: Object to form. 2 Q. (BY MR. SCHIRRMEISTER) -- with this 3 opinion? 4 A. This slide reads, "Mr. Wolfe was not 5 exposed to enough benzene to develop any form of 6 leukemia." 7 So, really, what we're going to talk 8 about the -- well, the fact that everyone is exposed 9 to some level of benzene, just in our normal 10 environment. So that's one aspect. And the other 11 aspect is that people have conducted quantitative 12 epidemiology to see and in -- and investigate and 13 evaluate how much benzene it takes before you start 14 meaningfully increasing someone's risk of developing 15 some form of leukemia. And we're going to put 16 Mr. Wolfe's estimated exposures into context with that 17 quantitative epidemiology. 18 Q. Okay. Now, would you explain -- first of 19 all, I'm going to offer -- I'm going to hand you what 20 has been marked as Defendants' Exhibit 23. Would you 21 identify Exhibit 23, please. 22 A. This is a picture of North Carolina with 23 all of the counties color-coded. And it really is 24 just to illustrate to -- to the folks in this trial 25 that there's benzene -- there's benzene everywhere. 73 1 We are all exposed to low levels of benzene just in 2 the ambient environment. 3 Q. Okay. 4 A. So in this room, in that room, there's 5 benzene in the air in the United States. 6 Q. Okay. So we're sitting in a conference 7 room here today in Colorado. Are we breathing 8 benzene? 9 A. We most certainly are. 10 Q. Okay. And the folks sitting in the 11 Courthouse before Judge Craig in Forsythe County, are 12 they breathing benzene? 13 A. They are. 14 Q. Okay. And what is the source for this 15 data? 16 A. The source for this data is the USEPA. 17 Q. Okay. And specifically what program from 18 the EPA there? 19 A. It looks like NATA, the National Scale 20 Air Toxics Assessment. 21 Q. Okay. 22 A. I'm not familiar with what they do, but 23 it came from USEPA. 24 Q. Okay. And describe for us the -- why are 25 there some higher elevated benzene concentrations in 74 1 certain areas of North Carolina than others? 2 A. The -- the -- the background benzene in 3 the atmosphere typically comes from vehicle exhaust, 4 so you're going to find increases in the amount where 5 there are major cities. So Charlotte, Asheville, 6 Winston Salem, Greensboro, those are the ones that 7 tend to have more benzene than more rural areas. And 8 it doesn't really matter about these numbers, but none 9 of these levels of benzene from high to low are 10 thought to have any toxicological relevance. So it's 11 just -- it's not to scare anyone, it's just to show 12 people that we are all exposed to benzene every day. 13 MR. SCHIRRMEISTER: Offer Defendants' 23. 14 Q. (BY MR. SCHIRRMEISTER) David, I'm going 15 to hand you what has been marked as Exhibit 24. And 16 what is this slide and what's the relevance, please? 17 A. This is just a continuation of that 18 concept and to show people that things that they are 19 exposed to in their daily life, that their diet has 20 benzene in it. Benzene is a ubiquitous chemical. 21 It's a really simple aromatic ring, and you find it 22 all over the place. You find it in drinking water, 23 you find it in air, you find it in bananas, you find 24 it in cake, pizza, fried chicken, et cetera. So no 25 matter what it is, what kind of diet you're on, there 75 1 is some low level of benzene that are -- are in those 2 products that you're eating. 3 Q. Okay. And what is the source for this 4 data? 5 A. This is from FDA, the Food and Drug 6 Administration. 7 Q. Okay. 8 MR. SCHIRRMEISTER: I'll tender Exhibit 9 No. -- offer Exhibit 24. 10 Q. (BY MR. SCHIRRMEISTER) Okay. David, I'm 11 going to hand you what's been marked as Exhibit 25. 12 Would you take a look at that, please. And explain to 13 us dose response, and specifically with regard to the 14 bullet points on Exhibit 25. 15 MR. GIANARIS: Objection, leading. 16 A. A dose response, it's not magical; but it 17 is the most important concept in toxicology. And I 18 will say, whether I'm teaching toxicology to medical 19 students, to physicians, to graduate students, it is 20 the very first thing that I teach them. And it is the 21 first thing on the first day; and at the end of the 22 course, it is the thing that I hope that they remember 23 the most. And that is that there has to be a 24 meaningful relationship between the dose and the 25 response. And if you increase the dose, if a person's 76 1 exposure increases, then the response needs to change 2 according to that change in dose. 3 So that's -- there has to be a connection 4 between the dose and the response. It doesn't always 5 have to go up. Sometimes it can go down. It can be 6 quite complicated, but there has to be a connection. 7 If you change the dose and the response does not 8 change, then probably, from a scientific point of 9 view, you are not looking at what you think you're 10 looking at, and the response is related to something 11 else other than the dose. That's why toxicologists 12 are so keenly interested in this notion of a dose 13 response relationship. 14 Q. (BY MR. SCHIRRMEISTER) Okay. I'm going 15 to offer 25 and hand you what has been marked as 16 Exhibit 26. It's a dose response chart. Would you 17 explain that to the jury, please. 18 A. So this is the simplist dose response 19 relationship that we could come up with. And down 20 here, you see the dose is increasing. And then 21 whatever you're defining as the response is on the Y 22 axis here, and so that's going up. And it's just 23 showing you that as the dose increases, you're 24 starting to see more of a response. 25 So down here, you don't have an effect. 77 1 So the dose is too low for there to be an effect. At 2 this dose, you start seeing a slight effect, a 3 moderate effect, a more serious effect. And then if 4 it's a really toxic chemical or exposure, you know, 5 perhaps it goes all the way to death of the animal. 6 So this is the simplest kind of dose 7 response; but it illustrates the point, you know, to 8 the jury, or to whoever is looking at this, that as 9 the dose is changing, the response is changing along 10 with it. 11 MR. SCHIRRMEISTER: Okay. I'll offer 26 12 and hand you 27, David. 13 Q. (BY MR. SCHIRRMEISTER) Now, this is 14 called Doses of Common Substances, a typical dose and 15 a toxic dose. And if you would explain this to the 16 jury; and then, secondly, explain the significance 17 with regard to the dose response concept. 18 A. Really, this -- this is -- when you talk 19 about a dose response, that means that it takes a 20 certain amount of the chemical to be toxic. So even 21 things like benzene, if you're exposed to low enough 22 levels of benzene, there's no evidence that it's 23 toxic. And even really common, what we consider to be 24 safe substances, like water, sugar, salt, if you're 25 exposed to too much of those things, then you can get 78 1 toxicity. 2 So as Paracelsus said -- and we kind of 3 skipped that, but that's fine. He was an early 4 toxicologist. He said probably the most famous quote 5 in this field is that the dose makes the poison. So 6 you can't say that a chemical is toxic unless you also 7 understand what the exposures are, unless you also 8 understand what the doses of that chemical that you're 9 talking about. 10 So a quart of the water is not toxic. 11 Seven-and-a-half gallons is typically lethal. It 12 messes up the electrolytes and causes cardiovascular 13 problems. So everyone has heard of people that drink 14 too much Gatorade and potentially died from it or, you 15 know, got really sick because of it. 16 So that's what this slide is showing you, 17 that a little bit of salt is okay, too much salt is 18 toxic. So it's -- it's a concept that most everyone 19 is familiar with. 20 Q. Okay. And does this concept of dose 21 response also apply to benzene? 22 A. Of course, it does. That's -- I mean, 23 the reason why we had those slides earlier was to show 24 people that we are all exposed to benzene every day of 25 our life all of the time. And there is no adverse 79 1 effects associated with those exposures. So those are 2 below a point where anyone is going to think that 3 there is adverse toxicity associated with it. 4 Q. Okay. And if a plaintiff's expert were 5 to testify that dose does -- dose of benzene -- dose 6 not matter, would you disagree with that? 7 A. I -- I would as well as the scientific 8 world would disagree with that statement. 9 MR. SCHIRRMEISTER: Offer 27. 10 Q. (BY MR. SCHIRRMEISTER) I'm going to hand 11 you what has been marked as Exhibit 28. David, this 12 is a slide called Dose Response Curve For Aspirin. 13 Would you explain this to the jury, please. 14 A. Sure. This is just a little more 15 complicated verse, but down here is the dose, over 16 here is the response. This one is a little different 17 because it makes a change or it delineates the 18 difference between a beneficial effect and a toxic 19 effect. And this dotted line here means that doses 20 below this line actually have a beneficial effect; 21 doses above this line, that's where you start seeing 22 toxicity. 23 So this red line here is the -- the dose 24 response curve. And we know from epidemiology that 25 low doses of aspirin are beneficial in that you 80 1 actually have a decreased risk of certain 2 cardiovascular problems. But if you start taking too 3 much aspirin, then you start getting GI bleeding and 4 other GI problems. So that's what this line is 5 depicting. But this is a standard kind of dose 6 response. 7 Now, this red line is actually supposed 8 to be touching there. And the idea is that that would 9 be called a threshold. And that is a dose below which 10 you really don't see anything going on. 11 So at doses of aspirin below the 12 threshold, you don't have a beneficial effect, you 13 don't have a toxic effect, you can't tell that a 14 person has been exposed to those levels of aspirin. 15 MR. SCHIRRMEISTER: Okay. I'll offer 28. 16 Q. (BY MR. SCHIRRMEISTER) David, the next 17 exhibit I'm going to hand you is 29 titled Dose 18 Response Curve For Alcohol. And would you, again, 19 explain this to the jury. 20 A. This -- we put this in here -- I have put 21 this in here just because this is something that most 22 people are going to be either firsthand or secondhand 23 familiar with. And that is that if you increase the 24 number of -- the amount of alcohol, ethanol that a 25 person is being exposed to, then you have a dose 81 1 response relationship. And a little bit of wine or a 2 little bit of alcohol, you get a giddy feeling. Then 3 you start becoming impaired from a driving point of 4 view. And, you know, you could argue about where 5 those are going to be. But as that increases, blurry 6 vision, alcohol poisoning, coma, and death. 7 So it just, again, depicts this notion of 8 a dose response. And that is what -- if you were 9 going to ask someone or someone was going to ask you, 10 Well, what will alcohol do to me? Will alcohol make 11 me sick or will alcohol have some effect on me? Your 12 question is -- your -- your answer is going to have to 13 be, well, it depends on how much you're exposed to. 14 If you're only exposed to a drop of alcohol, it's 15 probably not going to do anything to you. If you 16 drink two fifths of whiskey, you know, you're probably 17 going to be up here in this category if you do that in 18 a 24-hour period. So that's -- that's the purpose of 19 this slide. 20 MR. SCHIRRMEISTER: Okay. Offer 29. 21 Q. (BY MR. SCHIRRMEISTER) Okay. David, the 22 next I'm going to hand you is Exhibit 30. And what 23 I'd like you to do is explain to the jury, please, the 24 dose response concept that you just discussed and the 25 quantitative measurement of benzene, number one. And 82 1 then, secondly, I'm going to ask you once you've done 2 that to discuss the levels of permissible exposure 3 limits set by OSHA -4 A. Okay. 5 Q. -- for workplace exposure to benzene. 6 A. Yeah. Probably the easiest things is to 7 just kind of go through the slide. But benzene 8 exposures are described in the literature and probably 9 in this case, when it's actually happening, in terms 10 that not every one are familiar with. And the terms 11 that epidemiologists and benzene toxicologists and 12 people use to define or describe benzene exposure is 13 this concept of a part per million year or a ppm year. 14 And this really is not a -- a conceptually difficult 15 concept. The part per million is a concentration. 16 What that means, we don't need to get 17 into, but a ppm is a part per million and is a way of 18 measuring how much benzene is in the air. Okay. It 19 could also be in water and other things, but for our 20 purpose, it's in the air. So a part per million tells 21 you the concentration in the air. And then the time 22 or the duration, the years, tells you how long you've 23 been exposed to that concentration in the air. So 24 that's what a -- a ppm is. 25 Q. Okay. 83 1 A. All right. And then the second part 2 talks about what the Occupational Safety and Health 3 Administration -- what they regulate as a permissible 4 exposure to benzene. And they call that a PEL or a 5 permissible exposure level. And -6 Q. Okay. And -- and is that PEL set by 7 OSHA? 8 A. That's correct. 9 Q. Okay. 10 A. Right. And that is a legally enforceable 11 standard. So OSHA says this is -- the most that you 12 can have a person occupationally be exposed to is the 13 permissible exposure limit. And they do it over a 14 time-weighted average, which is how much they are 15 exposed to averaged out over an eight hour. And the 16 permissible exposure limit is 1 PEL. 17 So it is one part per million benzene 18 averaged out over -- that's what this TWA, 19 time-weighted average -- averaged out over eight 20 hours -- that's the permissible exposure level. 21 Q. Okay. And is this the permissible 22 exposure limit that was in effect all during the time 23 that Mr. Wolfe worked as a painter? 24 MR. GIANARIS: Object to foundation. 25 A. I don't recall exactly when the 1 ppm 84 1 became -- I think that was in '86. I don't -- he 2 might have started working in 1985, is my recall. So 3 I'm not positive about that. 4 Q. (BY MR. SCHIRRMEISTER) Okay. But at 5 least from -- from 1986 forward, you understood it to 6 be one part per million? 7 A. Correct. 8 Q. Okay. 9 A. Correct. 10 Q. So let's go to the next bullet point, 11 average of 8 hour TWA over year is a ppm year, which 12 would explain that concept. 13 A. Right. So that's just what we were 14 talking about. Up here where this is kind of the 15 metric, the way that people talk about benzene 16 exposures. And the jury and the court, they are going 17 to hear about this. You know, for as long as this 18 goes on, people are going to be talking about part per 19 million years. So a -- one part per million year is 20 -- this is one way to get to it, is a 1 ppm exposure. 21 And keep in mind that that is an 22 eight-hour time-weighted average, so it's not, I was 23 exposed to 1 ppm for two seconds during the day. 24 That's not going to be that much exposure. It's 1 ppm 25 averaged out over an entire working day, eight-hour 85 1 working day for one year. That is a 1 ppm year. 2 Here is an example of a much higher 3 exposure where the individual was exposed to 10 part 4 per million. Again, that's not a two-second peak of 5 10 ppm. That averaged out over an eight-hour working 6 day. And they maintained that exposure for 20 years. 7 All right. So that's much higher exposures, and that 8 would end up giving you a 200 ppm year cumulative 9 exposure to benzene. 10 Q. Okay. 11 A. This bullet here is what, basically, OSHA 12 will allow in United States, because they allow an 13 eight-hour time-weighted average of 1 ppm. And that's 14 the permissible exposure limit. And the -- the 15 estimated working lifetime is 40 years. So they 16 regulate benzene as if a 40 ppm year is an 17 occupational safe level. 18 Q. Okay. Now, this 40 part per million 19 years, is this benzene exposure measurement also used 20 in epidemiology? 21 A. It is. 22 Q. Okay. 23 A. It is. It's probably the most common 24 metric measurement of benzene exposure that you will 25 find in that the epidemiology -- particular the 86 1 epidemiology that is quantitative. And by that -- and 2 we'll see that in a second, but there's a lot of 3 epidemiology that doesn't really describe people's 4 exposures very well. And they are less useful when it 5 comes to trying to understand whether exposures cause 6 problems because of the dose response that we just 7 talked about. The quantitative epidemiology that is 8 in the literature with regard to benzene will almost 9 all use this metric of ppm years. 10 Q. And that's the same metric that the U.S. 11 government uses? 12 A. That's the same -- yes. Yeah. 13 Q. Okay. And what does the U.S. government 14 establish as a safe likely work life for benzene 15 exposure? 16 MR. GIANARIS: Object to the foundation. 17 A. Well, they base -- since the permissible 18 exposure limit is 1 ppm over a 40-year life span or 19 40-year working life, then that ends up being 40 ppm 20 years. 21 Q. (BY MR. SCHIRRMEISTER) Okay. All right. 22 MR. SCHIRRMEISTER: Offer Defendants' 23 No. 30. 24 Q. (BY MR. SCHIRRMEISTER) Now, David, the 25 next slide, I'll hand you Exhibit 31. Now, first of 87 1 all, tell us -- read the title and explain to us what 2 the -- what the title means. 3 A. Benzene and acute myeloid leukemia: Dose 4 Response, Quantitative Studies of Benzene and 5 Leukemia. So in the world's literature, these are the 6 studies that have actually gone and said how much were 7 people being exposed to benzene and what was their 8 risk of leukemia or AML associated with those 9 exposures. 10 And that's what the values in yellow 11 represent. Those are the exposures that were reported 12 in this quantitative literature. 13 Q. Okay. Now, the first one -- I see the 14 first two is called pliofilm. What is the pliofilm 15 study and how was that used by the U.S. government in 16 establishing a safe level of occupational exposure to 17 benzene in the workplace? 18 MR. GIANARIS: Object to the foundation. 19 A. Pliofilm is a nickname given to rubber 20 hydrochloride. It was like a -- a cellophane-like 21 material that they made in three facilities, Goodyear 22 facilities in Ohio. And the workers that made this 23 pliofilm, they were using pure benzene as a solvent. 24 So they were dissolving this material in pure benzene, 25 they were spreading this material out on big drums, 88 1 they were collecting the benzene above the facility. 2 So these workers were exposed to pure 3 benzene in -- in, by today's standards, really high 4 concentrations. And the workers that were making this 5 pliofilm at certain exposures did have an increased 6 risk of developing leukemia. 7 Since there was a dose response that was 8 evident, since these workers were not exposed to lots 9 of other chemicals that could confuse the analysis, 10 and since we really kind of had pretty good ideas 11 about what these workers were doing, how long they 12 were working there, that kind of thing, then the 13 pliofilm cohort and the various analysis thereof -14 and there's been probably 13 studies or 14 studies 15 published on this -- this cohort, that forms the basis 16 for all of our regulatory standards. In the United 17 States, that forms the -- the regulatory basis for our 18 understanding of benzene and leukemia. 19 Q. Okay. 20 A. EPA uses it, OSHA uses it, ACGIH uses it. 21 Everyone uses the pliofilm today. 22 Q. Okay. 23 MR. GIANARIS: Object to the form. Just 24 let me get it out before so I don't talk on you. 25 Object to the form, lack of foundation, move to strike 89 1 for lack of foundation, nonresponsive. 2 Q. (BY MR. SCHIRRMEISTER) And the -- the 3 first two studies, pliofilm, are those studies of that 4 pliofilm group from the Goodyear plants in Ohio? 5 A. Correct. The first one that Bob Rinksy 6 -- well, this actually wasn't the first one, but the 7 one that Dr. Rinsky published in 1987, they used all 8 leukemias combined. 9 There was a case of CML, there was a case 10 of ALL. And then Dr. Otto Wong in 1995 did a 11 subsequent analysis of this cohort, this group of 12 individuals that worked at these plants. And he 13 reevaluated only based on AML. So that's why those 14 are two different studies. But, you know, the date is 15 pretty similar. And they really were looking at the 16 same workers. 17 Q. Okay. And just so we're clear, there 18 were no APLs in any of these cases, correct? 19 A. You -- I can't say that. I don't know. 20 They didn't evaluate APLs. 21 Q. None were identified on these studies? 22 A. That's right. They didn't look. 23 Q. Okay. So the -- then -- then -- so what 24 is -- when the first two pliofilm -- significant 25 excess at greater than 200 part per million years in 90 1 those first two, what does that mean? Explain that to 2 the jury. 3 A. The significant excess -- and we'll talk 4 about this a little later, is -- from an 5 epidemiological point of view, it means that the 6 excess was statistically significant, which means you 7 can be reasonably confident that the excesses that you 8 saw were, in fact, related to the exposures and not 9 just random chance. 10 So statistical significance is a 11 relatively important aspect of epidemiological studies 12 and the evaluation of that data, because it allows you 13 to rule out the role that chance could play. And in 14 order to achieve a statistically significant excess, 15 it took 200 part per million years of benzene exposure 16 in these workers. 17 Q. The next one is NCI China. What is that? 18 A. That was a really large study that the 19 National Cancer Institute did over about a 20-year 20 period with the Chinese Academy of Preventative 21 Medicine. They looked at some 78,000 workers in China 22 employed in a variety of different occupations. They 23 were shoe workers and -- and rubber workers and 24 petroleum workers and painters, and all kinds of 25 different things. And they then reported out a 91 1 collective cumulative sort of analysis of the benzene 2 exposures. And in that analysis, they saw a 3 statistically significant increase at something 4 greater than 40 part per million years. 5 Q. Next one, Glass, Health Watch? 6 A. Deborah Glass published a paper in 2003, 7 which was the latest iteration. Health Watch is a 8 series of industry surveys that the Australian 9 Petroleum Institute funded through Monash University 10 and some others. And they basically followed these 11 refinery workers and petrochemical workers that were 12 employed in the petrochemical industry in Australia. 13 And she reported that there was an increase -14 significant increase in acute non-lymphocytic 15 leukemia, which is AML, essentially -- at something 16 greater than 8 ppm, but it wasn't any higher than 57 17 part per million years. 18 Q. Okay. Next one is the shoe worker study. 19 A. Costantini did a -- looked at Italian 20 shoe workers and reported a consistent finding with 21 the pliofilm that it took more than 200 p -- I think 22 it was actually 199. It had to be greater than 199 23 ppm years. 24 Q. Okay. And then the three find no stat -25 no significant access at different levels. Explain 92 1 those three to us. 2 A. Dr. Bloeman was doing a Dow Chemical 3 worker study. And he had exposures -- he had workers 4 in his study that were exposed to benzene 5 concentrations at greater than 79.1 part per million 6 years. And he did not report a statistically 7 significant excess. 8 So we don't know how far it has to go 9 before you would get one. All we know is that in his 10 study, you know, basically 80 part per million years 11 was not associated with an increased risk. And Rob 12 Schnatter, Dr. Schnatter and Leslie Rushton, these two 13 studies are very similar. Rob Schnatter did look at 14 refinery and petroleum workers in Canada. Leslie 15 Rushton looked at refinery and petroleum workers in 16 the UK. And they both had an exposure category that 17 was something greater than 45 ppm years. But in those 18 highest-exposed individuals, they did not see a 19 statistically significant increase, in -- in this 20 case, leukemia. 21 Q. Okay. Now, David, on Exhibit 31, are 22 these all the studies that exist that quantitatively 23 analyze benzene exposure and potential for increased 24 risk of leukemia? 25 A. The only one that I can think of that we 93 1 didn't put on here was a previous study to Bloeman and 2 it was by James Collins. And he had an exposure -- it 3 was pretty low. He had an exposure of 6 ppm years, 4 but there was number of statistically significant 5 increase. 6 So other than that one, if you slide that 7 one in here -- and, basically, he didn't see 8 anything -- that is it for the quantification of 9 benzene exposure and AML risk that -- that I have 10 seen. 11 Q. Okay. And how does OSHA use this data 12 that is in the quantitative studies? 13 MR. GIANARIS: Object to the form, 14 foundation. 15 A. My understanding is that -- I mean, at 16 least based on what they say in their documentation is 17 they are basing their dose response analysis on, not 18 Wong or Bob Rinsky, but what we don't have on here. 19 There -- there have been three separate exposure 20 calculations done on these workers. 21 I actually -- Bob Rinsky did do one, I 22 take that back. His '87 paper -- there were two 23 others that have tried to get their arms around what 24 these pliofilm workers were actually exposed to. EPA, 25 OSHA, all of these other regulatory agencies used 94 1 those three quantifications or those three estimates 2 of their exposures to set these standards. 3 Q. (BY MR. SCHIRRMEISTER) Okay. And is the 4 standard they set the one that we looked at earlier of 5 a likely work life of 40 part per million years? 6 A. Well, they set a standard of 1 part per 7 million year, which would equate to 40 over a normal 8 working lifetime. 9 MR. SCHIRRMEISTER: Okay. I'm going to 10 offer into evidence Defendants' 31. 11 Q. (BY MR. SCHIRRMEISTER) And, David, I 12 hand you Exhibit 32. Okay. What have we done in 13 Exhibit 32? 14 A. This -15 Q. There are four columns. 16 A. Right. This was just to depict these 17 kind of graphically in a -- in a simple histogram, 18 depict these various occupational levels. So here's 19 what we're talking about with OSHA. So that's 40 ppm 20 years. Here's the Rinsky and the Wong. So all of the 21 other ones would be on here somewhere. And this 22 little red box up here illustrates that it takes 23 exposures greater than that before you start seeing a 24 statistically significant increase in -- well, in this 25 case, it's leukemia; and in this case, it's AML. And 95 1 then this little line here, which you can barely see, 2 little tiny yellow line there, that's based on a 3 quantification estimation of Mr. Wolfe's benzene 4 exposure during his employment as a painter that was 5 done by Brad Russell. And his cumulative exposure as 6 still made by Brad Russell was .093 ppm years. 7 MR. GIANARIS: Just I want to make an 8 objection, because I think the question went -- the 9 answer went beyond the question, so I didn't have time 10 to -11 THE DEPONENT: Sorry. 12 MR. GIANARIS: -- inter -- interject the 13 objection before the question. But this goes beyond 14 the scope of his disclosure, beyond the scope of his 15 report, and lacks foundation as to Mr. Wolfe's 16 exposure. 17 Q. (BY MR. SCHIRRMEISTER) Okay. So let's 18 -- let's go through OSHA -- this one here, 40 part per 19 million. What does that represent? 20 A. What this -- this box represents the 40 21 part per million years. It's what OSHA allows in the 22 occupational workplace if a person is exposed at the 23 PEL, which is 1 ppm over a 40-year working life. 24 These other two boxes are where Dr. Rinsky and 25 Dr. Wong calculated a statistically significant 96 1 increase in either leukemia or AML. 2 Q. Okay. Now, is there any literature, 3 David, anywhere in the world that you're aware of that 4 finds an increased risk of leukemia when a person is 5 exposed to .093 part per million years? 6 A. That's -- no. No. That's not any 7 different, really, than a person's typical background 8 exposures would be through their life. But, no, there 9 is no evidence that that increases a person's risk of 10 developing leukemia generally, AML or APL 11 specifically. 12 MR. SCHIRRMEISTER: Okay. Offer 13 Exhibit 40 -- 32. 14 Q. (BY MR. SCHIRRMEISTER) Okay. Now we're 15 going to move on to your next opinion in this case, 16 David. Would you read page 35 into the record, 17 please. 18 MR. GIANARIS: Objection, leading. 19 A. Do you want me to just read this? 20 Q. (BY MR. SCHIRRMEISTER) Yes, sir. 21 A. "Painters as an occupational group are 22 not at an increased risk of developing leukemia." 23 Q. Okay. I'm going to hand you what has 24 been marked as Exhibit 33. And I think it might be 25 easiest for you to stand David, if you want to. 97 1 A. Sure. 2 Q. Explain some of these concepts to the 3 jury. 4 A. Well, what we needed to do in order for 5 the jury to really have some, you know, basis for 6 interpreting the literature, the literature being the 7 epidemiology studies that have looked at the 8 occupational risks associated with being a painter -9 and as you're going to see in these subsequent slides, 10 there is a great deal of literature on that topic. 11 Lots and lots of people have reported on the 12 occupational risks associated with being a painter. 13 Q. Okay. Now -14 A. But in order to do that, we needed to 15 provide at least a very superficial background on 16 epidemiology. 17 Q. So do you understand that Dr. Milman has 18 testified that a dose does not matter because 19 Mr. Wolfe was a painter, and there are studies that 20 say painters get leukemia? 21 A. That flies in the face of every 22 toxicological principle that exists. 23 Q. Okay. 24 A. We're all exposed to benzene, painters 25 are exposed to benzene, I'm exposed to benzene. You 98 1 have to quantitate the dose. You have to understand 2 what the exposures were before you can say that 3 there's an increased risk of -- of even developing the 4 disease. And then it's another whole step to say that 5 this person's disease was actually caused by those 6 exposures. But, no, I don't -- I do not agree with 7 that. 8 Q. Okay. Let's look at Exhibit 33, the 9 first one, and explain -- explain epidemiology and 10 what you're showing to the jury here, please. 11 A. So really epidemiology, in the simplest 12 terms, is the study of diseases in the human 13 population. So it's the study of the distribution of 14 disease and those causes, whether they are exposures, 15 or whatever else, in the human population. 16 So the purpose of all epidemiology is to 17 understand the cause of disease in humans. And this 18 is just to show here's a population, and those two 19 individuals have whatever the disease is that -- that 20 you're interested in looking for. 21 MR. SCHIRRMEISTER: Okay. Offer 33. 22 A. So these are very superficial in terms of 23 their explanation. 24 Q. (BY MR. SCHIRRMEISTER) Okay. Now, 25 David, I'm going to hand you Exhibit 34, which is one, 99 1 two, three, four, five, six slides. So let's go 2 through these. The first slide is called Cohort 3 Studies. Explain what you're showing here to the 4 jury. And before you do this, David, set the basis 5 for why these concepts are important for the jury to 6 understand when you will show them, in a few minutes, 7 paint slides or graphs from painter epidemiology 8 studies. 9 A. Okay. 10 Q. That -- I'm sorry, that's a poor 11 question. 12 A. No, I got it. 13 Q. But I think you understand what I'm 14 asking. 15 A. Yeah. I mean, as I said earlier, these 16 are just to give the court, the jury, whoever is 17 watching this -- just to give them a really basic 18 understanding of the science of epidemiology so that 19 when we start looking at data in these epidemiological 20 studies that they have the tools that they need to be 21 able to interpret and to understand what those studies 22 are really telling them. And it's not that hard. 23 It's not magic, and it's not -- you don't have to have 24 a Ph.D. in epidemiology to be able to look at the 25 studies and understand what that data tells you. 100 1 Having a Ph.D. epidemiology is important if you're 2 going to be doing the studies, but in terms of 3 interpreting them, we can all do that. 4 Q. Okay. And how do you use epidemiology in 5 your work? 6 A. I use epidemiology every day. I mean, I 7 am evaluating human studies in any of the 8 toxicological evaluations that I do for -- for any of 9 my clients with regard to -- because it's human data. 10 So you never have to worry about the 11 relevance of what this data means to people. When 12 you're looking at toxicological studies that have used 13 an inbred strain of mouse, while it's interesting and 14 it may give you some information on mechanism, but you 15 always have to ask yourself, Are we like that mouse? 16 Are we likely to get the same diseases that that mouse 17 is going to get? So you're always questioning the 18 relevance of that mouse data to humans. From an 19 epidemiological point of view, you've overcome that 20 hurdle. And that's a very big hurdle toxicologically. 21 This data is relevant because we are humans. 22 Q. Okay. And do you teach epidemiology as 23 well? 24 A. I do. I teach environmental epidemiology 25 class. I teach it with another person. 101 1 Q. Okay. Now, the first -- the first type 2 of epidemiology study is a cohort. What is a cohort 3 study? 4 A. Yeah, there are two -- there are two main 5 kinds of epidemiological analysis, and they are pretty 6 different in their design. And each -- all of these 7 studies have pros and cons, they have strengths, they 8 have weaknesses. The devil is in the details with an 9 epidemiology study, so they are not easy to conduct. 10 But the two basic kinds are cohort studies and case 11 controls. And cohort really just means group. So a 12 cohort is a group of people. 13 So when you're doing a cohort study, 14 you're looking at a group of people that had some 15 exposure, and you're comparing them to a group of 16 people that did not have that exposure. And so by 17 comparing these exposed people to what happened to 18 these unexposed people, they will allow you to start 19 making some statements about whether or not their -20 that exposure had an affect on them. 21 Q. Okay. Now, what are we seeing here in 22 the folks that are highlighted? 23 A. Okay. So this is exactly what I talked 24 about. The ones that are highlighted, they would be 25 the individuals that had the disease. So you're 102 1 looking at this cohort. This is my exposed cohort. 2 And we found two individuals that had the disease, 3 kidney cancer or -- or bladder cancer or lung cancer 4 -- whatever it is that you're looking at. 5 Cardiovascular disease. And then these were our 6 nonexposed -- our nonexposed group. And the 7 comparison here is only fair if this nonexposed group 8 is chosen very carefully; but, you know, that's more 9 than we need to talk about here. But, basically, you 10 also see two individuals that have the disease in the 11 nonexposed. So you have two in the exposed, two in 12 the nonexposed. 13 Q. Okay. And when you -14 THE VIDEOGRAPHER: Counsel, five minutes 15 until tape change. 16 Q. (BY MR. SCHIRRMEISTER) Okay. When we 17 look at this, what -- and this has cohort studies, 18 three possibilities. Explain what the three 19 possibilities are in a cohort study. 20 A. Sure. When you're making those 21 comparisons -- so you're comparing the exposed group 22 with the unexposed group, right? That's really what 23 you do on a cohort. No matter how sophisticated they 24 seem, that basic thing is happening. 25 You can either have one possibility that 103 1 it's the same. So you have two cases in the exposed. 2 You have two cases in the unexposed. So the incidence 3 of disease, the rate of disease is the same. 4 Q. Okay. 5 A. You can also -- in the exposed group, you 6 have four cases here, compared to only two in the 7 unexposed. And this is sometimes called the control 8 group. 9 Q. Okay. 10 A. You only see two in the control group. 11 So in that case, you see more cases of disease in the 12 exposed than you see in the unexposed. 13 Q. Okay. 14 A. So something like this, you would start 15 to think, well, maybe the exposures are having 16 something to do with this increased incidence of 17 disease. 18 Q. And what's a good example that we all 19 know -- I think we all know about or we do know about 20 with exposed folks getting more of a disease than 21 unexposed people? 22 MR. GIANARIS: Objection, leading. 23 A. Yeah, there's lots of examples, but 24 probably the easiest one that I think everyone would 25 have heard about would be lung cancer in cigarette 104 1 smoking. And that one is pretty -- pretty unequivocal 2 that people that are exposed to cigarette smoking, 3 because they are smoking all the time, have a higher 4 incidence of lung cancer than a controlled population 5 does. 6 Q. Okay. And what is group No. 3? 7 A. And the other -- the third possibility is 8 that when you look at your exposed cohort and you 9 compare it to your control or your unexposed cohort, 10 you actually see fewer cases in the exposed group than 11 you see in the unexposed group. So here you see two 12 cases of the disease and here you see four cases of 13 the disease. 14 Q. Okay. 15 A. So you certainly wouldn't say that the 16 exposure had an -- you know, influenced or had an 17 increase on the risk. You may even say perhaps this 18 exposure is somehow protecting these individuals from 19 getting whatever this disease is. 20 Q. And what would be an example of that? 21 A. Probably an example would be what I 22 showed with the aspirin where people that take an 23 aspirin a day actually have a lower incidence of 24 developing cardiovascular disease. So -25 Q. Excuse me. 105 1 A. That's fine. If you're looking at 2 cardiovascular disease, then the control people, these 3 people are not taking aspirin. They have a higher 4 rate than the people who are taking aspirin. And that 5 is the basis for us being able to say that taking an 6 aspirin is beneficial to your health, because they 7 aren't developing that disease as much as the 8 controls. 9 MR. SCHIRRMEISTER: Okay. I think we 10 have to change the tape, David. 11 THE VIDEOGRAPHER: This is the end of 12 tape No. 1. Going off the record. The time is 11:58. 13 (Recess taken, 11:58 a.m. to 12:11 p.m.) 14 THE VIDEOGRAPHER: We are back on the 15 record. The time is 12:11. This is the beginning of 16 tape No. 2. 17 Q. (BY MR. SCHIRRMEISTER) All right, David. 18 We had just finished discussing this slide, page 39 of 19 Exhibit 34. So go on to the next page. And explain 20 here no association in this example of a cohort study. 21 A. Yeah, really the only point out of this 22 slide, because this is the first example where the 23 number of cases in the exposed was similar to the same 24 as the number of cases in the unexposed. And then 25 basically in epidemiological studies, you set up a 106 1 ratio. So you put this number over this number. And 2 the math is not that important; but if that ratio is 3 1, that means that the top number and the bottom 4 number are the same, that means that the number of 5 cases in the exposed was the same as the number of 6 case in the unexposed. 7 So by definition, if you see a relative 8 risk, however that's defined, but that's a ratio 9 that's describing the risk of getting this disease 10 being exposed to whatever it is of 1.0, then there's 11 no association. 12 Q. Okay. So if when we -- when the jury 13 looks later at different epidemiology studies, if they 14 see 1, there's no association? 15 A. If they see 1.0, that means that in the 16 exposed group, they saw the same number of cases -17 exactly the same number of cases as they saw in the 18 unexposed group. 19 Q. Okay. Next slide is cohort studies with 20 a positive association. Explain that, please, David. 21 A. Right. So it's the same -- it's a ratio 22 of how many you saw in the exposed, in this case 8, 23 versus how many you saw in the unexposed, in this case 24 2; but you set it up as a ratio. Doesn't matter how 25 we got that. But in this case, the ratio is 4.0. So 107 1 that means that it was four times more likely in the 2 exposed to find people with the disease than you would 3 find in the unexposed. 4 So that would suggest that there might be 5 a relationship between whatever this chemical was and 6 this disease. So this is a positive association 4.0. 7 Q. And is that, for example, smokers more 8 likely to get lung cancer than nonsmokers? 9 A. I think in that case when it's lung 10 cancers and cigarette smoking, this relative risk is, 11 like, 20 or 30. It's very high. 12 Q. But that speaks to a positive 13 association? 14 A. That's correct. 15 Q. Okay. And then the next is cohort 16 studies, no association in this example. 17 A. Right. This is the third case where you 18 actually see fewer number of cases in the exposed 19 compared to the unexposed. And so the ratio is going 20 to be less than 1. 21 In this case, the ratio was .25, which 22 means that you have a reduced chance of finding people 23 with the disease associated with the exposure than you 24 have in the control group. 25 Q. Okay. 108 1 A. So this would not indicate an association 2 between exposure and disease, and could be used to 3 support the position that these exposures actually 4 protected the individuals from developing that 5 disease, like we talked about with cardiovascular and 6 aspirin. 7 MR. SCHIRRMEISTER: Okay. Offer 34. 8 Q. (BY MR. SCHIRRMEISTER) David, I'm going 9 to hand you what's been marked as Exhibit 35, which is 10 a two-page slide called Case Control Studies. 11 Now, how is a case control study 12 different from a cohort study? 13 A. In a case control study, you basically -14 and you use these if the disease is relatively rare. 15 And there are other characteristics of these types of 16 studies. But basically, you get a group of 17 individuals that have the disease that you're 18 interested in. 19 So you look at a bunch of people that 20 have kidney cancer and you call those the cases. And 21 then you get a group of individuals that you call the 22 controls, and these individuals should be as close to 23 these people as possible, with the exception that they 24 don't have kidney cancer. 25 So they are the same age, same gender, 109 1 ethnicity, occupation, all of those things are going 2 to be the same, except that they do not have -- they 3 do not have kidney cancer. And then through one 4 mechanism or another, you ask these people on 5 interview, questionnaires, other methodologies -- you 6 ask these people, Were you exposed to this chemical? 7 And you ask these people, Were you exposed to this 8 chemical? And then you look at the ratio of how many 9 of these people that said, Yes, I use that, or, Yes, I 10 worked with that, compared to this. So that is a case 11 control study. 12 Q. Okay. And then this is a -- a slide that 13 demonstrates a 2.5-fold association in a case control 14 study. Would you explain this, David. 15 A. Right. Really, it's the same -- the 16 ratio is the same. So this ratio is how many people 17 responded yes, Yes, we were exposed in the -- in the 18 cases versus how many people responded yes in the 19 controls. And you set it up as a ratio just like you 20 do with the cohort studies. 21 So in this case, the odds ratio is 2.5. 22 An odds ratios are what you're calculating for case 23 control studies. So this would suggest that there is 24 an association. There is a 2.5-fold association in 25 this example. This could be 1. And if it's 1.0, then 110 1 in this case control study, the same number of cases 2 as the number of controls said, Yes, we were exposed 3 to this or, Yes, we did this. And it can be less than 4 1. 5 MR. SCHIRRMEISTER: Okay. I'm going to 6 offer 35. 7 Q. (BY MR. SCHIRRMEISTER) And hand what you 8 has been mark as 36. This is Relative Risk and 9 explaining the 1.0. 10 A. Okay. So on both cohort and case 11 control, which we've just gone through, associations 12 between exposure and diseases are measured by relative 13 risk. And this relative risk can be called an odds 14 ratio, it can be called a standardized mortality 15 ratio. I mean, there's all kinds of ways, depending 16 on specific that you're looking at. But essentially 17 it's what we've been talking about. If it's 1.0, then 18 that means that the controls and the exposed had the 19 same probability or risk of developing the disease. 20 If it's greater than 1, then there were 21 more people in the exposed that had the disease than 22 than the unexposed, so that would suggest there might 23 be an association. If it's less than 1, then there 24 are fewer people in the exposed than you saw in the 25 unexposed. And that suggests that there might be a 111 1 protective effect from that. So this is really just 2 kind an overview of what we've been talking about. 3 MR. SCHIRRMEISTER: Okay. Offer 36. 4 Q. (BY MR. SCHIRRMEISTER) David, I'm going 5 to hand you 37, which goes on to a slightly different 6 topic, a two-page slide called Evaluating The Role Of 7 Chance. 8 Now, the first there -- would you just 9 read that to the jury and explain the P-value and the 10 95 percent confidence interval and explain how that is 11 used in epidemiology studies, both cohort studies and 12 case control studies. 13 A. Right. There's really no difference 14 between those. All you really need to know about this 15 slide is that when you're conducting an epidemiology 16 study, whether it's a cohort or a case control, it's 17 not a very precise science, and there is uncertainty 18 about your answer. There is variability around that 19 answer. And what you need to do, because of that 20 variability, is you want to -- to the best of your 21 ability scientifically, you want to be able to say 22 this is a real certification and not due to just 23 random chance. Not due to the fact that, you know, we 24 just flipped a coin, and it ended up heads six times 25 in a row. Okay. That there really is something going 112 1 on. 2 These two measures are ways that 3 epidemiologists mathematically -- it allows them to 4 account for the role that chance can play in their 5 studies, the P-value and the 95 percent confidence 6 interval. But really all you need to remember -7 that's fine. All you need to remember is that it's 8 ways that epidemiologists account for the role that 9 chance could play in their findings. 10 MR. SCHIRRMEISTER: Okay. Offer 37. 11 Q. (BY MR. SCHIRRMEISTER) David, I'm going 12 it hand you 38 and 39, which are two studies -- or two 13 slides that speak to confidence intervals. 14 A. Might we go back. We didn't do the P 15 value. 16 Q. I'm sorry. 17 A. So really, we'll just go through it. The 18 P-value is the probability that you could have 19 obtained the data that you got and the association 20 that you calculated from that data by chance alone. 21 Q. Um-hum. All right. 22 A. Okay. So that's what a P-value does. So 23 it tells you what's the probability that we really 24 don't have an association at all but that random 25 chance gave us the data that we're looking at. 113 1 So if the P-value is .01, then that means 2 that we are 99 percent sure that chance did not give 3 us the answer that the study reports. So that would 4 be a very good study. 5 So we are only 1 percent chance -6 there's only a 1 percent probability that chance is 7 the reason why we got the results that we got. And by 8 convention, scientifically, we say that of a P-value 9 of .05 or less means that it is statistically 10 significant, which means we are willing to accept -11 the scientific community is willing to accept, all of 12 us that, the EPA, the FDA with clinical trials, all of 13 us, the scientific community is willing to accept a 14 5 percent chance that -- that just dumb luck is what 15 we're looking at, but we are 95 percent sure that -16 that -- that, really, we are looking at the real data. 17 Q. Okay. So now on to Exhibit 38 and 39 18 called a confidence interval. The first slide speaks 19 to the president's approval rating or a president's 20 approval rating. And then the second describes a 21 relative risk. So would you explain Exhibit 38, 22 please, David. 23 A. Yeah, a confidence interval is just a 24 descriptor. And a lot of epidemiologists think that 25 this is actually the most important part of the 114 1 epidemiology data, that the number, the point estimate 2 doesn't tell you merely as much as the 95 percent 3 confidence interval. But what that is is that when 4 you calculate a relative risk, there's variability 5 around that, and you don't know what the exact answer 6 is. 7 So as an example, if they did a 8 president's approval rating and some poll and they 9 would say, yeah, their approval rating is 60 percent. 10 Okay. That's pretty good. But they would also say, 11 We don't know if it's exactly 60 percent. We say it's 12 60 percent, plus or minus 3 percent. So that plus or 13 minus 3 percent is the confidence interval. 14 They say, We don't know that the 15 confidence -- I mean, that the approval rating is 16 actually 60, but we are pretty sure that it's 17 somewhere between 57 and 63. Maybe it's 62, maybe 18 it's 59. We don't know, but we are 95 percent sure -19 if it's a 95 percent confidence interval, we're 20 95 percent sure that the real answer is from 63 to 57. 21 That's very important in evaluating epidemiology 22 studies. 23 Q. Okay. Now we have the next slide, which 24 is Exhibit 39. And this is the 95 percent confidence 25 interval. 115 1 A. So this is exactly what we were just 2 describing in the previous study, but it's looking at 3 real epidemiological data. 4 So you pick up a study and you show that 5 the relative risk is 2.0, which means that there were 6 more people in the exposed that had the disease than 7 were in the unexposed. All right. So this ratio was 8 greater than 1. But we don't know that the real 9 answer is 2.0. 10 Okay. All we know is based on the size 11 of the study and the -- and the conduct of the study 12 that we are 95 percent sure that the real answer is 13 within this range. And this range is the 95 percent 14 confidence interval. In this case, it's 0.9 to 4.4. 15 So we don't know if the answer is 2.0, we 16 don't know if the answer is 1.0, we don't know if the 17 answer is 4.0. Okay. And that's really important, 18 because if the answer is 4.0, that's a really 19 different interpretation than if the answer is 1.0. 20 1.0, no association; 4.0, a positive association. So 21 this 95 percent confidence interval really is 22 critically important in evaluating this study. 23 Q. Okay. Now, we did this originally, 24 David, to speak about painter epidemiology studies. 25 MR. SCHIRRMEISTER: Before we do that, 116 1 offer 38 and 39. 2 Q. (BY MR. SCHIRRMEISTER) I'm going to hand 3 you what has been marked as Exhibit 40. Would you 4 read the title of this study. 5 A. Studies show painters do not have an 6 elevated risk of AML or leukemia. 7 Q. Okay. Now, what have you done here, 8 David? 9 A. This slide just depicts -- and we 10 separated it out, I separated in cohort, because now 11 we know what those are, as opposed to case control 12 studies. These registry based -- this is a different 13 type of epidemiological study design, but it's looking 14 at the same thing. These are all the studies that -15 that I know of that specifically evaluated the 16 relationship between leukemia and/or AML and 17 occupation of being a painter. 18 Q. Okay. 19 A. And as you can see, there is a -- a lot 20 of studies. This has been looked at from an 21 epidemiological point of view for years. 22 Q. Okay. Now, Dr. Milman, one of 23 Mr. Wolfe's experts, has testified that painters are 24 at an increased risk for developing AML or leukemia. 25 Do you believe the epidemiology literature as set 117 1 forth on Exhibit 40 supports that? 2 A. Well, anytime you ask this question over 3 and over and over again, just by random chance, you're 4 likely to find some positives. And there are a few 5 positive studies scattered throughout the literature. 6 So if all you were going to do is look through the 7 literature and say, Well, here's a positive study or 8 two, and that's what's going to be the basis of your 9 opinion, you know, then -- then that's basically what 10 you would say. But, you know, a fair interpretation 11 is you've got to look at this overall literature. You 12 can't just pick out the sporadic positives. You have 13 got to look at the collective body of studies. And 14 there's a huge amount of data out there. And 15 collectively, this does not support that painters have 16 an increased risk of developing AML. 17 Q. Okay. How many cohort studies were you 18 able to identify? 19 A. I could find 19. 15 have some kind of 20 positives, so 19 -- I'm sorry, 15 have some -- 4 have 21 some positive finding, 15 are negative. So 15 out of 22 19 were negative. 14 out of 17 for the case controls. 23 Almost all of the registry studies were negative. 24 It's important to point out that simply 25 listing them and then counting up the number of 118 1 positives and negatives isn't really an appropriate 2 way of evaluating this literature, because these 3 studies are -- some of them are more important than 4 others. Some of them are more powerful, some of them 5 are bigger. And so, really, you -- you can't just, 6 you know, go like this and say, Well, there's more 7 papers on the positive side or the negative side. 8 You've got to look at what these individual studies 9 say. 10 MR. SCHIRRMEISTER: Okay. Offer 40. 11 Q. (BY MR. SCHIRRMEISTER) David, did you go 12 into all of these different studies and select those 13 that you thought were most important? 14 A. The ones that I picked out were the most 15 recent and they were also the largest. 16 Q. Okay. 17 A. So from a size point of view -18 Q. So -19 A. -- the bigger the study is, the better 20 able those investigators are going to be able to -- to 21 find a -- a potential association. 22 Q. Okay. I'm going to hand you what has 23 been marked as Exhibits 41 and 42. 41 is this slide. 24 42 is the underlying study. So describe this study. 25 First of all, it's -- what type of study is it? 119 1 A. Okay. This was an epidemiological study 2 that was conducted by Kyle Steenland and a 3 co-investigator from NIOSH, government-sponsored 4 study. And they were specifically looking at 5 mortality associated with being a painter. 6 Q. Okay. 7 A. And they evaluated the mortality 8 experience of 57,000 painters. 9 Q. Okay. And who -- and who sponsored this 10 study? 11 A. This was NIOSH, the National Institute of 12 Occupational Safety and Health. So this was done on 13 behalf of OSHA. 14 Q. Okay. And you have a -- and how many 15 painters did they look at? 16 A. They looked at 57,000. So this was a 17 really, really big study. And the larger the study 18 is, it allows them to be able to see potential changes 19 that are small. The bigger the study, the better able 20 the investigators to see if there are small increases 21 in risk. And 57,000, that's the biggest one that I -22 that I think is in existence right now on painters. 23 And they did look specifically at leukemia. And here 24 is their results from that leukemia. 25 Q. Okay. And what is the relative risk that 120 1 was found? 2 A. Yeah. So in this case, it was 3 standardized mortality ratio, which is their form of a 4 relative risk with the 95 percent confidence interval. 5 So, I mean, that's exactly what we were 6 just talking about. Think found an overall relative 7 risk of leukemia of .92. So that is actually less 8 than 1. So it does not support that there was an 9 association between being a painter and getting AML. 10 The 95 percent confidence interval -- so this is 11 really what we think the real answer is going to be. 12 Somewhere between .78 and 1.1. We don't know what it 13 is, but the overall risk does not suggest there's an 14 increase. The overall study does not suggest there's 15 an increase. 16 Q. Okay. And risk is actually below 1? 17 A. That's right. 18 Q. And the significance of that is? 19 A. Well, the significance is it clearly 20 doesn't support an association. If you have a number 21 that's below 1, then you could say, well, that 22 suggests there's a protective effect. But I don't 23 believe, unless it's statistically significant, you 24 can really rely on that. 25 So here we have one that's 1.3. Well, I 121 1 don't believe that is meaningfully elevated any more 2 than I believe this is more meaningfully depressed, 3 because you don't have statistical significance 4 associated with those. So while this is less than 1, 5 my interpretation is that just says there's no 6 association. 7 Q. Okay. And when you say no association, 8 no association between what and what? 9 A. No association between being a painter 10 and dying from leukemia, because this is a mortality 11 study. 12 MR. SCHIRRMEISTER: Okay. Offer 41 and 13 42. 14 Q. (BY MR. SCHIRRMEISTER) Okay. The next 15 one, David, is another study. And you selected the 16 second study, correct? 17 A. Yes. 18 Q. Okay. What is this study? Who performed 19 it? Who were the authors? What -- what did it do? 20 A. This was published in 2002. Dr. Brown, I 21 don't -- I don't actually know -- the National Cancer 22 Institute. Yep. So they were from NCI. So that's a 23 federal agency, NCI. 24 Q. And, again, National Cancer Institute 25 being the sponsoring organization? 122 1 A. Correct. Or where these people worked. 2 And they looked at exposures into painting trades and 3 paint manufacturing industry and risk of cancer among 4 men and women in Sweden. 5 Q. Okay. How many painters? 6 A. And they looked at 49,000 painters. And 7 in this case, they reported an SIR. The previous 8 study was SMR for mortality. So they were looking at 9 death certificates and how many people died. These 10 folks were looking at medical records and how many 11 people got the disease. So this is I for incidents, 12 SIR. But it's a relative risk. Same concept. 13 Q. Okay. And what was the relative risk 14 reported for leukemia and painters? 15 A. In this study, they look at leukemia 16 collectively. They had 115. That's what the N means. 17 That's how many cases they looked although. The SIR 18 or the relative risk was exactly the same as the other 19 one, .9, a little bit below 1. The 95 percent 20 confidence interval was .8 to 1.1. 21 Q. Okay. 22 A. So this very large study from the NCI 23 does not support that being a painter increases your 24 risk of developing leukemia. 25 MR. SCHIRRMEISTER: Okay. Offer 43 and 123 1 44. 2 Q. (BY MR. SCHIRRMEISTER) Okay. David, I'm 3 going to now point you to Exhibit 45 and 46. Would 4 you identify that for us, please. 5 A. Another recent study, 2002. This was a 6 registry-based study, Association Of -- Swiss Cancer 7 Registries. 8 Q. Okay. 9 A. Another really large one. 10 Q. How many painters? 11 A. 28 -- excuse me, 58,000 painters. And 12 they were looking at -- so this is kind of a case 13 control, which is why you have odds ratios. And this 14 043 at the beginning of the study, they listed all of 15 the various occupations and assigned a numerical code 16 to those occupations. And on 043 was the painter 17 occupation. 18 Q. Okay. 19 A. That's not on the slide. You just have 20 to take my word for it; but for the painters, for 21 leukemia, the odds ratio was .7. So that's below 1. 22 Here's the 95 percent confidence interval. And then 23 for myeloid leukemia -- which is a little more 24 relevant, because it includes chronic myelogenous, as 25 well as acute myelogenous, but the relative risks 124 1 really don't change -- it's 0.6, and the 95 percent 2 confidence interval is .6 to 1.2. 3 Q. Okay. And in each case, is the odds 4 ratio below 1? 5 A. In these cases, they are below 1; but 6 since it's not statistically significant to me, that 7 really just says, in this study, they did not see an 8 association or any hint of an association between 9 being a painter and developing either leukemia or 10 myeloid leukemia. 11 Q. Okay. So if we were to add the painters 12 together in all three studies, we would have 13 approximately how many painters? 14 A. I don't know, 150,000. 15 Q. Okay. 16 A. 160,000. 17 Q. Okay. And in those three studies, did 18 any of the authors find that increased risk between 19 being a painter and developing leukemia? 20 A. There were no increased risks of any of 21 those three which were relatively recent large, large 22 epidemiological studies, no. 23 Q. Okay. And do you believe that being a 24 painter puts you occupationally at an increased risk 25 for developing leukemia? 125 1 A. The only way you can answer that kind of 2 question is by looking collectively at the 3 epidemiology that investigates that question. And 4 that's what we've been doing. 5 These three largest, but as well as the 6 overall list that we showed earlier and collectively, 7 no, this literature does not support that painters, as 8 an occupational group, have an increased risk of 9 developing leukemia. 10 MR. SCHIRRMEISTER: Okay. Offer 45 and 11 46. 12 Q. (BY MR. SCHIRRMEISTER) Okay. Now, 13 David, we're going to go on to our final area here. 14 Would you read that, please. 15 A. "The best available scientific literature 16 does not support a link between formaldehyde and acute 17 myeloid leukemia or acute promyelocytic leukemia." 18 Q. Okay. Now, I'm going to hand you what 19 has been marked as Exhibit 47. Did you prepare a 20 supplemental report in this case regarding 21 formaldehyde and -22 A. I did. 23 Q. -- AML or APL? 24 A. I did. 25 Q. Okay. And is Exhibit 47 a 126 1 true-and-correct copy of your supplemental report 2 dated July 9, 2009? 3 A. It looks to be. I don't have any reason 4 to think you would have changed it. 5 Q. No. 6 A. Looks right, yes. 7 Q. Okay. 8 MR. SCHIRRMEISTER: Offer 49. Excuse me, 9 was that 47? 10 THE DEPONENT: It is 47. 11 MR. SCHIRRMEISTER: Okay. Offer 47. 12 MR. GIANARIS: Same objection. 13 Q. (BY MR. SCHIRRMEISTER) Okay. And just 14 so we're clear, your -- Exhibit 47 is a 15 true-and-correct copy of your report of your report -16 of your supplemental report dated July 9, 2009? 17 A. Correct. 18 MR. SCHIRRMEISTER: Okay. Offer 47. 19 Q. (BY MR. SCHIRRMEISTER) Okay. Now, what 20 did you do, David, to address the question of whether 21 formaldehyde exposure places folks at an increased 22 risk for developing leukemia or AML? 23 A. Well, really, in the report, I just 24 summarized the literature. I -- I have done some work 25 over the last two or three years interactive with EPA, 127 1 worked with some formaldehyde industries that use 2 formaldehyde on the biological basis and whether or 3 not the epidemiological literature supports that 4 formaldehyde is a -- a cause of human leukemia. 5 So I knew what the literature was 6 addressing this issue. So, really, all I did in my 7 report was describe it in a way that I hoped was 8 understandable. 9 Q. Okay. And did you select studies that 10 you believed best addressed -- best addressed this 11 question? 12 A. Yes. There's a lot of old literature 13 that -- that people talk about. And I've read them 14 all. But these are looking at workers that are 15 embalmers, funeral directors, pathologists. And while 16 they were exposed to formaldehyde, they were also 17 exposed to lots of other things. And so there are 18 some really small epidemiological studies that 19 evaluated the leukemia risk in those groups. But then 20 more recently, there have been really large cohort 21 studies of workers who were exposed to formaldehyde in 22 which they actually measured formaldehyde. 23 So there was a quantification of the 24 exposures and not just, yes, he was an embalmer, we 25 think he was exposed to formaldehyde. They have 128 1 actually done -- done the air monitoring and the 2 exposures. And so that's what I made some slides of, 3 those three big modern studies. 4 Q. Okay. And tell us what the first study 5 is, David. I'm going to -- I'm going to hand you -6 this is -- Exhibit 48 is the slide and Exhibit 49 is 7 the underlying study. 8 A. Right. So Dr. Pinkleton -- Pinkerton 9 worked for NIOSH, so did this out of NIOSH, and looked 10 at garment workers exposed to formaldehyde in an 11 update. So this was the most recent. I think there 12 were three -- two -- two prior to that. But in this 13 case, they specifically addressed the question in the 14 overall cohort, was there a risk associated with 15 myeloid leukemia. In this case, acute myeloid 16 leukemia, so -- I mean, they didn't do acute 17 promyelocytic leukemia, but this is as close as we 18 get. 19 And in that case, there was a slight 20 increase in the SMR of 1.34. But it was not 21 statistically significant, so my interpretation of 22 that is that it's -- there's -- there's -- this study 23 does not provide any evidence that being exposed to 24 formaldehyde as a garment worker increases a person's 25 risk of developing AML. 129 1 MR. SCHIRRMEISTER: Okay. Offer 48 and 2 49. 3 Q. (BY MR. SCHIRRMEISTER) David, I'm going 4 to hand you what has been marked as Exhibit 50 and 51. 5 The slide and the underlying Coggon study. 6 A. Right. I think Dr. Coggon was from the 7 National -8 MR. GIANARIS: I got to object. No 9 question pending. 10 THE DEPONENT: Oh, sorry. 11 Q. (BY MR. SCHIRRMEISTER) Who was 12 Dr. Coggon? 13 A. I don't know him, but he apparently was 14 working with the Medical Research Council in England. 15 And he published this paper, "Extended follow-up of a 16 cohort of British chemical workers that were exposed 17 to formaldehyde." 18 Q. Okay. And -- and did -- are there tables 19 contained within that study that measure -20 THE REPORTER: I'm sorry. Can we go off 21 the record. 22 THE VIDEOGRAPHER: Going off the record. 23 The time is 12:40. 24 (Recess taken, 12:40 p.m. to 12:42 p.m.) 25 THE VIDEOGRAPHER: We are back on the 130 1 record. The time is 12:42. 2 Q. (BY MR. SCHIRRMEISTER) Okay. David, 3 I've handed you what has been marked as Exhibits 50, 4 which is the slide pertaining to the Coggon 2003 5 study, and then 51, the underlying study. Tell us who 6 Dr. Coggon is and what his study was about. 7 A. I -- I don't know Dr. Coggon, but he 8 apparently, based on the affiliations, works for the 9 Medical Research Council, which is a federal agency in 10 the UK. That's my understanding. But he did a 11 follow-up of a large cohort of British chemical 12 workers that were exposed to formaldehyde. 13 Q. And was -- are there tables there 14 examining the relative risk of developing leukemia 15 following exposure to formaldehyde? 16 A. Yes. 17 Q. Okay. And there are -- just explain the 18 tables there, the three relative risks there. 19 A. What he did was looked at leukemia based 20 on these ICD codes, the International Classification 21 of Diseases, and did it based on the total cohort. 22 And then when -- segregated out certain segments of 23 the cohort. But in all cases -- and we put them up 24 here so that you could see the numbers a little 25 clearer. So this is the relative risk and this is the 131 1 95 percent confidence interval. And no matter how you 2 cut out the workers based on where and when, the 3 overall cohort was 0.91. So is less than 1. There is 4 no association with being a formaldehyde worker and 5 leukemia. And there's the 95 percent confidence 6 interval. Same -- basically the same all the way 7 across. 8 Q. Okay. And what is the significance of 9 the study with regard to Mr. Wolfe's claim that 10 exposure to formaldehyde caused him to develop 11 leukemia? 12 A. This study does not support the -- the 13 notion that even people that are working with a lot of 14 formaldehyde in the chemical industry have an 15 increased risk of developing leukemia. 16 MR. SCHIRRMEISTER: Okay. Offer 50 and 17 51. 18 Q. (BY MR. SCHIRRMEISTER) And, David, I'm 19 going to hand you what has been marked as 52 and 53. 20 52 is the slide. 53 is Dr. Beane Freeman's underlying 21 study. Who was Dr. Beane Freeman and what's the name 22 of -- well, what is her study about and who performed 23 it? 24 A. Dr. Beane Freeman is a researcher with 25 the National Cancer Institute. I don't know her. I 132 1 know some of the other authors. This was -- this was 2 published just this year. And it was their update of 3 the NCI cohort that they have been following now for 4 -- well, since '86, I think, was the first one. And 5 it was looking at the mortality from a 6 lymphohematopoietic malignancy. That's all of them. 7 That's lymphomas, multiple myelomas, Hodgkin's 8 lymphoma, all of the different kinds of leukemias. So 9 malignancies in workers in the formaldehyde industry. 10 So this is NCI's cohort. 11 Q. Okay. And what was the result of folks 12 who were exposed to formaldehyde? Did they have an 13 increased risk of developing leukemia? 14 A. This table was the overall workers in 15 this cohort. And the ones that were exposed to 16 formaldehyde, based on myeloid leukemia, so it's not 17 AML, but it at least segregates out the lymphoid 18 leukemias and the myelomas and the others. And as you 19 can see, the SMR, the Standardized Mortality Ratio, 20 relative risk, and the 95 percent confidence interval 21 is right here in the exposed group. And it does not 22 indicate that there was an association between myeloid 23 leukemia and working as a formaldehyde worker. 24 Q. Okay. And why did you select these three 25 studies to -- 133 1 A. These three, the last three, these are 2 the most important in the formaldehyde world, because 3 these have large numbers of workers and they have 4 quantification of the formaldehyde exposures. 5 So the older studies looking at embalmers 6 and pathologists, no one really knows what those 7 people were exposed to. So if you see an increased 8 risk or a decreased risk, it's specla -- it's 9 speculative to say, well, we think that's because of 10 formaldehyde or we think it's because it's some other 11 people, or whatever. You don't know. At least here 12 in these studies, they have gone in and quantitated 13 the formaldehyde exposures. 14 Q. Okay. So I'd like to go back to our 15 summary slide, David. So, again, opinion No. 1, would 16 you read that into the -- read that to the jury and 17 summarize your testimony. 18 A. That DuPont and PPG paint solvents do not 19 cause cancer or leukemia. So we discussed toluene and 20 xylene and the petroleum distillates, all the various 21 regulatory agencies that have evaluated those 22 chemicals. Those -- those toluene and xylenes all 23 have small amounts of benzene naturally occurring. 24 They always have. And so when these regulatory 25 agencies evaluate these chemicals and say they do not 134 1 cause cancer, they are basing that on the fact that it 2 has a little bit of benzene in there. 3 Q. Okay. And No. 2? 4 A. That APL, acute promyelocytic leukemia is 5 not just another subtype of AML, it is a -- a clearly 6 distinct clinical entity. It's treated differently. 7 It's diagnosed differently. The prognosis is 8 different. It's treated different. The cell of 9 origin is probably different. And as we discussed, 10 epidemiologically it appears that APL is a different 11 thing than AML. It behaves differently in these 12 epidemiological studies. 13 Q. Okay. Point No. 3? 14 A. That the best available scientific 15 literature does not support a link between benzene and 16 APL. So ignoring the fact that Mr. Wolfe really 17 wasn't ever using benzene, but was using solvents and 18 other things, but what -- what does the literature 19 tell us about people who were using benzene or that 20 had solvents -- used solvents with benzene in them and 21 APL. And that literature does not support that 22 benzene really causes this -- this disease. 23 Q. Okay. No. 4? 24 A. This was the quantification that 25 Mr. Wolfe was not exposed to enough benzene to develop 135 1 any form of leukemia. 2 Q. And does that include your discussion of 3 dose response? 4 A. That's right. So this was the dose 5 response and the quantitative epidemiology, who has 6 published papers and said benzene causes leukemia, 7 AML. We can all agree on that, but it takes a certain 8 amount. And that it takes a certain amount is what 9 that quantitative epi was important in understanding. 10 What is that line? How much does it take before we 11 would start saying, yes, that -- that's a reasonable 12 assumption that that exposure could have caused that 13 disease? 14 Q. Okay. And -- and you're familiar with 15 Mr. Russell's exposure estimate for Mr. Wolfe? 16 A. Mr. Russell's and Mr. Keller's for PPG. 17 And I've read all of them, yes. 18 Q. Okay. And do they approach the levels 19 that have been found to cause an increased risk in 20 disease? 21 A. They do not. As depicted on that slide. 22 And even if you don't agree and think that it's going 23 to be ten times more than what Mr. Russell potentially 24 estimated, it's still nowhere near enough to get to 25 where there's an meaningful increased risk of 136 1 leukemia. 2 Q. And you disagree -- or do you disagree 3 with Dr. Milman's opinion that dose is irrelevant? 4 A. I cannot understand the basis for that 5 statement. So, yes, I completely disagree with that. 6 Q. What is No. -- opinion No. 5? 7 A. That was the "Painters as an occupational 8 group collectively are not at an increased risk of 9 developing leukemia." 10 So the 40 or some studies that we talked 11 about, we chose the three largest and most recent; but 12 overall, that literature does not support that being 13 say painter, in and itself, increases your risk of 14 developing leukemia. 15 Q. Okay. And finally No. 6? 16 A. That even pretty high exposures to 17 formaldehyde -- you can't be exposed to really high 18 levels of formaldehyde, because it's so irritating. 19 So the exposures are relatively low even in these 20 industries where they are using formaldehyde. But 21 when they have quantitated and actually gone in and 22 said, Okay, these people were exposed to formaldehyde, 23 you do not see an increase in leukemia or AML. 24 There's no data to say whether you see an 25 increase in APL. There's certainly no information 137 1 that would suggest that you would. 2 Q. Okay. And you've done this work in this 3 case so far and appeared today on behalf of my client, 4 DuPont, and on behalf of Mr. Miller's client, PPG, 5 correct? 6 A. Correct. That's -- that's who I'm here 7 today on behalf of, yes. 8 Q. Okay. And what's your rate that you 9 charge us for the work that you've done in the case? 10 A. My hourly rate is $300 an hour -11 Q. Okay. 12 A. -- for this kind of work. 13 Q. And you've been paid for your work that 14 you've done so far today? 15 A. I -- I've been paid some, yes. 16 Q. Okay. 17 A. Yes. 18 Q. All right. And, again, you're not 19 going -20 A. We're not even, if that's what you're 21 implying. 22 Q. No, I'm not -- I'm not, sir. I'm not, 23 sir. And again you won't -- the jury will see you by 24 videotape, correct? 25 A. I guess. 138 1 Q. Right. Okay. And that's because you 2 have a long planned trip that requires you to be out 3 of the country? 4 A. Yes. I would like to be in North 5 Carolina, but I'll be in Nepal instead. 6 Q. Right. 7 MR. SCHIRRMEISTER: Okay. Finally, as a 8 matter of housekeeping, I want to offer 52 and 53. I 9 believe I've offered all Exhibits 1 through 53, but if 10 I have missed one in the course of my questioning, 11 David, I will just reoffer all Exhibits 1 through 53 12 and pass the witness. Thank you for your time, sir. 13 THE DEPONENT: You're welcome. 14 MR. GIANARIS: Renew all of my objections 15 and the standing objection to the admission of these 16 exhibits that were created for this trial. 17 THE DEPONENT: Could we take a 18 five-minute. Thanks. 19 THE VIDEOGRAPHER: Going off the record. 20 The time is 12:53. 21 (Recess taken, 12:53 p.m to 1:05 p.m.) 22 (The following testimony was on the 23 record, but not on the videotape record.) 24 MR. GIANARIS: For the record, this is a 25 voir dire of the witness outside of the presence of 139 1 the jury on the issue of some testimony regarding the 2 State of North Carolina. 3 VOIR DIRE EXAMINATION 4 BY MR. GIANARIS: 5 Q. Sir, for this part of the deposition and 6 for the remainder of my portion of the deposition, can 7 we agree, like you agreed with Mr. Schirrmeister, that 8 any opinions you give will be to the same legal and 9 scientific scrutiny that you agreed with 10 Mr. Schirrmeister on? 11 A. The standard? Sure. 12 Q. The standard. 13 A. Yes. 14 Q. Yes. Okay. Are you familiar with the 15 benzene regulations or regulations as to benzene 16 within the state of North Carolina? 17 A. No. 18 Q. Okay. Have you studied them in any way? 19 A. State of North Carolina? 20 Q. Yes. 21 A. I've never done any work for the State of 22 North Carolina. 23 Q. And preparing for this case and preparing 24 for the testimony you just gave on direct examination, 25 you didn't study the regulation as they related to 140 1 benzene within the state of North Carolina? 2 A. No. 3 Q. You didn't study what North Carolina said 4 or hasn't said about what different products can cause 5 cancer or not, have you? 6 A. No. 7 Q. And you don't know -- you're assuming, 8 but you don't know, what national organizations or 9 federal governmental bodies that do regulate these 10 topics or have spoken on these topics -- you don't 11 know which ones North Carolina has adopted or not 12 adopted, do you? 13 A. I can't specifically address each one. 14 My understanding -- and they had it on -- I think it 15 was the North Carolina Department of Labor -- on their 16 web site. My read of that was that they are deferring 17 to OSHA and ACGIH and EPA and all of the ones that are 18 listed. And they are -- they are adopting -- they are 19 not doing their same -- they are not conducting their 20 own epidemiological evaluation. That's -- that's my 21 understanding. 22 Q. Right. You don't know -- you have no 23 information that North Carolina has ever conducted 24 their own epidemiological investigations on these 25 topics? 141 1 A. I do not know that, no. 2 Q. And you've been to the web site for the 3 Department of Labor in North Carolina, and you see 4 that they have on their web site some other 5 organizations' epidemiological studies; is that right? 6 A. Right. That they -- my understanding was 7 that they are deferring to these national groups for 8 their own position, but I -- only that one page. 9 Q. You just read one page? 10 A. Yeah. 11 Q. Okay. All right. That's enough, thanks. 12 VOIR DIRE EXAMINATION 13 BY MR. SCHIRRMEISTER: 14 Q. Just take a question. So, David, your 15 testimony is that with regard to the standards -16 workplace standards followed by the state of North 17 Carolina, you examined the North Carolina Department 18 of Labor web site, which stated that it incorporated 19 the standards set by several federal or private 20 agencies; is that correct? 21 A. That's my understanding of what they did, 22 correct. 23 Q. Okay. As opposed to the North Carolina 24 Department of Labor going out and independently doing 25 its own studies? 142 1 A. That's -- that's exactly right, yes. 2 Q. Their web -- the North Carolina 3 Department of Labor web site indicates that they 4 incorporated the standards of the federal government, 5 which, in turn, did those standards or evaluations? 6 A. And did those studies, that's my 7 understanding, yes. 8 Q. Okay. And that forms the basis for your 9 testimony in which you describe the position of North 10 Carolina with regard to whether toluene, xylene, and 11 petroleum distillates with naturally occurring trace 12 benzene are capable of causing cancer or leukemia? 13 A. Correct. 14 VOIR DIRE EXAMINATION 15 BY MR. GIANARIS: 16 Q. Just so we're clear, can you tell me how 17 you got that web site, where that web site is, or if 18 you printed that page off? 19 A. You know, I did have it, and I didn't 20 bring it with me. It actually came from 21 Mr. Schirrmeister's office. 22 Q. Okay. So -- that's good to know. This 23 page of the web site was printed off and sent to you 24 by the lawyers? 25 A. It wasn't sent to me. It was present in 143 1 a meeting that I attended. 2 Q. Okay. So you attended a meeting with the 3 lawyers in this web -- and this page from the web site 4 had been printed off? 5 A. That's right. 6 Q. You've never even been to that web site? 7 A. We did look at it in that meeting. So I 8 did go to it then, yes. 9 Q. That particular page? 10 A. Yeah. 11 Q. Okay. And you're your original answer to 12 my question -- I think your answer to 13 Mr. Schirrmeister -- or Mr. Schirrmeister's question 14 was a little different than to my question. You said 15 that it's your understanding that that's what North 16 Carolina has done and deferred. I think he asked, Is 17 that what you read? He asked you, Did you read that 18 they deferred? It doesn't say on that page that they 19 deferred to other organizations, did it? 20 A. I don't remember the exact language. It 21 was just my understanding that they had deferred to 22 other federal agencies. And that's what they are 23 basing their position on. 24 MR. GIANARIS: Okay. All right. That's 25 all I have. I just ask that that page be produced to 144 1 me so we can have it for the judge when we go over 2 that issue. 3 MR. SCHIRRMEISTER: I'll be happy to do 4 that. Please send me a letter. 5 MR. GIANARIS: I might have to write on 6 my hand. 7 MR. SCHIRRMEISTER: We'll have it in the 8 transcript. It won't be a problem. The North 9 Carolina Department of Labor web site. I can give you 10 a piece of paper. 11 MR. GIANARIS: This is better. I won't 12 lose it. 13 MS. MANELA: Hopefully not. 14 MR. GIANARIS: Ready when you all are. 15 THE VIDEOGRAPHER: Okay. One moment, 16 please. I've finished with the voir dire. 17 (The following testimony was on the 18 record and on the videotape record.) 19 THE VIDEOGRAPHER: We are back on the 20 record. The time is 1:12. 21 CROSS-EXAMINATION 22 BY MR. GIANARIS: 23 Q. Good morning, Dr. Pyatt -- or afternoon 24 now. 25 A. Afternoon. 145 1 Q. How are you? 2 A. I'm good, thank you. 3 Q. Just so the jury can reorient now and 4 understand what we're doing. This is Ted Gianaris, 5 and I'm one of the lawyers along with Bo Drew for the 6 Wolfe family. You understand that? 7 A. Yes. 8 Q. Okay. And we're here in your home town 9 in Boulder, Colorado? 10 A. Yes. 11 Q. And we're at the St. Julien Hotel and 12 Spa; is that right? 13 A. I think they do have a spa here, yes. 14 Q. That's what the pens I think and the note 15 pads in front of us say? 16 A. Yeah. 17 Q. This is -- this is where you give 18 depositions; is that right? 19 A. I've given depositions here. It's not 20 the only place, but, yes, I have used these facilities 21 before. 22 Q. Okay. And you've given plenty of 23 depositions in your time as an expert witness; is that 24 right? 25 A. I -- I don't know what plenty means. I 146 1 -- I think at this point I've given 17. 2 Q. 17 depositions total? 3 A. Yes. 4 Q. Okay. And in all of those depositions, 5 you get paid just like you're getting paid here today, 6 right? 7 A. I -- in all of the work I do as a 8 toxicologist, I get paid for my time. 9 Q. Right. And you told the ladies and 10 gentlemen of the jury earlier that you took a vow of 11 poverty when you went to graduate school, right? 12 A. Yes. 13 Q. Okay. 14 A. It's kind of a joke among graduate 15 students, but, yes. 16 Q. I understand. And -- but you've sworn 17 off of that vow of poverty now, and now you have a 18 business of your own, a toxicology business? 19 A. I have a full-time job, yes. 20 Q. Okay. And you're getting paid $300 an 21 hour to testify here and do your work in this case? 22 A. That's correct. 23 Q. Okay. And that's being paid at this 24 point by DuPont and PPG? 25 A. At this point, I think that's right, yes. 147 1 Q. Okay. You've -- when you've worked on 2 cases in the past, it's been more than 17 cases, but 3 you've actually testified in deposition in 17 cases, 4 right? 5 A. That's true. 6 Q. Okay. Every case you've ever looked at 7 was a benzene case where a person, a worker mostly 8 claimed that they had been exposed to benzene, 9 breathed benzene on their job, and developed a -- some 10 form of blood disease; is that right? 11 A. That -- yes, that -- those are all the 12 cases that I've worked on, yes. 13 Q. And in every one of those cases, there's 14 been a medical doctor who has said, on behalf of the 15 worker that, yes, this benzene exposure caused this 16 man's blood disease, right? 17 MR. SCHIRRMEISTER: Object to the 18 residential? 19 A. That is -- that's incorrect. 20 Q. (BY MR. GIANARIS) That's incorrect? 21 A. Yes. 22 Q. In most of them, has it? 23 A. No. 24 MR. SCHIRRMEISTER: Object to the form. 25 A. Very rarely. As a matter of fact, I can 148 1 only think of, maybe, one or two that a treating 2 physician associated with the patient said, I think 3 this person's exposure had anything to do with their 4 work. 5 Q. (BY MR. GIANARIS) Right. That wasn't my 6 question. I said there was a medical doctor on the 7 other side of the case, just like you -8 A. Oh, oh, oh. 9 Q. -- on this case? 10 A. I'm sorry. 11 Q. You've been hired in this case -- first 12 of all, you're not a medical doctor, right? 13 A. I am not. I have a Ph.D. 14 Q. Ph.D. In science -- in type of science, 15 in toxicology? 16 A. Correct. 17 Q. Okay. And what I'm saying is the claims 18 that have been brought by these workers, more than 17 19 of them -- you've given 17 depositions, but more than 20 17 claims that you've worked on, there's been a 21 medical doctor on the other side, a trained medical 22 doctor who said, yes, that benzene exposure caused 23 that man's or that worker's blood disease? 24 MR. SCHIRRMEISTER: Object to the form. 25 A. Yeah. I'm sorry. I don't -- I mean, 149 1 there have been some cases where that's true for sure. 2 I don't know whether it's the majority. There have 3 been some cases where there wasn't an M.D. associated, 4 there was other toxicologists and epidemiologists. 5 But there have been some for sure. 6 Q. (BY MR. GIANARIS) Okay. Or a scientist 7 like a toxicologist or an epidemiologist? 8 A. Well, now, there's always that. 9 Q. Yeah. 10 A. That's always true. It was the M.D. part 11 that threw me off. 12 Q. Okay. 13 A. That's not always the case. 14 Q. Okay. And in every one of those 17 15 cases, you've worked for the defense; is that right? 16 Or more than 17 cases you worked for the defense? 17 A. At this point, that's true. 18 Q. Okay. And in every one of those cases, 19 you found no cause, right? 20 A. That's not true. In every one of the 17 21 cases that I've given depositions in, it was my 22 opinion that either the disease was not linked to 23 benzene exposure, that the disease characteristics 24 weren't consistent with our understanding of what a 25 benzene-exposed person would look like or, 150 1 alternatively, that the person was not exposed to 2 enough benzene to meaningfully increase their risks. 3 But that's not true for -- for all cases. I mean, I 4 have seen some cases where I was unable to 5 realistically say that I can -- let's put this way. 6 There were some cases that I was not able to say I 7 don't know whether the benzene had any effect or not. 8 Q. And in those cases, the defendants or it 9 is defendants' lawyers didn't use you as an expert, 10 right? 11 A. They didn't use me past that point, 12 that's true. 13 Q. Okay. 14 A. I don't think those cases went much 15 further. 16 Q. Okay. And you're -- you're a -- you're a 17 scientist who specializes his -- his toxicology or 18 focuses his toxicology on diseases of the blood, 19 correct? 20 A. That's true, yes. 21 Q. Okay. What's that called again? 22 A. Well, hematotoxicity, hematopoietic 23 toxicology, immunotoxicology. That's probably the 24 biggest category. 25 If you look at SOT, the Society of 151 1 Toxicology, and you look at all of the various 2 subspecialties, hematotoxicity there's maybe one me. 3 But immunotoxicity, there's going to be several. So 4 those are the categories. 5 Q. But there's a lot of doctors who study 6 these diseases of blood. In fact, you said you just 7 went over to Germany, and there was a big group of you 8 all got together and talked about the sciences; is 9 that right? 10 A. That's correct. And by doctor, of all -11 all denominations. 12 Q. Right. So kind of an ecumenical group. 13 A. Well, there was M.D.s, there were Ph.D.s, 14 you know, so -- so there were -- there were both. 15 Q. Okay. The stem cell, that is the basic 16 building block of the blood; is that right? 17 A. I think that's a fair assessment. It is 18 the most primitive cell that, to the best of our 19 ability, we believe gives rise to all the other blood 20 cells. 21 Q. And you told us earlier -- when 22 Mr. Schirrmeister asked you a question about the 23 definition of stem cells, you were kind of taken aback 24 and you were thinking about it, and you told us that 25 blood -- the scientists who study blood, when they get 152 1 together, they have passionate arguments over the 2 definition of a stem cell; isn't that right? 3 A. They do indeed. 4 Q. They do. But then you told us -- you 5 said but it's really irrelevant, didn't you? 6 A. Well, what I meant by that -- I mean, 7 they certainly would not think it's irrelevant and 8 then they would be passionately arguing with me over 9 that comment. What I meant is it wasn't that 10 important to our slide. 11 Q. Oh, okay. 12 A. To what we were discussing today in this 13 -- in this case. 14 Q. Okay. Let's look for a minute at 15 slide -- page 7, if we could. 16 MR. GIANARIS: We can go off for a 17 second. 18 THE VIDEOGRAPHER: Going off the record. 19 The time is 1:19. 20 (Recess taken, 1:19 p.m. to 1:20 p.m.) 21 THE VIDEOGRAPHER: We are back on the 22 record. Time is 1:20. 23 Q. (BY MR. GIANARIS) Okay. We put up what 24 is page No. 7 -- I think it was Defendants' 25 Exhibit 4 -- for a moment. 153 1 Now, I want to talk to you about these 2 categories for a minute: Toluene, xylene, and 3 petroleum distillates. Let's start with toluene. The 4 -- the toluene in DuPont and PPG's paints and solvents 5 is contaminated with benzene, isn't it? 6 MR. SCHIRRMEISTER: Object to the form. 7 A. Well, I think even -- even today, if you 8 hydro-treat toluene, which is a really sophisticated 9 process, you cannot get all of the benzene out. So 10 there is going to be some benzene that is part of that 11 toluene. So there's -- there's always going to be a 12 little benzene in toluene. 13 Q. (BY MR. GIANARIS) So DuPont and PPG's 14 toluene is contaminated with benzene? 15 MR. SCHIRRMEISTER: Object to the form. 16 A. It has some naturally occurring benzene 17 in it. 18 Q. (BY MR. GIANARIS) You don't like the 19 word contaminated? You're using naturally occurring 20 rather than contaminated? 21 A. Well, I think it's the same. 22 Q. Okay. It's the same. I thought so. 23 Okay. Xylene in DuPont and PPG's paints and paint 24 solvents is contaminated with benzene, isn't it? 25 MR. SCHIRRMEISTER: Object -- 154 1 Q. (BY MR. GIANARIS) -- that second box? 2 MR. SCHIRRMEISTER: Object to the form. 3 A. Because of the way they produced 4 xylene -- not they, but the way xylene is produced, I 5 don't think it's possible to get every molecule of 6 benzene out of xylene. 7 Q. (BY MR. GIANARIS) Okay. So it's 8 contaminated with -- DuPont and PPG's xylene is 9 contaminated with some benzene? 10 MR. SCHIRRMEISTER: Object to the form. 11 A. It has some benzene in it. Sorry. 12 Q. (BY MR. GIANARIS) And the petroleum 13 distillates -- distillates -14 A. Distillates. 15 Q. -- distillates. Easy for you to say. 16 A. Yeah. 17 Q. The petroleum distillates in the DuPont 18 and PPG paints and solvents are contaminated with 19 benzene, aren't they? 20 MR. SCHIRRMEISTER: Object to the form. 21 A. I would put those into the same category. 22 They all contain small amounts of benzene. 23 Q. (BY MR. GIANARIS) Okay. And then down 24 on the bottom of this slide, we have IARC and NIOSH 25 and ACGIH, which I think is the American Conference of 155 1 Government and Industrial Hygienists, NTP, ATSDR, EPA. 2 I just want to talk about those groups 3 for a minute and the heading there. This isn't 4 completely accurate, is it, this slide? 5 A. Well, you'll have to be a little more 6 specific. We -- this is one of the things that I 7 specifically went through and looked at these various 8 documents and piled up these documents from these 9 agencies and made sure that they had all weighed in on 10 these various classes of chemicals. 11 Q. Right. So when you went through the -12 you went through the IARC documents, piled them up and 13 you waded through them? 14 A. Yes. 15 Q. Same with the NIOSH documents, same with 16 the ICGIH documents, et cetera, right? 17 A. Well, I actually did it on a chemical -18 per-chemical basis. 19 Q. Okay. 20 A. I said, Okay, here's all of the things on 21 toluene. Do I have something that IARC said about 22 toluene? Do I have something that NIOSH said about 23 toluene? So I -- I did it that way. 24 Q. Okay. And none of these organizations 25 talked about what you -- you have up here in the 156 1 heading of this particular slide, right, they didn't 2 look at DuPont and PPG paints and solvents. They 3 didn't extensively evaluate and study DuPont and PPG's 4 paints and solvents, does they? 5 A. No, they didn't evaluate these specific 6 products. 7 Q. Okay. 8 A. But since those are the main ingredients 9 in those paint solvents, that's -- that -- it has some 10 bearing to what we were looking at. 11 Q. Right. It has some bearing; but by no 12 stretch of the imagination did any of these groups 13 down here at the bottom look at DuPont and PPG paints 14 and solvents and extensively evaluate and study them, 15 did they? 16 MR. SCHIRRMEISTER: Object to the form. 17 A. Oh, that's the part that you said is not 18 accurate. 19 Q. (BY MR. GIANARIS) Yeah. 20 A. Oh, I got it. Well, I guess it depends 21 on your definition. I mean, if the paint solvents 22 that you're referring to are toluene and xylene and 23 the petroleum distillates, then it is totally 24 accurate. 25 If you're saying did they go get a PPG 157 1 paint solvent that is something different than these, 2 then, you know, that would not be accurate. But these 3 are the PPG and DuPont paint solvents, the most 4 common. And they did look for those. So it depends 5 on your definition, but I think it's accurate. 6 Q. Okay. But you don't -- and maybe it's 7 tomato, tomato, but these groups down at the bottom, 8 so we're clear, did not in any way, shape, or form 9 evaluate DuPont and PPG paints and solvents? They 10 didn't actually go look at them and evaluate them and 11 write about them? 12 MR. SCHIRRMEISTER: Object to the form. 13 A. What they evaluated -- I think I see 14 where you're going. What they evaluated was toluene. 15 Q. (BY MR. GIANARIS) Okay. 16 A. So when you look at a DuPont paint 17 product and it has toluene in it, okay, well, that 18 evaluation, in my view, is relevant to the toluene 19 that's in a DuPont product. 20 Q. Okay. 21 A. Did they go and pull a DuPont product off 22 the shelf and say, Is this toluene any different than 23 all of this other toluene? I don't know the answer to 24 that. My guess is no. 25 Q. Right. Okay. Let's go to page 29, 158 1 please, Exhibit 27. Okay. You used this to describe 2 the dose response -- to describe dose response, right? 3 A. Well, kind of. What -- what we tried to 4 depict here was this notion that even very safe things 5 that everyone considers and are exposed to all of the 6 time, like water and salt, can be toxic if you are 7 exposed to enough of them. 8 Q. Right. And what we're talking about over 9 here in the red -- just so the jury -- we make sure 10 it's clear to the jury, in the red is an acute 11 overdose. That's -- that's getting 7 1/2 gallons of 12 water pretty fast or 5 pounds of sugar, I guess, 13 shoved down your throat, right? 14 A. Yes. 15 Q. Be kind of crazy scenario? 16 A. Yes. 17 Q. Okay. 18 A. That's true. 19 Q. That's not over time? I mean, you could 20 have 5 pounds of sugar maybe a week or maybe even 21 less. You might gain some pounds, but you're not 22 going to die? 23 A. You're absolutely right. And we even -24 I even thought about putting that this was acute. But 25 you're exactly right. It wasn't -- I was not trying 159 1 to make any claims about sugar's toxicity, only 2 illustrate to the jury that you need to understand how 3 much a person is exposed to before you can really get 4 an idea of the toxicity of that compound. 5 Q. Sure. But there's different types of 6 exposure? I mean, the length of time you're exposed 7 is important, right? 8 A. You're ab -- absolutely right. 9 Q. Chronic exposures over time are different 10 than acute exposures, like 5 pounds of sugar all at 11 once? 12 A. That is absolutely true. 13 Q. Okay. Let's go to page 30, please, which 14 is Exhibit 28. Okay. Now, this is also on that same 15 part of your testimony that you said is critical to 16 understanding toxicology. And here you're talking 17 about something that when it's on the left side of the 18 threshold for toxicity line is beneficial. Isn't that 19 right? In this -- in this case, this example? 20 A. Um-hum, yes. 21 Q. All right. We're talking about aspirin 22 and how it can help keep you from having a heart 23 attack? 24 A. Yes. 25 Q. And again -- I don't want to go back to 160 1 the last slide, but if you take a bunch of bottles of 2 aspirin all at once, you're doing to die? 3 A. Well, not even -- I mean, some of the 4 gastrointestinal bleeding, you would get that if you 5 took three or four aspirin on a chronic basis, so that 6 actually is not an acute -- aspirin -- well, I mean, I 7 understand what you're saying, and that's true. 8 Aspirin doesn't have that much of an acute toxicity, 9 but you certainly can OD on it. 10 Q. Okay. And but -- so the jury 11 understands, benzene does not -- this -- this isn't 12 really applicable to benzene. Benzene doesn't have a 13 beneficial effect below the -- the -- on the left side 14 of the broken line there, does it? 15 A. It was not my intent to imply that. 16 Q. Okay. 17 A. I don't think anyone has uncovered a -- a 18 potential beneficial effect of low exposures to 19 benzene. 20 There is a guy in the University of 21 Texas, Stephen Safe, who's -- he has put forth this 22 notion of -- it's called hormesis. And in hormesis 23 almost every dose response curve is biphasic, and that 24 really low exposures do have beneficial effects. We 25 just always don't know what those are. I'm not saying 161 1 that's true -- for benzene, I'm certainly not saying 2 that. 3 Q. Okay. Let's go to page 31, please, 4 Exhibit 29. Okay. Now, this is the same basic 5 testimony you gave. This illustrates the same basic 6 testimony about dose response. And here we're talking 7 about alcohol; is that right? 8 A. Correct. Ethanol, yes. 9 Q. Ethanol, which is in beer -10 A. It's what people drink, yes. 11 Q. Okay. And what you're illustrating here 12 is if you don't drink, you don't get drunk; but if you 13 drink way too much, you can have a coma or die, right? 14 A. Correct. 15 Q. Okay. This is -- again, this is an acute 16 exposure, right, something that happens fast and all 17 at once in a continuous exposure, not chronic over 18 time? 19 A. That's true. The chronic effects would 20 be cirrhosis of the liver and other kinds of effects 21 for chronic alcoholism. But, sure, this is more on -22 like a night out. 23 Q. Night out. Okay. Good night out, you 24 get giddy; bad night out, you go in a coma? 25 A. I would hope that doesn't ever happen to 162 1 anyone, but it does. 2 Q. Okay. And you just mentioned -- you kind 3 of anticipated my next question. About types of 4 injuries you can have exposures -- low, low exposures 5 to alcohol, drink a few drinks a day, never get 6 anything more than, maybe, giddy, but still have 7 injury, right, like cirrhosis of the liver? 8 MR. SCHIRRMEISTER: Object to the form. 9 A. Yeah, that might not be the best example. 10 For one thing, a few drinks a day, I wouldn't consider 11 that to be low exposure. Now, the giddy part is true. 12 People develop tolerances for that, and they may take 13 a lot more to have this, you know, euphoric, giddy 14 feeling. But cirrhosis is a complete reorganization 15 of a person's liver with scar tissue, and it takes a 16 lot of alcohol over a long period of time. 17 Q. (BY MR. GIANARIS) If you drink over 20 18 years, you never get drunk enough to have an acute 19 reaction injury, like coma or death, but you drink 20 over a long period of time, you can have chronic 21 injury, right? 22 A. That -- that's true. You may not have to 23 go -- in your individual episodes, you may not have to 24 go to alcohol poisoning to get cirrhosis. But I -25 you know, the lower end, I don't think evidence 163 1 supports that -- that these would give you cirrhosis. 2 Q. They could give you some injuries in a 3 susceptible person, couldn't they? 4 A. I'm not sure. I don't really know that 5 much about the dose response relationship with 6 cirrhosis; but looking at cirrhotic livers and what I 7 do know about that literature is that those people 8 that have it, they drink a lot. 9 Q. Over a long period of time -10 A. Correct. 11 Q. -- they drink? 12 A. Correct. 13 Q. Okay. Let's look at slide 33, please, 14 which is Exhibit 31. Now, this slide, you -- when you 15 were talking about it on direct examination with 16 Mr. Schirrmeister, he asked you if they saw any -- and 17 I'm paraphrasing here, but if they saw any APLs here. 18 And you kind of leaned back and said, Well, they 19 weren't looking for APLs in these cases -- in these 20 studies, right? 21 A. Well, he was asking about pliofilm. 22 Q. Okay. 23 A. So that -- that question you just asked 24 will vary depending on which of these studies you're 25 talking about. 164 1 Q. Let's talk about the study he was talking 2 about, the pliofilm studies, the two up at the top. 3 They weren't -- you wouldn't find any APLs because 4 they weren't looking for APLs, right? 5 A. They did not specifically look for APLs. 6 And it was a retroactive mortality study, so you're 7 basing the analysis on death certificates. 8 However, in these cases with the leukemia 9 cases, they did write up case descriptions of the 10 various types of leukemia. And they classified them, 11 like, erythroleukemia and other forms of AML. 12 So there are some examples where you can 13 say definitively this was not APL. There are two 14 cases in the pliofilm that I think you can't say 15 definitively that this was or was not APL. 16 So part of your question is right. They 17 didn't specifically look. But I don't think we're in 18 a complete vacuum in terms of the information, because 19 most of those were not APL. We do know that. 20 Q. Okay. Let's go -- let's go back -21 MR. GIANARIS: Let's go off the record. 22 THE VIDEOGRAPHER: Going off the record. 23 The time is 1:33. 24 (Recess taken, 1:33 p.m. to 1:34 p.m.) 25 THE VIDEOGRAPHER: We are back on the 165 1 record. The time is 1:34. 2 Q. (BY MR. GIANARIS) A moment ago, a few 3 moments ago, on direct examination, you all talked 4 about some studies where your testimony was they were 5 looking at APL. And you -- you gave a caveat that 6 they were very small studies. Do you remember that? 7 A. Some of them were small studies, yes. 8 Q. It's important to know the size of a 9 study, because the size of the study is -- correlates 10 to the study's power; is that right? 11 A. That much is true, yes. 12 Q. Okay. And the larger the study, the 13 higher the power, everything else being equal? 14 A. All things being equal, you're right. 15 The larger the study the -- the better the statistical 16 power. 17 Q. And statistical power has to do with the 18 likelihood that the results in the study aren't based 19 on chance, right? 20 A. It has to do -- that partially, but it 21 also has to do with the ability of the study to detect 22 subtle changes, small changes in risk. 23 For example, if you have smoking and -24 smoking and lung cancer or some other -- where the 25 risks are really high, you can see those in a 166 1 relatively small study. But if you have a 50 percent 2 increase in risk or a 75 percent increase in risk, you 3 may not see that in a little study. You have to -4 you need a bigger cohort to evaluate those. 5 Q. So small studies don't -- one thing they 6 -- they -- small studies are more likely to have their 7 results based on chance and they don't detect subtle 8 differences in risk; is that right? 9 A. I think the last part is -10 MR. SCHIRRMEISTER: Object to the form. 11 A. -- is accurate. 12 Q. (BY MR. GIANARIS) Okay. You talked 13 about chemotherapy and Mr. Wolfe's chemotherapy; is 14 that right? 15 A. Well, I think I -- I answered a question 16 about -- but I talked in specifics about 17 altransretonoic acid, the form of chemotherapy that -18 that you treat APL with. 19 Q. And you said that's what Mr. Wolfe had? 20 A. Right. 21 Q. Right. And you know Mr. Wolfe had rounds 22 of chemotherapy, correct? 23 A. Um-hum. 24 Q. And you know that he had a recurrence of 25 his disease, don't you? 167 1 A. I -- I do. I read all of his medical 2 records, but it's been some time; but I do recall 3 that, yes. 4 Q. And he had a stem cell transplant? 5 A. Right. 6 Q. Okay. And Mr. Wolfe's not cured, is he? 7 A. That, I don't know. 8 Q. Okay. 9 A. I really wouldn't be qualified to make 10 that determination. 11 Q. From what you've seen in the medical 12 records, you don't have an indication that he -- he's 13 been cured of his disease? It's in remission for 14 right now; is that right? 15 MR. SCHIRRMEISTER: Object to the form. 16 A. I don't remember how long it's been in 17 remission, and I don't remember the data associated 18 with that. If it's in cytogenetic remission and it 19 has been in remission for some time, then his 20 long-time -- long-term prognosis is pretty good, but 21 that's -- that's really not my area. 22 Q. (BY MR. GIANARIS) Okay. You know that 23 Andy Wolfe's blood cancer, his leukemia or APL, was 24 caused by -- or he claims it was caused by repeated 25 exposure to solvents in paint products over his 168 1 career? 2 A. That's my understanding of the 3 allegations, yes. 4 Q. Okay. And you've studied Andy Wolfe's 5 case, you've read his transcripts, you've read his 6 medical records, you've read exposure reports; is that 7 right? 8 A. All of that has been some time ago; but, 9 yes, at one point or another, I did. 10 Q. You needed to do that to give your 11 opinions that you talked about today. I mean, at one 12 to another, you had to do that to educate yourself 13 about the case, right? 14 A. Right. I mean, most of what I did to 15 educate myself on this case was the -- I mean, I'm a 16 toxicologist, so I was mostly interested in the 17 scientific data associated with his disease. 18 The various exposure experts, it was 19 their job to figure out what he did and where he did 20 it and what his exposures might have been while he was 21 doing that. So I read his report -- their reports and 22 I was interested in it, but I didn't do that. 23 Q. But you've read them? 24 A. Yes. 25 Q. Okay. You read -- I saw in your report 169 1 you read his deposition? 2 A. Yes. 3 Q. Okay. And you know he worked for over 20 4 years as a car painter? 5 A. '85 to 2004. I think -6 Q. Or almost 20 years? 7 A. I think that's right, yes. 8 Q. Started in high school. When he was in 9 high school, he started painting cars? 10 A. Right. Right. On the weekends and 11 things, yes. 12 Q. Okay. And you know, from what you've 13 read and what you've been told, that he regularly 14 worked with PPG paints and DuPont paints and the 15 products that go along with those paints, don't you? 16 MR. SCHIRRMEISTER: Object to the form. 17 A. That, I'm not so sure about. I mean, I 18 -- from reading the experts, the exposure reports, I 19 don't think he used PPG products as long as he did 20 some of the other products; but I'm -- that's not my 21 area. 22 Q. (BY MR. GIANARIS) So he used DuPont 23 products the most? 24 A. That -- that's my understanding, but that 25 could be wrong. 170 1 Q. Okay. But that's kind of important, 2 isn't it, to know what the guy was exposed to when 3 you're going to give opinions about what caused his 4 disease, isn't it? 5 A. Well, it depends. It depends on what 6 disease it is and what the exposures are. As I said, 7 there were five individuals, all of them trained in 8 industrial hygiene, and all of them more qualified 9 than me, that -- that quantitated or wrote detailed 10 reports about his exposures. 11 The other side of that is if a person 12 says, I'm exposed to toluene and I have a disease 13 that's associated with toluene, well, I mean, it's 14 useful and it's -- and it's informative to know what 15 his exposures to toluene were. But the first thing 16 I'm going to do is say, Well, can toluene exposure at 17 any level cause this person's disease? 18 Q. Okay. So, really, you didn't have to 19 read anything in this case, you just had to know what 20 his disease was, and you could have said right away 21 toluene, xylene, or any amount of benzene didn't cause 22 this disease? You could have done that without 23 reviewing anything? 24 MR. SCHIRRMEISTER: Object to the form. 25 Q. You already had that scientific 171 1 knowledge? In fact, the lawyers knew that opinion, 2 because you've given that opinion for them before. 3 MR. SCHIRRMEISTER: Object to the form. 4 A. Not -- no, not exactly like that. It 5 is -- I mean, I do like knowing what the individual 6 was doing. 7 Q. (BY MR. GIANARIS) Right. 8 A. But that was not part and parcel of my 9 opinion. I did base my opinion somewhat on the 10 quantitative exposure information that they said that 11 Mr. Russell provided in his report and Mr. Keller 12 provided in his report where they were looking -- they 13 quantitated the benzene exposure. But I don't believe 14 that -- I do not believe that toluene exposure at any 15 -- at any level is associated with an increased risk 16 of leukemia. 17 Q. Right. So -- and Mr. Schirrmeister and 18 the lawyers for PPG, they knew that opinion before 19 they ever brought you the Wolfe case, because you've 20 given them that opinion in other cases in the past? 21 MR. SCHIRRMEISTER: Object to the form. 22 A. That, I don't know about. I've never 23 given -- I've never worked in a specific toluene, 24 xylene, distillate case and acute promyelocytic 25 leukemia before. 172 1 Q. (BY MR. GIANARIS) So did you or did you 2 not have to review Mr. Wolfe's exposures to come up 3 with your opinions? 4 A. I wouldn't say that I had to, no. 5 Q. Okay. But you did read his transcripts. 6 And you know that he worked with paints and paint 7 products for over -- or almost 20 years or from high 8 school until he got sick? 9 A. That's my recollection of what he said, 10 yes. And it's also what the various exposure experts 11 summarized in their reports. 12 Q. And you know he used PPG products and 13 mostly used DuPont products? 14 A. That's my understanding, yes. 15 Q. You know he mixed paints? 16 A. I don't remember that specifically, but 17 that wouldn't surprise me based on what he did. 18 Q. Do you know he sprayed paints? 19 A. I think that goes -- yes, I do know that. 20 Q. You know he cleaned with solvents? 21 A. That's my understanding, yes. 22 Q. Okay. You know he was around these 23 paints and these solvents on a daily basis, at least, 24 you know, unless he was on vacation, five days a week 25 for his career? 173 1 MR. SCHIRRMEISTER: Object to the form. 2 A. I can't speak to that. I think that's 3 right, yes. 4 Q. (BY MR. GIANARIS) And the benzene 5 exposure that Mr. Wolfe would have had would have been 6 doing that occupation, it would have been to the -- to 7 the contaminants, the benzene contaminants in those 8 paints and solvents, right? 9 MR. SCHIRRMEISTER: Object to the form. 10 A. The occupational exposures that Mr. Wolfe 11 would have had would have been because it is a 12 naturally occurring component of those various 13 solvents. I don't know what else Mr. Wolfe did. And 14 we're all exposed to benzene. So he has some 15 background exposure to benzene, just like we all do. 16 Q. (BY MR. GIANARIS) Okay. And you've -17 you've written about those exposures in your -- your 18 report or your letter to the defense lawyers, haven't 19 you? 20 A. About what exposures? 21 Q. About the exposures we -- we talked 22 about. 23 A. I -- you're going to have to be more 24 specific. 25 Q. Well, we just talked about all the things 174 1 that Andy has worked with -- well, let me show you, 2 just so we're on the same page. Paragraph 18, why 3 don't you read that highlighted portion into the 4 record. 5 A. Okay. "Based on deposition testimony and 6 discovery responses, the only possible occupational 7 exposures to benzene that Mr. Wolfe potentially 8 received would have been as a contaminant of paints, 9 paint and lacquer thinners, adhesives, adhesive 10 cleaners, rubber compounds, other paint-related 11 products and various solvents, such as toluene or 12 mineral spirits." 13 Q. Okay. So that's -- that's -- you wrote 14 that? 15 A. Yes. 16 Q. Okay. Thank you. So it's your opinion, 17 it's in your report, that Mr. Wolfe was exposed to 18 benzene contamination in paints, paint lacquer 19 thinners, adhesives, adhesive cleaners, rubbing 20 compounds, other paint-related products and various 21 solvents? 22 A. Yes. 23 Q. Okay. And then you say that "In order to 24 achieve exposure of benzene required to meaningfully 25 increase one's risk of developing AML, there could 175 1 necessarily be concurrent exposures to other chemicals 2 present in these products." 3 So there's other -- there's other 4 product -- chemicals in the products that he used that 5 we just discussed and it would be concurrent 6 exposures, right? 7 MR. SCHIRRMEISTER: Object to the form. 8 A. What I meant by that -- I mean, I think 9 what you said is right, that if you're going to say 10 how much benzene is a person exposed to if they are 11 using a solvent that is mostly toluene or xylene and 12 you're going to calculate a dose of benzene, when they 13 are exposed to that benzene, they are also being 14 exposed to other aromatic things that are in that 15 mixture. They are being exposed to toluene, they are 16 being exposed to xylene, they are being exposed to 17 other things. That was -- that was what I intended to 18 convey in that paragraph. 19 Q. (BY MR. GIANARIS) What does 20 hematological toxicity mean? 21 A. Hematological just means the blood. So 22 it would be toxicity to the blood or the blood-forming 23 organs. 24 Q. And you write also in your report, "As 25 hematological toxicity is universally observed 176 1 following exposure to benzene, this indicates that 2 either there is some type of interaction that reduced 3 benzene toxicity or that there is simply not enough 4 benzene present to be a toxicological issue." 5 I want to ask you what you mean by 6 hematological toxicity is universally observed 7 following exposure to benzene. 8 A. Right. 9 Q. What does that highlighted sentence mean? 10 A. Right. So -- well, what I mean is that 11 occupational workers who were exposed to high levels 12 of benzene, they get hematological toxicity associated 13 with them, cytopenias and hypocellular marrows and 14 aplastic anemia, depending on the dose and the 15 longevity and other things. But when you're looking 16 at people that are exposed to toluene, methylbenzene 17 toluene, you don't -- you don't see that. You don't 18 see it in the animals, you don't see it in the human 19 studies. 20 So while those animals are being exposed 21 to benzene through the toluene, you don't see the same 22 profile of toxicity that you see when those animals 23 are exposed to pure benzene. So there's something 24 else involved, whether it's the toluene decreasing the 25 toxicity or whether there's just not enough benzene in 177 1 the mixture to cause those effects. That's what that 2 paragraph was intended to imply. 3 Q. Okay. When a solvent gets on a person's 4 skin, can the -- can the chemicals in that solvent 5 pass through the barrier of the skin and get in the 6 bloodstream? 7 MR. SCHIRRMEISTER: Object to the form. 8 A. I think as a -- just a general principle, 9 some can. But it varies considerably, depending on 10 the solvent. It varies considerably, depending on 11 characteristics of the skin and where that, you know, 12 exposure occurs, how long it's -- I mean, there's so 13 many variables. But as a general principle, yes, 14 dermal exposure can occur. 15 Q. (BY MR. GIANARIS) That's a pathway of 16 exposure just like inhalation? 17 A. It is a pathway of exposure for benzene. 18 It is certainly not considered to be nearly as 19 important as inhalation, but you can't totally rule it 20 out. 21 Q. How about ingestion? Is that a pathway 22 of exposure? I mean, if -- if chemicals or solvents 23 get on some -- in someone's coffee or their hands and 24 they rub their mouth, can you ingest benzene that way, 25 too? 178 1 A. You know, that's so -- well, okay, yeah. 2 I mean, benzene in experimental animals that is given 3 via injection as a bolus, it goes right in. So the 4 absorption through the GI tract is thought to be very 5 high. 6 Now, how realistic is it, from an 7 occupational setting standpoint, that someone is 8 getting solvent in their mouth and ingesting them, 9 that's really not my area. But if it got in, if 10 benzene got into the GI tract, it would be absorbed. 11 That's our understanding. 12 Q. And once -- once benzene is inside the 13 body, whether it comes in through inhalation or 14 through the skin or through ingestion, what organ does 15 it go to from the blood? Where does it get 16 metabolized? 17 A. Once it gets into the blood. 18 Q. Um-hum. 19 A. You know, because inhalation is going to 20 the lungs first. 21 Q. Right. 22 A. So that's a little different. And even 23 the GI tract is a little different because of 24 something that we call first-pass metabolism. But 25 ultimately the benzene that's in the blood is -- we 179 1 believe that it's -- it starts its metabolic pathway 2 in the liver. 3 Q. And then the metabolites from that 4 benzene can go to the bone marrow? 5 A. That is our general -- sort of our 6 working hypothesis at this point is that the benzene 7 goes to the liver, depending on where and how and 8 other things; but that it produces metabolites that 9 are long-lived enough to get back into the circulation 10 and travel to the bone marrow. 11 Not -- not all metabolites will -- will 12 ever get out of the liver, but some probably do. And 13 then they are subsequently metabolized in the bone 14 marrow. That -- that's our understanding. 15 Q. And when benzene causes cancer, that's 16 where the cancer begins, isn't it, in the bone marrow? 17 A. Well -18 MR. SCHIRRMEISTER: Object to the form. 19 A. Yeah, cancer is too general of a term. 20 Q. (BY MR. GIANARIS) Leukemia? 21 A. And I don't even believe that benzene 22 causes all forms of leukemia. AML -23 Q. You have it. 24 A. Okay. 25 Q. Let's say when benzene causes AML, that's 180 1 where the cancer begins, in the -2 A. That is our -3 Q. -- bone marrow? 4 A. That is our understanding, yes. 5 Q. Okay. Tell us -- tell the jury why a 6 healthy and properly functioning bone marrow is so 7 important. 8 A. The bone marrow is the source of our 9 blood. So in order for us to have adequate oxygen 10 distribution, get rid of carbon dioxide, fight 11 infections, wound healing, all of the things -- clot 12 blood, all of the things that we associate with blood 13 cells in the periphery, we believe most of that 14 development occurs -- not all of it, some of it occurs 15 in the lymphoid system. But a lot of it occurs in the 16 bone marrow. 17 So the stem cell that we were talking 18 about earlier, how -- whatever you want to say about 19 it, it likely lives in the bone marrow. And it starts 20 its developmental process to these various cell types 21 inside the bone marrow. 22 Q. And let's talk about exposures that can 23 damage the bone marrow and exposures that can't. You 24 talked about, sort of, a background exposure. And 25 it's your opinion that -- tell me if I'm wrong -- that 181 1 a guy who, let's say, works in this hotel, okay? 2 St. Julien Hotel. And he walks around on the streets 3 and he drives his car and he pumps his gas and he mows 4 his lawn. He is breathing some benzene, right? 5 A. He is. 6 Q. Okay. But he is below a threshold. That 7 benzene won't hurt that guy? 8 A. There is no scientific evidence to 9 suggest that those levels have benzene are having any 10 effect on him. It -- adverse effect on him. 11 Q. And it -- but it's your opinion that 12 there are some groups of workers that are exposed to 13 enough benzene that they are above the threshold and 14 that exposure can put them in increased risk or cause 15 damage to the bone marrow and maybe acute myelog -16 AML? 17 A. Or aplastic anemia. Absolutely. 18 Q. Okay. And it's your opinion that 19 Mr. Wolfe is -- despite his 20 years of work as a 20 painter is below that threshold. He's in the same 21 group as the guy working at this hotel, mowing his 22 lawn, pumping his gas, right? 23 A. Well, he's in the same group in that I 24 don't believe that he had a sufficient exposure to 25 benzene to cause bone marrow toxicity. 182 1 I would -- I wouldn't say that he had the 2 same exposures to -- as a guy that works in this 3 hotel; but as that slide indicates, we're not 4 completely in the dark about how much benzene it -5 that we believe that it takes to meaningfully increase 6 a person's risk of AML. And it's far higher than what 7 the estimates that I've seen of Mr. Wolfe. 8 Q. Okay. But if you draw that little line 9 you drew, that broken line threshold, Mr. Wolfe would 10 be below the threshold, just like the guy working in 11 the hotel? He wouldn't be above the threshold like 12 the group -- some groups of workers who are at an 13 increased risk? 14 A. That's true. 15 Q. Okay. Chronic exposures to high 16 concentrations of benzene are toxic to the blood and 17 the bone marrow; is that right? 18 MR. SCHIRRMEISTER: Object to the form. 19 A. Chronic exposures to high concentrations 20 of benzene? Yes, we've known that for a hundred 21 years. 22 Q. (BY MR. GIANARIS) And the flip side of 23 that is that the risk of developing AML associated 24 with benzene exposure below the threshold that we 25 talked about is indistinguishable from background. In 183 1 that a guy like Mr. Wolfe who worked for 20 years as a 2 painter, he doesn't have any more risk than a guy 3 walking down the street? 4 A. He doesn't have an increased risk that 5 can be identified epidemiologically. I mean, it 6 depends on how you -- how you regulate benzene and 7 what you think about the dose response for benzene, 8 but he has not even approached the levels that we 9 believe are required in order to meaningfully increase 10 his risk of bone marrow damage. 11 Q. Okay. Let me -- let me just show you 12 your report, because that's what you -- you wrote 13 exactly what I said. 14 A. Okay. 15 Q. Right here. That is the risk of 16 developing AML associated with benzene exposure below 17 this threshold would be indistinguishable from 18 background. 19 A. Right. 20 Q. Right? 21 A. Yes. And I said -- I mean, it may not be 22 exactly background, but with current epidemiological 23 methods, you won't be able to tell those apart. 24 Q. It's indistinguishable from the 25 background? 184 1 A. Exactly. 2 Q. Okay. So just so the jury understands, 3 it's your opinion that Mr. Wolfe, with his 20 years of 4 painting, with potential inhalation, ingestion, and 5 dermal contact to solvents, is below that threshold, 6 and his risk of developing AML is indistinguishable 7 from background? That's your opinion in this case? 8 A. Yes. 9 Q. Okay. 10 MR. GIANARIS: Let's go off for a moment. 11 THE VIDEOGRAPHER: Going off the record. 12 The time is 1:55. 13 (Recess taken, 1:55 p.m. to 2:02 p.m.) 14 THE VIDEOGRAPHER: We are back on the 15 record. The time is 2:02. 16 Q. (BY MR. GIANARIS) Dr. Pyatt, just 17 refresh the jury's memory what IARC is? 18 A. IARC. The International Agency for the 19 Research on Cancer. 20 Q. And you're a cancer researcher, aren't 21 you? 22 A. Sure. 23 Q. Okay. IARC is well-respected by cancer 24 researchers, isn't it? 25 A. Yes. Yes, IARC -- yes, it is a 185 1 well-respected group of scientists. 2 Q. And I want to ask you about some other 3 groups. Are you familiar with the National Safety 4 Council? 5 A. The National Safety Council? I've seen 6 them, but I'm not as familiar with them -- I've never 7 read anything that they have written. 8 Q. Okay. I'm going to ask you about that in 9 a moment. I want to tell you the National Safety 10 Council has its headquarters in Chicago, and it's a 11 trade organization, has members from industry and 12 product manufacturers, worker representatives, unions, 13 safety men, scientists. And their -- their mission is 14 to -- is to disseminate information to create safer 15 workplaces. 16 A. Okay. 17 Q. You're familiar with them and you 18 understand that concept that type of group? 19 A. I do now, yes. 20 Q. Okay. Let's talk historically for a 21 minute so the jury can put things in perspective. Way 22 back in 1950, the National Safety Council wrote 23 benzene is one of the most poison -- one of the most 24 insidious poisons ever to find in industrial use. And 25 then they wrote in the same -- in the same article a 186 1 victim may become incurably poisoned before he feels 2 ill. 3 So I mean, is -- is that still the 4 understanding today, that benzene is one of the most 5 insidious poisons ever to find in industrial use? 6 MR. SCHIRRMEISTER: Object to the form. 7 A. I -- that's hard to answer. And I don't 8 quite know what insidious means. So are you asking me 9 if -- is that what people still think now? 10 Q. (BY MR. GIANARIS) Yeah. 11 A. There -- there might be some people that 12 still think that. 13 Q. Okay. And does that surprise you that 14 that was -- that was known and published back in 1950? 15 MR. SCHIRRMEISTER: Object to the form. 16 A. I -- I'm not surprised nor un -- un -17 not surprised. I mean, we've -- we've known about 18 benzene's toxicity for -- for some time. 19 Q. (BY MR. GIANARIS) Okay. Are you 20 familiar with the American Petroleum Institute? 21 A. Yes. 22 Q. Okay. And you've -- you've testified in 23 the past for defendants -- you've worked on cases for 24 defendants who were members of the American Petroleum 25 Institute; is that right? 187 1 MR. SCHIRRMEISTER: Object to the form. 2 A. I would assume that they -- they are 3 members, yes. 4 Q. (BY MR. GIANARIS) You've worked for oil 5 companies? 6 A. Correct. Yes. 7 Q. Okay. And oil companies make up the 8 American Petroleum Institute, among other -- among 9 other members, right? 10 A. That's correct. 11 Q. Are you familiar -- you've been shown 12 that way back in the 1940s, the American Petroleum 13 Institute reviewed the toxicology of benzene? 14 A. I've seen that 1948 Drinker paper, if 15 that's the one you're referring to. 16 Q. Yeah, that's the one I'm talking about. 17 So you're familiar with that? 18 A. Yes. 19 Q. We'll mark that as Exhibit 1. And I'll 20 show you here -- read the highlighted portion there 21 from the Drinker paper you just mentioned. 22 A. "Insomuch as the body develops no 23 tolerance to benzene, and as there -- and as there is 24 wide variation in individual susceptibility, it is 25 generally considered that the only absolute safe 188 1 concentration for benzene is zero." 2 Q. Okay. And that's what the API was saying 3 back in 1948, correct? 4 A. That's what this -5 MR. SCHIRRMEISTER: Object to the form. 6 A. -- Professor Drinker wrote in this paper. 7 Q. (BY MR. GIANARIS) Published by the API? 8 A. Yeah. But I don't know what the API was 9 -- I mean, I -- that's a big group, but that's what 10 this one individual said, yes. 11 Q. Okay. And you've -- you've -- you've 12 read and heard working in these cases about similar 13 sentiments the N -- the NS -- what the National Safety 14 Council said what Professor Drinker wrote for the 15 API -- you've heard and read those over the years 16 working on these cases, haven't you, that there's no 17 safe level to exposure of benzene? 18 MR. SCHIRRMEISTER: Object to the form. 19 A. Well, I don't think that's the first 20 thing. The -- the thing that you wrote from 1950 from 21 the National Safety Council, that wasn't my 22 interpretation that there's no safe limit. And even 23 in the Drinker study, they go on to recommend a air 24 concentration of -- of 50 part per million that they 25 consider to be regulatory and -- and safe. And you 189 1 also have to put it in the context of what our ability 2 -- what the science allowed these people to actually 3 measure back in the '40s in terms of benzene. 4 You know, we can measure benzene at way 5 lower concentrations than they were able to then. So 6 what they considered to be zero, now we know that's 7 not zero. There's benzene there. 8 Q. (BY MR. GIANARIS) Okay. So -- but way 9 back then in 1948, Dr. Drinker was saying the only 10 absolutely safe concentration of benzene is zero? 11 A. That's what he said, yes. 12 Q. Okay. And DuPont agreed with that, 13 didn't they, back in the -- in the 1950s? 14 MR. SCHIRRMEISTER: Object to the form. 15 A. That, I can't speak to. 16 Q. (BY MR. GIANARIS) Have you ever looked 17 at any DuPont documents? Has DuPont given you any 18 internal correspondence or memos about what they knew 19 about the -- about the dangers of benzene exposure? 20 A. No. 21 Q. Have you ever asked to see those? 22 A. No. 23 Q. Okay. Tell me what -- what you know 24 about Andy Wolfe's disease, how it came on, how it 25 progressed, how he was cared and treated for, et 190 1 cetera. 2 A. Can I refer to my report? 3 Q. Sure. 4 A. Because I just -- I don't -- it's been 5 awhile since I've looked. I meaning, I can at least 6 tell what you I had in my report. I think we did talk 7 about it. 8 MR. GIANARIS: We can go off the video 9 while he finds it. 10 THE VIDEOGRAPHER: Going off the record. 11 The time is 2:09. 12 (Discussion off the record.) 13 THE VIDEOGRAPHER: We are back on the 14 record. The time is 2:09. 15 A. My understanding that he presented with 16 blood abnormalities in 2004, was diagnosed with APL. 17 This is from memory. And I may be wrong, but that he 18 was treated with altransretonoic acid, entered 19 remission, relapsed, maybe put into remission again, 20 had a stem cell transplant that seemed to take, and 21 now is in long-term remission. That's my 22 understanding. 23 Q. (BY MR. GIANARIS) Okay. Dr. Pyatt, I 24 just asked you about his treatment and you asked to 25 see your report. You didn't put anything about his -- 191 1 his care and treatment or the progression of his 2 medical condition in your report, did you? 3 A. No. 4 Q. You went through and couldn't find 5 anything? 6 A. That's right. Sometimes, I do. 7 Sometimes, I write little medical histories; but this 8 time, I didn't. 9 Q. Okay. And do you remember much about -10 you gave us a little summary -- a couple of sentences 11 about his medical. How about his exposure? Do you -12 do you remember much about what Andy did on a daily 13 basis, how he worked, how he was exposed? 14 A. No. 15 Q. Okay. 16 A. Other than he was, you know, painting 17 cars. 18 Q. I'd like you to tell me, please -- or 19 give me a definition or an example of what you feel is 20 appropriate for an ethically responsible company to 21 tell the users of its products when its products 22 contain a dangerous substance. 23 MR. SCHIRRMEISTER: Object to the form. 24 A. I don't understand that question. 25 Q. (BY MR. GIANARIS) Okay. Some products, 192 1 the people use in their work places contain dangerous 2 substances, right? 3 A. Right. 4 Q. Toxic substances? 5 A. Correct. 6 Q. Substances that can cause severe 7 injuries? 8 A. Sure. 9 Q. Okay. What is the appropriate -- the 10 ethically responsible thing for a company that makes 11 products like that that contain chemicals that can 12 cause those kinds of injuries to tell the end user? 13 MR. SCHIRRMEISTER: Object to the form. 14 A. It's really not my area. I mean, this 15 whole warnings and how you word things and how you 16 print things out and how big it is and color and 17 signs, that's a whole area of science that I'm just 18 not familiar with. 19 So I really -- that's just outside of my 20 area to discuss. I mean, there are people that 21 specifically understand that and what people pay 22 attention to and what they read. And that's just not 23 anything that I know anything about. 24 Q. (BY MR. GIANARIS) Well, you know what -25 what an ethical company ought to do, don't you, I 193 1 mean, if they -- if they ought to tell people about 2 the dangers of their products or not? 3 A. Well, at that level, that's a relatively 4 simplistic level. And I think absolutely they should. 5 Q. Okay. Do you agree -6 A. But what I was saying is I don't know 7 how, what's the best mechanism for disseminating that 8 information. That's -- that is not my area. 9 Q. Do you agree that it's a good rule that a 10 company should tell workers using its products about 11 all of the dangers that come from using the products? 12 MR. SCHIRRMEISTER: Object to the form. 13 A. That's a harder question to answer. I 14 mean, I think that gets into this notion of warnings 15 and what you say and what you don't say and just -16 I'm just not comfortable answering that. 17 I mean, some of the -- at the superficial 18 level, yes; but if it's an exceedingly rare side 19 effect or it occurs at exposures that aren't going to 20 happen, you know, I don't -- I don't know. I mean, I 21 think some companies do that. They put all that on 22 MSDS sheets and some -- I -- I don't know. I just 23 don't know -- I don't know about that. Sorry. 24 Q. (BY MR. GIANARIS) Have you ever -- have 25 you ever thought about that? Have you -- when you 194 1 testify in cases like this, have you listened to other 2 experts testify and sat and thought I wonder -- I 3 mean, what -- what -- what I feel in my gut they ought 4 to do, a company ought to do? 5 MR. SCHIRRMEISTER: Object to the form. 6 A. Well, most -- the times that I've looked 7 at it -- and I haven't looked at it as a scientist, 8 just like you said, just kind of on the periphery, it 9 seems like they are. 10 The -- the companies that I work for, 11 they have made a good faith effort to disseminate this 12 information where it was required. But how and when 13 and what information you specifically include on 14 these, that's just not my area. 15 Q. (BY MR. GIANARIS) So it's a good thing 16 for a company to make a good faith effort to 17 disseminate the information they have to the workers? 18 MR. SCHIRRMEISTER: Object to the form. 19 A. Say that again. 20 Q. (BY MR. GIANARIS) It's a good thing for 21 a company to disseminate the information they have 22 regarding these possible harmful effects to the 23 workers? 24 MR. SCHIRRMEISTER: Object to the form. 25 A. Yes. 195 1 Q. (BY MR. GIANARIS) Okay. 2 A. At that level, yes. 3 Q. All right. 4 MR. GIANARIS: That's all I have. 5 Thanks. 6 MR. SCHIRRMEISTER: Jim? 7 MR. MILLER: Nothing. 8 MR. SCHIRRMEISTER: No questions. Thank 9 you, Dr. Pyatt. 10 THE DEPONENT: You're welcome. 11 THE VIDEOGRAPHER: This is the end of 12 tape 2 of 2. Going off the record. The time is 2:14. 13 WHEREUPON, the within proceedings were 14 concluded at the approximate hour of 2:14 p.m. on the 15 23rd day of September, 2009. 16 17 18 19 20 21 22 23 24 25 196 1 ***** 2 I, DAVID W. PYATT, Ph.D., do hereby 3 certify that I have read the above and foregoing 4 deposition and that the same is a true and accurate 5 transcription of my testimony, except for attached 6 amendments, if any. 7 Amendments attached ( ) Yes ( ) No 8 9 10 __________________________ DAVID W. PYATT, Ph.D. 11 12 13 14 The signature above of DAVID W. PYATT, 15 Ph.D., was subscribed and sworn to before me in the 16 county of ______________, state of 17 _____________________ , this _____ day of 18 ________________, 2009. 19 20 21 _________________________ Notary Public 22 My commission expires 23 24 Andrew Wolfe 9/23/09 (tc) 25 197 1 REPORTER'S CERTIFICATE 2 STATE OF COLORADO ) ) ss. 3 CITY AND COUNTY OF DENVER ) 4 I, TERESA COOGLE, Shorthand Reporter and Notary Public, State of Colorado, do hereby certify 5 that previous to the commencement of the examination, the said DAVID W. PYATT, Ph.D., was duly sworn by me 6 to testify to the truth in relation to the matters in controversy between the parties hereto; that the said 7 deposition was taken in machine shorthand by me at the time and place aforesaid and was thereafter reduced to 8 typewritten form; that the foregoing is a true transcript of the questions asked, testimony given, 9 and proceedings had. 10 I further certify that I am not employed by, related to, nor counsel for any of the parties herein, 11 nor otherwise interested in the outcome of this litigation. 12 IN WITNESS WHEREOF, I have affixed my 13 signature this 1st day of October, 2009. 14 My commission expires May 8, 2010. 15 16 __X__ Reading and Signing was requested. 17 _____ Reading and Signing was waived. 18 _____ Reading and Signing was not required. 19 20 21 22 23 24 25 198 1 October 1, 2009 2 DAVID W. PYATT, Ph.D. 3 1944 Cedaridge Circle Superior, Colorado 80027 4 Re: Andrew Wolfe and Denise Wolfe v. 5 E.I. DUPONT DE NEMOURS AND COMPANY, et al. Deposition of: David W. Pyatt, Ph.D. 6 Dear Dr. Pyatt: 7 Enclosed you will find a complimentary copy of your 8 deposition taken in the above matter. Also enclosed are amendment sheets for changes if necessary. Please return 9 the signed and notarized signature page and amendment sheet(s), if any, to our office on or before October 19, 2009, 10 in order that the deposition may be filed in time for trial. 11 Thank you for your attention to this matter. 12 Sincerely, 13 14 Teresa Coogle, RPR 15 HUNTER + GEIST, INC. Registered Professional Reporters 16 c: Ted N. Gianaris, Esq. 17 James R. Miller, Esq. Andrew C. Schirrmeister, Esq. 18 19 20 21 22 23 24 25 199