Document OEOOkq1Y56mOY252Ym9L9L7QQ

1 2 IN THE SUPERIOR COURT OF THE STATE OF ARIZONA IN AND FOR THE COUNTY OF MARICOPA 3 Case No. CV-07-005399 4 __________________________________________________ 5 VIDEO DEPOSITION OF DAVID PYATT October 8, 2009 __________________________________________________ 6 RAUL ZENDEJAS and ARACELI ZENDEJAS, 7 Plaintiffs, 8 vs. 9 SHELL OIL COMPANY; SHELL CHEMICAL LP, Individually 10 and as successor-in-interest to SHELL CHEMICAL CORPORATION; CONOCOPHILLIPS COMPANY, VON VERDE CITRUS 11 PACKING HOUSE, INC., an Arizona corporation; VON VERDE HARVESTING, INC., a dissolved Arizona 12 corporation; and VON VERDE CITRUS GROWERS COOPERATIVE, INC., a dissolved Arizona Corporation, 13 Defendants. 14 __________________________________________________ 15 APPEARANCES: 16 SHRADER & ASSOCIATES By Keith E. Patton, Esq. 17 3900 Essex Lane, Suite 390 Houston, Texas 77037 18 713-782-0000 Appearing on behalf of Plaintiffs. 19 20 HAYNES AND BOONE, LLP By Stan Perry, Esq. 21 One Houston Center 1221 McKinney Street, Suite 2100 22 Houston, Texas 77010-2007 713-547-2039 23 Appearing on behalf of Defendant Shell Oil Company and shell Chemical LP. 24 25 Also Present: Nick Borgia, Videographer 1 1 Pursuant to Notice and the Arizona Rules of 2 Civil Procedure, the video deposition of DAVID PYATT, 3 called by Plaintiffs, was taken on Thursday, 4 October 8, 2009, commencing at 9:34 a.m., at 5 7001 Yampa Street, Board Room 1, Denver, Colorado, 6 before Janet Lee Priestley, Registered Professional 7 Reporter and Notary Public within and for the State 8 of Colorado. 9 10 11 I N D E X 12 13 VIDEO DEPOSITION OF DAVID PYATT 14 EXAMINATION BY: 15 Mr. Patton 16 Mr. Perry 17 PAGE 5, 191 188 18 EXHIBITS INITIAL REFERENCE 19 Exhibit 1 Notice of deposition of David -- 20 Pyatt, Ph.D. 21 Exhibit 2 Curriculum vitae for David W. 23 Pyatt, Ph.D. 22 Exhibit 3 List of testimony given in 23 lawsuits by Dr. Pyatt 24 Exhibit 4 4-14-08 report prepared by 23 31 Dr. Pyatt 25 2 1 I N D E X (Continued) 2 EXHIBITS INITIAL REFERENCE 3 Exhibit 5 Article titled "Reducing the 79 Risk of Cancer" 4 Exhibit 6 Book chapter titled "Benzene: an 80 5 historical perspective on the American and European occupational 6 setting" 7 Exhibit 7 Article titled "Are Occupational, 141 Hobby, or Lifestyle Exposures 8 Associated with Philadelphia Chromosome Positive Chronic 9 Myeloid Leukaemia" 10 Exhibit 8 Article titled "Occupation and 141 Leukemia Mortality Among Men 11 in 16 States" 12 Exhibit 9 Article titled "Acute Myeloid 143 13 Leukemia among Petrol Station Attendants" 14 Exhibit 10 Article titled "Occupational 148 15 History and Exposure and the Risk of Adult Leukemia in 16 Shanghai" 17 Exhibit 11 Article titled "Mortality of 151 of Filling Station Attendants" 18 Exhibit 12 Article titled "Proportionate 151 19 Mortality Ratio Analysis of Automobile Mechanics and 20 Gasoline Service Station Workers in New Hampshire" 21 Exhibit 13 Article titled "A Case-Control 152 22 Study to Investigate the Risk of Leukaemia Associated with 23 Exposure to Benzene in Petroleum Marketing and Distribution 24 Workers in the United Kingdom" 25 3 1 I N D E X (Continued) 2 EXHIBITS INITIAL REFERENCE 3 Exhibit 14 Article titled "Further Follow 155 Up of Mortality in a United 4 Kingdom Oil Distribution Centre Cohort" 5 Exhibit 15 Article titled "A Retrospective 157 6 Mortality Study among Canadian Petroleum Marketing and 7 Distribution Workers" 8 Exhibit 16 Article titled "The 158 Relationship Between Low-Level 9 Benzene Exposure and Leukemia in Canadian Petroleum Workers" 10 Exhibit 17 Article titled "A Mortality 161 11 and Morbidity Study of Refinery and Petrochemical 12 Employees in Louisiana" 13 Exhibit 18 Article titled "Cytogenetic 164 Studies on Gasoline Attendants" 14 Exhibit 19 Article titled "Landmarks in 167 15 the History of Cancer Epidemiology" 16 Exhibit 20 7-6-06 University Medical 174 17 Center medical record for Raul Zendejas 18 Exhibit 21 4-20-06 University Medical 175 19 Center medical record for Raul Zendejas 20 Exhibit 22 4-4-06 medical record from 175 21 Dr. Hayder for Raul Zendejas 22 Exhibit 23 4-10-06 medical record from 176 Giangreco Medical Group for 23 Raul Zendejas 24 25 4 1 PROCEEDINGS 2 THE VIDEOGRAPHER: We're on the record at 3 9:34 a.m. Today is October 8, 2009. This begins the 4 videotape deposition of David Pyatt Ph.D. taken by 5 the plaintiff in the matter of Raul Zendejas and 6 Araceli Zendejas vs. Shell Oil Company, et al. We're 7 located at Embassy Suites, 7001 Yampa Street, Board 8 Room 1, in Denver, Colorado. The court reporter is 9 Janet Lee Priestley, and the videographer is Nick 10 Borgia. 11 Counsel will now introduce themselves and 12 the parties they represent beginning on my left. 13 MR. PATTON: Keith Patton for plaintiff. 14 MR. PERRY: Stan Perry for shell. 15 THE VIDEOGRAPHER: Will the court reporter 16 please swear in the witness. 17 DAVID PYATT, 18 being first duly sworn in the above cause, was 19 examined and testified as follows: 20 EXAMINATION 21 BY MR. PATTON: 22 Q Please introduce yourself for the record. 23 A David Pyatt. 24 Q Mr. Pyatt -- or is it Dr. Pyatt? 25 A I have a Ph.D. in toxicology. 5 1 Q Okay. Dr. Pyatt, you are a toxicology 2 expert, correct? 3 A Yes, sir. 4 Q Were you hired by Shell in this case? 5 A I was hired by. Shell and I think when I 6 first got involved, ConocoPhillips might have been 7 involved, as well. 8 Q Dr. Pyatt, were you hired by Shell to give 9 an opinion in this case? 10 A Yes. 11 Q Have you testified or been retained on 12 behalf of Shell in other benzene exposure cases? 13 A There was other case for sure that I 14 worked with Mr. Perry on. Shell may have been a 15 defendant in some other cases that I've worked on, 16 along with others, but I don't specifically recall 17 that. But I wouldn't say absolutely that they have 18 not been involved. 19 Q Can you explain to us your experience in 20 the area of benzene in working with industry? 21 A Working with industry? 22 Q And by example, sir, today you're working 23 with industry? 24 MR. PERRY: Object to form. 25 Q (By Mr. Patton) Do you agree? 6 1 A Today I'm providing my professional 2 opinion on a toxicological issue that Mr. Perry asked 3 me to evaluate. I'm not sure that -- I mean, I have 4 done projects for the American Petroleum Institute. 5 And in that case, I guess you would say that I was 6 working on behalf of industry. 7 Q Tell us about your experience in working 8 on behalf of industry with the American Petroleum 9 Institute or the API. 10 A Well, even when I was a graduate student 11 and was doing toxicological research, we -- my -- the 12 laboratory that I worked in had some funding from API 13 so I guess it would have started 15 years ago. And 14 then since then I've had various projects as a 15 consultant for that trade group. 16 Q Can you estimate how many various projects 17 you've been a consultant for the API on? 18 A Three. 19 Q And are any of those active right now? 20 A I would say no, equivocating a little, but 21 essentially no. 22 Q What were the three projects you did for 23 the API? 24 A Probably the longest one was, we conducted 25 a -- and actually, technically, that wasn't API. 7 1 They were involved in it, but it was also with the 2 American Chemistry Council. They kind of had this 3 giant group called the benzene consortium. And what 4 we were tasked with doing was conduct a risk 5 assessment for children with regard to benzene 6 exposure for EPA. So EPA put out this -- they called 7 it the VCCEP program. Are you familiar with that? 8 VCCEP stands for Voluntary Chemical Children's 9 Exposure Program. 10 So they said anyone out there that's 11 making chemicals that could potentially -- that 12 children could potentially be exposed to, we would 13 like for you to conduct a risk assessment 14 specifically for children, using children-specific 15 factors, and things like that. And so this group 16 decided to do it for benzene, and they hired us to do 17 that part. And so my job was the hazard assessment 18 portion of that project as well as some of the 19 children-specific sensitivity issues. So that was 20 one. Then we presented that to EPA. 21 Q Okay. Finish your thoughts on this 22 project because I want to talk about it before we go 23 to Nos. And 3. 24 A Okay. And then -- yeah, so we presented 25 to EPA, they came back with comments, we responded to 8 1 those comments, and now it's in the public domain. 2 Q Okay. 3 A If you go to TERA's Web site, T-E-R-A, you 4 can find what we said, what we did, and what EPA said 5 in response. 6 Q Okay. So he so if I understand you 7 correctly, EPA told the general public and chemical 8 manufacturers, Hey, if you're manufacturing chemicals 9 that children are going to be exposed to, we'd like 10 you to do a risk assessment; is that accurate? 11 A That's correct. And that was the 12 voluntary part. 13 Q Okay. And then the API said, Okay, we're 14 making chemicals, kids are exposed to chemicals, 15 we'll do a study on it, correct? 16 A API was involved. But like I said, it was 17 this kind of benzene consortium, and I don't know 18 even know if that's still in existence any longer. 19 So it was sort of a collaborative effort between the 20 American Chemical Council and API. 21 Q It was a collaborative effort initiated by 22 industry, right? 23 A Oh, yes; yeah, yeah, just I don't know 24 which -- which one of the industry members, you know, 25 took a lead. I don't know how all that worked out. 9 1 Q Okay. And you studied benzene exposure 2 and its possible effect on children? 3 A Right. We did a formal risk assessment 4 for children with regard to environmental benzene 5 exposures. 6 Q Okay. Kids living near gas stations, 7 things of that nature? 8 A Correct; attached garages, cigarette 9 smoke, you know, living next to roads, all of the 10 various exposure pathways that could -11 Q Did your -- I'm sorry. 12 A I was thinking. Go ahead. I'm done. 13 Q Did your consortium group conclude that 14 kids are exposed to benzene by living near gas 15 stations? 16 A We're all exposed to benzene so they do 17 have background exposures to benzene, just like all 18 of us do. Actually, living next to a gas station or 19 living in proximity to a refinery was a relatively 20 minor contributor. So while it probably did 21 contribute some, just like it would to anyone's 22 background exposures, it was a relatively minor 23 contributor. The biggest contributors were cigarette 24 smoking and having an attached garage. 25 Q Children are exposed to benzene above 10 1 background levels simply by virtue of having an 2 attached garage in their home? 3 A I wouldn't say their -- I would say that 4 makes -- no. What I would say is that we are 5 describing their background exposures. 6 Q Fair enough. When you are -- in a risk 7 assessment you are studying exposure to a substance 8 and the incidence of disease; is that a fair 9 statement? 10 A We were studying -- no. We were doing a 11 risk assessment, so not really -- it wasn't an 12 epidemiology study. We were actually looking at the 13 incidence of disease. It was a formal, EPA based 14 risk assessment where you use their potency factors 15 and their slope factors and their tox values. And 16 you basically multiply that by the exposures, and you 17 come up with a theoretical risk to children. And 18 then they have guidelines as to when that risk 19 becomes unacceptable. And, you know, it's just a 20 basic risk assessment. 21 Q What diseases were you looking at in that 22 study or evaluation of risk assessment? 23 A Well, it doesn't work that way. I mean, 24 what you use is, you use EPA's toxicity values, and 25 those are based on specific end points. So, you 11 1 know, that -- we can discuss that. But you don't -2 it's not a disease specific risk assessment. You're 3 just looking at what EPA says -- you have to kind of 4 understand how a cancer slope factor works and how 5 you would use it in risk assessment. But it is based 6 on -- I mean, ultimately if you go back far enough, 7 it's based on AML, and the noncancer toxicity is 8 based on lymphocytopenias. 9 Q Did you look at the relationship between 10 benzene exposure to children and the incidence of 11 leukemia in that risk assessment? 12 A Not per se, no. 13 Q Okay. In what way -- if not per se, in 14 what way did you evaluate leukemia, childhood 15 leukemia in relation to benzene exposure in that 16 project? 17 A Well, you didn't do childhood leukemia 18 because there's no -- there's no data that children 19 have gotten leukemia from benzene. So what you have 20 to do is use the cancer slope factor, which basically 21 says by EPA's calculations, here is the risk for 22 developing AML if you are exposed to X amount of 23 benzene. So then at the simplest level, you take 24 what the kids' exposure to benzene is, you put it 25 into that equation, and it spits out a risk number. 12 1 As then long as that risk number is below 1 times 10 2 to the minus 6, everyone ignores it. If it's below 1 3 times 10 to the minus 4, you discuss it, but then you 4 ignore it. If it's greater than 1 times 10 to the 5 minus 4, then you do something about it. 6 Q So you did look at AML in relation to 7 exposure in that study? 8 A Insomuch as that that is the basis for the 9 cancer slope factor. 10 Q Okay. 11 A I mean, we weren't doing an epi study. We 12 weren't going out -13 Q I understand. 14 A -- counting diseases. 15 Q How much benzene did you conclude that the 16 children were being exposed to? Was there a range? 17 A There was a range, and you can find it, 18 but I don't remember specifically. I mean, the risk 19 numbers associated with those exposures were less 20 than 1 times 10 to the minus 4, so that I remember. 21 Q So you didn't find an increased risk? 22 A Well, it depends on your definition of 23 "increased." I mean, if your definition of 24 "increased" is zero, then sure, it was increased. If 25 your definition of "increased" is something that the 13 1 federal government feels like is an issue, then no, 2 we didn't find one. Because the federal government, 3 EPA, did not consider those exposures, which they 4 agreed with, to pose an undue risk to children. 5 Q What were the second and third studies you 6 did? 7 A The second study had to do with chemical 8 sensitivity, which was connected to that. And then 9 the third study, third project, if you will, was a 10 re-re-revaluation of the Pliofilm cohort. And we 11 didn't -- I've only done a little on it. We 12 conducted Phase 1, as it were, and we haven't done 13 anything else. We haven't been able to do the 14 interesting stuff yet. I'm trying to think of 15 everything that I've done for them. 16 Q For the API? 17 A Correct, yes. So there was that little 18 Pliofilm one. There was the children's risk 19 assessment. There was the sensitivity paper. 20 Q Let me ask you this. In the first study 21 you did, the API one about benzene in children with 22 the benzene consortium, were any of your -- did the 23 results of any of your work in that risk assessment 24 then translate into additional measures that would 25 protect people? 14 1 A No. 2 Q The chemical sensitivity -- well, let me 3 ask you. The reevaluation of the Pliofilm cohort, 4 did any of your work in that project then translate 5 into other work which would go on to further protect 6 workers? 7 MR. PERRY: Object to form. 8 A Well, I'm not quite sure about the way you 9 worded that question. But if that were completed, 10 once we complete that project -- and I can explain to 11 what you we're doing, if you'd like. But once we 12 complete that project, it could impact on 13 regulatory -- a decision that involves the regulation 14 of benzene. The childhood leukemia risk assessment 15 could have if there was a need. 16 Q (By Mr. Patton) What is the chemical 17 sensitivity project you worked on, No. 2? 18 A That one had to do with the -- what I did 19 essentially was say, you know, there are other things 20 in the world that give people leukemia. And two of 21 those things that we know give people leukemia are 22 chemotherapeutic agents. And they give adults 23 leukemia, and they give children leukemia. And the 24 leukemias that children get are remarkably similar to 25 the leukemias that adults get and the doses. 15 1 So with that as kind of a theoretical 2 framework, what I went and did was looked at all of 3 the clinical literature that I could find, 250 some 4 studies, and evaluated on a study-by-study basis 5 whether or not they had separated out the various 6 ages. And the idea was, does age, as an independent 7 variable, affect a person's risk of developing 8 leukemia from these chemicals. And it did not appear 9 that the children, just by virtue of being children, 10 were any more susceptible to developing AML following 11 chemotherapy than adults were. In fact, most of the 12 studies would suggest that they were less 13 susceptible. 14 Q So the chemical sensitivity project you 15 did was also relevant to children? 16 A Yes. 17 Q It dealt with children? 18 A Yes. 19 Q It focused on children? 20 A Correct. 21 Am I providing too much detail. I can -22 Q It's all right. 23 Are you involved in -- where is it that 24 you work, the University of Colorado Health Sciences 25 Center in Denver? 16 1 A I work for Summit Toxicology, which is my 2 consulting firm. But I have appointments at CU, in 3 various departments at CU. 4 Q Are you familiar with an ongoing benzene 5 study in Shanghai? 6 A Yes. 7 Q Are you involved in that? 8 A No. 9 Q Do you know why you're not involved? 10 MR. PERRY: Object to form. 11 A No. 12 Q (By Mr. Patton) It's a weird question. 13 A Well, I mean, I'm probably on -- to answer 14 that question, no. Let me just tell you the story. 15 I mean, Rich Irons was my thesis advisor, and he's 16 the PI of that study. He's the principal 17 investigator of that study. When I was still at the 18 university and still working with him, he was 19 conducting the feasibility portion of that study, and 20 I was peripherally involved at that point. In fact, 21 I taught an immunology class on his behalf so that he 22 could go spend time in China to figure out whether or 23 not they could actually do this study. After that I 24 had my own grants funded. I was doing my own thing. 25 We kind of parted ways, like every graduate student 17 1 and their advisor does, and so we had separate career 2 paths. 3 Q Rich Irons -- Richard Irons, his career 4 path has involved a tremendous amount of work on 5 behalf of industry related to benzene; do you agree? 6 A I wouldn't agree that that's the only 7 thing that he's done. 8 Q I didn't say it was the only thing, sir. 9 I said a large amount. Would you agree that a large 10 amount of his work has been on behalf of industry in 11 relation to benzene? 12 MR. PERRY: Object to form. 13 A Yes, yes. 14 Q (By Mr. Patton) And in fact, it sounds 15 like that's how you got started in doing benzene work 16 on behalf of industry; is that a fair statement? 17 A No, no. I mean, I said that there was 18 funding from API in the lab where I started with 19 Dr. Irons. But we also had a really big NIH grant, 20 and I think I was working on the NIH grant. I'm not 21 positive about that. 22 Q What is -- you're a toxicologist, correct? 23 A Yes. 24 Q What is toxicology? What is it the study 25 of? 18 1 A Toxicity, poisons. I mean, if you look at 2 Casserett and Doull, which is our primary textbook, 3 it says Toxicology, the basic study of poisons. 4 Q Is benzene a poison? 5 A Benzene can be toxic. 6 Q What is the objective of studying poisons, 7 of being a toxicologist? 8 A That's a good question. It depends. I 9 mean, there's lots of objectives. There are -- you 10 want to understand the dose response relationship. 11 You would like to know how much of the chemical can 12 actually make a person ill, can exert a toxic effect. 13 You would like to understand, if that occurs, is 14 there some way to treat it, is there a way to 15 mitigate that toxicity. 16 Every toxicologist that I'm aware of -17 and certainly in my own research -- we all have a 18 keen interest in the underlying disease process. So 19 while we were looking at benzene and its ability to 20 cause AML, we were also researching the basic 21 pathology of that disease. So, I mean -- and people 22 that look at kidney toxicity, they are also 23 uncovering basic physiological mechanisms for kidney 24 function. 25 Q Is there something of a loftier objective 19 1 in the study of toxicology? That's to say, there's 2 an end goal to help people? Would you agree with 3 that? 4 A That's pretty lofty. Yes. I mean, it 5 certainly isn't the other way, at least today. In 6 medieval Europe, all the courts had toxicologists. 7 The kings employed toxicologists. And in that 8 situation, those individuals were not necessarily 9 employed to help people. 10 Q As a toxicologist do you personally 11 consider yourself somebody who is in the business to 12 help people, make people safer? 13 A I've never really thought about it in 14 those terms, but yes. 15 Q I mean, do you want the end work of your 16 body of work, all the studies that you've done, all 17 the information that has went into your curriculum 18 vitae, do you want that ultimately to go to help 19 people, make the world a better place and make people 20 safer? Is that part of your sort of mission, as a 21 toxicologist? 22 A I've never really thought about it that 23 way. 24 Q So you don't know one way or the other? 25 That's your -- 20 1 A I certainly wouldn't say that it's the 2 other way, to make people less safe. 3 Q Okay. 4 A So sure, I would agree with that. 5 Although I'm just telling you, I've never looked at 6 myself in the mirror and said, Okay, today we're 7 going to go out there and make the world a safer 8 place. I just haven't done that. But I do agree 9 with you. I mean, ultimately by improving our 10 understanding of chemical toxicity, that is 11 ultimately the goal. 12 Q Improving our understanding of chemical 13 toxicity can help to protect people, can help to 14 protect certain types of workers; fair statement? 15 A Sure. 16 Q You said that part of the study of poisons 17 or part of toxicology is to evaluate ways to mitigate 18 tox -- to mitigate toxicity. That's to say, part of 19 toxicology is to evaluate and study ways so that 20 people aren't exposed as toxically. Is that fair, or 21 am I saying that wrong? 22 A Well, I understand what you're saying. I 23 think toxically is -24 Q It's probably not even a word? 25 A Yeah, but that's all right. I understand 21 1 where you're going. No. I would say that part of it 2 would be industrial hygiene, where you're actually 3 figuring out engineering ways to limit, reduce 4 exposure. What I meant -- and that's really the dose 5 response relationship, how much can a person be 6 exposed to, without any anticipated adverse effects. 7 And that is certainly an important part of what we 8 all do. 9 Q Industrial hygienists, they have the -10 part of their job involves the ability, to some 11 extent, to put engineering controls in place, do 12 things to reduce workers' exposure to benzene to 13 mitigate toxicity; do you agree? 14 A I do agree. And they would base that 15 decision on our toxicology -16 Q Right. 17 A -- dose response information. 18 Q Right. So you could give those more 19 engineering type folks the scientific and medical 20 information so that they could go do things to 21 mitigate exposure and protect workers. Do you agree 22 with that? 23 A Yes. 24 (Exhibits 1 through 3 marked.) 25 Q (By Mr. Patton) Okay. We've got your CV, 22 1 which I've marked as Exhibit 2. It likes like it's 5 2 or 10 pages. It talks about your professional, 3 studies you've done, consulting work, editorial 4 review, et cetera. We have Exhibit 3. This is a 5 list of all the testimony you've given in lawsuits. 6 Is there anywhere on Exhibit 2 or Exhibit 3 where you 7 did something in your body of work as a toxicologist 8 that contributed to industrial hygienists or other 9 folks actively doing something to mitigate toxicity? 10 MR. PERRY: Object to form. 11 A It would be a pretty crooked line. I 12 mean, most of the research that I was doing in the 13 lab would -- you would not expect that exposures 14 typically encountered today that you would expect 15 those toxicities to occur. 16 Q (By Mr. Patton) Sir, maybe my question 17 wasn't clear. Are you a health scientist? 18 A Well, I'm a toxicologist. 19 Q My question is this, sir. In Exhibit 2 20 and Exhibit 3, is there anywhere in there where you 21 can point to your personal work that resulted in 22 changes down the road, so to speak, that helped to 23 mitigate toxicity such that workers were directly in 24 safer conditions? 25 MR. PERRY: Object to form. 23 1 A I -- I don't know whether that's happened 2 or not. 3 Q (By Mr. Patton) Okay. You mentioned 4 earlier -- well, hold on a second. Does any part of 5 your -- how old are you? 6 A I'm 51. 7 Q Does any part of your remaining career -8 does it interest you to do things that would make the 9 world a safer place or maybe protect certain classes 10 of workers? 11 MR. PERRY: Object to form. 12 A Well, yeah. That interests me. I mean, I 13 worked at EPA for two years. So that was -- you 14 know, at a lofty level that was to protect the 15 public, to protect the environment. So, I mean, 16 there have been -- maybe I'm being too literal, but 17 I'm trying to think of a specific experimental work 18 that I've come up with myself in the lab that I can 19 draw a straight line to a change in regulation on 20 benzene exposure, and I can't do that. 21 Q (By Mr. Patton) Or any other exposure, 22 for that matter, correct? 23 A I can't do that. That's not to say that 24 things that I have published have not been part of a 25 decision-making process. But I can't point to a 24 1 straight line and say, okay, because of this study 2 that I did, people went out there and said, yeah, 3 these exposures are too high, and people are getting 4 sick from it. 5 Q Right. Is it fair to say that you've kind 6 of done the opposite? For instance, Exhibit 3, your 7 deposition testimony, in each of these cases did you 8 testify that the chemical agent did not cause a 9 person's disease? 10 MR. PERRY: Object to form. 11 A I wouldn't say that's the opposite. 12 Q (By Mr. Patton) Okay. Sir, on Exhibit 3 13 you've testified in 20 depositions involving chemical 14 exposure as the cause of disease, correct? 15 A Say that again. 16 Q Chemical exposure as a cause of disease or 17 illness. 18 MR. PERRY: You're saying all of those on 19 Exhibit 3? 20 A I'm not -21 Q (By Mr. Patton) Let me be a little more 22 clear. 23 A Please. 24 Q Dr. Pyatt, the deposition testimony marked 25 as Exhibit 3, these are all the cases you've 25 1 testified in, correct? 2 A Yes, sir. 3 Q Okay. Have you ever been hired by an 4 injured worker or lawyers or families, people 5 involving an injured worker? 6 A I have not yet, no. 7 Q Have you always been retained on behalf of 8 industry or chemical companies? 9 A So far, yes. 10 Q Okay. Do all -- excuse me. All of these 11 cases that you've testified in as a toxicology 12 expert, you testified on behalf of industry or 13 chemical companies, correct? 14 A That's right. 15 Q In each of these cases -- in any of these 16 cases -- let me ask a better question. 17 How many of these cases involve benzene? 18 A They all do. 19 Q All 20 of them? 20 A Yes, sir. 21 Q In any of these cases did you testify that 22 benzene exposure caused the person's disease? 23 A No; not in those 20, no. 24 Q Okay. Is it leukemia in all these 20? 25 A No, sir. 26 1 Q Are there -- what are all the diseases 2 reflected in this list? 3 A Can I see it? I'd have to go through it. 4 Q Let's go through and just write what 5 disease it is right next to each case. 6 A Right now? 7 Q Sure. 8 A Okay. 9 Q You can write it next -10 A You want me to do it out loud, or you just 11 want me to do it quietly? 12 Q Let's do it out loud. 13 A Okay. Wilkerson, this was a nonHodgkin's 14 lymphoma. Remboldt, this was a nonHodgkin's 15 lymphoma. Barker, this was an AML. Detel, this was 16 an ALL. Reed was a Hodgkin's lymphoma. Solis was a 17 nonHodgkin's lymphoma. Behymer, this was a chronic 18 lymphocytic leukemia and a multiple myeloma. 19 Henrickson was an AML, and that actually was a 20 gasoline case. 21 Q Yeah. If there are any others in there 22 that involve gasoline, please mark them. 23 A Barker was a gasoline case. Saltonstall, 24 that's an NHL. Baker, this was a monoclonal 25 gammopathy of undefined significance. 27 1 THE REPORTER: Say that again. 2 MR. PATTON: Worry about it later. 3 A A monoclonal gammopathy of undefined 4 significance. This was an idiopathic myelofibrosis. 5 This was an AML. This was an AML. This was an APL. 6 Q (By Mr. Patton) APL, acute promyelocytic 7 leukemia, right? 8 A Right. 9 Q It's still a myeloid disease, right? 10 A Yes. This was a nonHodgkin's lymphoma. 11 Bishop was multiple myeloma. Knapper was an AML. 12 This was an AML. We've already done that one. This 13 was an APL/AML. And this one was paints. And this 14 one, Remboldt, this was crude oil. So was this one. 15 So saying these are all benzene-related, it's not 16 totally accurate. The hearing stuff, you want those, 17 too? 18 Q Sure. 19 A Okay. Cantu, that was a nonHodgkin's 20 lymphoma. 21 THE REPORTER: I can't hear you. 22 THE DEPONENT: I'm sorry. I'm talking to 23 myself. 24 A Milward, we already talked about that one. 25 So there was a deposition, and then there was a 28 1 hearing so it was really the same thing; and Wolfe, 2 the same. 3 Q (By Mr. Patton) Dr. Pyatt, we just took 4 some time, and you went through Exhibit 3 and you 5 marked next to each of these cases in which you 6 testified on behalf of industry or you were hired by 7 industry. You testified in some 20 cases involving 8 benzene or benzene-containing products which the 9 plaintiffs alleged caused a form of myeloid or 10 lymphocytic leukemia, fair statement? 11 A Sometimes, not always. 12 Q What do you mean, "not always"? 13 A Well, like, for example, the idiopathic 14 myelofibrosis, which was Stromberg, they were 15 claiming that that was toluene. And while they 16 discussed the possibility of a minute amount of 17 benzene in the toluene, they still said, We think 18 it's toluene that's doing it. Thorpe was mineral 19 spirits. 20 Q Mineral spirits, do those contain benzene? 21 A At low levels, yes. 22 Q Does toluene contain benzene? 23 A It depends. I mean, even if you hydro 24 treat it, you can probably find a molecule or two. 25 Q Crude oil contains benzene, yes? 29 1 A Crude oil has benzene in it. 2 Q Gasoline contains benzene, correct? 3 A Yes. 4 Q You mentioned earlier part of your work as 5 a toxicologist involves an interest in underlying 6 disease progress. You remember saying that? 7 A Process. 8 Q Underlying disease process. Okay. Would 9 you agree with me that diseases such as the myeloid 10 leukemias, diseases -- I only want to talk about the 11 myeloid leukemias, okay? 12 A Okay. 13 Q Would you agree with me, Dr. Pyatt, that 14 the myeloid leukemias, they do progress through a 15 series of different myeloid disorders before they 16 ultimately arrive at a firm diagnosis? And then once 17 that happens, they might progress to a different 18 myeloid firm diagnosis? Would you agree with that? 19 MR. PERRY: Object to form. 20 Q (By Mr. Patton) I probably didn't phrase 21 that real good, but do you understand what I'm 22 asking? 23 A Kind of. 24 Q Well, let me ask it in a different way. 25 A Okay. 30 1 Q You issued a report in this case. We'll 2 mark it as an exhibit, right? 3 A It is. Oh, it's not, but we will sure. 4 Q Okay. And you talk about my client, Raul 5 Zendejas, having, CML or atypical CML. And I 6 think -- do you say in your report about maybe he has 7 MDS? 8 A I don't think so, no. 9 Q Let's get your report, just to be fair. 10 We'll mark that one as an exhibit. 11 (Exhibit 4 marked.) 12 A "I have been asked to evaluate the 13 allegation that Mr. Zendejas' atypical CML was caused 14 by gasoline, diesel, or other chemical exposure, 15 including benzene." 16 Q Okay. As we sit here today, do you 17 understand what disease Mr. Zendejas has? 18 A I think I do, yes. 19 Q What does he have? 20 A I think he has atypical CML. 21 Q As we sit here today? 22 A Well, as we sit here today, it went -- as 23 we sit here today, I think he's in remission. But it 24 went through a blast crisis. 25 Q Okay. Did you review the deposition of 31 1 Dr. Carroll, who is -- who was Raul's main treating 2 doctor? 3 A Yes. 4 Q Did you read the deposition of Dr. Gore in 5 this case? 6 A Yes. 7 Q You understand Dr. Gore is a world 8 renowned hematologist oncologist at Hopkins? Do you 9 understand that? 10 A No. 11 MR. PERRY: Object to form. 12 Q (By Mr. Patton) Are you a hematologist or 13 an oncologist? 14 A No. 15 Q Have you ever diagnosed anybody with a 16 type of leukemia? 17 A No, sir. 18 Q Have you ever saw someone in a clinic or 19 looked at pathological findings and said, Hey, you 20 have this specific type of leukemia? Have you ever 21 done that with a patient or person? 22 A Well, I did that a lot through my 23 training, but it was not the formal diagnosis that 24 went on people's charts. 25 Q Have you ever formally diagnosed anyone 32 1 with any type of leukemia? 2 A No. 3 Q Okay. Dr. Carroll, do you understand he 4 held some type of leadership position at the 5 Arizona -- University of Arizona Cancer Center? Do 6 you understand that? 7 A No. 8 Q In his deposition he says that Raul 9 Zendejas went through atypical CML, ultimately was 10 treated, and then came back with AML. He calls it 11 AML. Did you see that in his deposition? 12 A I recall that. 13 Q Okay. Dr. Carroll is a bone marrow 14 transplant doctor, and he saves people's lives. And 15 he saved Mr. Zendejas' life. 16 A I did see that, yes. 17 Q Okay. And he says that Raul had AML. As 18 we sit here today, are you telling this judge and 19 this jury that Raul did not have AML? 20 A Well, what I'm saying is that when you 21 have CML first, atypical or otherwise, and it goes 22 into blast crisis, that is usually what most 23 hematologists will say, that he's in blast crisis. 24 It can look like AML. It can be indistinguishable 25 from AML, but it doesn't always look like AML. 33 1 Sometimes it's a lymphoid malignancy. Whether or not 2 he called it AML, I'm calling it blast crisis, it was 3 an acute manifestation of his disease. So it was, 4 clearly, an acute myeloid disease. 5 Q He's got AML, right? 6 MR. PERRY: Object to form. 7 A He would have AML if there wasn't the 8 preceding process. With the preceding process, most 9 hematologists in the field would describe that as 10 blast crisis. 11 Q (By Mr. Patton) Can you hold up this 12 notebook and show it to the camera. 13 A (Deponent complied.) 14 Q Okay. Can you hold up this notebook and 15 show it to the camera. 16 A I think they probably saw it when you 17 handed it to me. Okay. 18 Q Can you hold up this notebook and show it 19 to the camera. 20 A Okay. 21 Q Doctor, all these papers in front of you, 22 these are some of the studies that you're relying on 23 in giving your opinions in this case, correct? 24 A Yes. 25 Q Is it your opinion in this case that 34 1 benzene did not cause Mr. Zendejas' form of leukemia? 2 A Yes. 3 Q Okay. And are you testifying that based 4 on all this literature, you therefore feel that 5 benzene played zero role in Raul's leukemia? Is that 6 your testimony? 7 A Well, I don't believe the scientific 8 literature supports that benzene can cause atypical 9 CML, A. B, I don't believe Mr. Zendejas ever used 10 pure benzene. So the literature that's far more 11 appropriate to evaluate a causal relationship with 12 Mr. Zendejas is gasoline because that is ostensibly 13 the thing that he was the most exposed to. And I 14 think that literature is pretty clear that gasoline 15 exposure does not cause CML or AML. 16 Q So your testimony is yeah, he has 17 leukemia, but he doesn't have AML, right? 18 A Well, now you're asking a different 19 question. 20 Q I am. 21 A Okay. My testimony is that he has 22 atypical CML. And when chronic myelogenous leukemias 23 progress, they will frequently go into what is 24 usually termed blast crisis, which is an acute 25 manifestation of their disease. 35 1 Q All these studies that you just showed the 2 camera, did any of those people in those studies with 3 leukemia go through an acute blast crisis before they 4 arrived at their AML? 5 A You would have to go through the studies 6 specifically to answer that question. 7 Q Have you went through any of these studies 8 to determine if some of these patients -- before they 9 were classified as an AML in the study, to determine 10 whether or not they went through an MDS phase or they 11 went through a CML phase or an atypical CML phase? 12 Have you done that evaluation? 13 A Yes. 14 Q And what did you find? 15 A I didn't see any evidence of that. I 16 mean, CML -- the only way -17 Q Hold on. Hold on. 18 MR. PERRY: Let him finish. 19 A They only way that could occur is that 20 someone does not ever get -- seek medical treatment 21 for the first part of that disease. So they walk 22 around with CML for however long it takes, their 23 spleen keeps getting bigger, their white count keeps 24 increasing. They ignore all that symptomatology 25 until it goes into blast crisis, and then they show 36 1 up and say, Yeah, you're in blast crisis or, you have 2 AML. 3 So I guess theoretically, if you took a 4 study that was just purely a retrospective mortality 5 study and all they did was look at death certificates 6 and they said, okay, this person died from AML, 7 there's no way to know what happened prior to that 8 diagnosis. But that is not -- or prior to what the 9 funeral director -- or whoever filled out the death 10 certificate, because those things can be fairly 11 inaccurate. But many of the studies, that's not the 12 way they work. I mean, they knew the person. They 13 could do a work history on the person. There's no 14 evidence that that person had a chronic 15 myeloproliferative disorder before they developed 16 AML. 17 Q (By Mr. Patton) Do you believe that any 18 of the folks with AML in any of these studies in 19 front of you ever experienced a myeloproliferative 20 disease or form of MDS or CML before they were 21 designated in the study as AML? 22 MR. PERRY: Object to form. 23 A Ask that again. 24 Q (By Mr. Patton) Do you believe that any 25 of the individuals in any of these studies who were 37 1 called persons with AML, do you believe, as a 2 scientist, that none of them went through phases 3 where they had atypical CML or MDS or 4 myeloproliferative disease or aplastic anemia or 5 anything else? 6 A There's no evidence that that occurred, 7 but I can't say unequivocally that it has not. 8 Q Sir, as a scientist you would respect and 9 acknowledge and you would agree with me that it is 10 certainly possible, if not likely, that these folks 11 with AML, they had other specific disease 12 characteristics and disease precursors, other forms 13 of myeloid diseases before they were called AMLs in a 14 study? 15 MR. PERRY: Object to form. 16 Q (By Mr. Patton) Would you agree with 17 that? 18 A No. 19 THE REPORTER: Excuse me. You need to 20 slow down a little bit. I have you saying, "Object 21 to form" and then "No." Give him a little time. 22 THE DEPONENT: Sure, you bet. Sorry. 23 MR. PERRY: Object to form. 24 Q (By Mr. Patton) Let me ask -25 A No -- 38 1 Q -- the question again, Doctor. 2 A -- because many times AML is diagnosed 3 de novo. Sometimes there is a -- sometimes there is 4 a progression. I'm not arguing that the progression 5 can occur. And frequently people that are diagnosed 6 with myelodysplastic syndrome, based on the form, 7 some percentage will convert to AML. But I think 8 those people will show up in the studies as MDSs. 9 Q Why do you believe that? 10 A Because that's when they would have gone 11 to the doctor, and that's when they would have been 12 pulled into these studies as a myelodysplasia. 13 Q So let's say somebody goes into the study 14 as an MDS. The study's published. When the person 15 goes back to the doctor two months later, they're 16 diagnosed with AML. 17 A That's possible. 18 Q Do the study authors ever go back to the 19 study and redraft and say, Hey, by the way, you know, 20 we just looked at these people who were subjects of 21 the study. They're not MDSs anymore. They're AMLs. 22 Has that ever happened? 23 A I don't think it's needed. 24 Q Okay. What about CML? Would you agree 25 that some patients get CML and then they end up with 39 1 AML? 2 A Well, they end up in blast crisis. Almost 3 all of them will end up in blast crisis, I mean, 4 unless they get cured or with a bone marrow 5 transplant and you end the disease process. But that 6 is historically the way people with CML die. They 7 went with their CML up to the point where they went 8 into blast crisis; AML, if you want, fine. With 9 acute manifestation, blast cells pour out of the 10 marrow into the periphery, and then that ends up 11 being insurmountable. They don't survive that. 12 Q Most people with CML, their CML eventually 13 evolves into a blast crisis or an AML? 14 MR. PERRY: Object to form. 15 Q (By Mr. Patton) Right? Isn't that what 16 you just said? 17 A Historically. 18 Q If a patient in the study like a mortality 19 study where you're looking at death certificates, 20 okay, if they're called an AML on their death 21 certificate, they're designated as an AML in the 22 mortality study, correct? It's a mortality study. 23 It looks at death certificates, right? 24 A Well, some only look at death 25 certificates. Some may be more involved. They may 40 1 have hospital records. They may have interviews with 2 treaters. I mean, there are -- there is a spectrum 3 of specificity with how epidemiologists go about 4 doing the studies. Some, yes, just look purely at 5 death certificates or cancer registry data. And then 6 they really -- there's no way to know what happened 7 before. But that's not the case in all of them. 8 Q Had Raul Zendejas died during his second 9 bone marrow transplant, do you know what he would 10 have been called on a death certificate? 11 MR. PERRY: Object to form. 12 A I would assume that he would have been 13 called atypical CML. 14 Q (By Mr. Patton) He could have been called 15 blast crisis, though, correct? 16 A They might have put that in there, yes. 17 Q And they might have put AML on there, 18 correct? 19 A That, I don't know. 20 Q Would they be wrong if they put AML or 21 blast crisis on there? 22 MR. PERRY: Object to form. 23 A They wouldn't be wrong if they put blast 24 crisis. I think if they listed AML, that would 25 really not be enough information to understand what 41 1 Mr. Zendejas actually went through. 2 Q (By Mr. Patton) Consistent with your 3 other experience in industry, would you agree with me 4 that it is easier for you to testify on behalf of 5 industry in this case because Raul didn't die? He's 6 not called an AML; therefore you can call him an 7 atypical CML and stratify him out of the literature? 8 Is that accurate? 9 MR. PERRY: Hold on. Objection; form, 10 unfounded, argumentative. Go ahead. 11 A No, no. I mean, because he had atypical 12 CMA, that brings in a different body of literature 13 that is appropriate and relevant to discuss. And 14 most of that is in this binder, the CML literature. 15 But he was exposed to gasoline and diesel fuel. 16 Gasoline is not considered to be a carcinogen by any 17 regulatory body. Neither is diesel fuel. 18 So whether he had AML or blast crisis or 19 CML or myelodysplasia or any other myeloid disease 20 that you would like to categorize him as, I do not 21 believe that gasoline -- that there is sufficient 22 literature for the gasoline to have caused that 23 malignancy. So no, what you're saying is incorrect. 24 The CML brings in a different body of literature. If 25 it were a pure AML case, no one ever said that he had 42 1 CML, it was just straight AML, then that would be a 2 different body of literature. But it would still be 3 related to gasoline. 4 Q (By Mr. Patton) Some of the citations or 5 the references in support of your report talk about 6 refinery workers and talk about benzene exposure and 7 talk about leukemia, correct? 8 A I would have to look. I suspect that's 9 true, yes. I mean, I printed out a few refinery 10 worker studies. 11 Q Are those guys exposed to all benzene all 12 the time? Is it all 100 percent benzene? 13 A Not at all. 14 Q What do they make in refineries? Do you 15 know? 16 MR. PERRY: Object to form. 17 A I think that depends on the refinery. 18 Q (By Mr. Patton) Would you agree with me 19 that some oil refineries make gasoline? 20 A That's a good question. I don't -- I 21 think some might. I actually thought they all did. 22 But I was informed just recently at the Munich 23 meeting, talking to a toxicologist for a refinery, 24 and he said they don't make gasoline. So I thought 25 they all did, but apparently that's not true. 43 1 Q The studies that connect -- first of all, 2 the Pliofilm cohort, you talked about you're 3 currently doing a re-revaluation of the Pliofilm 4 cohort, correct? 5 A Kind of tongue in cheek because it's been 6 evaluated to death, but yes. 7 Q Okay. So the Pliofilm cohort, what was 8 that? 9 A The Pliofilm cohort is the most important 10 cohort in the U.S. with regard to benzene exposures 11 and the risk of AML. 12 Q Who performed that study? 13 A Which study? 14 Q The Pliofilm cohort. 15 A The first one? 16 Q Yes. 17 A I mean, there's like 30. 18 Q Dr. Infante was involved in that, correct? 19 A Peter Infante was the first person who 20 responded from NIOSH to Dr. Sakol's observations that 21 we're seeing too many of these erythroleukemias in 22 this population. But the first quantitative study, 23 the first quantitative epi, was not done by 24 Dr. Infante. It was done by Dr. Rinsky. 25 Q In any event, the Pliofilm cohort helped 44 1 lead to the increased -- or to the new benzene 2 standard in the late '70s, correct? 3 A That is my understanding, yes. 4 Q It's my understanding, too. 5 And is Pliofilm benzene? 6 A Pliofilm is rubber hydrochloride. 7 Q It doesn't -- it's not pure benzene, is 8 it? 9 A Well, Pliofilm, that's a thing. That's a 10 material. And it's kind of like Saran Wrap. When 11 they were making this Saran Wrap, thick Saran Wrap, 12 which is called Pliofilm, which is rubber 13 hydrochloride, they used pure benzene as a solvent. 14 So they dissolved this stuff in pure benzene. They 15 spread this out on this big table in pure benzene. 16 They allowed the benzene to evaporate up. They tried 17 to collect it overhead in tanks. That's why it gives 18 us such good data on the benzene/AML association. 19 Q But weren't the folks who were making that 20 Pliofilm, weren't they exposed to other chemicals 21 besides just the benzene? 22 A No. That's the reason why the US EPA, 23 OSHA, all these people, all the regulatory groups in 24 the US rely on Pliofilm to set our regulatory 25 standards, because there was not a lot of confounding 45 1 chemical exposures in those workers. And we had a 2 reasonable dose response. So we knew some people 3 were dry side workers. They weren't exposed very 4 much. There were wet side workers, five or six job 5 categories. They had varying levels of exposures so 6 it allowed us to do a pretty detailed dose response 7 analysis. 8 Q You bring up dose response, which is an 9 interesting point. Does everyone respond the same 10 way to the same dose of a given substance? 11 MR. PERRY: Object to form. 12 A It depends on the substance. It depends 13 on the dose. I mean, I think what you're asking me 14 is, is there individual susceptible? 15 Q (By Mr. Patton) Yes, sir. 16 A And the answer is, or course. 17 Q Of course there is individual susceptible? 18 A Yes. Now, whether or not that impacts on 19 any observation that you might see epidemiologically 20 or pharmacologically or toxicologically, that's going 21 to be a discussion for the chemical and the end point 22 and what we know about that scenario. But yes, as a 23 general rule, we all respond differently to different 24 chemicals. 25 Q Because we all respond differently to 46 1 different chemicals, and specifically to benzene, 2 would you agree with me that different workers will 3 respond differently to benzene? 4 MR. PERRY: Object to form. 5 A I was talking more generally. 6 Q (By Mr. Patton) I want to talk a little 7 more specifically. 8 A About benzene specifically? 9 Q Yes, sir. Will you agree with me when 10 we're talking about benzene that all workers respond 11 to benzene in the same way (sic)? 12 MR. PERRY: Object to form. 13 A It depends on the end point. 14 Q (By Mr. Patton) What do you mean, "end 15 point"? 16 A Well, like we know that people who were 17 exposed to thousands of part per million in a short 18 term benzene suffer CNS, depression, and they lose 19 consciousness and pass out. There doesn't appear -20 I mean, there's not many people that have ever been 21 exposed like that, but there doesn't appear to be a 22 clear-cut distinction in one person versus another. 23 So I think there is no evidence to say that there 24 would be individual susceptibility with regard to 25 that end point. So that's what I meant by end point. 47 1 Now, if you're talking about cytopenias or 2 you're talking about aplastic anemia, then that's a 3 different question. 4 Q If benzene is going to hurt someone, what 5 organ of the body would it hurt? 6 MR. PERRY: Object to form. 7 A That would depend on the dose. 8 Q (By Mr. Patton) Does benzene -9 A It would depend on the exposure duration. 10 MR. PATTON: Objection, nonresponsive. 11 Q (By Mr. Patton) Does benzene affect the 12 bone marrow? 13 A It can. 14 Q It can. And what does it do to the bone 15 marrow? 16 A That depends on the dose. 17 Q Okay. And what dose does it take of 18 benzene to affect the bone marrow, to create a 19 harmful effect on the bone marrow? 20 A In experimental animals, it depends -- you 21 know, I could quibble. It would depend on your 22 definition of a harmful effect. But in experimental 23 animals, you know, the levels were pretty high, 24 300 PPM, five days a week, et cetera, and then you 25 saw pretty severe toxicity in their bone marrow. 48 1 More subtle changes you could see at about 10 part 2 per million. 3 And as far as people go, if that's the end 4 point, which most people would agree is the most 5 sensitive end point for benzene toxicity, that being 6 a cytopenia, it appears to be happening somewhere 7 between, say, 5 and 10 part per million. 8 Q Okay. So let's kind of start over based 9 on what you started to explain. Benzene can affect 10 the bone marrow, correct? 11 A Yes. 12 Q Okay. And benzene can create harmful 13 effects on the bone marrow, right? 14 A It can if it's high enough and long 15 enough. 16 Q Sure. And benzene can cause -- you said 17 cytopenia? 18 A Correct. 19 Q What is cytopenia? 20 A The penia means there's too few. So a 21 cyto is a reduction in cells. So you can have a 22 lymphocytopenia, which would be something you would 23 measure in the peripheral circulation, and you would 24 see a decrease in the lymphocytes. And EPA's 25 reference concentration, which is their regulatory 49 1 standard for noncancer end points, is based on 2 lymphocytopenia. So according to the EPA and Nate 3 Rothman's study, that is the most sensitive end point 4 for humans exposed to benzene, lymphocytopenia. 5 Q And that is observed at what amount of 6 benzene exposure? 7 A In that study it was 7.2 PPM -8 Q Okay. 9 A -- over an eight-hour time weighted 10 average. 11 Q Okay. So let's say I go work all day, and 12 I'm loading gasoline. Let's say Raul Zendejas is 13 working all day, and he's loading gasoline, okay? 14 You agree with me that gasoline contains benzene, 15 correct? 16 A Yes. 17 Q You agree with me that workers -- gasoline 18 distribution workers can and sometimes are exposed to 19 measurable amounts of benzene while performing 20 certain loading and unloading operations? Do you 21 agree with that? 22 MR. PERRY: Object to form. 23 A We can measure benzene in really low 24 levels so we're all going to be exposed to measurable 25 amounts of benzene. 50 1 Q (By Mr. Patton) Would you agree with 2 me -3 A So I'm not sure that's a good adjective to 4 use. 5 Q Okay. Would you agree with me that 6 gasoline distribution workers at least had the 7 potential, if they're not, in fact, sometimes exposed 8 to measurable amounts of benzene around or -- above, 9 actually, background levels? Would you agree with 10 that? 11 MR. PERRY: Object to form. 12 A For the period when they're loading, I 13 think that seems to be borne out in the literature, 14 yes. 15 Q (By Mr. Patton) Would you agree with me, 16 Dr. Pyatt, that the literature tells us that gasoline 17 distribution workers, when they're loading gasoline, 18 they are exposed to measurable amounts of benzene 19 above background levels, correct? 20 MR. PERRY: Object to form. 21 A Yes. 22 Q (By Mr. Patton) And they are sometimes or 23 can sometimes be exposed to benzene above or close to 24 or around the amount that is a PEL or a TLV, correct? 25 Does the literature show us that? 51 1 MR. PERRY: TLV or PEL for benzene or 2 gasoline? 3 MR. PATTON: Benzene. 4 MR. PERRY: Because there's one for both. 5 MR. PATTON: Benzene, sir. 6 MR. PERRY: Object to form, unfounded. 7 A That, you've exceeded my knowledge of the 8 industrial hygiene for distribution workers. 9 MR. PATTON: Let's take a break. Off the 10 record. 11 THE VIDEOGRAPHER: The time is 10:28. 12 We're going off the record. 13 (Recess from 10:28 a.m. to 10:39 a.m.) 14 THE VIDEOGRAPHER: We're on the record at 15 10:39. This is the beginning of Tape 2. 16 Q (By Mr. Patton) Dr. Pyatt, must someone 17 be exposed to pure benzene to be exposed to benzene? 18 A No. 19 Q Okay. Must I be exposed -- well, first of 20 all, alcohol can make someone intoxicated, right? 21 A Ethanol. I mean, there's lots of kinds of 22 alcohol. 23 Q Okay. But as far as -24 A Ethanol alcohol can. 25 Q Okay. If somebody's going to go out to 52 1 dinner and have a couple cocktails, okay, that can 2 cause intoxication, right? 3 A That's true. 4 Q What is it in the cocktails that causes 5 intoxication? 6 A Ethanol. 7 Q Ethanol, okay. So must someone be exposed 8 to pure ethanol to be intoxicated, or can the ethanol 9 be diluted with other products like in a cocktail to 10 make someone intoxicated? 11 A Both. 12 Q Okay. But you would agree with me that 13 someone who is exposed to alcohol or ethanol in a 14 cocktail is ultimately being exposed to alcohol or 15 ethanol, correct? 16 A Yes. 17 Q The fact that the alcohol or ethanol is in 18 the cocktail doesn't change the fact that they're 19 still exposed, right? 20 A No. 21 Q Okay. You talked about individual 22 susceptibility and dose response. Is there a dose of 23 alcohol or ethanol in cocktails that causes 24 intoxication? 25 A You'll have to define "intoxication." 53 1 Q Well, does it -- my point, sir, is doesn't 2 that differ among the individuals? 3 A It does down at the low end. I'm not sure 4 that it does up at the high end. I mean, people -5 if you drink enough alcohol and you go into a coma 6 and respiratory arrest, I don't know that that 7 happens at different levels. But certainly down at 8 the low end of that dose response, the Asian 9 population, they have this so-called flushing 10 reaction. And they get a profound metabolic change 11 at really, really low levels of ethanol that I don't 12 get. So there are some differences. That's what I 13 mean. You just have to define what you mean by 14 "intoxication." 15 Q Okay. Well, let's take, for example, 16 drunk driving, okay? 17 A Okay. 18 Q The blood alcohol content I think in most 19 of the U.S. is .8; is that right? 20 A I thought it was 1.0, but maybe it has 21 dropped. I don't know. 22 Q Let's say it's 1.0. 23 A Okay. 24 Q How much alcohol must someone drink to 25 reach a 1.0 blood alcohol level such that they are 54 1 drunk, according to the police? 2 A I don't know the answer to that. It would 3 depend on like what they ate prior, their size, the 4 content, how quickly they did it. I mean, there's a 5 lot of variables, and there are charts that can 6 predict that. But I'm -- I don't know what those 7 are. 8 Q So different folks are going to -- their 9 blood alcohol level is going to respond differently 10 or arrive at a different number depending on various 11 factors, correct? 12 A That I think is fair, yes. 13 Q Okay. If someone's exposed to benzene, 14 okay, would you agree with me that there are 15 different various factors that would affect that 16 person's uptake or metabolic effect, so to speak, of 17 benzene? Or is it just uniform across the board? 18 A Well, there's a lot involved in that. The 19 uptake -- which I'm assuming you man absorption? 20 Q Yes, sir. 21 A There doesn't appear to be any differences 22 in absorption. 23 Q Is it your opinion, Doctor, that all 24 people absorb benzene at the same rate? 25 A There doesn't appear to be much 55 1 difference. So, I mean, you're going to have 2 differences in breathing rates. So differences in 3 breathing rates will affect the absorption. But on a 4 given amount of benzene that's in the lungs, there 5 doesn't appear to be differences in the ability of a 6 molecule of benzene to cross those membranes and get 7 into the blood. That's absorption. So that, there 8 doesn't appear to be -- or I certainly can't think of 9 a biological reason why that would be different. 10 The next part of your question, the 11 metabolic, I think -- what did you say? Behavior? 12 Q Let me stop you real quick, and then I 13 want you to start with the metabolic -14 A Sure. 15 Q For absorption of benzene purposes, is it 16 your opinion that all human beings absorb benzene at 17 the same rate regardless of race, age, gender, 18 weight, what they had for breakfast, things of that 19 nature? 20 A We're talking about inhalation, 21 breathing -22 Q Sure. 23 A -- breathing it in? I've not seen any 24 information that would indicate that people absorb 25 benzene differently. The amount of benzene that you 56 1 can pull into your lungs, which would then dictate 2 how much gets into your -- the bloodstream, that 3 could vary. Children breathe quicker. Workers 4 working harder, they're breathing in more air. So 5 those things can change. 6 But, I mean, if you said here's 7 100 people, here's 100 molecules of benzene into each 8 one of those people's lungs, how much of that 9 100 molecules of benzene are to get into each of 10 those people's bloodstreams, I've never seen any data 11 to indicate that there would be any difference in 12 that. 13 Q Okay. Is it your opinion that the 14 literature says -- does, in fact, support your 15 opinion, that the benzene absorption rate is the same 16 for pretty much everyone across the board? 17 A I've never seen anything contrary to that. 18 Q Okay. So the next step is metabolism of 19 benzene? 20 A Correct. 21 Q Okay. What is metabolism of benzene when 22 it's affecting the body? 23 A The first thing that benzene's going to 24 do -- and it would be irrespective of the route of 25 administration, whether it's inhalation or 57 1 whatever -- it goes to the liver. And it is oxidized 2 by a variety of enzymes in the liver, and it produces 3 a variety of metabolites that I can describe for you, 4 if you care. But some of those are excreted right 5 away. Some are exhaled. Benzene is exhaled right 6 away so it doesn't get metabolized. You know, kind 7 of like ethanol goes right back out, and people can 8 detect it in these Breathalyzer tests. So benzene 9 does the same thing. 10 Some of the metabolites that are formed in 11 the liver then travel through the bloodstream to the 12 bone marrow where additional metabolic processes take 13 place. And that is thought to be underlying some of 14 the toxicity associated with benzene in the bone 15 marrow. 16 Q Okay. Let's go through those in a little 17 more detail. So someone absorbs benzene at a given 18 rate that is shown to be clear, across the board, 19 right? 20 A There hasn't been information that I'm 21 aware of that shows that it's different. 22 Q I'm not challenging you on that. 23 A Well, yeah. I just want to make sure. 24 I'm not saying that everyone -- that we know 25 definitively, but that there's not been any evidence 58 1 to show that it's different. 2 Q Okay. And then benzene is being 3 metabolized by the body. That means that the body's 4 taking it in, kind of like someone drinking a 5 cocktail is metabolizing the alcohol; is that fair? 6 A It's exactly like that. 7 Q Okay. And so the benzene's being 8 metabolized in the body. It goes through the kidneys 9 or liver? 10 A The liver is the first part where it is 11 metabolized, but the kidneys certainly play an 12 important role in the excretion of those metabolites. 13 Q Got it. So the benzene's being processed 14 through the liver. Some of it makes its way to the 15 kidneys. People urinate it out, correct? 16 A Yes. 17 Q And then some of it makes its way to the 18 lungs, and then you exhale it out, correct? 19 A More it's still in the lungs from 20 breathing it in, but yes. 21 Q Okay. 22 A It comes back out of the blood, goes into 23 the lungs, you exhale it, yes. 24 Q Got it. And then some of it goes to the 25 bone marrow, correct? 59 1 A Correct. 2 Q Before we talk about the bone marrow, does 3 some of it go anywhere else? 4 A Well, it's in the systemic circulation so 5 it's going to go anywhere the blood's going. 6 Q Okay. So by that time, benzene has 7 metabolized into the blood and into the bone marrow, 8 correct? 9 A By that time, the metabolites have left 10 the liver. Some of those have been conjugated, and 11 they're being excreted. That's part of this process 12 because that's how they get transported to the 13 liver -- to the kidneys and throughout. Some of them 14 are in transit anywhere that the blood is taking 15 them. And then there are specific enzymes in the 16 bone marrow that can take those metabolites and 17 further metabolize them. 18 Q Okay. And so is there a uniform or a -19 is it the same rate of benzene metabolism among 20 everyone? 21 A No. 22 Q Okay. That differs? 23 A Absolutely. 24 Q Okay. A kid who weighs 20 pounds at 25 infant age compared to a pro football linebacker, 60 1 they're going to metabolize benzene differently, 2 right? 3 A Probably not; probably not. 4 Q Probably not? 5 A No. 6 Q Not differently? 7 A No. 8 Q Where are we missing each other? 9 A Well, I said that people can be different, 10 and they can. Your question posed, is it because of 11 age or because of weight. And those two things -12 after a certain age, children express the same 13 profile of enzymes that the pro football players are 14 going to express on a per gram basis. And so they're 15 going to be, on a per gram basis, equally -- they 16 have an equal ability to metabolize benzene. So 17 based on those two, on the information you provided, 18 there's no evidence to think that they would handle 19 it any differently. 20 Q Okay. What about men who are in their 20s 21 and 30s and 40s, they have different diets, they're 22 different weights, they're different races, are there 23 similarities or are there differences in the 24 metabolic rates of benzene for those individuals? 25 A There's not -- let's try to talk a little 61 1 more specifically. The first metabolic step and the 2 most important step in the so-called bioactivation of 3 benzene -- because benzene is not toxic. You 4 understand that? It has to be metabolized to be 5 toxic. Okay. That first metabolic step, that first 6 step that it takes is catalyzed by an enzyme 2E1. It 7 doesn't matter what it does, why it's doing it. But 8 about 2E1 expression does not seem to change from 20 9 to 30 to 40. 10 Now, there are other enzymes in the 11 process of how benzene is metabolized. It's a very 12 complicated process. Some of those steps we have 13 found. "We" being the scientific community -- that 14 there are racial differences. African-American is 15 not one of them, but there are some differences. 16 Asian populations have a different expression of 17 those enzymes and, as such, they will metabolize 18 benzene -- potentially metabolize it differently. So 19 it certainly can happen. Your examples just aren't 20 good examples of where it would happen. 21 Q Okay. Do Asians metabolize benzene such 22 that -- how do you explain it as far as more harmful 23 or less harmful when comparing Asian to white 24 Americans, let's say? 25 A There is an enzyme called NQ01, and NQ01 62 1 is something that is thought to be a detoxification 2 step. So 2E1 is making toxic metabolites. NQ01 3 detoxifies those metabolites. If you have a mutation 4 in NQ01, then you have a reduced ability to detoxify 5 the metabolites. 6 Q Okay. So -7 A As such -8 Q Go ahead. 9 A -- then it's going to ostensibly be more 10 toxic. That mutation is present in a higher percent 11 of the Chinese population than it is in the U.S. 12 population. So based on that one end point alone, 13 you would say that Chinese people, the population, 14 they have a reduced ability to detoxify benzene. So 15 ostensibly they could be more susceptible to benzene 16 toxicity. 17 Q Asian folks are more susceptible to the 18 toxicity of benzene, correct? 19 A Chinese, if they have that mutation in 20 that enzyme. 21 Q Depending on little -- depending on 22 individual characteristics in their DNA? 23 A Sure. 24 Q Okay. Would you agree with me -- you said 25 earlier that individual susceptibility varies, 63 1 correct. 2 A Yes. 3 Q Would you agree with me that individuals 4 in the U.S., whether Hispanic or African-American or 5 white, based on other biological factors, DNA, what 6 have you, different people -- their ability to 7 detoxify or get rid of the harmful benzene before it 8 gets into the bone marrow, that's going to differ 9 among people, right? 10 A You certainly see a kind of a dose 11 response relationship anytime you look at 12 populations. 13 Q My question isn't -14 A I'm getting there. 15 Q I don't mean to cut you off. Okay. 16 A So this dose response relationship, say, 17 with benzene toxicity, it is likely due to variations 18 in these various enzymes that we're discussing. We 19 don't know what all those are so I can't tell you 20 definitively, yes, here is a profile of a person who 21 is going to be more susceptible or less susceptible 22 to benzene, with the exception of NQ01. That is one 23 that we sort of have a pretty good handle on. 24 Q For Asian folks, for Chinese people? 25 A Well, it would be the same. They just 64 1 have a higher population -- they have a percentage of 2 that mutation in their population. In the U.S. it's 3 about 5 percent. So 5 percent of the U.S. population 4 would possess that mutation and based on that one end 5 point alone could be susceptible -- more susceptible 6 to benzene toxicity. 7 Q Folks in the U.S. who have the NQ1 (sic) 8 mutation are more susceptible to benzene toxicity, 9 correct? 10 A Benzene toxicity. 11 Q Okay. And that makes up 5 percent of the 12 U.S. population? 13 A That's correct. 14 Q How do you find out if someone has an NQ1 15 mutation? 16 A NQ01. 17 Q NQ01. 18 A That's fine; get some DNA and look for it. 19 Q And those people who do have that 20 mutation, benzene is more likely to hurt them than 21 the people without the mutation? 22 A I mean, there is a study that suggests 23 that. It's not the strongest piece of evidence in 24 the world. But I don't know many people who have 25 done research on benzene that do not believe that 65 1 it's meaningful. But the degree of vulnerability 2 does not appear to be very much. I mean, so there's 3 a lot of caveats to it, but it does appear to hold 4 true. 5 Q It has some merit? 6 A I think it does, yes. 7 Q Okay. When did this NQ01 thing first -8 when was it first realized or understood by industry? 9 A By industry? I can't answer that. 10 Q Ten years -11 A I can tell you -12 Q -- ago? 20 years ago? 13 A -- it was first published. 14 THE REPORTER: Excuse me. 15 THE DEPONENT: Sorry. 16 Q (By Mr. Patton) What year was that first 17 published? 18 A Probably the mid, early '90s is when 19 people started recognizing the importance -- then it 20 was called DT diaphorase, the same enzyme. People 21 started recognizing that there were differences in DT 22 diaphorase that impacted on this ability to handle 23 chemotherapeutic drugs. And then there was a pretty 24 important paper that was published in 1997 from 25 research at the University of Chicago, '96, where 66 1 they reported that individuals that had this NQ01 2 mutation had a higher risk of developing leukemia 3 secondary to chemotherapy. 4 Q And is that akin to developing leukemia 5 secondary to benzene? Doesn't chemotherapy and 6 benzene act similarly? 7 A That certainly would be debatable, 8 depending on who you were asking, but I believe 9 there's some -- there is some value in evaluating the 10 chemotherapeutic literature with regard to 11 understanding what benzene is doing. 12 And then there was one more piece. NCI 13 researchers evaluated -- and this was '99 or 2000 14 where at high exposures, 30 PPM time weighted average 15 and up, they saw an increased hematotoxicity 16 associated with benzene exposure in those workers. 17 So the final step, does this mutation actually 18 increase a person's ability -- increase their risk of 19 developing AML from benzene, that hasn't been done. 20 But, you know, the pieces are all lining up, and I 21 believe it's a legitimate theory. 22 Q So in the late '90s there were two 23 studies, and they examined the role of this NQ01 as 24 increasing someone's likelihood of receiving the 25 harmful effects of benzene because they can't 67 1 detoxify it as quickly, correct? 2 A The first study was looking at the risk of 3 secondary leukemia following chemotherapeutic agents, 4 nothing to do with benzene. 5 Q Okay. And then the second study -- what 6 was it, again? 7 A The second study was looking at 8 hematotoxicity as evidenced by cytopenias, which we 9 talked about earlier, and whether people that have 10 this mutation, whether they have an increased 11 susceptibility to this cytopenia. And at high 12 exposures, it appeared that they did. 13 Q Okay. The combination of which increases 14 someone's -- based on their genetic factors, it 15 increases their likelihood of getting a secondary 16 leukemia from benzene or even chemotherapy 17 therapeutic agents, correct? 18 A The first part of that would be 19 speculation; supportable, but still speculative. The 20 second part of that, I think Richard Larson's group 21 pretty convincingly demonstrated, and that was the 22 chemotherapy. The benzene is speculative. The 23 chemotherapy I think is pretty solid. 24 Q And you think because they act similarly 25 enough it lends itself to being instructive on 68 1 benzene? 2 A I would think so, yes. 3 Q It's helpful to determine what folks might 4 be extra susceptible to get a secondary leukemia from 5 benzene exposure, true? 6 MR. PERRY: Object to form. 7 A Well, I mean, no. It wouldn't be helpful 8 at all if there's no evidence that anyone is going to 9 be exposed to the levels of benzene that can cause 10 leukemia, so there would be no real value in knowing 11 that. I don't even think -- you know, from an 12 academic point of view, it was very interesting. But 13 even knowing that in the clinic, you've got to treat 14 these patients. So whether you think they have an 15 increased risk of developing leukemia from your 16 treatment or not, they're not not treating them with 17 these chemotherapeutic drugs because they're going to 18 die of the primary malignancy. So it's interesting 19 academically, but I don't know that it has that much 20 bearing. 21 Q Can you examine a person's breath and 22 evaluate their level of benzene, the level of benzene 23 being metabolized by their body? 24 A The level of benzene being metabolized? 25 Q Well, let me ask a better question. 69 1 A I don't know the answer to that. 2 Q If someone is drinking alcoholic 3 beverages, they can take a Breathalyzer and you can 4 evaluate the blood alcohol content of that person, 5 correct? 6 A Yes. 7 Q Okay. Can you examine a person's breath 8 and learn anything about benzene? 9 A You might be able to if you did it really, 10 really quickly. But you blow off benzene really 11 fast. So, you know, if you look in my breath today, 12 you might can say what might be in this room or what 13 I might have been exposed to when I went to the 14 restroom, but you're not going to learn anything 15 about what I was doing yesterday. 16 Q Okay. But if we took a snapshot of your 17 breath yesterday, we could tell if you were being 18 exposed to more benzene, correct. 19 A Perhaps. 20 Q Okay. So like today you're sitting in a 21 hotel conference room. If we were to detect your 22 breath, you certainly wouldn't -- would you -- or 23 would you expect to find any appreciable amount of 24 benzene? 25 MR. PERRY: Object to form. 70 1 A Yeah. I don't know what mean by -- you 2 could measure it. 3 Q (By Mr. Patton) Okay. 4 A You certainly could measure it. 5 Q Okay. And then what if tomorrow you and I 6 go work on a gasoline loading rack and we top-load 7 without vapor recovery? Could we then evaluate our 8 breath and determine how much benzene is being 9 exhaled? 10 MR. PERRY: Object to form. 11 A Yes. You could certainly measure the 12 benzene that would come out of a person's breath, no 13 matter what they're doing. 14 Q (By Mr. Patton) Okay. But you're saying 15 that it happens quickly, such that you have to take 16 the snapshot kind of as it's happening? 17 A I don't actually know the kinetics so it 18 wouldn't have to be instantaneous. But it's not 19 going to stick around very well. 20 Q Okay. And then what about someone's 21 blood? Can you evaluate people's blood to determine 22 the benzene metabolism or benzene toxicity being 23 experienced at a given moment in time? 24 A You asked two questions. 25 Q Can you answer them both? 71 1 A Not together. We actually believe now -2 we've looked at urinary metabolites. We've looked at 3 all these different things. They're not specific. 4 There's problems with them. What seems to be the 5 best way at this point to biomonitor people for their 6 exposures is benzene in blood. Because if they have 7 benzene in their blood, then it had to have come from 8 benzene externally. If you see these metabolites in 9 their urine, maybe it came from benzene. Maybe it 10 came from the fact that they ate tuna fish the night 11 before. So there's all kinds of problems 12 interpreting it. So benzene in the blood does seem 13 to be the best biomarker for -- you know, exposure 14 marker with the caveat that it also is very quickly 15 metabolized so you've got to do it fast. 16 Q Are there -- I don't want to say 17 standards, but are there -- is there information out 18 there indicating the importance of benzene levels 19 when detected in the blood? Like how are they 20 measured? 21 A That's a great question. The only -- the 22 only chemical that is regulated today based on 23 internal levels is lead. So they say, Okay, you've 24 got too much lead in your blood. We need to kelate 25 you. You need to get out of this apartment complex, 72 1 you know, whatever -- whatever the situation is. 2 All the other chemicals, benzene included, 3 is regulated on external concentrations. So at this 4 point we can't say definitively if you have this much 5 benzene in your blood, you have been overexposed, or 6 here's what your exposures were. All the regulations 7 are external concentrations, how much benzene is in 8 the room. Five years from now, 10 years from now, 9 maybe it changes. We certainly understand the 10 pharmacokinetics -- well, I wouldn't say that. We 11 might at some point be able to understand the 12 pharmacokinetics of benzene to be able to make that 13 extrapolation, but right now we don't. We can't. 14 Q How did we -15 A Sorry -- the scientific community. 16 Q I'm with you on that. 17 How did the scientific community 18 ultimately arrive at those lead numbers? 19 A That's a good question. I don't know the 20 answer. I mean, I would guess that it was through 21 animal data and extensive epidemiological research 22 and looking at various children exposed to these and 23 doing these subtle cognitive tests. 24 I mean, at a certain height, a hundred 25 micrograms per deciliter, people are sick. So, you 73 1 know, at those levels it's easy to say, You've got 2 too much lead. We need to get it out of you. 3 At 10 micrograms per deciliter, you know, 4 there's not going to be any overt manifestation of 5 that so it's a much harder question to answer. 6 Q If the oil and gasoline producers or 7 manufacturers and the API, if they wanted to 8 determine the amounts of benzene in blood which 9 correspond with certain levels of exposure, external 10 exposure and safe limits and things of that nature, 11 do you believe the chemical companies and the API 12 have the amount of resources to figure that out? 13 MR. PERRY: Object to form. 14 A I'm not sure. I mean, it's not a matter 15 of -- there is a lot of research going on right now 16 on benzene metabolism. There's several people -17 that's what we did in this Munich meeting. People 18 from all over are researching benzene and its 19 metabolism. So it's not -- it's just a very 20 complicated -- it's a very hard question. 21 Q (By Mr. Patton) The scientific community 22 at some point years ago decided to evaluate lead, and 23 reached conclusions -- they performed studies and 24 they reached conclusions, and they decided what a 25 safe amount of exposure to lead was, right, or what 74 1 an acceptable amount of exposure is -2 A That's -3 Q -- in the blood? 4 A That's true. 5 Q Okay. Are you aware of any efforts by the 6 oil and gasoline companies and/or the API to evaluate 7 the amount of exposure or the amount of benzene in 8 the blood to determine more acceptable or safer 9 levels of exposure? Are you aware of any efforts by 10 the API right now? 11 A Yes. 12 Q With that end goal? 13 A We're doing it. 14 Q Are you doing it with the end goal of 15 increasing regulations? 16 A Well, we're doing it with the end goal of 17 understanding the relationship between benzene and 18 blood and what the external -- what a regulatory 19 limit would look like. What we're doing is 20 calculating what's called -- what we call a 21 biomonitoring equivalent, looking at internal blood 22 levels and how they would correlate with external 23 concentrations. 24 Q And is it your position that that research 25 is being done to find a regulatory limit? Is that 75 1 the purpose of the research? 2 A We have regulatory limits. We have all 3 kinds of regulatory limits. We have environmental 4 limits. We have occupational limits. There's all 5 kinds of limits for benzene. What we're doing is 6 trying to take those regulatory limits and say, okay, 7 if a person was exposed to what EPA says is safe -8 we're all exposed to benzene all the time, right? So 9 if a person was exposed to what EPA says, this is 10 okay, this is -- you're all right with these levels 11 of benzene, how much benzene in the blood would you 12 see. That's what we're trying to determine. 13 Q Okay. 14 A So then if you have benzene in the blood, 15 then I could say, Okay, based on this calculation, 16 EPA would say -- so we're doing exactly what you were 17 asking with lead. The internal concentration of lead 18 in blood correlates with an external exposure. 19 That's exactly what we're doing with benzene. 20 Q Is industry funding that? 21 A Yes. 22 Q Okay. Did you -- would you anticipate 23 that the results of all the scientific activity which 24 industry is a part of, do you anticipate that 25 industry would support lower levels of exposure to 76 1 benzene at the end of that research some? 2 MR. PERRY: Object to form. 3 A Would I -- would they support it? 4 Q (By Mr. Patton) Correct. 5 A Well -6 MR. PERRY: Object to form. 7 A I'm trying to think. I don't see how what 8 we're doing could ever -9 Q (By Mr. Patton) Let me ask the question a 10 little differently. 11 A Okay. 12 Q Let's say the scientific community reaches 13 conclusions about the amount of benzene detectable 14 when found in certain types of workers' blood. 15 A Okay. 16 Q And the scientific community says, Hey, 17 these people are being overexposed, okay, and we can 18 quibble about that term. But the scientific 19 community says if someone has X amount of benzene in 20 their blood, they're being exposed to too much 21 benzene, okay? 22 A Yes. 23 Q Then let's say the scientific community 24 went to the government and said, Hey, we suggest 25 increased safety limits to better protect workers by 77 1 evaluating benzene in the blood. Okay. Are you 2 following me? 3 A Uh-huh. 4 Q Would you anticipate that industry would 5 be onboard with those stricter safety requirements, 6 or would they oppose those stricter safety 7 requirements, based on your experience with industry? 8 A I think that would depend 100 percent on 9 the strength of the science that was presented on 10 behalf of, you know, this scenario that you just 11 described. I mean, if that science is unequivocal 12 and we all agree, yeah, this is -- this is pretty 13 solid, no, I don't think they would -- I don't think 14 they would oppose it. 15 If it is not unequivocal and there are 16 holes in it, they may not oppose it, but they may 17 say, you know, we don't know that that's true, and we 18 need to do these other things to fill up those data 19 gaps. 20 Q And what did industry do in that regard in 21 the late 1970s with benzene? Can you explain that 22 process, how it kind of compares to the scenario I 23 set forth? 24 MR. PERRY: Object to form. 25 A I can't. I wasn't around then. Sorry. 78 1 Q (By Mr. Patton) OSHA wanted to increase 2 workers' safety by decreasing the acceptable amount 3 of benzene exposure in the late 1970s, correct? 4 MR. PERRY: Object to form. 5 A That's my general understanding, yes. 6 Q (By Mr. Patton) You weren't around back 7 then, but that's your understanding, right? 8 A Yes. 9 Q And industry opposed those stricter 10 guidelines, correct? 11 A I think that's a simplistic view, but yes. 12 I mean, ultimately they opposed it for, you know, 13 whatever their scientific reasons were. 14 Q Okay. Did you know that part of the 15 reason that they opposed it was because they were 16 concerned about the gross national product? Did you 17 know that? 18 A I did not. 19 MR. PERRY: Object to form. The Supreme 20 Court of the United States opposed it, too, and 21 rejected it. 22 Q (By Mr. Patton) I'll show you what I'll 23 mark as Exhibit 5. Have you ever seen this document 24 before? 25 (Exhibit 5 marked.) 79 1 A No. 2 Q (By Mr. Patton) Can you take a minute to 3 read through it? 4 A The whole thing? 5 Q Well, if you want to read the whole thing, 6 that's fine. But I want to point your attention to a 7 couple portions. 8 A Yeah. If you're going to quiz me on it, 9 I'd like to read it. 10 Q Okay. 11 A (Deponent examined exhibit.) 12 Q Actually, Doctor, I don't -- let me -- I'm 13 not going to ask you a question. I want to give you 14 a chance to read it. 15 A Okay. 16 Q But what I'd like to do is if I can give 17 you that document and another document, and then 18 we'll take -- and then I'll let you read them and 19 then ask you some questions after that. Can we do 20 that? 21 A Sure. 22 Q Okay. And I will show you what I will 23 mark as Exhibit 6, and this is an article called 24 "Benzene: an historical perspective on the American 25 and European occupational setting." This is a study 80 1 by Dr. Infante. Are you familiar with this? 2 A No. 3 Q Have you ever seen that article before? 4 A No. 5 Q Okay. What I'd ask you to do is, I'd like 6 to go off -7 A This isn't an article. This is a book 8 chapter. 9 Q Okay. What I'd like to do is go off the 10 record, and I'd ask you to do two things. With 11 Exhibit 5, the Shell Views paper, if you could read 12 that. 13 A Okay. 14 Q And then with respect to Exhibit 6, if you 15 can go through each paragraph -- and do you consider 16 yourself an expert on benzene? 17 A I consider myself an expert on benzene 18 toxicology -19 Q Okay. 20 A -- not historical activities associated 21 with the regulation of benzene. 22 Q Okay. Can you go through this Exhibit 6 23 and mark next to each paragraph agree, disagree, or 24 no opinion? Can you do that for us? 25 A I'll try. 81 1 Q Okay. Let's go off -2 A Each one of the paragraphs? 3 Q Yes, sir. 4 A Okay. 5 MR. PATTON: Let's go off the record. 6 THE VIDEOGRAPHER: We're off the record at 7 11:11. 8 (Recess from 11:11 a.m. to 11:48 a.m.) 9 THE VIDEOGRAPHER: We're back on the 10 record at 11:48. 11 Q (By Mr. Patton) Dr. Pyatt, if you could 12 take a look at Exhibit 5, turn to Page 6. Did you 13 have a chance to read this document during the break? 14 A Yes. I read both of them. 15 Q Would you look at Page 6, please. It says 16 6 in the lower left-hand corner right there. 17 A Okay. 18 Q Do you see near the top in the left-hand 19 corner -20 A What am I looking for? 21 Q The paragraph beginning "Certainly." Do 22 you see where it says, "Certainly we are not 23 considering maintaining exposures that are clearly 24 unsafe. Such risks are unacceptable and must be 25 eliminated by reducing exposure drastically or, if 82 1 the risk cannot be sufficiently reduced, stop 2 manufacture." Do you see that? 3 A I see that paragraph, yes. 4 Q And then you see it goes on there, and it 5 talks about an example of the benzene case? And then 6 if you look in the right-hand column near the bottom, 7 the paragraph starting, "The industry's argument 8 goes, if all of society's resources were allocated 9 with the cost-ineffectiveness of the benzene 10 standard, the total gross national product would soon 11 be exhausted before making a dent in the vast array 12 of health and safety problems confronting workers and 13 others in our society." 14 This is a position by Shell. It's called 15 a Shell Views, this document on the front page. Do 16 you understand that? 17 A I do. I mean, you skipped over. You kind 18 of picked and choosed (sic) what you wanted to read 19 out loud. You skipped over the paragraph right 20 underneath the "certainly" where it says, We are 21 considering the fact that industries are disrupted 22 and society loses in the long-term when no tangible 23 benefits result from expenditures of large amounts of 24 talent, time, and money. An example of this is the 25 benzene case." 83 1 So what they were describing was that 2 benzene was not related to the paragraph that you 3 read, where clearly there was a health hazard and 4 they were going to stop manufacturing. With regard 5 to this other paragraph that you read down here, I 6 don't -- I don't know what the GNP is. I don't 7 know -- I mean, I can't comment on that. 8 Q Okay. Sir, I'm not implying that they 9 should stop producing benzene or producing gasoline. 10 But my question for you is based on this document, do 11 you believe that Shell's view, as reflected on the 12 front page, is in favor of increased safety or 13 against increased safety, or do you not have an 14 opinion, as a health professional? 15 A I think in 1980, which is when this 16 document was produced, I read this, and I agreed 17 with -- I agreed with it. I thought it was pretty 18 well written, pretty well considered. I think they 19 would be for increased safety. 20 Q You think Shell would be for increased 21 safety -22 A Correct. 23 Q -- even though they joined with the API in 24 opposing increased safety? 25 MR. PERRY: Object to form. 84 1 A Well, that's your interpretation of that 2 argument. And I don't know enough about it to say 3 whether you're right or wrong. But you're 4 interpreting that debate as to whether or not we 5 should be reducing the acceptable amounts of benzene 6 based on leukemia risks that went on in the late '70s 7 and early '80s as these guys saying we don't care 8 about safety. And what they said was, we're not 9 convinced that the science supports that reducing the 10 risks -- excuse me -- reducing the concentration is 11 really going to make any difference in the leukemia 12 risk. 13 Q (By Mr. Patton) As a toxicologist would 14 you agree with me that the less people -- the less 15 workers are exposed to benzene, the less likely they 16 are to suffer leukemia as a result of benzene? 17 MR. PERRY: Object to form. 18 A No. 19 Q (By Mr. Patton) You don't agree with 20 that? 21 A No. 22 Q So if the -- if the whole classification 23 of -- let's say workers who work with benzene, okay? 24 If all the benzene workers in the country, whether 25 gasoline distribution workers or they are refinery 85 1 workers, if somehow, some way, they are exposed to 2 less benzene, what effect do you think that would 3 have on their risk of getting leukemia as a result of 4 benzene? 5 A It depends on how you define "risk." It 6 depends on what the concentrations are. If the 7 concentrations for this population of individuals 8 that are exposed to benzene are not going to increase 9 the risk of leukemia to any meaningful degree, 10 cutting it down by a factor of 10 or a factor of 100 11 or a factor of 10,000 isn't going to impact on the 12 risk because it's not elevated because of those 13 exposures. That's why I disagree with that. 14 Q Do you believe people who work with and 15 around benzene in refineries have an increased risk 16 of getting leukemia, yes or no? 17 A I can't answer that yes or no. 18 Q Do you believe that folks who are gasoline 19 distribution workers who are exposed to benzene on a 20 daily basis have an increased risk of getting 21 leukemia? 22 A Well, that one, there's actually studies 23 that people have exactly answered that question. And 24 the answer is no. They do not have a meaningful 25 increase in their risk of leukemia in distribution 86 1 workers exposed to gasoline. 2 Q What do you mean, "meaningful increase"? 3 A Well, it depends on -- that's why I said 4 it depends on your definition of "risk." If you're 5 going to draw a line through zero and you're going to 6 model benzene leukemia risk as a straight, linear 7 line through zero, then by definition any increase in 8 exposure is corresponding with an increased risk of 9 leukemia. Which means if I eat a banana for 10 breakfast, theoretically I now have an increased risk 11 of leukemia from eating that banana because it has 12 benzene in it. Well, I don't agree with that. 13 But if you are going to take that linear 14 approach, then any exposure, whatever it comes from, 15 Diet Coke, decaffeinated coffee, or loading gasoline 16 into a tanker -- all of those are going to have an 17 increased risk of leukemia just because of your 18 model. 19 Q Occupationally speaking, do you believe 20 that low benzene exposures cause blood effects? 21 MR. PERRY: Objection to form. 22 A Occupationally speaking, do I believe low 23 concentrations of benzene cause blood effects? Okay. 24 What do you mean by "low," and which blood effects 25 are we talking about? 87 1 Q (By Mr. Patton) That's what I'm trying to 2 understand. As a toxicologist, how would you define 3 low level benzene exposure? 4 A We already talked about that. I thought 5 we clarified it. What you're going to say is low or 6 insignificant or toxicologically irrelevant or safe, 7 however you want to describe it, is going to be 8 solely dependent on the end point in question. I 9 mean, what I consider low as far as neurological 10 dysfunction and coma and respiratory distress and 11 passing out, that's a very different level than what 12 I would consider low with regard to cytopenias. So 13 that question, the way you worded it, can't be 14 answered. 15 Q Have you ever seen documents from -- well, 16 first of all, were you provided documents from Shell 17 in this case as far as actual Shell documents, 18 memorandums, studies, memos, things like that 19 discussing benzene and gasoline? Were you provided 20 those? 21 A I was provided as part of the discovery 22 response that had a long list of -- I guess these 23 were lots of gasoline produced, tanks of gasoline 24 produced. I don't know exactly what they were. But 25 it listed all of the benzene content of all of that 88 1 gasoline that Shell produced. And that was part of 2 the discovery. That's the only thing that I have. 3 Q Sir, I'll represent to you that some of 4 the documents produced by Shell in this case talk 5 about prolonged exposure to low levels of benzene. 6 Have you ever heard that phrase before, prolonged 7 exposure to low levels or low concentrations of 8 benzene? Have you ever heard that phrase? 9 A I've heard all those words, sure. 10 Q Okay. Have you heard the phrase? 11 A All the words put together, prolonged -12 yeah, sure. 13 Q Okay. Do you know what that means? 14 MR. PERRY: Object to form. 15 Q (By Mr. Patton) What is meant by the word 16 "prolonged" in that phrase, and what is meant by the 17 term "low levels of exposure"? 18 MR. PERRY: Object to form. 19 A No. 20 Q (By Mr. Patton) Have you ever asked Shell 21 what they meant by prolonged exposure to low levels 22 of benzene? 23 A I have had no reason to do that. 24 Q Do you believe there's an increased risk 25 for AML in persons exposed to more than 20 part per 89 1 million years cumulative dose exposure in the 2 workplace? 3 A I don't believe there's an increased risk 4 of AML at those exposures to gasoline. 5 MR. PATTON: Objection, nonresponsive. 6 MR. PERRY: You didn't specify. You 7 didn't say "gasoline" or "benzene." 8 A You didn't. Sorry. 9 Q (By Mr. Patton) I know. I'll ask a new 10 question. 11 A Okay. 12 Q Sir, do you believe there's an increased 13 risk for AML in individuals exposed to greater than 14 20 part per million of benzene exposure? 15 A The way you worded it, yes. At something 16 greater than 20 PPM years, there will be an increased 17 risk. The critical question is at what level above 18 20 are you going to start seeing that increased risk. 19 So I don't believe that 21 will get you there, but 20 somewhere above 20, yes, you're going to have an 21 increased risk of developing AML. 22 Q Okay. If someone -- can somebody be 23 exposed to 20 part per million benzene by working 24 in a -- 20 part per million cumulative dose of 25 benzene from working in a refinery with pure benzene? 90 1 Is that plausible, that someone might be exposed at 2 that level over their career? 3 MR. PERRY: Are we talking PPM years or 4 PPM time weighted average? 5 Q (By Mr. Patton) Let me ask a different 6 question. First of all, let me back up. 7 Have you seen -- do you have any -- have 8 you seen any information in this case as to how much 9 benzene Raul Zendejas was exposed to in the course of 10 his work? 11 A The only thing that I've seen that was not 12 just the published literature, but -- the only thing 13 that I've seen is a report written by your -- by 14 Stephen Petty. 15 Q Let me ask a more clear question. Have 16 you seen any information in this case besides the 17 report from Steve Petty which discusses specific to 18 Raul Zendejas how much benzene he was exposed to? 19 A Well, I mean, we know -- we know -- "we" 20 being the scientific community -- there are papers 21 out there regarding what people that are loading 22 trucks with gasoline, what their potential exposures 23 could be. We know what the background exposures are. 24 I mean, there's information, but I haven't seen 25 anything specific to Mr. Zendejas. 91 1 Q Besides the report from Petty? 2 A Right. 3 Q As we sit here today, do you have any 4 opinions on the range of exposure to benzene commonly 5 experienced by gasoline distribution workers? 6 A That is outside of my area of expertise. 7 But I will tell you that irrespective of what those 8 end up being, the literature is pretty clear that 9 those workers do not have an increased risk of 10 leukemia. So whatever it is, it's going to be 11 something less than a threshold amount where you're 12 going to start seeing an increased risk of leukemia, 13 AML, in the literature. 14 Q The report by Steve Petty indicates that 15 Raul Zendejas was exposed to an estimated amount of 16 25 PPM year cumulative dose to benzene. Is that your 17 understanding of his report? 18 A That's my understanding of his report. 19 Q Do you have any reason to disagree with 20 his report? 21 A Yes. 22 Q What are those -- what are your opinions 23 in that regard? 24 A Well, in order for that to have occurred, 25 since most of that exposure that I could tell, 92 1 reading his report -- in order for that to have 2 occurred, most of that is going to occur in the last 3 two years of his career when he was driving a truck, 4 which means that his time weighted average exposures 5 would have had to have been 10 part per million over 6 an eight-hour time weighted average. 7 That's unbelievable. That just is not 8 scientifically defendable. He wouldn't be able to 9 defend it. It's not defendable. Those levels of 10 exposure are higher than most people working in the 11 Pliofilm cohort where they were actually using pure 12 benzene, 100 percent benzene, as a solvent, spreading 13 it out on a table, letting it evaporate. Those 14 people didn't have exposures like that, the vast 15 majority of them. So to think that he did it from 16 loading gasoline in a tanker truck three times a day, 17 twice a day, however often he did it, is just not 18 scientifically believable. 19 Then when you go and say, Okay, well, that 20 clearly is exaggerated, why is it exaggerated? Well, 21 the math I don't know. I mean, that's -- somebody 22 else is going to deal with that. But he clearly has 23 exaggerated on the amount of benzene that is in the 24 gasoline. He assumes 2.4 percent. And the data that 25 I looked at, that's incorrect. This was part of the 93 1 discovery so I'm assuming that it was available for 2 everyone. I mean, I didn't see but just one or two 3 where it was over 1 percent; most of the gasoline 4 that was produced for this area, .7, .6, .5 percent 5 benzene. So if it's .5 and he's estimating 2.5, 6 there's a -- there's a 20 percent -- an 80 percent 7 exaggeration of what it could possibly be. 8 Then he mistook -- I'm doing this from 9 memory. But he read something that Mr. Horton said 10 that he had done in his career, and he extrapolated 11 and said that Mr. Zendejas had done that same thing, 12 spilled gasoline on himself a hundred times. That's 13 incorrect. And at least in one of the calculations 14 that he had done, he did not account for the fact 15 that Mr. Zendejas was not working with gasoline 16 100 percent of the time, but only -- I think by his 17 own estimation, only 20 percent of the time, and the 18 rest of it was diesel fuel. 19 So all of those things combined, plus 20 whatever was going on in the Monte Carlo part that I 21 didn't evaluate, it is a gross overestimation of what 22 his likely exposures were. 23 Q Your opinion is that Dr. Petty's opinions 24 are -- Steve Petty's opinions are a gross 25 overestimate of Raul's exposure? 94 1 A Yes. 2 Q Do you have any opinions on what would be 3 a fair estimate of Raul's exposure? 4 A Something much less than that. I mean, 5 even if you just take the factors that I just told 6 you, you know, you divide that by 5; okay, 5 PPM 7 years, even that's really high. That's a lot. Over 8 an eight-hour time weighted average, it takes a lot 9 of benzene to get those numbers up. But even that I 10 think is probably too high. 11 Q Have you seen any data from Shell 12 estimating the amount of cumulative dose of benzene 13 Raul may have experienced in his work? 14 A From Shell? 15 Q Yes, sir. 16 A I have not, no. 17 Q Have you seen any evidence or any 18 documents from Shell of any air monitoring performed 19 at facilities similar to the McNeece Brothers 20 facility? 21 A That I couldn't tell you. I haven't seen 22 it, but I think it exists. 23 Q Have any Shell experts provided you with 24 any numbers or estimates of how much benzene Raul was 25 exposed to in his work? 95 1 A Not at this point. I haven't specifically 2 asked for that. 3 Q Are you an industrial hygienist? 4 A No, sir. 5 Q Have you ever performed an exposure 6 analysis where you've estimated how much benzene 7 someone is exposed to while working with gasoline? 8 A Yes. Actually, I have. 9 Q Tell us about that. 10 A Well, I mean, I was kind of on the 11 sideline, but it was looking at what people using 12 chainsaws -- tree trimmers using chainsaws with 13 gasoline -- gasoline-driven chainsaws, what their 14 personal exposures to benzene would be from using a 15 gasoline-driven chainsaw. So we estimated it, 16 they -- we calibrated pumps. We looked at the data. 17 So yes, at least once, but I'm not an industrial 18 hygienist. I don't -- I'm not pretending to be one. 19 Q Have you ever -- are you familiar with 20 Dr. Neitzel? 21 A No. 22 Q Have you ever worked with him before? 23 A No. I'm not familiar with him. 24 Q Have you ever seen any of his work for 25 this case? 96 1 A No. 2 Q Do you have any understanding of what he 3 is going to -- what the purpose of his role in this 4 case is? 5 A Mr. Perry said something to me about it 6 yesterday, but I honestly don't remember, so no. 7 Q Dr. Ijazz Jamall, do you know him? 8 A I do not. 9 Q Have you ever worked with him before? 10 A No. 11 Q Have you seen any of his work in this 12 case? 13 A No. 14 Q Do you have an understanding of what he -15 the subject of his testimony will be? 16 A Yes. 17 Q What is that? 18 A My understanding is that he will talk -19 kind of follow the same lines that he wrote in his 20 paper about why gasoline is not just a vehicle for 21 distributing benzene to people but it is its own 22 unique chemical, and it has its own unique 23 toxicology. And I think he's going to, on a more 24 quantitative basis, evaluate Mr. Petty's report. 25 Q Have you seen any more specific 97 1 evaluations from Dr. Jamall as to Petty's report? 2 A I just understand that he's doing it. 3 Q Did you ask him for that information? 4 A I've never spoken with him. 5 Q What if Raul was exposed to 5 PPM years? 6 What if based on your calculations you cut his 7 benzene exposure from 25 to 5 PPM years? Would he 8 still be at an increased risk of getting leukemia? 9 A Well, I mean, even if you accepted the 10 first number, the 25 PPM years, which I don't, but 11 even if you were to accept that number, that number 12 of benzene doesn't cause CML. So even if we said, 13 This is fine, this is okay, we agree with Mr. Petty, 14 this is what his exposures were likely to be, there's 15 clear literature that those exposures and exposures 16 much higher than that does not increase one's risk of 17 developing CML. 18 Q If I understand your opinions in this 19 case, you're saying we're not talking about AML. 20 You're choosing to talk about CML, correct? 21 MR. PERRY: Object to form. That's the 22 medical diagnosis in the lawsuit. He didn't choose 23 anything. That's the -- every medical doctor agreed 24 the man had atypical CML. 25 Q (By Mr. Patton) Dr. Pyatt, in defending 98 1 industry in this case you have chosen to classify and 2 analyze Dr. (sic) Raul Zendejas' disease as CML or 3 atypical CML and not consider AML in forming your 4 opinions, correct? 5 MR. PERRY: Object. 6 A Well, I always -- I mean, he didn't have 7 AML. He had CML. And that was the consistent 8 diagnosis your experts, our experts, the medical 9 records -- everything says he had CML. 10 Q (By Mr. Patton) Would it be harder for 11 you to defend this case on behalf of industry if it 12 was AML, if it was clear AML? 13 A No. 14 MR. PERRY: Object to form. 15 Q (By Mr. Patton) Why not? 16 A Because gasoline doesn't cause leukemia of 17 any kind, any flavor; AML, CML, ALL, CLL, it doesn't 18 happen. So it doesn't matter from a gasoline point 19 of view whether he had CML or AML or any other type 20 of leukemia or myelodysplasia. Gasoline is not 21 carcinogenic. No one thinks that it's carcinogenic: 22 IARC, ATSDR, ACGIH, OSHA. None of these large 23 regulatory bodies out there that have evaluated all 24 of this science that was in this binder that you set 25 in front of me a little while ago, none of those 99 1 groups think gasoline is carcinogenic. 2 Q Just because gasoline is not carcinogenic, 3 does that mean that gasoline distribution workers who 4 are exposed to higher levels of benzene in their work 5 and work with gasoline all the time, does that mean 6 that they just can't -- they can't get leukemia from 7 benzene exposure? Is that your testimony? 8 A Well, my testimony is there's no evidence 9 that they have. 10 Q Well, hold on a second. First of all, I'm 11 with you that all these government groups, they say 12 what they say, and what they -- they do not classify 13 gasoline as a carcinogen. Okay. I understand that 14 part. I think a jury will understand that part, too. 15 But what I'm trying to understand is if 16 you're telling this jury that just because gasoline 17 isn't designated as a carcinogen, that folks who work 18 with gasoline on a daily basis under unsafe 19 conditions where they are exposed to a tenfold amount 20 of benzene than compared to other loading operations, 21 are you telling the jury that there's no way they 22 could get ben -- could get leukemia from benzene 23 because gasoline's just not a carcinogen? Is that 24 what you're telling us? 25 THE DEPONENT: I thought you were going to 100 1 object. 2 MR. PERRY: Objection. 3 Q (By Mr. Patton) You want him to object 4 because that's a good question, isn't it? 5 A Well, there was just a whole lot of kind 6 of stuff in there -7 Q Well, he had 10 seconds that he could have 8 -9 A -- that we have to -10 THE REPORTER: Excuse me. I need you to 11 go one at a time. 12 THE DEPONENT: Sorry. 13 A I'm not a lawyer. Okay. Lots of things 14 that you said I would have a problem with; whether or 15 not that really represents an unsafe work 16 environment, whether or not they're really -- when 17 you say a tenfold increase, okay, well, tenfold, if 18 the first exposure's really, really low and now 19 you've multiplied it by 10, yeah, it's higher, but it 20 still may be safe. So all of that, you know, I'm not 21 going to agree with. 22 Your question I think, in essence is, is 23 it possible for someone to get enough benzene 24 exposure from gasoline to get leukemia? 25 Q (By Mr. Patton) That's my question. 101 1 A However you want to phrase it, is that 2 possible? And the answer is, I don't know. But what 3 I can tell you is, the scientific literature that has 4 evaluated gasoline workers of all types and 5 denominations, they do not support that an increased 6 risk of leukemia or any other human cancer follows 7 those exposures. That's why OSHA, ACGIH, all of 8 these regulatory agencies do not regulate gasoline as 9 a carcinogen. 10 If that wasn't true and under some extreme 11 exposure conditions you could, in fact, get leukemia 12 from gasoline, that would be represented in these 13 studies, and then these agencies would not take that 14 position. 15 Q Do you have any understanding of whether 16 Raul's exposure to benzene from gasoline was, in 17 fact, extreme conditions? Do you have any 18 understanding of that one way or the other? 19 A He only did it for two years. It was in 20 2004, 2005, 2006. So we're not talking about 21 historical exposures back in the '40s and '50s. I 22 don't know what the numbers are. 23 Q Sir, the man worked from 2000 to 2006. 24 A Well, he was a truck driver from '04 to 25 '06. 102 1 Q Did you -- did you read his deposition? 2 A I did. 3 Q Did you read the other depositions in the 4 case? 5 A Yes. 6 Q Did you see where he testified that he 7 loaded fuel before he was a driver? 8 A That's true. 9 Q Would you agree with me that he's exposed 10 to benzene while loading fuel? 11 MR. PERRY: Object to form. It depends on 12 the fuel. 13 MR. PATTON: On gasoline. 14 A Well, I mean, he's going to be -- there's 15 going to be benzene exposure in any of these things, 16 just like there's benzene exposure from drinking that 17 Diet Coke, so that's a given. But yes, you're right, 18 he did testify that during that four-year period -19 that's fine. Six years. 20 Q (By Mr. Patton) Then why did you say two 21 years earlier? 22 A Well, because I was thinking about being a 23 truck driver and loading gasoline in those big tanker 24 trucks. That's where -- that's where I thought your 25 question was going. 103 1 Q Do you know that he was loading without 2 vapor recovery? 3 A I've seen that. I don't -- I don't know 4 enough about what that means in terms of his 5 exposures. 6 Q Of any of the studies that you brought 7 with you today, do they focus on the group of workers 8 who top-loaded without vapor recovery in extreme 9 heat? Do any of those studies focus on that? 10 A That, I couldn't answer. 11 Q Wouldn't that be the most relevant body of 12 literature, folks who top-loaded gasoline without 13 vapor recovery under the conditions that they did at 14 small bulk terminals -15 A Well, the only -16 Q -- and their incidence of leukemia, rather 17 than just looking at, oh, petrol station attendants? 18 Well, Mr. Zendejas wasn't a station attendant, was 19 he? 20 A Were you done? 21 Q Yes. 22 A Okay. No, he wasn't. But the answer to 23 your question is, you only need to do that if you 24 have -- you have some reason to believe that his 25 exposures were so enormous that these studies aren't 104 1 going to include those. And even your own expert, 2 Stephen Petty, that's not the case. I mean, his 3 cumulative exposures to benzene are well within those 4 that are represented in this binder of gasoline 5 studies so he clearly was not somewhere so far out 6 that these studies don't apply to him. Your own 7 expert would agree with that. 8 MR. PATTON: Let's take a break and change 9 the tape. 10 THE VIDEOGRAPHER: The time is 12:14. 11 We're going off the record. This is the end of 12 Tape 2. 13 (Recess from 12:14 p.m. to 12:20 p.m.) 14 THE VIDEOGRAPHER: We're back on the 15 record at 12:20. This is the beginning of Tape 3. 16 Q (By Mr. Patton) Dr. Pyatt, as a 17 toxicologist and when it comes to testifying in a 18 case like this, do you believe you are biased? 19 MR. PERRY: Object to form. 20 A No. 21 Q (By Mr. Patton) Why not? 22 A Well, I mean, when I was being trained at 23 the University of Colorado, all of the graduate 24 students in toxicology -- we all knew that to one 25 extent or another, all of us would be faced with 105 1 litigation as being part of our professional career, 2 one way or another. And there was a course that 3 several of the faculty taught called toxicology in 4 the courtroom. And I was pretty early in my 5 training, but in that course what they stressed over 6 and over is that irrespective of who hires us, it is 7 our job as toxicologists to give as fair a 8 representation of the science as we can. So I'm not 9 an advocate for you. I'm not an advocate for 10 Mr. Perry. I am an advocate for the science as best 11 as I understand it. And so no, I don't believe I'm 12 biased. I believe the science supports what I'm 13 saying completely. 14 Q What if you wanted to say the opposite, 15 okay, that benzene did cause or contribute to Raul's 16 leukemia, okay? There's two sides to every argument, 17 right? 18 A I guess that's how the saying goes. 19 Q What arguments could you make and what 20 references in the science and references in causation 21 theory and so on and so forth could you point to that 22 support the proposition that Raul's exposure to 23 benzene did cause or contribute to his leukemia? 24 MR. PERRY: Object to form. 25 A That's hard. It's a really hard sell. I 106 1 mean, there are a lot of cases that I've seen, three 2 or four that I've said, I can't really make a 3 determination here. It's just too close for me to 4 call. But this is not one of them. I mean, it's not 5 a benzene case. It's a gasoline case. His exposures 6 to benzene, wherever they came, were from gasoline. 7 The gasoline literature is completely free of any 8 risks of CML. And even AML, I don't believe you can 9 get there. I don't know what studies you could pull 10 out that would support this position. 11 Q (By Mr. Patton) Well, besides studies, 12 let's just think of some arguments, okay? First of 13 all, there is some showing that individuals' 14 susceptibility varies and that some people would 15 argue and some studies may show that there is no safe 16 level of exposure to benzene. Do you agree with 17 either of those principles? 18 A Well, we need to explore that a little. 19 As we discussed earlier, I do believe -- and then 20 provided you with at least one biologically plausible 21 mechanism where that susceptibility could occur. I 22 suspect there are others. We just haven't identified 23 them. 24 Q Raul could have been more biologically 25 susceptible to benzene exposure or to suffer leukemia 107 1 as a result; possible? 2 MR. PERRY: Objection. 3 A It is possible that he could have had an 4 NQ01 mutation and thereby increasing his 5 susceptibility to hematotoxicity. But the levels of 6 benzene were really high in that one study so I don't 7 even think that would necessarily hold up. 8 The other thing that -- the problem with 9 the theory, as I understand your question, is that we 10 now have -- we can explain to some extent this 11 biological susceptibility: NQ01, glutathione 12 transferase, 2E1, epoxy-hydrolase, myeloperoxidase, 13 all these enzymes that have something to do with 14 benzene metabolism and toxicity. So we can start to 15 explain that. But those things are not new. NQ01 is 16 not new. People in the Pliofilm had NQ01 mutations. 17 People in the China study had NQ01 mutations. 18 So when we set a regulatory limit or when 19 we say this is a safe dose or this is how much it 20 takes in order to see toxicity, the people that are 21 getting sick, that are exhibiting that toxicity, they 22 are the susceptible people. So to then take this 23 number of 40 PPM years or 100 PPM years or whatever 24 and say, well, that's really not protecting a 25 susceptible person, is it, I disagree. I think that 108 1 it is. I think that is the basis for those numbers. 2 MR. PATTON: Objection, nonresponsive. 3 Q (By Mr. Patton) Have you seen the Hayes 4 study? 5 A Yes. 6 Q What does the Hayes study tell us about 7 the amount of benzene shown to cause an increased 8 risk of leukemia? 9 A It depends on the form of leukemia. 10 Q You're just going to stratify every 11 question of mine right back out, aren't you? 12 A Well, we can get out the study. That's 13 the way they do it. They stratify out -- there's 14 no -- well, there is actually one category for 15 leukemia. You're right. 16 Q Let's get the Hayes study out. 17 A Sure. This is the whole NCI series. 18 Q First of all, are there any criticisms 19 that you have the Hayes study as a whole before you 20 look to the certain pages of it? 21 A Well, you know, this was a complicated 22 process that was ongoing before NCI, Richard Hayes, 23 and these other guys -- before Martha Linet, before 24 they got involved. The Academy -- Chinese Academy of 25 Preventive Medicine had started this study in the 109 1 '80s. It was a mess. They came in, tried to make 2 sense of this mess, but it was not an easy task. So 3 before I list any criticisms, it's not of these 4 investigators. It's that this was a really difficult 5 task. 6 I think the epidemiology is credible as 7 far as the disease end points, but I think the 8 exposure levels are not credible. So to look at this 9 and say this tells us something about how much 10 benzene it takes to do things, I don't think that 11 it's correct. And in fact, EPA agrees. OSHA agrees. 12 Just about everyone agrees that this is not reliable 13 enough from a quantitative point of view to use for 14 risk assessment purposes or for, you know, regulatory 15 limit setting. So that's my criticism. 16 Q Doctor, I think I can probably shorten 17 your whole deposition here. And I'm going to try 18 to -- try to see to the extent that I can work 19 through it. 20 First of all, have you read Dr. Infante's 21 deposition? 22 A No. 23 Q Why not? 24 A I don't think I have it. 25 Q Have you read any of his work in other 110 1 cases? 2 A Yes. I can't say I've read one 3 specifically in a CML case. 4 Q Have you ever agreed with any of the 5 opinions that Dr. Infante gives in a given case about 6 benzene exposure causing someone's leukemia? 7 A Say that again. 8 Q Have you ever agreed with Dr. Infante's 9 opinion that benzene exposure caused a certain 10 person's certain type of leukemia? Have you ever 11 agreed with that? 12 A That, I don't know. I mean, like I said, 13 there have been some cases where I said, I can't 14 really get involved here. I can't tell you one way 15 or the other. And Dr. Infante may very well have 16 been on the other side. I don't know. To the extent 17 that I have seen his reports or depositions in cases 18 that I've been retained in, no, we have not agreed. 19 Q Have you ever given the opinion in 20 litigation that benzene caused someone's leukemia? 21 A No. 22 Q Have you ever given the opinion in 23 litigation for industry that benzene contributed to 24 someone's leukemia? 25 MR. PERRY: Object to form. 111 1 A I'm not even sure how that would work, so 2 no. 3 Q (By Mr. Patton) Well, for instance, 4 myeloid leukemia's caused by smoking, radiation, 5 chemotherapy drugs, benzene, right? 6 A No. 7 Q You disagree with that? 8 A Yes. 9 Q Why do you disagree with that? 10 A Because myeloid leukemia includes chronic 11 and acute. Chronic leukemia, all of those things 12 that you just mentioned, none of those will work. 13 Chemotherapy doesn't cause chronic leukemia. 14 Cigarette smoking doesn't cause chronic leukemia, the 15 other form of ionizing radiation -- ionizing 16 radiation does so that's one. But the other ones 17 that you mentioned, they don't form, cause, myeloid 18 leukemia. They cause acute myeloid leukemia, not 19 chronic. 20 Q Dr. Gore in this case, did you read his 21 deposition? 22 A Yes. 23 Q What do you agree with in his deposition, 24 and what do you disagree with? 25 MR. PERRY: Object to form. 112 1 A I can't answer -- I can't answer that. I 2 mean -3 Q (By Mr. Patton) Well, let me ask you in 4 an easier way. Is there -5 A I agree that he had CML. I agree that he 6 went into blast crisis. That's what Dr. Gore said. 7 He said he would call it blast crisis. I'd agree 8 with that. I agree with what he said about 9 treatment. I mean, there's lots of things that I 10 agree with. 11 Q What do you disagree with? 12 A I disagree when he said that diesel fuel 13 is a carcinogen. Okay. I'd like to see him prove 14 that in a court of law, that diesel fuel is a 15 carcinogen. So that's one thing I disagree with. I 16 disagree when he says gasoline is a carcinogen. I 17 disagree when he said that all of these things cause 18 CML. No, they don't. So I disagree with the real 19 pertinent issues of his opinion. 20 Q He gives the opinion that benzene caused 21 Raul's form of leukemia, whatever you might choose to 22 call it. You're not a hematologist, right? 23 A I am not. 24 Q Okay. So whatever it is that Dr. Gore 25 chooses to call Raul's complicated disease process, 113 1 he concludes that benzene caused it. And you 2 disagree with that, right? 3 A I do. He calls it the same thing I'm 4 calling it, atypical CML that went into blast crisis. 5 So I agree with him there. There's no disagreement 6 on that front. 7 Q What about Dr. Carroll? He opined that 8 benzene caused Raul's disease. Do you agree with 9 that? 10 A He opined that he believed that his 11 occupation had something to do with it. But when 12 pushed for the literature supporting that, there 13 really wasn't very much. And it looked to me like he 14 was kind of backing off that. 15 Q I believe I saw the Adegoke study in some 16 of your materials. 17 A Uh-huh. I have that. 18 Q Does that support plaintiffs' argument, or 19 does that not support our argument in this case? 20 A Well, it depends on -- that one study 21 shows an increased risk of CML for benzene exposure. 22 Q But Raul was exposed to gasoline, correct? 23 A That's correct. And this actually has a 24 specific type for gasoline, and there is not an 25 increased risk of CML for gasoline. So why would 114 1 anyone ignore the thing that he was really exposed 2 to, which is gasoline, and focus on this other 3 category which really is irrelevant for that study? 4 That doesn't make sense to me. 5 Q Have you ever given your -- given the 6 opinion in your career that exposure to any chemical 7 for a certain person caused a certain resultant 8 disease? Have you ever given that opinion in any 9 context? 10 A Say that again. 11 Q Have you ever given the opinion in your 12 career as a toxicologist that someone -- we'll call 13 them Jim, that Jim's exposure to Chemical X or 14 Substance X caused Disease Y? Have you ever given 15 that opinion? 16 A Yes. 17 Q Can you give us some examples? 18 A There was a situation -- I mean, it wasn't 19 a formal setting, but the guy had -- how did it work? 20 He was having something done in his mouth, and they 21 were rooting out a tooth with hydrochloric acid. And 22 the little dam thing broke, and the hydrochloric acid 23 that they were using on his tooth flooded his mouth, 24 and then he said, I can't taste anything anymore. 25 Q That's pretty simple. 115 1 A Well, you asked for an example. 2 Q No. I -3 A I'm giving you an example. 4 Q I'm not -5 A I think -6 THE REPORTER: Excuse me. 7 A I think the guy's hydrochloric acid 8 exposure caused his loss of taste. 9 Q (By Mr. Patton) Okay. Give me some other 10 examples where you've concluded that a man's or 11 woman's exposure to Chemical or Substance X caused 12 Disease Y. 13 A I'm trying to think of when I've been 14 asked. That's the only time that I can think that 15 anyone has specifically asked. Now, there have been 16 some cases, examples, where people have called me and 17 said, Will you take a look at this, and I say yes. I 18 take a look at it, and they send me the information. 19 And they call me back, and I say, I don't know. 20 It -- maybe it did, maybe it didn't. I don't -- I 21 cannot defend that it did not. And then so -- to my 22 way of thinking I said, yeah, it could be. It could 23 be. So that's happened several times in my career, 24 but it did not happen in this case. 25 Q So if I understand your testimony, 116 1 you've -- besides the hydrochloric dentist example, 2 you've never had an occasion as a toxicologist to 3 conclude that someone's exposure to Chemical X 4 caused -- a 51 percent chance, okay, more likely than 5 not, caused Disease Y? 6 A I haven't. That's just not how my career 7 has progressed. I mean, I was in the lab doing that 8 kind of work, doing risk assessment work, consulting 9 work. It just never has -- you know, I think maybe 10 medical toxicologists or clinical toxicologists like 11 Richard Dart at the Rocky Mountain Poison Control 12 Center, he probably makes those determinations all 13 the time. But I haven't ever been asked to. 14 Q How do you -- can you explain to the jury 15 why you think it is fair for you to give the opinion 16 in this case or as you have in 20 other cases where 17 benzene or other chemical exposure didn't cause this 18 person's certain type of leukemia or other disease 19 when throughout your career you've never given 20 opinions otherwise? How is that fair? 21 A Well, I disagree with that. I have given 22 that opinion otherwise, and I think we just went over 23 that. But what I would tell the jury is, they don't 24 have to take my word for it. We're going to show 25 them the science. We are going to show them what 117 1 ATSDR, what IARC, what all these people say about 2 gasoline. I'm going to show them the studies where 3 people have specifically looked at the kind of 4 disease that Mr. Zendejas has and what exposures are 5 or are not linked to that disease. They don't have 6 to take my word for it. This -- this (indicating) 7 speaks for itself. And that's what my job will be if 8 this goes to trial, to explain to the jury here is 9 this huge body of scientific evidence that does not 10 support that Mr. Zendejas' disease was caused by his 11 occupational exposures. That's what my job will be. 12 Q Do you feel good about your job? 13 A Yes. 14 Q Do you have any opinion as to what 15 occupations outside of a refinery are exposed to the 16 highest levels of benzene? 17 A Today? 18 Q Yes, sir. 19 A Working today, '09, no. 20 Q You don't have any opinions? 21 A I don't know. 22 Q Do you have any opinions as to what 23 occupations do lend themselves to an increased risk 24 of AML or another form of myeloid leukemia? 25 MR. PERRY: Object to form. 118 1 A Well, I don't think the occupation is 2 really the question. So yes, the Pliofilm 3 occupation, for some of those workers clearly 4 increased their risk of developing AML. Some of the 5 shoe workers clearly had an increased risk of 6 developing AML. Rubber workers in some of the older 7 studies clearly had an increased risk of developing 8 AML. 9 MR. PATTON: Objection, nonresponsive. 10 Q (By Mr. Patton) My questions is, as we 11 sit here today do you have an opinion as to what 12 occupations lend themselves to the highest exposures 13 to benzene? Do you have an opinion? 14 A It would be pretty speculative on my part. 15 Q Okay. Do you have an opinion as we sit 16 here today what occupations that people could perform 17 today lend themselves to the highest increased risk 18 of development of AML? 19 A As associated with a benzene exposure? 20 Q Yes, sir. 21 A They would really be essentially the same 22 question. 23 Q And you don't know? 24 A I'm not an industrial hygienist. I just 25 can't really answer that. 119 1 Q Do you have an opinion as to what amount 2 of exposure to benzene is necessary for it to be a 3 causative factor in someone's AML? 4 A Yes. 5 Q Tell us that. 6 A I think the quantitative epidemiology 7 supports 40 part per million years at the low end. 8 Q Okay. Must those people exposed to 40 PPM 9 years be exposed to pure benzene? 10 A No. 11 Q They can be exposed to benzene as a 12 constituent in other chemicals? 13 A Yes. 14 Q But not gasoline, right? 15 A Well -16 Q Is that your opinion? 17 A I don't know that you could achieve those 18 with gasoline, quite honestly, without the other 19 chemicals in gasoline being acutely toxic and someone 20 passing out or dying from it. But gasoline has its 21 own set of epidemiology. So while gasoline has 22 benzene in it, I don't think anyone is ever going to 23 argue that it doesn't. It seems counterproductive to 24 ignore this binder -- wherever it went -- this binder 25 of gasoline studies and say, Well, we're going to 120 1 ignore all this, and we're going to ignore what all 2 these federal agencies said about gasoline, and we're 3 just going to focus on the benzene part of the 4 equation. That doesn't make sense to me. 5 Q What does chronic alcoholism cause in the 6 body? Do you know? 7 MR. PERRY: Object to form. 8 A It can cause cirrhosis of the liver as 9 well as other, you know, nutritional problems and 10 pernicious anemia. 11 Q (By Mr. Patton) If someone were to be 12 diagnosed with cirrhosis of the liver and you found 13 out that they weren't alcoholic, would you be able to 14 give the opinion that their alcoholism caused or 15 contributed to their cirrhosis? 16 A Say that again. 17 Q If someone were -18 A Go ahead. 19 Q If someone were diagnosed with cirrhosis 20 of the liver, okay, and you asked them what about 21 their exposure to -- I'm sorry -- what about their 22 drinking habits and their alcoholism, and they 23 explained to you that they considered themselves an 24 alcoholic and that they were drinking alcohol on a 25 quite frequent basis, would you then draw the 121 1 conclusion or give the opinion 51 percent that their 2 alcoholism caused or contributed to their cirrhosis? 3 Would you give that opinion? 4 A Probably. But without having reviewed 5 that literature -- I mean, I don't know if there's a 6 clear-cut dose response relationship. I don't know. 7 So I don't know whether there's -- you know, maybe 8 someone can be an alcoholic their whole life but not 9 consume enough alcohol to give them cirrhosis. I 10 don't -- you know, the term "alcoholic," okay, that 11 implies some kind of psychological dependency on the 12 alcohol. Maybe that occurs at lower levels. I don't 13 know the answer to that. But I do know that alcohol 14 at sufficient quantities can cause cirrhosis of the 15 liver, so certainly they have causation. 16 Q Okay. What if they told you that they 17 were drinking only Jack Daniels? 18 A That wouldn't matter. 19 Q Why not? 20 A Well, because my understanding of the 21 alcohol literature, which is very different than 22 gasoline with benzene in it, but my understanding of 23 the alcohol literature is that we can see that people 24 who live in Germany and who drink beer, they get 25 cirrhosis. We can see people that live in Italy and 122 1 drink mostly wine, they can get cirrhosis. We can 2 see people in Russia that drink mostly vodka, they 3 end up with cirrhosis. So it's not the water or the 4 orange juice or the hops or the barley or the grapes. 5 It's the ethanol that's doing it. That's a very 6 different situation than the benzene in gasoline. 7 Q Can you tell us as we sit here what the 8 range of benzene exposure estimated in these gasoline 9 studies is? 10 A What the range of benzene -- no, not 11 sitting here. I mean, it's in some of them. We 12 could pull them out and look. 13 Q You just believe that Raul was not exposed 14 to enough gasoline to cause significant benzene 15 exposures that would cause his leukemia? Is that 16 your opinion? 17 MR. PERRY: Object to form. 18 A Well, what I believe is the scientific 19 literature does not support that gasoline exposure at 20 any level causes CML. 21 Q (By Mr. Patton) Have you seen scientific 22 literature that studies benzene exposure in the 23 context of gasoline distribution workers at small 24 bulk terminals? 25 A I think I have, but I would have to look 123 1 through the literature to see. I mean, there's -2 Otto Wong looked at 18,000 distribution workers. 3 Lesley Rushton looked at 20,000 distribution workers. 4 Rob Schnatter looked at distribution workers. 5 Sorahan looked at distribution workers. I've got to 6 believe that a lot of those people that they pulled 7 into those studies would fit into that category. 8 Q Are there any criticisms of the Wong study 9 that you just mentioned? 10 A I think you can probably find criticisms 11 of every paper. 12 Q Do you believe that the less a gasoline 13 distribution worker is exposed to benzene, the safer 14 he is? The better off he is? 15 MR. PERRY: Object to form. 16 A That the less a gasoline distribution 17 worker is exposed to benzene, the better off he is? 18 Q (By Mr. Patton) Let me ask it in a 19 different way. 20 A Okay. 21 Q Let's say we have two gasoline 22 distribution terminals 10 miles away from each other, 23 okay, and at one of the terminals the men are loading 24 in -- they're loading with vapor recovery, okay. 25 That's to mean they are exposed to fewer gasoline 124 1 hydrocarbon and benzene vapors than the guys working 2 at Terminal No. 2, okay? At Terminal No. 2 they're 3 top-loading without vapor recovery. They're being 4 exposed to more benzene and hydrocarbon vapors. And 5 I'll represent to you, sir, that the evidence from 6 Shell in this case shows that the folks at Terminal 7 No. 2 are exposed to more benzene, generally 8 speaking. 9 A Okay. 10 Q Would it -- do you believe it's safer to 11 work at Terminal 1 or safer to work at Terminal 2? 12 MR. PERRY: Objection. 13 Q (By Mr. Patton) From a general sense, can 14 you give us any answer on that? 15 MR. PERRY: Objection to form. 16 A With the situation as you described it, 17 there would be no way for me to answer it. We're all 18 exposed to benzene. If the benzene exposures in this 19 terminal over here, the one with the lack of vapor 20 recovery, top-loading, whatever you said, if those 21 exposures are not harmful and there's no evidence 22 that those exposures matter from a toxicological 23 point of view, then they're just as safe as these 24 other people. 25 Q (By Mr. Patton) Right. That's what I 125 1 thought your answer would be. Your answer is that 2 under no circumstances can gasoline -- can benzene 3 exposure from gasoline cause someone's leukemia; is 4 that your opinion? 5 A Well, my opinion -- and you've already 6 asked that. My opinion is the scientific literature, 7 as illustrated by this binder -- and I don't think 8 there's any other one -- does not support that 9 gasoline is a risk factor for leukemia. 10 Q Right. So it doesn't matter how much 11 benzene the guys at Terminal 2 are being exposed to? 12 It's just not a factor? That's your opinion, 13 correct? 14 A That's what the literature would state, 15 yes. 16 Q I'm asking you what the literature states, 17 sir. I'm asking you your opinion in this case. 18 A But my opinion is based on the literature. 19 They're not separate. 20 Q Then tell me that. Say my opinion is that 21 under no circumstances can someone's exposure to 22 benzene via gasoline be a factor in their leukemia. 23 Can you tell me that? 24 MR. PERRY: Objection. He's already done 25 it. 126 1 Go ahead and do it again. 2 A My opinion is, the scientific literature 3 does not support that gasoline is an established risk 4 factor for leukemia, period. 5 Q (By Mr. Patton) Is it your opinion, then, 6 that under no circumstances can a worker's exposure 7 to benzene from gasoline be a causative factor in his 8 leukemia? That's my question. 9 A We've done this three times now. 10 Q And you keep going back to, Oh, I think 11 the literature says this. I'm not asking you what 12 the literature says, sir. 13 A Well, no. 14 MR. PERRY: Let me object, Keith. This is 15 not where experts make up what they think. And maybe 16 some of your guys have done that. This guy's based 17 on the science and the literature. This is not a, 18 come in and tell me what you believe. It's what does 19 the scientific, medical literature support. That's 20 what he's going to testify to. This is not the time 21 for personal opinions. 22 MR. PATTON: Objection, nonresponsive. 23 MR. PERRY: Objection, nonresponsive. 24 Q (By Mr. Patton) Dr. Pyatt, is it -25 A I'll try. I'll try. I mean, we did it 127 1 once before, and what I said -2 Q Let me try to ask it differently. I 3 understood what you said before, okay? 4 A Okay. 5 Q I just want to go through this, get this, 6 and go to lunch, okay? 7 A Take as long as you need. 8 Q Is it your opinion that exposure to 9 benzene above 40 PPM years can cause someone's AML? 10 A That's what the literature would support, 11 yes. 12 Q Is it that -- is it therefore your 13 opinion? 14 A My opinion is that that's what the 15 literature supports, yes. 16 Q So if someone came to you with solid 17 evidence that a worker was exposed to benzene above 18 40 PPM years, would you then be willing to give the 19 opinion that that benzene exposure was a causative 20 factor in his AML? Would you be willing to do that? 21 A Perhaps; other considerations, but 22 perhaps. 23 Q Is it your opinion that the literature 24 does not support benzene exposure via gasoline as a 25 causative factor in AML? Is that your opinion, yes 128 1 or no? 2 A Yes. That is my opinion -3 Q Okay. 4 A -- as based on the scientific literature. 5 Q Is it therefore your opinion that under no 6 circumstances, based on the literature, could 7 someone's exposure to benzene via gasoline, that 8 whatever amounts they are, they could not be a 9 causative factor in someone's AML? 10 A See, I can't answer that. I mean, I can't 11 say what is possible, what's not possible. All I can 12 tell you -- and we did talk about this. I said what 13 you're really asking me is, is it possible for a 14 person to get exposed to enough benzene to give them 15 leukemia from gasoline. And I don't know that it is 16 because, A, I don't believe that you can take the 17 amount of benzene that a person gets from gasoline 18 and just extrapolate it directly to someone being 19 exposed to pure benzene. That's because of 20 competitive inhibition and all there other chemicals 21 going in. So that is an uncertainty. 22 Also, I don't know if someone is going to 23 achieve, say, 40 or 50 PPM years of benzene, how much 24 toluene are they going to have? How much n-hexane 25 are they going to have? How much of these other 129 1 chemicals are they going to have? I don't know the 2 answer to that. What I can tell you is the 3 literature is clear that gasoline does not cause CML. 4 Q Does the literature say anything about 5 gasoline causing AML? 6 A Oh, sure. 7 Q What does it say? 8 A It says it doesn't happen. 9 MR. PATTON: Okay. Off the record. 10 THE VIDEOGRAPHER: We're going off the 11 record at 12:48. 12 (The deposition recessed at 12:48 p.m., 13 to be reconvened at 1:30 p.m.) 14 15 16 17 18 19 20 21 22 23 24 25 130 1 AFTERNOON SESSION 1:40 p.m. 2 THE VIDEOGRAPHER: We're back on the 3 record at 1:40. 4 EXAMINATION (continued) 5 BY MR. PATTON: 6 Q Dr. Pyatt, in your experience working with 7 industry, has industry ever asked you to help improve 8 nonindustry, meaning nonAPI member work sites or work 9 environments based on what industry knows about the 10 harmful effects of any chemicals? 11 MR. PERRY: Object to form. 12 A I can't think of anything that would fit 13 into that category, no. 14 Q (By Mr. Patton) Aside from defending 15 industry in litigation and aside from the studies 16 that you mentioned earlier in your deposition, is 17 there any work that you've done on behalf of 18 industry, the API, which would directly help the 19 working man? 20 MR. PERRY: Object to form. 21 A Well, I mean, I think you could take a 22 fairly lofty approach to that question and say 23 anything that we've done to understand the toxicity 24 of benzene is to the benefit of the working man, 25 public health. So all of the basic research that I 131 1 did and did with Dr. Irons and others, looking at the 2 toxicity of benzene, I think that's useful 3 information. 4 Q (By Mr. Patton) Have you ever done any 5 work which resulted in more stringent workplace 6 controls on benzene exposure? 7 A I don't know the answer to that. 8 Q Do you have any opinions in this case as 9 to whether or not the Shell material safety data 10 sheets -- do you have any opinions on those in this 11 case? 12 A No. 13 Q Do you have any opinions on whether or not 14 Shell adequately warned McNeece Brothers about the 15 dangers of benzene? Do you have any opinions? 16 A No. 17 Q Do you have any opinions on whether or not 18 Shell adequately warned Raul Zendejas about anything? 19 A No. 20 Q Do you have any opinion on whether or not 21 gasoline distribution workers as a whole are 22 adequately warned about the dangers of benzene? 23 A I have no opinion about that. 24 Q Do you think they should be warned about 25 anything? 132 1 MR. PERRY: Object to form. 2 A Who? 3 Q (By Mr. Patton) Gasoline distribution 4 workers. 5 A Who should warn them? I mean -6 Q The manufacturers of the gasoline that 7 they're working with. Do you have any opinions on 8 whether or not the gasoline companies like Shell 9 should even warn gasoline distribution workers about 10 anything? 11 A Well, I'm not a warnings expert, and in a 12 formal setting like this, no, I'd say I don't have an 13 opinion about that. I would let others argue for or 14 against whatever. 15 Q As a toxicology expert, do you have any 16 opinions on whether or not gasoline is capable of 17 causing any type of disease? 18 A In humans -19 Q Yes. 20 A -- or in experimental animals? 21 Q Humans. 22 A Humans. The only -- the only 23 toxicological -- well, yes. I mean, if you are 24 exposed to a lot of gasoline, there are neurological 25 symptoms. There is respiratory depression, which 133 1 really seems to be true for any organic solvent at 2 very high exposure. So that's a toxic end point 3 associated with gasoline that I think can happen. 4 Q How much is a lot? 5 A I think thousands of parts per million, 6 but I'm not sure exactly where the cutoff would be. 7 Q Do you think gasoline is causally 8 associated with any type of long-term disease 9 process? 10 MR. PERRY: Object to form. 11 A The only one that's even been really 12 speculated on or maybe, perhaps, probable, however 13 they've worded with it for gasoline, is kidney 14 cancer. And that's based on the male rat and the 15 studies that have been conducted on these 16 experimental animals. Whether or not that holds up 17 under the epidemiology studies, I'm not prepared to 18 talk about because I haven't evaluated that 19 literature specifically lately. But I think that 20 would be the one that -- I mean, when IARC says 21 gasoline is a probable human carcinogen, that's what 22 they're talking about. 23 Q (By Mr. Patton) So IARC has designated 24 gasoline as a probable human carcinogen, right? 25 A That's correct. 134 1 Q Have you ever seen industry issue a 2 questionnaire among any group of chemical workers in 3 the United States? Have you ever been involved in 4 any of that activity? 5 A No. 6 Q As we sit here today can tell me an 7 example of any research that you know that Shell as 8 done specific to gasoline distribution workers? 9 A I would have to look, but it seems like 10 Sean Tsai has done some studies for Shell looking at 11 hematopoietic effects in the refinery workers. And I 12 would suspect there are some distribution workers 13 that are included in what he did. 14 Q And he works for Shell? 15 A Uh-huh. 16 Q If he were to conclude as an employee or 17 studying and working on behalf of Shell that there 18 was, indeed, an increased risk, would you suspect 19 that they would publish that information? 20 A I would suspect that they would, yes. I 21 mean, it would depend on the nature of the study, how 22 reliable the study was, but sure. 23 Q I mean, if API and/or Shell were to 24 perform a study about gasoline and conclude that 25 there was an increased risk, a statistically 135 1 significant increased risk of leukemia related to 2 gasoline or benzene exposure, would you expect them 3 to publish that study? 4 A It's hard for me to answer, but I think 5 they would, yes. 6 Q Wouldn't it be incredibly detrimental to 7 them because that study would then link benzene and 8 gasoline exposure with leukemia, such that they could 9 be held responsible? 10 A I don't know about all that, but I think 11 they have an interest, as do all the rest of the 12 companies and researchers, to publish their results 13 and make sure that we all know what's going on with 14 these exposures. 15 Q You would agree with me that if Shell were 16 to perform a study and they were to conclude that 17 there was an increased risk related to gasoline, 18 whatever that risk might be, whatever disease 19 process, they would have a problem because they could 20 then be responsible for their product causing 21 someone's disease? 22 MR. PERRY: Object to form. 23 A Your question is would they have -- would 24 they be responsible, or would they -- I'm sorry. 25 What was your question? 136 1 Q (By Mr. Patton) It's all right. 2 Do you require scientific certainty in 3 terms of causality for every specific 4 lymphohematopoietic disease related to exposure by 5 benzene by exposure level? 6 MR. PERRY: Object to form. 7 A Are you asking whether -- what my criteria 8 would be before I could say that benzene can cause a 9 disease? 10 Q (By Mr. Patton) I'm saying would you 11 require scientific certainty in terms of causality 12 for every subtype of a leukemia? 13 A Of leukemia? 14 Q Of a given -- let me start again. 15 A Okay. 16 Q For you to testify that benzene caused 17 someone's leukemia -- and again, you -- besides the 18 dental example you've never testified or given the 19 opinion that Chemical X caused Disease Y, correct? 20 MR. PERRY: Object to form. 21 A Well, like I said, there have been three 22 or four times when I've had that opinion, and then 23 they either settled the case or went somewhere else. 24 Q (By Mr. Patton) You didn't say that 25 earlier, sir. 137 1 MR. PERRY: Yes, he did. 2 A Yes, I did. 3 Q (By Mr. Patton) Would you require 4 scientific certainty in terms of causality for every 5 specific subtype of myeloid leukemia related to 6 benzene by exposure level before you would give an 7 opinion on that causality? 8 A No. 9 Q When have you given the opinion to Shell 10 or to industry that benzene did cause someone's 11 disease? 12 A Well -13 Q Because that's not what I understood you 14 testified to this morning. The transcript will say 15 it, but I just want to understand where our 16 disconnect is. 17 A Like I said, there have been three times 18 where they called me up and said, We'd like for you 19 to help with this case. And the way I always do it 20 is, okay, what are the issues, what's going on. Send 21 me the medical records. 22 They did. I looked at all the exposure 23 information they provided, talked to them. We had a 24 follow-up call, and I said I can't -- I can't help 25 you. I mean, I cannot say definitively that these 138 1 people's -- that this disease was not caused by their 2 exposure. And that's happened three times that I can 3 think of, sitting here. 4 Q What were the chemicals in question? 5 A Benzene. 6 Q What kind of exposure was it? Pure 7 benzene? 8 A Working at a benzene unit, yes; pretty 9 much, yes. 10 Q What were the diseases? 11 A The diseases were AML. 12 Q What kind of AML? 13 A That, I don't recall. 14 Q Wouldn't that matter to you? 15 A Not really. I mean, it would matter -16 there is one subtype of AML called acute 17 promyelocytic leukemia, which is the M3 designation, 18 and that one is unique enough that it has had 19 epidemiology studies conducted on it by itself. None 20 of the other like erythroleukemias, none of the other 21 subtypes of AML have had that extensive research done 22 on them independently. 23 Q Do you have any opinions as to what 24 McNeece Brothers should have done differently in this 25 case? 139 1 A No. 2 Q Do you have any opinions as to what Raul 3 should have done differently? 4 A No. 5 Q Do you have any criticisms of the way Raul 6 worked with gasoline? 7 A Well, I mean, just kind of general. If 8 what Stephen Petty said was true and he really did 9 spill gasoline on himself 100 times while he's 10 loading up tanks, I might say you might want to be a 11 little more careful and pay attention to what you're 12 doing. 13 Q But from a leukemia standpoint, if 14 gasoline can't cause leukemia anyway -15 A No, I agree. 16 Q -- what does it matter if he spills any on 17 himself? 18 A I agree. 19 Q Okay. So is it your opinion that it 20 doesn't matter how much Raul -- or how he was working 21 with the gasoline or even if he spilled it on 22 himself, because it still wouldn't cause his form of 23 leukemia? Is that your opinion? 24 A That's what the literature would support, 25 yes. 140 1 Q And therefore that is your opinion? 2 A Based on the literature, correct. 3 Q Why do you always qualify it, "based on 4 the literature"? 5 A Because I want the jury to understand that 6 my opinion is solidly based in the literature. This 7 is not an authority based, look at me, I've got all 8 these publications, I know this much about benzene. 9 My opinions in this case are based on these binders 10 of studies. 11 (Exhibit 7 marked.) 12 Q (By Mr. Patton) Let's talk about some of 13 your studies. I've marked as Exhibit 7 a study about 14 occupational hobby or lifestyle exposures associated 15 with Philadelphia chromosome positive CML. Is that 16 what Mr. Zendejas had? 17 A No. 18 Q Okay. 19 A But it was a lot closer to him than AML. 20 (Exhibit 8 marked.) 21 Q (By Mr. Patton) Exhibit 8, "Occupation 22 and Leukemia Mortality Among Men in 16 States." Are 23 you familiar with this study, Loomis? 24 A I can't tell from you holding it way over 25 there. I mean, it was one of my papers that I 141 1 referenced in my report so I'm -2 Q Does this study show all leukemias 3 combined, there's an increased risk of all leukemias 4 from workers in the petroleum industry? 5 A The relevant data in this study is on 6 Page 512. I'll give it back to you. And no, it 7 doesn't -- I mean, there is the CNLL which is the 8 disease that Mr. Zendejas had. 9 Q Hold on a second. I thought you said he 10 had CML? 11 A Same thing. 12 Q What is it? 13 A This is chronic nonlymphocytic leukemia. 14 It's just a different epidemiological classification, 15 but it is chronic myeloid leukemia. So there's 16 petroleum refineries, they had no cases of CML so 17 they couldn't do any math on it. Then there's motor 18 mechanics and service station attendants, which would 19 be relevant to gasoline, and the relative risk of CML 20 was .5. So it actually would suggest that there 21 would be a protective effect, based on that study. 22 MR. PERRY: Who's the lead author of that 23 study? 24 THE DEPONENT: It was Loomis and Savit, I 25 think, David Savit at UNC; is that right? Is it 142 1 David Savit? 2 MR. PATTON: Yes. 3 Q (By Mr. Patton) But this says only 4 petroleum refining and rubber manufacturing had 5 excess deaths for all leukemias combined. 6 A You know, the pertinent data is on that 7 table. I'm not sure exactly what he's talking about. 8 And you could say that something with a relative risk 9 of 1.2, that there was an excess death. But does 10 that mean that it is meaningful? That's where you 11 have to start applying statistics and see whether it 12 really is different or not. 13 (Exhibit 9 marked.) 14 Q (By Mr. Patton) The Jakobsson study, 15 you're familiar with this one, correct? 16 A Yes. 17 Q This shows an increased risk of AML among 18 petrol workers, correct? 19 A Correct. 20 Q Is Mr. Zendejas a petrol worker? 21 A Well, I think those were like gasoline 22 station attendants. But I think it has relevance to 23 the gasoline -- I mean, that is certainly one that I 24 consider when I evaluate the gasoline literature. 25 Q Would you agree with me that someone who 143 1 bulk-loads gasoline has more exposure to benzene than 2 a service station attendant? Or do you have an 3 opinion either way? 4 A I don't have an opinion either way. 5 Q But nevertheless, your Exhibit 9 shows 6 that the risk of AML was increased for petrol 7 workers, right? 8 A That's correct. 9 Q Statistically significant, correct? 10 A Yes. 11 Q Why doesn't that study by Jakobsson 12 support your -- I'm sorry. Why doesn't that support 13 the argument that benzene did cause Raul's leukemia? 14 A Well, because you can always find -15 anytime a question has been asked 50 times, a hundred 16 times in the epidemiological literature, you can 17 always find a single positive study here and there. 18 You can't just pull out one positive study or one 19 positive finding from a study and say, okay, this is 20 it. See, I have a positive study; therefore, 21 gasoline causes AML. 22 When you look collectively at that overall 23 literature, the vast majority of that literature does 24 not support that, which is why it is not generally 25 accepted that gasoline is a human carcinogen, 144 1 leukemia being one of the end points that they were 2 evaluating. 3 Q You said something about -- you mentioned 4 earlier a competitive inhibition. What does that 5 mean? 6 A When we were discussing earlier this 7 morning about benzene's metabolism -- you remember? 8 Q Yes. 9 A Benzene has to be metabolized by the 10 liver, and there are certain enzymes in the liver 11 that take -- that are responsible for that 12 metabolism. Well, there are other chemicals that 13 also go through the liver and are acted on by that 14 same enzyme. So the idea is that if a person -- and 15 there's good data to show this. Whether or not it 16 was happening in Mr. Zendejas or not, I don't know. 17 But there's clear evidence in the 18 experimental animal literature that if you take an 19 animal and you expose them to benzene, you see 20 effects. You take that same animal and you expose 21 them to benzene and a lot of toluene at the same 22 time, you don't see those same benzene effects 23 because the toluene has prevented the liver from 24 metabolizing the benzene. That is the general 25 consensus. And so that inhibition is what 145 1 competitive inhibition is. The competitive means 2 toluene is outcompeting the benzene for that spot in 3 the enzyme. 4 Q And the position that you're stating 5 there, is that -- is that from gasoline analysis? 6 A There are certainly studies that say that 7 that does happen with gasoline. There are other 8 studies that say it may not even just be the toluene, 9 but that clearly benzene's toxicity in gasoline is 10 different than benzene's toxicity is by itself. 11 Q Is it your opinion that therefore, then, 12 benzene's toxicity by itself is different -- I'm 13 probably just rephrasing, saying this over. 14 Is it your opinion that benzene toxicity 15 in and of itself is much different than benzene 16 toxicity when somebody's exposed to additional other 17 chemicals, toluene being one of them? 18 A Yeah. You can't just say additional other 19 chemicals. Toluene, it is possible, and there is 20 evidence to support it. You can't -- any chemical is 21 not going to matter, necessarily, because it's only 22 going to be chemicals that are impacting on benzene's 23 metabolism. 24 Q What other chemicals impact on benzene's 25 metabolism? 146 1 A I think all of the aromatic hydrocarbons 2 do -3 Q Okay. 4 A -- xylene, trimethyl benzene, all of them. 5 Q And that doesn't -- doesn't that defeat 6 the refinery studies? Because those folks are 7 exposed to benzene, and they're exposed to all other 8 aromatic hydrocarbons, generally speaking, and 9 there's still an increased risk of AML for refinery 10 workers, correct? 11 MR. PERRY: Object. 12 A Well, I would disagree. I mean, I think 13 if you look at the refinery workers overall as a 14 total body of literature, they do not seem to really 15 be at an increased risk. You can certainly find 16 positive studies here and there, and maybe they were 17 working in a benzene unit. I mean, I don't know 18 exactly why that happens. But the overall literature 19 for refinery workers does not support that those 20 individuals have an increased risk of AML. 21 Q (By Mr. Patton) Do you know if Shell ever 22 studied its own refinery workers and found an 23 increased risk of AML? 24 A That, I don't know. 25 Q If they did, it wouldn't make sense 147 1 because of competitive inhibition, right? 2 A No. I mean, all that competitive 3 inhibition means is if it's occurring, all it's going 4 to do is shift the dose response. And if you would 5 see a certain effect at 10 PPM, maybe you need 15 PPM 6 if they're being co-exposed to toluene to see that 7 same effect. It doesn't ameliorate it. It just 8 changes it. 9 (Exhibit 10 marked.) 10 Q (By Mr. Patton) Are you familiar with the 11 Adegoke study, Exhibit 10? 12 A I'm familiar with that study, yes. I 13 didn't know it was Exhibit 10. 14 Q Let me read for you a portion real quick, 15 and then I'll let you see this. 16 A Okay. 17 Q "The odds ratio among those ever exposed 18 to benzene was 1.7, 95 percent confidence interval, 19 1.1 to 2.6." So that is statistically significant, 20 correct? 21 A That's correct. 22 Q For total leukemia? 23 A That, I don't remember. 24 Q I'll let you read it here in a second. 25 A Okay. 148 1 Q So this study also analyzed total leukemia 2 without subsetting it into CML, MDS, AML. Would you 3 agree with that? 4 A I think they did. They also broke out 5 CML. 6 Q It shows the ever exposed category had a 7 significantly increased risk for CML. Odds ratio 8 2.5, a 95 percent confidence interval, 1.3 to 4.9. 9 That's statistically significant, correct? Here you 10 go. 11 A I think I might have another copy so we 12 can both be looking at it. 13 Q Is what I just read at the right-hand 14 column of Page 47 incorrect (sic)? 15 MR. PERRY: Is it correct or incorrect? 16 Q (By Mr. Patton) Is it correct? 17 A Let's see. The ever exposed category had 18 a significantly increased risk for CML. Odds ratio 19 2.5, 95 percent confidence interval, 1.3 to 4.8. So 20 yes, that is -- that one finding is statistically 21 significantly elevated. 22 Q So if you wanted to make an argument in 23 favor of benzene causing Raul's leukemia, you could 24 cite that study, right? 25 A No. 149 1 Q No? Why not? 2 A Because when you look where they've 3 divided up the all leukemias, the less than 15 year 4 category, which Mr. Raul would -- I'm sorry -5 Mr. Zendejas would fit into, that is not 6 statistically significant or even elevated and for 7 CML or all leukemias. And then like we talked about 8 earlier, the benzene category -- sorry -- the 9 gasoline category, which is the most pertinent to 10 this case and Mr. Zendejas, does not support an 11 increased risk of leukemia. 12 Q This is kind of a futile exercise, isn't 13 it? I mean, just as you've done in the other 14 20 cases that you've testified for on behalf of 15 industry, you and I could go through all these 16 studies, and you could just carve it out as you see 17 fit? And that's what you're doing, correct? 18 MR. PERRY: Object to form. 19 A I don't think I'm carving it out at all. 20 I mean, like I said, I will show the jury and they 21 will see the word "gasoline" and the risks associated 22 with gasoline exposure. I'm not carving it out. 23 That's what this study supports. 24 Q (By Mr. Patton) Do you believe that the 25 health impact of exposure to gasoline has been fully 150 1 elucidated? 2 A Say that again. 3 Q (By Mr. Patton) Do you believe the health 4 impact of exposure to gasoline has been fully 5 elucidated? 6 A Well, I think we know a lot about it. 7 We've been doing animal studies for some time. We've 8 got a lot of epi. I wouldn't say we know everything 9 there is to know about it. 10 (Exhibit 11 marked.) 11 Q (By Mr. Patton) So this person, Lagorio 12 from the National Health Institute in Rome, 13 Exhibit 11, one of your studies, concludes that 14 "Filling station attendants are exposed to gasoline 15 vapors and seem at risk of cancer at various sites. 16 But due to the power limitations of this study, a 17 precise estimate of the risk for many causes of death 18 was not achievable. Further cohort studies of 19 greater size are warranted." 20 And this is from 1994. Do you agree with 21 that statement? 22 A I don't have any reason to disagree with 23 that. 24 (Exhibit 12 marked.) 25 Q (By Mr. Patton) "Workers in the gasoline 151 1 service station industry experienced a leukemia 2 mortality excess. PMR equals 328. N equals 3. 3 P less than 0.05." What does that mean? This is 4 from the Schwartz study. 5 A Yeah, Schwartz. He did a proportional 6 mortality study which -- you know, it's better than a 7 case report because it is at least analytical, but it 8 isn't much better than a case report. And that means 9 that it was a statistically significant finding. But 10 the problem with the PMR, proportional mortality, is 11 that it takes all of the deaths and forces them into 12 a percentage so that the total number of death has to 13 equal 100. So if you see an increase in one death -14 one cause of death, then there have to be subsequent 15 decreases in others so that the total amount ends up 16 being 100. So it's not a very good study design. 17 (Exhibit 13 marked.) 18 Q (By Mr. Patton) Rushton 1996, Exhibit 13, 19 he (sic) concludes there's "some suggestion of a 20 relation between exposure to benzene and myeloid 21 leukemia; in particular, for acute myeloid and 22 monocytic leukemia. Peaked exposures seemed to be 23 experienced for this disease." I don't understand 24 that. He says, "Further work is necessary," 1997, 25 correct? 152 1 A Yes. And Lesley is a woman. 2 Q What does it have to do with your 3 opinions, that study, Exhibit 13? 4 A Well, this is a -- this is a very 5 important study. This was looking at a large number 6 of distribution workers, which I think would be 7 relevant to Mr. Zendejas. They looked at various 8 forms of leukemia. They looked at various forms of 9 leukemia associated with cumulative exposures, peaks, 10 intensities, a variety of exposure metrics associated 11 with those workers. And there is a chart 12 specifically for chronic myeloid leukemia along -13 associated with various benzene exposure metrics. 14 Q What kind of benzene exposure were these 15 workers experiencing via gasoline operations? 16 A You mean in terms of quantification? 17 Q Yes, sir. 18 A I don't -- well, yeah. I mean, there was 19 less than 4.5. There was a 4.5 to something. There 20 was a greater than 45 PPM years. I don't know 21 whether those were the distribution workers or not. 22 But at no point in that dose response was there an 23 increased risk of CML, which I think is directly 24 germane to what we're doing here. 25 Q So even when it shows like all leukemias, 153 1 your response is then to say, yeah, but it doesn't 2 deal with -- but it doesn't help it -- help the case 3 to support CML and gasoline exposure, correct? 4 A Well, I don't believe -- and, you know, we 5 can talk about this as much as you like. But 6 epidemiologists and hematologists and toxicologists 7 we've known for a long time that the etiological risk 8 factors for different kinds of leukemia are clearly 9 different. 10 Q Do you believe that there's no reason for 11 these researchers to even mention all leukemias? 12 Like what's the point in that? Because if you can't 13 connect it with the disease until you cut it down to 14 the subtype or the division, what's the point in 15 these researchers, in their published studies, to 16 even mention what the odds ratio or what the risk is 17 for all leukemias? 18 A Well, I mean, that's a fair -- that's a 19 fair question. And I don't know the answer to it. 20 Q There must be some value because they do 21 it, right? 22 A Well, I mean, it can go both ways. It can 23 hurt both ways. For example, let's say that you do 24 not find an increased risk of total leukemia, but 25 then when you subdivide it out you see that there, is 154 1 in fact, an increased risk of AML, but there's no 2 increased risk of these others so that it kind of 3 dilutes that finding. And so the overall risk, you 4 don't see it elevated. I think it hurts both ways. 5 Q Have you ever wrote to any of these 6 researchers and said, Hey, you shouldn't deal with 7 all leukemias because it doesn't really matter? 8 A I've actually had that question with 9 Lesley Rushton, but epidemiologists are going to do 10 what they're going to do. 11 (Exhibit 14 marked.) 12 Q (By Mr. Patton) Exhibit 14 is a follow-up 13 from Rushton. It concludes, "Mortality from 14 leukaemia was high at one company and in drivers 15 overall." This is specific to gasoline distribution, 16 right? 17 A I would have to look at it, but that -- I 18 think that's correct. 19 Q It shows here that "Several studies have 20 carried out personal air sampling or taken urine 21 samples to investigate the exposure of workers to 22 benzene at bulk marketing terminals or service 23 stations." You see that where I circled that on 24 Page 14? 25 A Yes. 155 1 Q Are you aware of Shell ever performing 2 that type of investigation for gasoline distribution 3 workers? 4 A I don't know. Are these studies Shell 5 studies? 6 Q I don't think that one is. My question is 7 a little different. 8 Are you aware of Shell ever conducting air 9 monitoring, blood samples, urine samples, for 10 gasoline workers outside of Shell's own refineries? 11 Do you know? 12 A Well, I mean, what I'm saying is, she 13 referenced several studies in support of that 14 sentence. And perhaps they were Shell, but I don't 15 know. You'd have to go and pull these studies and 16 look to see where the people worked and where they 17 were doing the measurements. 18 Q In this case that we're here for today, 19 has Shell shown you any information indicating that 20 they carried any of those that types of investigation 21 for workers? 22 A No. 23 Q Okay. Do you think it would be helpful so 24 that we could be better elucidated when it comes to 25 the relationship between benzene via gasoline and 156 1 various forms of leukemia? Do you think it would be 2 helpful for Shell to perform some tests in that 3 manner? 4 MR. PERRY: Objection, form and vague. 5 A Well, I think there is a lot of data on 6 what the potential benzene exposures are in these 7 various tasks. I don't think they're very high, but 8 there are plenty of studies, and that's what others 9 in this case will discuss. 10 THE VIDEOGRAPHER: One minute, Counsel. 11 MR. PATTON: Off the record. 12 THE VIDEOGRAPHER: We're off the record at 13 2:10. This is the end of Tape 3. 14 (Recess from 2:10 p.m. to 2:14 p.m.) 15 THE VIDEOGRAPHER: We're back on the 16 record at 2:14. This is the beginning of Tape 4. 17 Q (By Mr. Patton) I'll mark as Exhibit 15 18 the Schnatter study. What does this have to do with 19 your opinions? 20 A Rob Schnatter did the same basic design 21 that we were just talking about with Lesley Rushton 22 where they looked at a variety of worker types in 23 refineries, distribution workers, et cetera. 24 Q Schnatter worked for Exxon, right? 25 A Yes. 157 1 Q If the results of the Schnatter study 2 would have been such that, Hey, it looks like benzene 3 causes an excess risk of leukemia, that could have 4 been bad for industry, would you agree? 5 MR. PERRY: Object to form. 6 A I know Rob Schnatter personally, and he 7 would publish his findings. And, in fact, Jeff 8 Lewis, Dr. Lewis, who is a colleague of Dr. 9 Schnatter, has published papers that show an 10 increased risk of this or that in various refineries, 11 you know, because that's what the science said. 12 Q (By Mr. Patton) Schnatter performed 13 another study -- I'll mark it as Exhibit 16 -- "The 14 Relationship Between Low-Level Benzene Exposure and 15 Leukemia in Canadian Petroleum Workers." Are you 16 familiar with this? 17 A Yes. 18 Q It says here, "This study" -- and this is 19 1996. "This study is consistent with other data in 20 that it was unable to demonstrate a relationship 21 between leukemia and long-term low level benzene 22 exposure. The power of the study was limited. Thus, 23 further study on benzene exposures in this 24 concentration are warranted." 25 My question for you, sir, is, doesn't it 158 1 benefit industry when the studies specific to 2 gasoline are inconclusive? 3 MR. PERRY: Object to form. 4 Q (By Mr. Patton) I mean, as far as 5 responsibility and liability goes, industry is better 6 off when there are inconclusive studies rather than 7 positive studies, true? 8 MR. PERRY: Object to form. 9 A I mean, I think we want to know the right 10 answer. 11 Q (By Mr. Patton) Did you want to know the 12 right answer in this case? 13 A Absolutely. 14 Q Is there anything you asked Shell or its 15 attorneys to do to provide you different -- better 16 information so that you could give a right answer? 17 A I think I had everything I needed. 18 Q But you don't believe Steve Petty's 19 opinions on how much benzene Raul was exposed to, you 20 don't believe those are accurate, correct? 21 A No. 22 Q So wouldn't you require accurate estimates 23 for you to be able to give your opinions? 24 A I don't understand why I would. Even if 25 you accept his number, that's not going to get you to 159 1 an increased risk of CML and really not even going to 2 get you to an increased risk of AML, even if you 3 wanted to accept that this is an AML case. I just 4 don't think those are scientifically defendable. 5 Q (By Mr. Patton) Gerhard Raabe did a study 6 on -- a mortality study of workers at a refinery in 7 Beaumont. Do you know what he found? 8 A Gerry Raabe, no. I mean, I'd have to 9 review that study. He's done several. 10 Q He works for industry, right, works for 11 Mobil, or worked for Mobil? 12 A He did, yes. I think you'll find through 13 the literature that most of the epidemiology studies 14 for refineries were done by people that had a vested 15 interest in those refineries. 16 Q Because refiners are the ones who can 17 afford to do those studies, correct? 18 MR. PERRY: Object to form. 19 Q (By Mr. Patton) And they have the access 20 to the people and the information, right? 21 MR. PERRY: Object. 22 A I think all of that is probably true to 23 some extent. 24 Q (By Mr. Patton) Would you agree with me 25 that the body of literature you brought with you 160 1 today is at least suggestive of a responsibility or 2 of a relationship between benzene exposure and 3 leukemia, or you just -- you just disagree? 4 A Well, I think the literature that we've 5 been discussing and others is clear that at certain 6 exposure levels to benzene, you get an increased risk 7 of AML. 8 Q I guess I just don't understand why there 9 are still studies into the '90s and into the 2000s 10 about gasoline, benzene, and leukemia if the 11 question's already settled. Can you explain that, or 12 do you have any understanding? 13 A The question's not settled. There's a 14 whole lot of information that we would like to know 15 about the process and characteristics and morphology 16 and progression and treatment and response and all 17 kinds of things that aren't settled. 18 (Exhibit 17 marked.) 19 Q (By Mr. Patton) Exhibit 17 is the Tsai 20 study, T-s-a-i. What does this have to do with your 21 opinions? 22 A Sean Tsai I just mentioned earlier. He 23 works for Shell so I think the studies that Sean Tsai 24 has published are going to probably be on Shell 25 employees. But that particular study, I don't -- 161 1 you'll have to show it to me. 2 Q I'm handing you Exhibit 17. What does 3 that have to do with your opinions in this case? 4 A I think I referenced this to just 5 illustrate what we were talking about earlier, and 6 that is that the majority of the literature on 7 refinery workers does not support that they have an 8 increased risk of AML or leukemia. 9 Q Do you know if Raul Zendejas had any 10 chromosome damage? 11 A My understanding is no, he did not. 12 Q Do you believe if someone has chromosome 13 damage, that increases the likelihood that they have 14 a benzene-related leukemia? 15 A I think that based on our understanding of 16 what benzene can do, based on our understanding of 17 what the AML's following chemotherapeutic agents look 18 like, based on our understanding of what AML 19 following radiation exposure looks like, that yes, 20 cytogenetic changes are certainly consistent with a 21 chemical etiology. Cytogenetically normal AMLs would 22 be inconsistent with a chemical etiology. 23 Q Are you aware of -- in your opinion are 24 there any specific cytogenetic abnormalities that 25 tend to be -- that are really high on the list of 162 1 chemically related, so to speak? 2 A I mean, there's a lot of discussion. It 3 depends on the chemical. If you're talking about 4 alkylating chemotherapeutic agents -5 Q I'm talking about benzene. 6 A Oh. 7 Q It's benzene, benzene, benzene all day, 8 every day of the week. 9 A You don't see -10 Q That's my life. Let me ask -11 A I'm sorry about that. 12 Q -- the question, sir. Is there a specific 13 cytogenetic abnormality that you, as an expert, 14 attribute to benzene exposure? 15 A There are some studies that have shown 16 trisomy 8 might have something to do with benzene, 17 involvement of Chromosome 8 with an 8;21 18 translocation. Martyn Smith's group out of Berkeley 19 published that. It hasn't been reproduced, but 20 nonetheless, that data's out there. They have shown 21 Chromosome 5, some involvement of Chromosome 7. So 22 there are -- there are some cytogenetic changes that 23 people have said, you know, benzene can probably do 24 this. 25 Q So if someone had a myeloid leukemia and 163 1 they had a minus 5 and a minus 7 chromosome, you 2 would believe that, hey, it increases the chances 3 that it was chemically induced or benzene induced? 4 A If it was an AML and it had a 5 or a 7, 5 then yes, I would say those were both consistent with 6 a chemical etiology. 7 Q What if it's MDS? 8 A Same. 9 Q The same. 10 A You want this one back? 11 Q Sure. Let's put it in the pile. 12 (Exhibit 18 marked.) 13 Q (By Mr. Patton) Exhibit 18 is the 14 Santos-Mello "Cytogenetic Studies on Gasoline 15 Attendants." I don't have any questions on that one 16 for you right now. 17 A Okay. 18 Q What is the amount of benzene that 19 somebody can be exposed to on a cumulative level that 20 would not put them at risk of leukemia? Like if I 21 want to go be exposed to benzene, okay? I just want 22 to do it. 23 A Okay. 24 Q But I don't want to get leukemia. 25 A Okay. 164 1 Q What are those numbers that I want to make 2 sure I don't get over? 3 A If you're concerned about -- you're 4 probably going to get mad at this. But if you're 5 concerned about CML, I don't think it matters. 6 Q I can just go work with benzene all day? 7 A That seems to be the case. But if you're 8 concerned about AML, then the epidemiology literature 9 supports that somewhere around 40 PPM years over a 10 cumulative exposure basis is where the risk becomes 11 statistically significant. It doesn't mean you would 12 get it at 40. Lots of people exposed to that much 13 didn't get it. But you at least would be at a 14 statistically significant increased risk. 15 Q Are you familiar with the work being done 16 at the University of Colorado Health Sciences Center 17 in relation to the Shanghai study? 18 A Well, I mean, I worked with Dr. Irons, and 19 I'm in that department. But Rich Irons has retired 20 from the university so I'm not sure -- in fact, I 21 think as of November the funding being run through 22 the university has ended. So I don't think there's 23 anything going on at Colorado. 24 Q Nevertheless, in those activities haven't 25 they concluded that it is accepted that there's an 165 1 increased risk for AML above 20 PPM cumulative years 2 of benzene exposure? You're putting it at 40. And 3 what I'm saying to you is I believe others on your 4 side of the -- on your side of the battle, so to 5 speak, have put it down to 20. Do you have any 6 opinion either way on that? 7 A I haven't seen that -- I haven't seen the 8 data that could be used to support that. 9 Q The Australian Health Watch study puts 10 that lower number down around 1 PPM, right? 11 MR. PERRY: Object to form. 12 A I disagree with that. 13 Q (By Mr. Patton) You disagree with that? 14 A Yes. 15 Q Am I just saying it wrong, or they're 16 saying it and you disagree with them? 17 A No, you're saying it wrong. What she says 18 for -- okay. For CML, there is no risk. 19 Q What about for all leukemias? 20 A I don't remember the numbers for all 21 leukemias. For AML, then the risks are statistically 22 significant at something greater than 8 but less than 23 57. So to me, that is consistent with many of the 24 other studies that show an increase somewhere around 25 40 to 50 PPM years. 166 1 Q I'm going to mark Exhibit 19. This is 2 Peter Greenwald, "Landmarks in the History of Cancer 3 Epidemiology." 4 (Exhibit 19 marked.) 5 A How did that get in there? That was in 6 the causation binder? 7 Q (By Mr. Patton) Maybe. 8 A I just printed it out because I thought it 9 was an interesting title. 10 Q I did, too. 11 I'm going to read something, and then can 12 you explain it to me? 13 A I can try. 14 Q Okay. "Quantitative" -- and this is on 15 Page 2158 -16 A Okay. 17 Q -- of Exhibit 19. "Quantitative 18 assessment of exposure is difficult, posing 19 challenges to epidemiological investigation of 20 occupation/cancer relationships." Do you agree with 21 that? 22 A Yes. 23 Q "Whereas individuals usually can describe 24 their smoking histories and eating habits reasonably 25 well, they're often relatively ignorant about their 167 1 work exposures." Do you agree with that? 2 A Not completely. I mean, I think -- well, 3 they could describe their smoking, but I think 4 frequently they don't. But yes, it's hard to 5 measure -- the occupational exposure part of an epi 6 study is frequently the weakest part. 7 Q Right. I mean, you ask a guy what he ate 8 for lunch or how much he smokes, he can tell you 9 about that? 10 A Correct. 11 Q You ask him how many PPM he's exposed to 12 of benzene when he's working with whatever solvent, I 13 mean, you wouldn't expect a guy to know that, would 14 you? 15 A He wouldn't know, I agree. 16 Q "Moreover, because of long latency periods 17 between exposure and cancer diagnosis and because 18 working conditions change over time, data on current 19 workplace exposures may not reflect those experienced 20 by past workers," correct? 21 A Yes. 22 Q You agree with that? 23 A Yes. 24 Q And you would also agree that workplace 25 exposures in past data like some of the numbers we 168 1 might find in these studies you're relying on, those 2 might not accurately reflect exposure data for a 3 given situation like Yuma, Arizona, a small bulk 4 terminal, top-loading, no vapor recovery; would you 5 agree with that? 6 A Well, in terms of your specific scenario 7 with that case, I mean, all I could say is that even 8 if you accepted Stephen Petty's assessment, then yes, 9 that cumulative exposure is absolutely encompassed in 10 these studies. That is not something that's so far 11 out there that we don't have a study that would tell 12 us about the risk associated with those exposures. 13 Q So you would agree with me that the 14 studies -- some of the studies do show exposures at 15 the level that Petty estimates? However, you're 16 critical of Petty for other reasons? 17 A I would say that this literature does have 18 people that are exposed at that level but not from 19 working five years and not from being -- well, I'm 20 not sure about the tank truck drivers. But the ones 21 I'm thinking about are the Pliofilm workers, the 22 rubber workers, the shoe workers. These people have 23 really high benzene exposures. 24 Q "Epidemiologists" -- and I'm still reading 25 from Exhibit 19. "Epidemiologists often have had to 169 1 rely on proxy measures of exposure and studies of 2 occupational cancer." What does that mean, "proxy 3 measures"? 4 A Like duration. 5 Q Surveys? 6 A No. Like instead of actually having 7 quantitative air monitoring data that might be 8 lacking or problematic, they would just say, Okay, 9 well, this guy worked there for five years, these 10 guys worked there for ten years, all those people 11 over there worked there for 20 years, so let's see 12 whether or not there's changes in their risk. So in 13 that case, duration would kind of be a proxy for 14 exposure. 15 Q Reading on in Exhibit 19, "For example, 16 the epidemiological studies which showed that 17 physicians who specialized in radiology prior to 1950 18 were at an increased risk of leukemia because of high 19 radiation exposure relied primarily on knowledge of 20 typical radiation protection practices in different 21 time periods, rather then on specifics about the 22 exposure of particular individuals." Does that make 23 sense to you? 24 A No. I'd have to read it again and look at 25 it in the context of that. 170 1 Q "Difficulty in obtaining accurate exposure 2 data remains a problem today, hampering recent 3 efforts such as the determination of whether 4 occupational exposure to pesticides and 5 electromagnetics fields influence cancer risk." Do 6 you agree that difficulty in obtaining accurate 7 exposure data remains a problem today? 8 A It depends on what it is you're looking 9 for. Certainly something like electromagnetic 10 fields, that's really problematic; benzene, less so. 11 But in an epidemiological study, the exposure 12 assessment is always the weakest part. 13 Q Because the exposure assessment is always 14 the weakest part in these epi studies, doesn't it 15 make a little more sense to look at the group of 16 workers a little more specifically with a little more 17 care, so to speak, to draw conclusions? 18 A I don't understand. I think they have 19 done that. 20 Q Well, I mean, I think that's what 21 Dr. Carroll did and Dr. Gore did for Raul. I mean, 22 they look at -- looked at his specific circumstances. 23 It's in the medical records that the guy's exposed to 24 gasoline and hydrocarbons. They considered the 25 unlikelihood that he would get his disease at his 171 1 age, and they concluded that benzene caused it. Why 2 isn't that fair? 3 MR. PERRY: Object to form. 4 Q (By Mr. Patton) I mean, you've got all 5 these problems with these epi studies, but epi 6 studies are what you're relying on to disprove 7 causation. Why isn't it fair to do what Dr. Gore and 8 Dr. Carroll did? 9 A It's not just me. Epi studies are what 10 EPA, IARC, OSHA, ATSDR -- I mean, this is the gold 11 standard for what we're doing. These are human 12 studies with toxicity. The difference is whether 13 you're going to have an authority based kind of 14 opinion or whether you're going to have a science 15 based opinion. And I think that will be evident if 16 this goes to trial when they start asking, Well, what 17 is the scientific basis in support of your opinion. 18 And that's going to be lacking. 19 Q You believe there is a -- that the 20 scientific basis supporting those experts' opinion is 21 lacking? 22 A Yes. 23 Q Isn't it easier, though, to use the 24 epidemiology to carve out a certain disease or a 25 certain specific circumstance to say it did not cause 172 1 it? Isn't that easier to do than collect the 2 literature to say it did cause it? 3 MR. PERRY: Object to form. 4 A I don't -- I don't how to answer that 5 question. I don't think that I have carved out 6 anything. I have brought in the literature that is 7 related to gasoline that is related to CML. That's 8 what he was exposed to. That's what everyone said. 9 That's the disease that he had. That's agreed upon 10 with everyone. I don't -- I don't see how I've 11 carved out something specific out of the literature. 12 Q (By Mr. Patton) He's got AML. I mean, if 13 he died tomorrow, it's AML. 14 MR. PERRY: Object to form. 15 A We've gone through that. I mean, your own 16 expert said that he would call it blast crisis. 17 Q (By Mr. Patton) Dr. Carroll already 18 called it AML. 19 A Dr. Gore called it blast crisis, and 20 that's what -- if you pick up any hematology textbook 21 and you're talking about a person who has his disease 22 following atypical or typical CML, they will call it 23 blast crisis. 24 Q Your job is easier because you can quibble 25 with these -- with calling it atypical CML? 173 1 MR. PERRY: Object to form. 2 A I'm not sure about that. I don't think my 3 job is easy, although -- I take that back. In this 4 case, it was pretty straightforward. 5 Q (By Mr. Patton) Was it easy for you to 6 conclude that Raul's exposure to benzene via gasoline 7 did not cause his form of leukemia? 8 A I wouldn't say it's easy, but I think the 9 literature is less schizophrenic with regard to 10 gasoline and CML than it is a lot of other diseases. 11 I think that literature is pretty clear, pretty 12 clearly negative. 13 (Exhibit 20 marked.) 14 Q (By Mr. Patton) Exhibit 20, this is one 15 of the medical records you have. I circled the 16 portion about cytogenetics. Does that indicate he 17 had a translocation? 18 A In one cell, which in a cytogenetic point 19 of view is insufficient. They have to see it in at 20 least three cells, or they don't count it. 21 Q Are you a cytogeneticist or a pathologist? 22 A I took a lot of pathology. Pathology and 23 toxicology in my institution were hand in hand. And 24 I wasn't intimately involved with the studies, but we 25 published -- out of the lab that I worked in, we 174 1 published several cytogenetic papers on benzene 2 metabolites and various lymphocytes. I know the 3 person who did the cytogenetics. I mean, I'm not a 4 cytogeneticist, but I'm familiar with the techniques. 5 Q The term "atypical CML" did not exist 6 before 2000, correct? 7 A I think they called it Philadelphia 8 negative -- Philadelphia chromosome negative. And I 9 don't remember when they stopped doing that. 10 Q Because the definition atypical CML was 11 not even used until around 2000 or so, you wouldn't 12 expect that term to be reflected in the literature, 13 would you? 14 A I think that's right, yes. 15 (Exhibits 21 and 22 marked.) 16 Q (By Mr. Patton) Exhibit 21 is another 17 medical record. 18 Exhibit 22, upon diagnosis Dr. Fayssoux 19 and Dr. Abdella, they mentioned occupation and 20 habits: "He works as a delivery man or a truck 21 driver for diesel fuel and gasoline." Why should 22 they even bother to mention that? 23 A You'll have to ask them. I mean, I think 24 as Dr. Nadelson described in his deposition, that is 25 something that they typically do, take an at least 175 1 brief occupational history of people that have 2 leukemia. 3 (Exhibit 23 marked.) 4 Q (By Mr. Patton) Exhibit 23, Dr. Fayssoux 5 originally called Raul's disease a myeloid 6 proliferative disorder, MDS, right? 7 MR. PERRY: Objection, form. 8 Q (By Mr. Patton) MPD? 9 A A myelo -- a myeloproliferative disorder 10 is CML. CML is a myeloproliferative disorder. 11 Q It's a myeloid leukemia, a myeloid 12 illness, right? 13 A Which one? 14 Q MPD or CML or MDS, all of them? 15 A They are -- no. Okay. MDS -16 Q Let me ask a better question. 17 A Okay. 18 Q Is MDS a bone marrow disease? 19 A Yes. 20 Q Is PMD a bone marrow disease? 21 A Yes. 22 Q Is CML a bone marrow disease? 23 A Yes. 24 Q Is atypical CML a bone marrow disease? 25 A Correct. 176 1 Q Is AML a bone marrow disease? 2 A Yes. 3 Q Is CMML a bone marrow disease? 4 A Yes. It's a form of MDS, or used to be. 5 THE DEPONENT: Is this the exhibit pile 6 here (indicating)? 7 MR. PERRY: Yes, sir. 8 THE DEPONENT: You want my report in that 9 pile? 10 MR. PERRY: Yeah. I've just been kind of 11 gathering them as we go. 12 THE DEPONENT: These are the ones that he 13 asked me to read. 14 Q (By Mr. Patton) Let's go through your 15 report. 16 A I need it back. Sorry. 17 Q First of all, do you know when benzene was 18 first associated with any form of bone marrow 19 disease? Do you know approximately what year? 20 A I can't tell you when it was first 21 associated. I can tell you when the first 22 publication came out. 23 Q When was that? 24 A 1897, I think it was. 25 Q And they drew the conclusion that benzene 177 1 is toxic to the bone marrow, correct? 2 A Yes. 3 Q And they drew that conclusion before we 4 have modern science today and before we started 5 classifying and reclassifying, for treatment and 6 prognosis purposes, the different forms of bone 7 marrow disease or myeloid diseases, correct? 8 MR. PERRY: Object to form. 9 A I don't understand that question. It was 10 aplastic anemia. It was a fairly specific diagnosis. 11 Q (By Mr. Patton) Do you know when benzene 12 was first connected with any type of myeloid leukemia 13 rather than aplastic anemia? Do you know what 14 decade? 15 A The first publication of benzene leukemia 16 was in 1828 -- sorry -- 1928, but it was actually a 17 lymphoid leukemia. So based on what we know now, 18 they were probably -- they were incorrect, and that 19 wasn't a benzene-related malignancy. But 20 nonetheless, that's when the first paper came out, 21 Delores and something. 22 Q "In summary, there is" -- this is Page 10 23 of your report. 24 A Okay. 25 Q "In summary, there is no consistent 178 1 evidence in the existing body of scientific 2 literature that occupational exposure to gasoline 3 results in an elevated risk of developing CML, MDS, 4 or any other human cancer." Do you still agree with 5 that? 6 A Absolutely. 7 Q I mean, we went through some of these 8 studies, and I pointed out to you a handful of them 9 that did show evidence of an increased or elevated 10 risk of developing leukemias. Didn't we do that? 11 A No, no. That's why no consistent 12 evidence -- and that's why Bradford Hill in his 1965 13 paper said, Here's what you've got to do in order to 14 establish causation. That was the whole idea. 15 Because we know that you're going to have, just by 16 random chance, a positive finding here or a positive 17 finding there. When you look collectively at that 18 overall literature, it does not support an 19 association. 20 Q Exhibit 5 or Exhibit 6 -- I'm not sure 21 which one it is. 22 A Okay. Well, I'll have to get those back. 23 I'm sorry. 24 Q It's Infante's paper. 25 A Okay. It's in here. I think it's on the 179 1 top, maybe just right under those medical reports. 2 All right. It's in there. 3 Q Exhibit 6. 4 A Okay. 5 Q Turn to Page 43. 6 A Okay. 7 Q See the upper right -- the right-hand 8 column? Or can you just start at the lower left-hand 9 corner. Can you read aloud for us, "In the 1970s." 10 A I'll try. "In the 1970s benzene 11 manufacturers and users began a new approach for 12 conveying knowledge about the toxicity of benzene to 13 the public, in general, and to workers and plant 14 managers specifically which contributed to a 15 continuation of overexposure to benzene. This is the 16 period when manufacturers began to hire consultants 17 to downplay the importance of scientific observations 18 related to the toxicity of benzene and to introduce 19 unresolvable arguments about dose response analysis, 20 which had an impact in delaying much-needed 21 government regulations that sought to reduce benzene 22 exposure in the workplace." 23 Q Let's stop right there. 24 MR. PERRY: Wait. What page is that? 25 THE DEPONENT: 43. 180 1 MR. PERRY: 43 of Exhibit 6. 2 Q (By Mr. Patton) Dr. Pyatt, manufacturers 3 like Shell have hired you as consultants, correct? 4 A I am a consultant, yes. 5 Q Do you believe it is fair to say that you 6 are downplaying the importance of the scientific 7 observations related to the toxicity of benzene? Do 8 you believe you're doing that? 9 A No, absolutely not. I think that's what 10 your experts are doing. 11 Q Do you believe you're introducing 12 unresolvable arguments about dose response analysis? 13 A No. 14 Q Do you believe to better understand the 15 relationship between -- well, let me look at it a 16 different way. 17 You have essentially three things going on 18 for a worker like Raul in a case like this. You have 19 benzene exposure, gasoline exposure, and him as a 20 gasoline distribution worker, okay? Wouldn't it be 21 helpful to study gasoline distribution workers who 22 worked in similar environments to him to better 23 understand the significance of benzene exposure to 24 that class of worker? 25 A We have; Schnatter, Rushton, Wong, 181 1 Sorahan, other refinery studies that have included 2 distribution workers. 3 Q Sir, I'll represent -4 A We have. 5 Q I'll represent to you that none of the 6 studies that we went through talked about top-loading 7 without vapor recovery. Do you have any reason to 8 disagree with me? 9 A I don't know whether they specifically 10 addressed that or not. But when they're looking at 11 18,000 distribution workers, I would assume that some 12 of them are doing exactly what Mr. Zendejas did. 13 MR. PATTON: Off the record. 14 THE VIDEOGRAPHER: We're off the record at 15 2:46. 16 (Recess from 2:46 p.m. to 2:47 p.m.) 17 THE VIDEOGRAPHER: We're back on the 18 record at 2:47. 19 Q (By Mr. Patton) Dr. Pyatt, do you believe 20 that industry is responsible to anyone or any class 21 of workers who have suffered leukemia as a result of 22 chemical exposure? 23 MR. PERRY: Object to form. 24 A What do you mean, "responsible"? I don't 25 think -- 182 1 Q (By Mr. Patton) Your answer says enough, 2 sir. 3 A Okay. 4 Q Do you believe there's a difference in 5 something like gasoline being called a carcinogen or 6 not and someone being exposed in a manner and at a 7 rate that exposes them to dangerous levels and an 8 increased risk? 9 MR. PERRY: Object to form. 10 A I'm not quite sure how to answer that. 11 But I would go back to what we've talked about 12 before, and that is even if you accept Stephen 13 Petty's quantitative exposure assessment, which 14 should take care of all of these other things that 15 you're addressing -- heat and Yuma and this, that, 16 and the other, top-loading -- it's not enough. It 17 just is not sufficient exposure. 18 Q (By Mr. Patton) Do you believe benzene 19 exposure played any role, even a 1 percent role, in 20 causing Raul's leukemia? 21 A I don't know how to answer that question. 22 Q Why not? Why can't you answer it? 23 A I just can't. I just don't know how to 24 say, well, it's a 6.5 percent probability or it's an 25 8 percent probability or it's 1 or 80. I just don't 183 1 know how to answer that. What I can tell you is the 2 scientific literature clearly does not support an 3 increased risk of CML from gasoline exposure. To me, 4 that's what this case is about, CML and gasoline. 5 And it does not establish a causal association. 6 Q Are there any other opinions that you 7 intend to offer in this case that are not described 8 in your report or that we haven't talked about? 9 A I don't -- I can't imagine what those 10 would be, no. 11 Q Have you been asked to testify at trial in 12 this case? 13 A Yes. 14 Q Do you know when that is? 15 A Yes, vaguely. 16 Q What's that? 17 A Yes. 18 Q Is there any additional information you'd 19 like to see in this case before you testify live in 20 front of a judge and a jury? 21 A The only thing that I would like to see 22 is -- and mainly just curiosity -- what Dr. Jamall 23 ends up saying about Stephen Petty's report and if he 24 does a cumulative exposure estimate. 25 Q Putting benzene aside, aren't there other 184 1 chemicals out there and other substances out there 2 for which there are no safe levels of exposure? 3 MR. PERRY: Object to form. 4 A I don't think that's true for benzene. 5 Well, that's what you said, putting benzene aside. I 6 mean, I do believe there are safe exposure levels to 7 benzene. I don't know of a chemical -- I mean, 8 methylmercury is really, really toxic, and it's 9 really, really toxic at really low levels. I don't 10 know whether you could actually be exposed to 11 measurable amounts of methylmercury and not have some 12 kind of toxicity, but I'm not positive. 13 Q (By Mr. Patton) What if someone had AML 14 with minus 5 minus, minus 7 chromosomes, and they 15 worked with gasoline for six years? Would you 16 believe that gasoline could have possibly played a 17 role in that person's disease? 18 A That's not what the literature would 19 support. 20 Q It's got to be pure benzene? 21 A It's got to be benzene at a high enough 22 level to put them into an increased risk based on the 23 quantitative epi. The other things, the minus 5 and 24 the 7, that's what we would expect the disease to 25 look like if it were, in fact, caused by benzene, 185 1 perhaps. You can't take those features and say, 2 Okay, because we've got these features, we don't care 3 about exposure anymore, it must have been caused by 4 benzene. 5 They're not that specific. People get 5 6 and 7, monosomy 7 and interstitial deletions in 5Q31. 7 They get that all the time without any exposure. So 8 that is just a description of what a person would 9 look like -- potentially look like if they had a 10 benzene induced leukemia. 11 Q Some of these studies in the exhibits, 12 they talk about the relationship between benzene and 13 specific types of leukemias or all leukemias. Some 14 of these studies don't even do a dose analysis, do 15 they? 16 A That's true. And from a public health 17 point of view, those studies are not very useful. 18 Q So all the studies that we've marked as 19 exhibits that don't look at benzene exposure in a 20 quantitative or an exposure or dose type viewpoint, 21 those just do not have much value to the public 22 health perspective; is that your testimony? 23 A No. I mean, if you -- you can look at -24 say, you can do an epi study, and you can say, never, 25 ever, okay? And one of those that we talked about 186 1 did, never, ever; exposed to gasoline, yes; exposed 2 to gasoline, no. All right. So what if the answer 3 is yes; people who say, yes, I was exposed to 4 gasoline, I have an increased risk of lung cancer. 5 Okay, well, a public health official who 6 is tasked with setting an exposure level for gasoline 7 to protect workers from getting lung cancer, a yes/no 8 answer doesn't help them. A high, low, medium 9 doesn't help them unless someone can go in and say, 10 Okay, when they said "low," here's what the exposures 11 were. When they said "medium," here's what they 12 were. 13 So the more quantitative information you 14 have about dose, the more useful it is from a risk 15 assessment public health causation basis. 16 Q On those three cases that you said you've 17 told industry, Hey, I can't testify for you, did you 18 tell them that you thought benzene, 51 percent 19 chance, did play a role? 20 A What I told them was, I cannot rule it 21 out. 22 Q But if you -- could you not rule it out to 23 51 percent? 24 A They didn't ask, and I just -- I can't do 25 that. I mean, I don't know how to do this 8, 75. 187 1 You know, I just said I can't rule it out. I can't 2 say definitively that there is evidence to support 3 this person's disease wasn't caused by their 4 occupation. 5 Q Putting aside the person who had the 6 dental work and the hydrochloric acid, can you cite 7 for me another example where you've given the opinion 8 in literature or elsewhere in your work that exposure 9 to Chemical or Substance X caused Disease or Health 10 Effect Y? 11 A No, other than the ones that we've talked 12 about. 13 Q Okay. Thank you for your time. 14 A You're welcome. 15 EXAMINATION 16 BY MR. PERRY: 17 Q Can you please state your name. 18 A David Pyatt. 19 Q And what is your occupation? 20 Is it Mr. Pyatt or Dr. Pyatt? 21 A My family calls me David or Dad, but 22 students usually call me Doctor. 23 Q And do you have a Ph.D? 24 A I do, in toxicology. 25 Q And what is your current occupation? 188 1 A I am a toxicologist. 2 Q With which company? 3 A I started my own company in 2005 called 4 Summit Toxicology, but I have been with the 5 university since 1996 teaching, sitting on 6 committees, doing research, that kind of thing. 7 Q And it's October 8, 2009, and we're 8 outside of Denver, Colorado, correct? 9 A That's right. 10 Q And when you say "the university," which 11 university are you referring to? 12 A I'm talking about the University of 13 Colorado. We've only got one really big one here in 14 Colorado so that's probably why we say that. 15 Q And really, today we've been -- we started 16 your deposition this morning around 9:30 mountain 17 time. And there's been lots of questions about lots 18 of literature, and I want us to kind of focus on the 19 ultimate issue. And this is the question, Dr. Pyatt, 20 I'm asking you as a professional toxicologist with 21 university appointments, with membership in 22 professional societies dealing with toxicology, and 23 the question is this: Is it generally accepted in 24 the scientific community that gasoline exposure 25 causes leukemia? 189 1 MR. PATTON: Objection, form. 2 A No. 3 Q (By Mr. Perry) And why do you say that? 4 A Well, because if you put quotations around 5 generally accepted, how would you know whether 6 something is generally accepted? You know, did you 7 go out and do a survey of all the toxicologists? 8 Well, in fact, in this case, that is what has been 9 done. And IARC, ATSDR, The Agency For Toxic 10 Substances and Disease Registry, a bunch of 11 toxicologists, physicians, epidemiologists, they 12 don't believe gasoline is carcinogenic. 13 IARC, the International Agency for the 14 Research on Cancer, preeminent physicians, 15 toxicologists, epidemiologists that evaluate any 16 chemical that has the potential to be a human 17 carcinogen, they don't believe gasoline is a human 18 carcinogen, let alone causing leukemia. OSHA, United 19 States Environmental Protection Agency, the American 20 Conference of Government Industrial Hygienists -- I 21 mean, collectively that is a lot of really talented, 22 really smart epidemiologists and toxicologists that 23 collectively say gasoline is not a carcinogen. So I 24 believe saying it is not generally accepted is 25 totally supportable. 190 1 Q Is it generally accepted in the scientific 2 community that gasoline exposure causes CML or 3 atypical CML? 4 A Absolutely not. If you can't even say 5 that it causes cancer as a collective group of 200 or 6 so miscellaneous diseases, the answer to that is no. 7 There is -- no. 8 Q Is it generally accepted in the scientific 9 literature that benzene exposure, regardless of the 10 level of exposure, causes CML, including 1atypical 11 CML? 12 A That has not been shown in the scientific 13 literature. We know that high dose exposure to 14 benzene can cause acute myelogenous leukemia; some 15 types, certain situations, but it can happen. That 16 is the only form that has been clearly established. 17 And CML, there is -- there is no association with 18 high dose -- even high dose exposure to benzene in 19 CML. 20 MR. PERRY: No further questions. 21 EXAMINATION 22 BY MR. PATTON: 23 Q Dr. Pyatt, if it is so clearly established 24 in the relevant scientific community that exposure to 25 gasoline isn't going to cause any leukemia, why did 191 1 all these people and all these journals and all these 2 resources study benzene exposure in the context of 3 gasoline? And why did some of them find an increased 4 risk of certain types of leukemia among gasoline 5 distribution workers? 6 A Which one would you like for me to answer? 7 Q Both. 8 A Okay. Can you start again with the first 9 one? Why they do the studies with gasoline? 10 Q Let me back up. 11 A Okay. 12 Q If it is so widely accepted, as Mr. Perry 13 just asked you, in the scientific community that 14 gasoline exposure just doesn't cause leukemia, why is 15 it still studied in the context of gasoline 16 distribution workers? And more importantly, if it is 17 so widely accepted, how do you reconcile that with 18 the fact that some of these studies do show an 19 increased risk of certain types of leukemia among 20 gasoline distribution workers? 21 A Fine. The reason why I say it is widely 22 accepted in these scientific agencies -- I mean, a 23 lot of the data that's in this pile and a lot of the 24 data that's not in this pile that's in this binder, 25 that is why they know what they know. So this 192 1 literature -- I mean ATSDR, it was 2005 when they 2 came out. IARC's going to reevaluate everything this 3 year. I don't know if gasoline's on that list or 4 not. I actually don't think that it is. They feel 5 like they've -- they know enough about gasoline from 6 the last time they did it. The ACGIH, when they 7 write their TLVs, which they do every year, they 8 update it with the literature. So all of that 9 science has gone into this general acceptance. 10 Now, your question -- which now this is 11 probably the third time -- you can always find 12 spotty, you know, quirky findings here and there. 13 That Jakobsson was a real -- that is a positive 14 study. Jakobsson is a positive study, but it's 15 really small. And there was like three or four 16 leukemias that maybe were associated with petroleum 17 workers. When you look at it collectively, the 18 overall literature, it doesn't -- it's not 19 consistent. It doesn't hold up. And that's what you 20 have to do to say gasoline is or gasoline isn't a 21 carcinogen. 22 Q What gives you the authority, you 23 personally as Dr. Pyatt, to say that it's just not 24 widely accepted? I mean, where do you get that power 25 from? 193 1 A It's not my power. He asked the question. 2 And what I said was, ATSDR said no. There's no power 3 with me. I'm just telling you what they said. If 4 you don't believe it, you know, I can pull up their 5 Web site and show you what they say about gasoline. 6 Q We're misunderstanding each other here. 7 Do you believe it is widely accepted in the relevant 8 scientific community that gasoline exposure and 9 exposure to benzene as a gasoline distribution worker 10 does not create an increased risk of leukemia? Do 11 you believe that? Do you believe it's widely 12 accepted as to those -- what I just stated? 13 A That was kind of a double negative. I 14 believe it is widely accepted in the scientific 15 community, as evidenced by what we were just 16 discussing, that gasoline is not a carcinogen. 17 Q Okay. I heard that part already. 18 A Okay. 19 Q Do you believe it is widely accepted in 20 the scientific community that exposure to benzene 21 from gasoline as a gasoline distribution worker does 22 not cause or cannot cause an increased risk of 23 leukemia? 24 A I don't see that as being any different. 25 Q Okay. What gives you the power -- what 194 1 makes you the guru to say that it's widely accepted 2 as it relates to benzene via gasoline, specific to 3 gasoline distribution workers? 4 A There's no guruness here. I'm not being a 5 guru. You are emphasizing the benzene in the 6 gasoline, as if that is something unique to 7 Mr. Zendejas and it is not commonly found in every 8 other form of gasoline. Benzene is in gasoline in 9 every one of these studies. Benzene is in gasoline 10 that ATSDR evaluated. OSHA, US EPA, ACGIH -- all of 11 those have gasoline that has benzene in it. 12 Q Do you believe there's -13 A Wait a minute. I'm not done yet. 14 Q Okay. I'm sorry. 15 A So collectively, all of those studies have 16 said that gasoline with benzene in it is not 17 carcinogenic. If it's not carcinogenic, it's not 18 causing leukemia. It's not causing atypical CML. 19 It's not causing myelodysplasia. It's not causing 20 whatever you want to say. 21 Q Do you believe there is an increased risk 22 of leukemia by gasoline distribution workers? 23 A By gasoline distribution workers? 24 Q For gasoline distribution workers. 25 A No. 195 1 Q Let me say it in a different way. Do you 2 believe gasoline distribution workers have an 3 increased risk of leukemia? 4 A If you're talking about collective 5 leukemias, no. We've gone through that several 6 times, and we've also discussed what do you mean by 7 an increased risk. 8 Q What about AML? Do gasoline distribution 9 workers have an increased of AML? 10 A That would not be supportable by the 11 scientific literature. 12 Q That's your opinion? 13 A That's the scientific literature's 14 opinion. 15 Q But you're the one making the conclusion 16 that it's not supportable? 17 A That's true. 18 MR. PATTON: Okay. Thank you. 19 THE DEPONENT: Are you done, too? 20 THE VIDEOGRAPHER: We're off the record at 21 3:03. This concludes today's deposition of Dr. David 22 Pyatt. 23 (The deposition concluded at 24 3:03 p.m., October 8, 2009.) 25 196 1 I, DAVID PYATT, do hereby certify that I 2 have read the foregoing transcript and that the same 3 and accompanying amendment sheets, if any, constitute 4 a true and complete record of my testimony. 5 6 7 ________________________________ 8 Signature of Deponent ( ) No Amendments 9 ( ) Amendments Attached 10 Subscribed and sworn to before me this 11 _____ day of ______________, 2009. 12 13 Notary Public: ________________________ 14 Address: _____________________________ 15 _____________________________ 16 My commission expires _________________ 17 Seal: 18 19 20 JLP 21 22 23 24 25 197 1 STATE OF COLORADO) 2 ) ss. REPORTER'S CERTIFICATE 3 COUNTY OF DENVER ) 4 I, Janet Lee Priestley, do hereby certify 5 that I am a Registered Professional Reporter and 6 Notary Public within the State of Colorado; that 7 previous to the commencement of the examination, the 8 deponent was duly sworn to testify to the truth. 9 I further certify that this deposition was 10 taken in shorthand by me at the time and place herein 11 set forth, that it was thereafter reduced to 12 typewritten form, and that the foregoing constitutes 13 a true and correct transcript. 14 I further certify that I am not related to, 15 employed by, nor of counsel for any of the parties or 16 attorneys herein, nor otherwise interested in the 17 result of the within action. 18 In witness whereof, I have affixed my 19 signature and seal this 12th day of October, 2009. 20 My commission expires October 29, 2009. 21 22 ____________________________ Janet Lee Priestley 23 216 - 16th Street, Suite 650 Denver, Colorado 80202 24 25 198 1 - AMENDMENT SHEET - 2 Video Deposition of DAVID PYATT October 8, 2009 3 Zendejas vs. Shell Case No. CV-07-005399 4 The deponent wishes to make the following changes in 5 the testimony as originally given: Page Line Should Read Reason 6 ____ ____ ______________________________ ______ 7 ____ ____ ______________________________ ______ 8 ____ ____ ______________________________ ______ 9 ____ ____ ______________________________ ______ 10 ____ ____ ______________________________ ______ 11 ____ ____ ______________________________ ______ 12 ____ ____ ______________________________ ______ 13 ____ ____ ______________________________ ______ 14 ____ ____ ______________________________ ______ 15 ____ ____ ______________________________ ______ 16 ____ ____ ______________________________ ______ 17 ____ ____ ______________________________ ______ 18 ____ ____ ______________________________ ______ 19 ____ ____ ______________________________ ______ 20 Signature of Deponent: ____________________ 21 Subscribed and sworn to before me this ____ day of 22 ______________, 2009. Notary's signature ________________ 23 (seal) Notary's address __________________ __________________ 24 My commission expires ____________. 25 199