Document gDwVOY5xgKG5X7j1Oq7E8j5ge

CHARLES DOUGLAS YORK vs. TEXACO INC., ET AL NO. E-149,519 IN THE DISTRICT COURT OF JEFFERSON COUNTY, TEXAS 172ND JUDICIAL DISTRICT DEPOSITION OF RICHARD IRONS, Ph.D. On October 26, 1998, the oral deposition of RICHARD IRONS, Ph.D., a witness in the above-styled cause, was taken at the instance of the Plaintiff in the offices of Fulbright & Jaworski, 1301 McKinney, Houston, Texas, pursuant to Stipulation attached hereto. 2 1 Those persons present were as follows: 2 3 MR. HERSHEL HOBSON Attorney at Law 4 2190 Harrison Avenue Beaumont, Texas 77701 5 Counsel for Plaintiff, 6 CHARLES DOUGLAS YORK 7 8 9 MR. LARRY THORPE 10 Reaud, Morgan & Quinn 801 Laurel Street 11 Beaumont, Texas 77701 12 Counsel for Plaintiff, CHARLES DOUGLAS YORK 13 14 15 16 MR. STEPHEN DILLARD Fulbright & Jaworski 17 1301 McKinney Houston, Texas 77010 18 Counsel for Defendants, 19 Mobil Chemical Company, Inc. Texaco, Inc., 20 Texaco Chemical Company Texaco Refining and Marketing 21 Chevron, U.S.A., Inc., Chevron Chemical Company 22 Unocal Corporation 23 24 25 3 1 MR. CHARLES STANTON PERRY Mehaffy & Weber 2 500 Dallas Street, Suite 1200 Houston, Texas 77002 3 Counsel for Defendant, 4 Du Pont 5 6 7 MR. KIRK MARTIN 8 Jenkins, Grove & Martin 2615 Calder Avenue, Fifth Floor 9 Beaumont, Texas 77702 10 Counsel for Defendant, American Petrofina 11 12 13 14 STARLA LEE FOUST, CSR Charlotte Smith Reporting, Inc. 15 235 Orleans Street The Kyle Building 16 Beaumont, Texas 77701-2399 17 18 19 VIDEOTAPE OPERATOR/TECHNICIAN: 20 Warriene Flatt 21 Legal Images P.O. Box 315 22 Gilchrist, Texas 77617 23 24 25 4 1 EXHIBITS INDEX 2 DEPOSITION OF RICHARD IRONS, Ph.D. 3 4 October 26, 1998 5 6 EXHIBIT NO. DESCRIPTION PAGE 7 8 NOS. 1 THROUGH 41 76 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 5 1 THE REPORTER: Please state the 2 stipulations on the record. 3 MR. HOBSON: Texas Rules of 4 Civil Procedure. 5 MR. DILLARD: He will read and 6 sign. 7 THE VIDEOGRAPHER: We're on the 8 record at 2:02 p.m. 9 10 RICHARD IRONS, Ph.D., 11 having been duly sworn, testified as follows, 12 to-wit: 13 14 EXAMINATION BY MR. HOBSON: 15 Q What questions have you been asked to 16 answer in this case, Dr. Irons? 17 A Basically I was asked to evaluate the case 18 materials that were provided to me and to render an 19 opinion as to whether or not Mr. York's aplastic 20 anemia, in fact - whether it was more probable than 21 not that it was associated with exposure to benzene 22 and that it was a benzene-induced aplastic anemia. 23 Q The last answer that you gave there about 24 his aplastic anemia and his exposure and whether or 25 not his aplastic anemia was caused by benzene - is 6 1 there a sequence there that you went through? Did 2 you evaluate exposure first and then the kind of 3 aplastic anemia he has, or how did you do that in 4 your mind? 5 A Based upon the order in which the 6 materials were made available to me, the first 7 analysis that I performed was to evaluate the 8 medical records and the pattern of presentation and 9 the characteristics of his aplastic anemia in the 10 context of what I would expect to see associated 11 with benzene, and subsequent to that to review the 12 documentation and the depositions that were made 13 available to me in order to evaluate the - his 14 potential likelihood that exposure to benzene was 15 associated with that. So, the pattern and 16 presentation of aplastic anemia first and the 17 opportunity for exposure second. 18 Q On behalf of which Defendants are you 19 appearing as an expert witness in this case? 20 A You would have to ask someone with 21 expertise other than mine for that. I believe 22 Texaco. I am not certain what other Defendants are 23 involved in this case. 24 Q So, I take it your contact so far in this 25 case has been through Mr. Dillard, then -- 7 1 A That's correct. 2 Q -- and not any other attorneys associated 3 with the case? 4 A Not to the best of my recollection. 5 Q You said that you started off with 6 evaluating the case materials. What case materials 7 have you been provided with and in what order and 8 when? 9 A I made a brief list of what I received in 10 this case: The medical records in general - and I 11 haven't in my notes distinguished those, although, 12 they are rather massive - and a variety of different 13 depositions. 14 Q Did you delineate whose depositions you 15 have been provided? 16 A Yes. 17 Q May I have who those were, please? 18 A Charles Douglas York, Frank Gardner, Ethan 19 Natelson, John Bickers, John Dement, Frank Parker, 20 Craig Morin. 21 Q That's all the depositions you have been 22 provided in this case? 23 A That's correct. 24 Q And about when did you receive those 25 depositions? 8 1 A Certainly the major - most of them, I 2 received in March and April of this year, between 3 January and March and April of this year. 4 Q And when were you first contacted about 5 being an expert in this case? 6 A I believe the first time I had any kind of 7 conversations at all would have been by telephone 8 with Mr. Dillard; and to the best of my recollection 9 it was in 1997, probably in the summer of 1997. 10 Q Besides Mr. York's medical records and the 11 depositions you listed, what else have you been 12 provided? 13 A I believe that's it. 14 Q Did you receive the attachments to any of 15 the depositions that you were provided? 16 A Yes. The -- I have received the exhibits 17 to some of these, not all of them. 18 Q Did you receive the documents that 19 Mr. Morin had been provided? 20 A No. 21 Q Let's talk about the first part of what 22 you did. The pattern of exposure I think is what 23 you said was the first element that you considered; 24 is that right? 25 A No, the pattern of presentation -- 9 1 Q I beg your pardon 2 A -- of Mr. York's disease. 3 Q The pattern of presentation. Tell me what 4 you saw in the way of pattern of presentation, 5 please. 6 A Well, essentially there were some records 7 and some analyses that were performed on bone marrow 8 and peripheral blood immediately preceding the 9 definitive diagnosis, suggesting sideroblastic 10 anemia. 11 This was immediately followed by an 12 extensive workup and diagnosis of aplastic anemia. 13 The presentation was that of a classic idiopathic 14 aplastic anemia, primary aplastic anemia, 15 pancytopenia, and acellular bone marrow with ringed 16 sideroblasts, initial treatment refactory to B12 and 17 folate. These were the principal characteristics 18 that were important to me. 19 Q All right. What literature do you have 20 that says that this is a characteristic pattern of 21 presentation for an idiopathic aplastic anemia? 22 A What literature do I have? 23 Q Yes, sir. 24 A Certainly this is a pattern that is 25 described throughout the literature - certainly the 10 1 articles and books published by Dr. Young; Jandl in 2 his hematology text describes a similar pattern. 3 Certainly the characteristics of a primary aplastic 4 anemia are found in many articles. I provided 5 some - brought some with me here today. 6 I would say that the best central source 7 for a description of this pattern would be the work 8 by Dr. Young. Dr. Natelson, who I believe is a 9 treating doctor in this case, has also published 10 cases describing this pattern. 11 Q Well, sir, I'm trying to find out can you 12 point me to a page in a text or an article that says 13 that this is a pattern of presentation that is 14 typical for idiopathic aplastic anemia? 15 A No. I don't have Dr. Young's book here, 16 but that would be the first place that I would look 17 for a general description. 18 Q Yes, sir. Just so I'm clear, I'm looking 19 for a statement that idiopathic aplastic anemia 20 follows this pattern of presentation. 21 A Yes. Well, first of all, the criteria for 22 aplastic anemia include pancytopenia and an 23 acellular marrow. So, those would be two criteria 24 that I would expect to see. 25 Q Is that in any kind of aplastic anemia or 11 1 only idiopathic aplastic anemia? 2 A Idiopathic, most certainly; it would not 3 apply in general to any aplastic anemia. Certainly 4 in the case of benzene, the prevailing presentation 5 would be different. -For one thing one does not 6 usually expect to see in the majority of patients an 7 acellular marrow. Those aplastic anemias that have 8 been associated with benzene tend to have a moderate 9 cellularity or even hypercellularity. 10 Also, the pancytopenia is usually preceded 11 by in many cases a lymphocytopenia and in some cases 12 a thrombocytopenia. 13 The other characteristic that is really 14 quite remarkable for benzene is the absence of 15 demonstration or at least recognition of ringed 16 sideroblasts associated with benzene-induced 17 aplastic anemia. 18 Q Okay. But you still haven't told me the 19 reference for idiopathic aplastic anemia. 20 A Well, I have referred you to Neal Young's 21 book. I don't have a copy of it here. I'm trying 22 to see whether in the materials I have brought I see 23 a general description. So far, I haven't seen one. 24 (Reviewing documents) I don't think I have 25 precisely what you are asking for with me. 1 Q All right. Let's turn to what you 2 answered a moment ago. 3 Do you have any human epidemiological 4 studies that show that benzene-induced aplastic 5 anemia meets the criteria that you previously 6 described? 7 A In terms of the characteristics that I 8 described for benzene-induced aplastic anemia? 9 Q Yes, sir. 10 A There are several descriptions in the 11 literature in collections of cases associated with 12 characterizing individuals poisoned by benzene and 13 benzene-induced aplastic anemia and bone marrow 14 suppression. The principal authors that I would 15 refer you to are Goldwater and Greenburg, their 16 analysis of rotogravure workers and benzene 17 suppression and the aplasia associated with benzene 18 poisoning. 19 Certainly the collective cases of Aksoy 20 and I brought at least one reference with me there, 21 but there are several. And he describes these same 22 characteristics in both his book on benzene 23 carcinogenesis, as well as some of the manuscripts. 24 Those would be the principal references. 25 There are a number of other reports that 13 1 describe various aspects of this. The most recent 2 would be a study of the workers in Brazil, I believe 3 by Ruiz, that describes some of these same 4 characteristics. 5 Q Are any of the those - the Goldwater and 6 Greenburg, the Aksoy articles, or the Ruiz article 7 human epidemiological studies? 8 A The closest that comes to it is basically 9 Greenburg and Goldwater, which is a controlled 10 study. The Aksoy study really represents a 11 collection of cases. The Ruiz study, I believe, is 12 a collection; but let me look at it again. 13 (Reviewing document) It's basically a 14 series. It's not a quantitative study. 15 Q "It's" being the Ruiz study? 16 A Yes. 17 Q Okay. Let's talk about Goldwater and 18 Greenburg for a moment then. 19 Do they report relative risk or 20 statistical significance for their publication? 21 A No, they don't. 22 Q How many aplastic anemias did Goldwater 23 and Greenburg report on? 24 A It is certainly based upon the criteria 25 that they are using at that time. They have a 14 1 fairly -- They have approximately -- They have 2 80-plus individuals that have some evidence of bone 3 marrow suppression or benzene poisoning. In their 4 follow-up over several months, they have at least 5 four that show persistent abnormalities over a year 6 later. 7 Q Did the 80-plus total individuals that you 8 told me about initially all have aplastic anemia? 9 A No. 10 Q How many had aplastic anemia? 11 A Well, using their criteria for persistent 12 changes, they have at least four that are candidates 13 based upon the current - what we would currently 14 define as aplastic anemia. 15 Q Well, can you tell by looking at the 16 Goldwater and Greenburg paper of those four that had 17 persistent problems whether or not they, in fact, 18 have or had what we would today call aplastic 19 anemia? 20 A If we were going to reevaluate or 21 rediagnose these patients based upon current 22 criteria, it's not clear to me which of these would 23 be reclassified as having a definitive aplastic 24 anemia. Certainly many of them would be classified 25 as having persistent hematopoietic abnormalities 1 associated with exposure. 2 Q Do Goldwater and Greenburg use the term 3 "aplastic anemia" in their paper? 4 A No, they don't. 5 Q For the 80-plus total individuals who were 6 initially seen, what were the controls? 7 A The controls were taken from individuals 8 that had -- (Reviewing document) I'm trying to see 9 if I can find a precise description. I have seen it 10 before. The controls were matched to the extent 11 that they provided a reasonable control for the 12 working conditions except for the exposure to 13 benzene. I do recall that. It was the first real 14 control study of benzene-exposed workers, and the 15 control group is included. I'm looking for a 16 description. 17 Okay. 81 industrial workers that were 18 employed in a factory where no demonstrable exposure 19 to benzene existed was their description of the 20 control group. 21 Q So, one control person for each case? 22 A I'm not exactly sure whether it's 23 one-to-one. I think it was based more on the 24 availability of individuals that fit the criteria. 25 I'm not sure if it's one-to-one. 16 1 Q So, more just happenstance of who they 2 could find and how many they needed? 3 A I think -- My understanding is it was a 4 single group of workers. I don't think they 5 collected them, but I'm not seeing a description of 6 it right here. 7 Q But no attempt that you can see to match 8 by age or sex or race or any other parameter? 9 A The age distribution was similar to those 10 that were in the exposed group is all that is in 11 this particular study. I do recall -- Well, I have 12 had conversations with Dr. Goldwater about this 13 group many years ago; but as I sit here, I can't 14 recall what the nature of the description is. 15 Q Is there anyplace in Dr. Goldwater's and 16 Dr. Greenburg's paper that says that this particular 17 kind of disease presentation is the only kind you 18 should expect to see from benzene? 19 A Well, at this point in time this was the 20 only reasonably carefully studied large group of 21 benzene-exposed - highly-exposed workers that had 22 been conducted; so, I don't think that you would 23 expect to see that kind of a conclusion. 24 Q And, in fact, don't see that kind of 25 conclusion? 17 1 A No. This basically is the first carefully 2 characterized exposure group that had any kind of 3 controls done. 4 Q In any of the items that you brought, is 5 there such a statement that benzene will produce 6 only the pattern of presentation that you described 7 earlier to the exclusion of others? 8 A Well, as I said before, one would not 9 reasonably expect to see that; and they haven't said 10 that. It's also impossible to prove a negative; so, 11 I would be very surprised to see anyone make an 12 affirmative statement that this should exclude all 13 other possibilities. I certainly wouldn't say that. 14 Q I take it you would classify Mr. York's 15 aplastic anemia as idiopathic? 16 A Yes. 17 Q Now, you said that another part of your 18 presentation - I'm sorry - your evaluation was 19 looking at opportunity for exposure? 20 A Yes. 21 Q What did you find in the way of 22 opportunity for exposure to benzene for Mr. York? 23 A Well; the first thing that struck me was 24 in the medical records there's an indication that 25 certainly a diagnosis - he had no previous 18 1 recollection of exposure to benzene. More 2 importantly, the symptoms that he described were not 3 consistent with those that -- Or the lack of 4 symptoms was significant to me with respect to 5 consistent with exposure levels that I expect to see 6 associated with aplastic anemia. 7 So, in the initial material that I 8 reviewed, that was all the information that I had 9 that really provided me with any indication of what 10 his exposure might have been or might not have 11 been. 12 Mr. Morin's deposition is basically what I 13 used in confirming my own impression that there is 14 just no evidence that Mr. York was exposed to levels 15 of benzene that would be consistent with the 16 development of aplastic anemia. 17 Q Let's start with your assessment of what 18 level of benzene exposure is necessary to produce 19 aplastic anemia. 20 A Certainly if we read through the 21 collection of cases, the anecdotal cases and the 22 descriptions of hygiene conditions that are 23 associated with the body of cases that exist in the 24 literature today, most of these coming from the 25 first half of the century, we are talking about 19 1 massive exposure levels, certainly exposures on the 2 order of 100 parts per million or greater, repeated 3 exposures, high levels. Those are actually low for 4 some of the descriptions. So, certainly exposures 5 in that, above 100 parts per million, are associated 6 with the risk of developing aplastic anemia. 7 There may or may not be exposures in the 8 50 to 100 parts per million range that may be 9 associated with aplastic anemia. I don't think the 10 literature is particularly clear on that. And 11 these exposures are usually associated with a 12 variety of other symptoms, as well. 13 Q Do you have any literature that you can 14 cite me to that says that exposure below 100 parts 15 per million to benzene will not produce aplastic 16 anemia? 17 A Well, we have had this discussion before 18 in different contexts. I don't think that it's 19 appropriate and certainly it's not a scientifically 20 valid exercise to try to prove a negative. What one 21 does is look at what associations and what exposures 22 have been associated with the development of the 23 disease. And certainly in the case of aplastic 24 anemia, we are dealing with what is widely 25 considered to be a high-dose phenomenon. 20 1 The vast majority of cases involve 2 exposures of 300, 600, 1,000 parts per million or 3 greater. These are clearly associated with bone 4 marrow suppression and aplastic anemia development. 5 There are some references in the Greenburg 6 work that some of the exposures may have been 7 100 parts per million or lower; but in the context 8 in which they are reporting, you have to realize 9 that these would be considered relatively low 10 exposures. 11 So, I don't know of any study that would 12 that has even been designed to allow for -- As I 13 said before, science, you don't prove a negative. 14 So, I can't point to a study that says that 15 exposures below 100 parts per million don't cause 16 aplastic anemia. There are no credible exposure 17 scenarios that I know of that would certainly 18 associate aplastic anemia with actual exposures that 19 didn't involve scenarios involving 50 ppm, 100 ppm, 20 or greater. 21 Q What studies can you cite me to where 22 exposures of less than 50 parts per million have 23 been demonstrated in the work force 24 epidemiological studies, I'm talking about now - and 25 where aplastic anemia was an outcome that was looked 21 1 for? 2 A Well, with the caveat that the exposure 3 certainly the low level exposures are, I have some 4 real problems because they were modeled rather than 5 actually measured. The China study certainly has 6 evaluated aplastic anemia and has looked at exposure 7 paradigms that at least ostensibly involve lower 8 than 50 parts per million exposure. 9 There is no evidence that I have seen in 10 those studies that aplastic anemia is associated 11 with those particular exposure groups. And I must 12 add also that the exposure scenarios that are 13 described there are particularly unreliable for low 14 level analysis, and that's been the subject of a 15 number of discussions and published opinions. 16 Q When you say "low level" in that context, 17 how do you use it? 18 A I believe their low level or their lowest 19 level of exposure scenario bounds a range of 1 to 20 10 ppm years. I don't believe there are 21 Certainly Dr. Hayes hasn't indicated that there are 22 any aplastic anemias in that group. 23 In general that study is divided into at 24 least three different scenarios - 1 to 10, 10 to 25 and it depends upon the particular analysis they are 22 1 doing - what they call 10 to 30, and then greater 2 than 30. Some of their exposure levels are greater 3 than 100, however. 4 Q So, if I look in the Hayes papers, I will 5 find the analysis that you are speaking of? 6 A If you look across the board, you will see 7 the overall analysis of the modeling of the 8 exposures. There are problems with that. The 9 actual modeling only accounts for about 30 percent 10 or about a third of the overall exposures they are 11 attempting to in terms of overall exposure metric 12 and probably only 3 percent of the high exposure 13 groups. 14 They had nine aplastic anemias in the 15 entire cohort. I don't believe any of them were 16 associated with the lower exposure group. And even 17 that group is consistent -- The exposure metric is 18 consistent with excursions above 100 parts per 19 million. 20 So, I don't think that study provides any 21 indication that exposures of less than 100 or 22 50 ppm's on a repeated basis in ambient air is 23 associated with aplastic anemia; but it certainly 24 provides additional evidence that high-level 25 exposure is associated with aplastic anemia. 23 1 Q Any other papers that you would cite me to 2 for this proposition? 3 MR. DILLARD: Herschel, y'all 4 talked about several propositions. 5 Just to make sure that the record is 6 clear, which one are you referring 7 to? 8 MR. HOBSON: The papers that 9 demonstrate no association between 10 aplastic anemia where they 11 specifically looked for - and 12 exposures to benzene below 50 parts 13 per million. 14 15 (By Mr. Hobson) 16 Q That was what you were answering, I think, 17 was it not? 18 A Well, as I said before, I don't know any 19 study that is going to demonstrate no association. 20 There are numerous studies in the petroleum industry 21 looking at mortality in the petroleum industry that 22 provide a surrogate for benzene exposure, and you 23 certainly don't see any increases in aplastic anemia 24 in those studies. 25 So, conversely if what you are asking is: 24 1 Are there any studies associated with either 2 specifically benzene or where benzene is certainly a 3 potential agent in the occupational setting, that 4 have evaluated mortality rates that would have 5 encompassed aplastic anemia, there are several 6 petroleum refinery studies - Wong, some of the more 7 recent studies by Schattner - that demonstrate no 8 increased mortality and certainly have not observed 9 an increased incidence of aplastic anemia in those 10 populations. 11 Q In the -- Let's take the Wong petroleum 12 refinery studies then. Which of those can you show 13 that breaks out the refinery workers with 14 occupational exposure to benzene? 15 A I don't have those with me today. I'm not 16 in a position where I could do that. 17 Q Are you telling me that they do break out 18 the refinery workers with occupational exposure to 19 benzene and quantitate or semiquantitate those 20 exposures? 21 A Dr. Wong's studies certainly have looked 22 at exposure in the petroleum industry. I believe, 23 if I'm not mistaken - and I may be not citing this 24 exactly right - but I think that Dr. Schnatter has 25 recently published at least one, if not more than 25 1 one, study looking at mortality in the refinery 2 industry in a variety of different plants. And I do 3 not recall seeing any increased incidence of 4 aplastic anemia in those studies. 5 Q Well, let's go at it this way: Is 6 everyone who works in a petroleum refinery equally 7 exposed to benzene? 8 A Surely not. 9 Q Which ones are more highly exposed than 10 others? 11 A Well, certainly those that have the 12 potential for exposure are going to be those who 13 work in a benzene production area or an area where 14 the solvent content of - or the benzene content in 15 the solvents is going to be higher and where there 16 is an opportunity for exposure. 17 Q And what percentage of the particular 18 refinery population would that be? 19 A That, I couldn't tell you as I sit here. 20 Q Half of them or more? 21 MR. PERRY: I'll object to the 22 form. 23 A As I sit here, I couldn't tell you. I 24 think it's going to vary with the individual cohort 25 that you are looking at or evaluating. 26 1 Q So, in order to know the answer to that 2 question, one would have to evaluate the exposures 3 of the cohorts specifically for benzene? 4 A At least in terms of whatever the 5 surrogate for exposure is. What I'm saying is I 6 know of no studies in that industry or in refinery 7 studies, of which there are some recent studies, 8 that I recall showing any increased incidence of 9 aplastic anemia in those studies. 10 So, certainly if, in fact, one were going 11 to define a potential group that would have higher 12 exposure to benzene than others, refinery workers in 13 an environment where there is potential for exposure 14 to benzene would certainly qualify. 15 Q Well, surely it would depend on how 16 diluted you made the benzene-exposed group - would 17 it's not - as to whether you would find any outcome? 18 A Not necessarily. It would depend -- If, 19 in fact, the exposure is the critical issue here, 20 then the level of exposure would be a major 21 determinant of whether you would see an increase at 22 all. 23 Q Did you say two different names? I'm 24 having a hard time following you. You said 25 "Shattner" and then you just said -- 27 1 A "Schnatter." 2 Q "Schnatter." And that's only -- You did 3 not say "Shattner"? 4 A I don't believe so. 5 She is a candidate for governor in 6 Colorado. 7 Q Schnatter? 8 A Schattner. 9 Q Easy for you to say. Let's spell the one 10 you said so that we will have it right. 11 A I believe that he spells it 12 S-c-h-n-a-t-t-e-r. 13 Q And you say you believe that Schnatter has 14 published studies of refinery workers? 15 A That's correct. 16 Q That break out their benzene exposure? 17 A That at least evaluate benzene exposure, 18 yes. 19 Q And whose refinery was being studied - or 20 refineries? 21 A There's a series of companies. I can't 22 tell you as I sit here. 23 Q You didn't bring those with you? 24 A No, I did not. 25 Q All right. Let's go back to our pattern 28 1 of presentation. Is there anything about the 2 genetics of Mr. York that you think is germane to 3 this case one way or the other? 4 A It would have been useful to have had 5 cytogenetic data at the time of his diagnosis. That 6 apparently was not done. And the reason for that is 7 that in, certainly, cases of secondary aplastic 8 anemia and in cases of benzene poisoning, it is not 9 unusual to see clonal chromosomal aberrations. 10 However, I think a functional surrogate to 11 that certainly in the context of reaching my opinion 12 is the fact that he was, in fact, successfully 13 treated with anticlonacyte globulin, which is 14 clearly a pattern that is seen in primary idiopathic 15 aplastic anemia. Certainly in aplastic anemias with 16 clonal injury, that is not usually the most 17 prevalent outcome. 18 So, his successful treatment with 19 immunosuppressive therapy is consistent, more 20 consistent with a primary than a secondary. Other 21 than that, I have no cytogenetic information one way 22 or the other. 23 Q Let's talk about how you are using primary 24 versus secondary. 25 A Primary is basically -- What I mean as 29 1 primary idiopathic aplastic anemia, secondary would 2 be aplastic anemia, in this case obviously secondary 3 to benzene. 4 Q So, secondary aplastic anemia is any 5 aplastic anemia caused by something? 6 A Yes, or with a known cause. 7 Q Are you saying, then, that all aplastic 8 anemias with a known cause are fatal? 9 A No. Secondary aplastic anemias tend to 10 have a poorer prognosis, and certainly the 11 literature description of cases associated with 12 benzene have a poor prognosis. 13 Q Does that mean that the cases that are 14 secondary to benzene exposure in the literature 15 don't survive? 16 A It means they have a poor prognosis. They 17 have a less likelihood of survival. And certainly 18 those that have clonal lesions independent of their 19 origin have a poorer survival. 20 Q But they are not always fatal? 21 A Not always fatal, no. They have a less 22 favorable prognosis than primary idiopathic 23 following treatment. 24 Q So, you are saying that the fact that 25 Mr. York didn't die from his aplastic anemia is 30 1 indication that benzene didn't cause it? 2 A No. I'm saying that his very positive 3 in fact, remarkable response to immunosuppressive 4 treatment is more consistent with a primary 5 idiopathic aplastic anemia than one that has a 6 clonal lesion or one that would be associated with 7 benzene exposure. 8 Q But one doesn't exclude the other? 9 A I'm not sure what you mean. I wouldn't 10 exclude anything. What I'm saying is that the 11 likelihood, it's much more probable that a favorable 12 response to treatment is associated with the primary 13 idiopathic aplastic anemia than a secondary or one 14 that has a clonal lesion. That's well-described in 15 the literature. 16 Q Are you saying that you can show me a 17 case -- I'm sorry. 18 Are you saying that there are no cases 19 recorded where benzene is reported to be the 20 causative agent of aplastic anemia where a rapid 21 recovery was made? 22 A To my knowledge I know of no studies that 23 have described any group of patients with a 24 benzene-induced aplastic anemia where 25 immunosuppressive therapy has proved successful. If 31 1 you look at the aplastic anemia literature in 2 general, those with clonal lesions which would be 3 more consistent with the benzene exposure have a 4 poorer prognosis. 5 That doesn't mean that none of them 6 survive. It simply means that they have much less 7 likelihood. Certainly in the case of Mr. York, we 8 are dealing with an individual who had an extremely 9 favorable response to therapy - remarkable, even. 10 It was very early. It was complete with one series 11 of treatment, and it's been a persistent recovery 12 remission for the better part of 15 years. That's 13 an incredibly favorable response. 14 Q Is there no other 15-year survival 15 reported in a benzene-induced aplastic anemia? 16 A Where you have a diagnosis of aplastic 17 anemia, I'm sure there have been some cases of 18 recovery. I wouldn't exclude that possibility. 19 It's not impossible. I don't know of any series 20 that I can point to where one has even a significant 21 subgroup of individuals like that. Certainly the 22 prevailing description of those cases is a fairly 23 poor prognosis, either with respect to lack of 24 response to therapy or a subsequent relapse. 25 Q In the four patients that Drs. Goldburg 32 1 and Goldwater - I'm sorry - Goldwater and Greenburg 2 reported, did all four of those people with 3 persistent disease die -4 A I'm not sure. 5 Q -- from the disease? 6 A I'm not sure. I'm not sure how far they 7 go. 8 (Reviewing document) No. They only went 9 out two years, and those four individuals had 10 distinctly abnormal blood pressures at two years. 11 Q But no report as to whether they resolved 12 or did not? 13 A I have no information on that. 14 Q Is there anything in any of the references 15 that you brought that says that the pattern of 16 presentation that you describe for benzene and 17 aplastic anemia is typical for benzene? 18 A Well, if you look at them as a whole, you 19 see a picture that is reasonably consistent and is 20 not consistent with what you expect to see in 21 primary idiopathic aplastic anemia. 22 Probably the closest to describing a 23 consistent pattern or at least recognizing a 24 consistent pattern is that of the study of Ruiz, et 25 al. It's a relatively recent study. Most of the 33 1 rest of these were performed in a context where it 2 was the state of the art, this was the disease at 3 hand, and they were characterizing what was seen. 4 So, they weren't really referring to older 5 literature in terms of consistency. The Ruiz study 6 does make some references to what is seen in the 7 older literature. 8 Q Well, I guess what I'm trying to find out 9 is that what I hear you saying is it's your 10 assessment, your opinion, that there is this pattern 11 of presentation that is typical for benzene; and I'm 12 trying to find out is that something that other 13 people have said in writing? 14 Oh, yes. Certainly if you look at Aksoy 15 and in his book, to a lesser extent the publication 16 I brought - but there are several - he describes the 17 characteristics that are seen associated with 18 benzene - the aplasia - and with benzene poisoning. 19 And he describes essentially these same features. 20 Ruiz, as well, describes some of the same 21 features. It's a pattern that has been seen and 22 that is basically not a pattern that I have 23 devined. I'm reflecting what these authors have 24 said. 25 Yes Sir. But do they say - these 34 1 authors - that it's typical for benzene? 2 A Certainly Aksoy describes the prevailing 3 presentation with lymphocytopenia as being 4 characteristic of benzene and has been repeatedly 5 reported. Ruiz notes the nature of the bone marrow 6 cellularity. Vigliani -- Some of your original 7 Vigliani studies suggest that the benzene presents 8 with a relatively unique presentation. 9 So, I think if you take these authors as a 10 group, this particular pattern has been described; 11 and several aspects of it appear to be consistently 12 seen in benzene-exposed populations in different 13 decades and on different continents. 14 Q Yes, sir. But can you show me in their 15 papers where they say that this is a typical 16 presentation for benzene-induced aplastic anemia? 17 A I can show you in these various papers 18 where each of the aspects that I am describing are 19 reported as being consistent with and typical of 20 benzene-exposed individuals. And, so, taken as a 21 whole I think this literature supports a relatively 22 unique presentation for benzene compared to that 23 which you expect to see in primary idiopathic 24 aplastic anemia. 25 This opinion is shared by the authors that 35 1 I am citing. 2 Q All right. If it's that pervasive 3 throughout the papers, can you show me one where it 4 uses the term "typical"? 5 A That particular wording? No. As I said 6 before, the characteristics that they are describing 7 are typical. They are describing a prevailing 8 pattern of presentation. 9 In the case of Aksoy, he's describing a 10 prevailing pattern of presentation; and he describes 11 the initial changes that are seen with benzene that 12 are not seen in other cases of aplastic anemia. 13 In the case of Ruiz, for example, he 14 points out in none of the patients ringed 15 sideroblasts were observed. 16 Ringed sideroblasts are a very frequent 17 observation in cases of primary idiopathic aplastic 18 anemia. I can't think of a single case in the 19 benzene literature where that has been observed. 20 Q Can you show me, then, where it says in 21 the benzene literature that if you find ringed 22 sideroblasts, you should ignore any benzene exposure 23 and attribute this to idiopathic aplastic anemia? 24 A I never said that. 25 As I said before, my opinion in this case 36 1 is based upon two observations: One, that the 2 presentation of Mr. York - of Mr. York's aplastic 3 anemia is more consistent a priori with a primary 4 idiopathic aplastic anemia than with a pattern I 5 would expect to see with benzene; and, two, that I 6 have seen no evidence that he was exposed to benzene 7 at concentrations or in a scenario of exposures that 8 would be anything like what is associated with 9 development of aplastic anemia secondary to benzene. 10 Q In your assessment of Mr. York's exposure 11 to benzene, did you consider whether or not he was 12 washing his hands or tools in benzene? 13 A I have seen no evidence that would lead me 14 to believe that that, in fact, was the case. 15 Q Would washing your hands and tools and 16 clothes in benzene present a significant exposure to 17 benzene in your view? 18 A If what you are asking me is would washing 19 your hands and clothes and tools in benzene provide 20 the kind of exposure that would be consistent with 21 the development of aplastic anemia if, in fact, one 22 were to do that day in and day out repeatedly for 23 some period of time depending upon the 24 susceptibility of the individual from six months to 25 20 years, that would certainly be consistent with an 37 1 exposure level that could lead to the development of 2 aplastic anemia. 3 But then, again, there would be other 4 symptomatology that I don't see in the records, I 5 don't see in his medical records; and it's 6 inconceivable to me that he could experience such an 7 exposure without additional symptomatology. 8 Q What other symptomatology would you expect 9 one to have who washed their hands and tools and 10 clothes in benzene? 11 A Dizziness, headaches, central nervous 12 system effects, dermatological abnormalities, 13 problems with -- Certainly the hands would be 14 subject to a great deal of damage, defatting. 15 I don't see anything in any of the records 16 that would lead me to believe that he had 17 encountered these kinds of exposures. 18 Q So, without those kinds of exposures 19 I'm sorry. 20 Without those kinds of symptoms, you say 21 it just can't be possible for a person to wash their 22 hands and tools and clothes in benzene on a regular 23 basis? 24 A What I'm saying is in the absence of 25 industrial hygiene data or evidence to support that 38 1 kind of exposure, that the lack of that collateral 2 symptomatology is not consistent with exposure to 3 the levels necessary to produce aplastic anemia. 4 That is not to exclude the possibility 5 that anyone might have occasion - although certainly 6 I wouldn't recommend it - to wash their tools in 7 benzene. It would require not just a single 8 exposure at that level, but multiple exposures for a 9 considerable duration of time to produce the kind of 10 exposure necessary to produce aplastic anemia based 11 upon what we know about the disease. 12 Q So, washing your tools every day for six 13 months, every workday for six months, five days a 14 week? 15 A If an individual did that, I would expect 16 to see additional evidence of toxicity, if only 17 dermal. There is no evidence anywhere in the 18 medical records that I can see that those complaints 19 were made. 20 And, in fact, Mr. York testified or at 21 least said to his treating doctors that he did not 22 know that he was exposed to benzene. He certainly 23 didn't describe that in his initial presentation. 24 And I think it's inconceivable that an individual 25 would work in that environment, have that kind of 39 1 exposure and not at least be cognizant of the 2 exposure. 3 Q I'm interested in your concepts. I would 4 like to talk more about people washing their hands 5 with benzene or washing their tools with benzene or 6 washing their clothes with benzene. 7 Would you know one way or the other if 8 this has gone on in the Gulf Coast refineries in the 9 Beaumont/Port Arthur area in the past? 10 A I have no knowledge with respect to that 11 and have never seen any demonstrable evidence that 12 that, in fact, has occurred. 13 I am saying that in the case of Mr. York, 14 that indicating that he was not previously exposed 15 to benzene at the time of his diagnosis is not 16 consistent with someone who had repeatedly washed 17 his clothes and tools in benzene. He would be aware 18 that he had been exposed to benzene. 19 Q I'm interested in the symptomatology - the 20 dizziness, the dermatitis, the other things that you 21 describe. Are you saying that if a person regularly 22 washed their hands or tools or clothes in benzene, 23 maybe not every day, but on a regular basis, that 24 that would just be something totally inconsistent 25 with having no reports of dermatitis and dizziness 40 1 in the work force? 2 MR. PERRY: Object to the form. 3 A It is not -- I find it highly unlikely and 4 I don't see how it's consistent that you can 5 describe a scenario in which an individual was 6 exposed to levels that have been associated with the 7 development of aplastic anemia in the past without 8 incurring those types of symptomatology. 9 The exposures that have been described in 10 the past, it's charitable to say that exposures at 11 100 parts per million are associated with aplastic 12 anemia. The vast majority have involved exposures 13 that probably exceeded 300 and maybe as much as 14 1,000 parts per million; but you would expect to 15 have some central nervous system minor 16 symptomatology at least between 50 and 150 parts per 17 million. 18 And to not recognize any exposure is not 19 consistent with exposure at those levels. 20 Q I take it, then, that Drs. Goldwater and 21 Greenburg reported central nervous system effects in 22 the people with aplastic anemia that they studied? 23 A Goldwater and Greenburg focused on the 24 hematologic abnormalities that are associated with 25 benzene exposure. I don't recall whether they 41 1 discussed other symptomatology at all. 2 Certainly there are a number of other 3 references, including those that I brought with me 4 here today, that describe exposures associated with 5 the development of frank aplastic anemia in which 6 those types of symptoms are frequently reported. 7 And those levels of exposure - the levels of 8 exposure that have been documented exceed - greatly 9 exceed the symptomatology that we have discussed. 10 Q I guess I'm having a little bit of a 11 problem. Are you saying that these symptoms are 12 frequently reported or that they are always reported 13 for benzene-induced aplastic anemia people? 14 A They are very frequently reported. I 15 would -- Without scouring the literature, I'm not 16 prepared to tell you always ever. 17 Q What about in the ones that you have 18 brought? Can you tell me for the papers that you 19 have brought where you have a benzene-induced 20 aplastic anemia that there were reports from the 21 victims that they had dizziness, they had 22 dermatitis, that they had the other symptoms that 23 you described earlier? 24 A It will take me a minute. 25 (Reviewing documents) Certain -- 42 1 Parenthetically certainly Aksoy describes these 2 types of symptoms in shoe workers exposed. 3 Q What do you mean by "parenthetically"? 4 A If you read his book, he describes the 5 symptomatology. 6 Q Is that what you are reading now? 7 A (Reviewing document) I am looking now at 8 one of the papers that I brought with me that is 9 from - that is looking at hematological effects in 10 chronic benzene poisoning in 217 workers. And it 11 clearly describes the hematological abnormalities. 12 I'm seeing whether they report some of the other 13 findings. 14 They don't describe any collateral 15 symptomatology in this paper, but in his book he 16 definitely does. 17 This is typical of several that I brought 18 that basically examine -- They are either from the 19 U.S. Public Health Service or the National Safety 20 Council that describe exposure scenarios for benzene 21 in industry in the Twenties and Thirties. And it 22 describes a variety of conditions in which 23 hematologic abnormality has been found in patients 24 and where symptoms included not only blood changes, 25 but seen as symptoms, gastrointestinal symptoms, 43 1 irritation of the respiratory tract, weakness, 2 headache, eye irritation, which is expected or 3 typical in individuals exposed to extremely high 4 levels. 5 Q Is what you are saying that you think it's 6 probable that a person would experience these 7 systems if they develop a benzene-induced aplastic 8 anemia, but not necessarily so? 9 A I think it is much more probable, much 10 more likely than not, that individuals exposed to 11 levels of benzene that are associated with aplastic 12 anemia are going to have these other types of 13 symptomatology. 14 Q But they may not. 15 A I think that it's possible they may not, 16 but highly unlikely. 17 Q Now, this list of symptoms that you just 18 read to me, what were the exposure levels that are 19 associated with each of those? 20 A Well, here in one case it says that The 21 term "benzol" is used because this is the old 22 nonenclature. Benzol concentration in the air and 23 this is from the description that I was just reading 24 you in the air of five of the rooms was fairly 25 low. And they are referring to 200 parts per 44 1 million. 2 Another group that they are looking at, 3 they have low level in summer of 130 parts per 4 million to a high of 330. 5 Here is one 430 to 500 parts per million. 6 Here is another where the average was 1800 parts per 7 million and the maximum was 4,140 parts per 8 million. 9 Here is a table looking at concentration 10 of vapors in parts per million that ranges from 11 70 parts per million to the 4,140 that I described. 12 Q Well, does the table give the range of 13 concentrations for exposure, the places where the 14 aplastic anemia were found, and the symptoms for 15 each of the 16 A No, it doesn't outline it. It basically 17 outlines created fashion, the different - describes 18 or categorizes rooms in terms of what they are 19 calling relatively low, intermediate, to high 20 exposure. The 21 Q Are all the symptoms reported in all the 22 rooms? 23 A I would imagine without even going through 24 and trying to look at this in the context in which 25 you have put the question, you would expect to see 45 1 headache, fatigue, dizziness associated with any 2 exposures above 100 parts per million, for sure. 3 And as you approach 4,000, you expect to see 4 confusion, listlessness. 5 Actually this refers to a report by Arnold 6 Leeman showing that 4700 parts per million benzene 7 produces listlessness and confusion after half an 8 hour and within a few hours may cause loss of 9 consciousness. I would say that's unusually 10 charitable. I would imagine that some individuals 11 would probably lose consciousness at 5,000 parts per 12 million in less than an hour. 13 Here's a description by dose from the OHIO 14 PUBLIC HEALTH JOURNAL. 6,000 parts -- 6,260 parts 15 per million causes local symptoms. 15,000 parts per 16 million is poisonous. 4,000 parts per million is 17 poisonous. 900 parts per million caused local 18 symptoms. There are a variety of different 19 collections and descriptions like that throughout 20 this. We are talking about incredibly high exposure 21 levels. 22 Q And what are you reading from? 23 A This is a report by the National Safety 24 Council on Benzol, May, 1926. 25 Q How did you happen to find that particular 46 1 article, Dr. Irons? 2 A I don't know how I found this. I don't 3 know when I got this. 4 Q Where was it published? 5 A National Bureau of Casualty and Surety 6 Underwriters. It's one of several aspects of the 7 literature that I have acquired on benzene over the 8 years. 9 Q But it was distributed by the National 10 Safety Council, you said? 11 A Yes. 12 Q In 1926? 13 A Yes. 14 Q Well, would workmen tolerate working with 15 benzene where they have to wash their hands and 16 tools and clothes with benzene, with all these 17 symptoms? 18 A I have no knowledge of that. I wouldn't. 19 But I can't -- I have no basis for giving you an 20 informed opinion on what others might or might not 21 tolerate. 22 MR. HOBSON: Let's take a short 23 break, if you don't mind. 24 THE VIDEOGRAPHER: We're off the 25 record at 3:22. 47 1 (A BRIEF RECESS WAS TAKEN.) 2 3 THE VIDEOGRAPHER: We are on the 4 record at 3:34. 5 6 (By Mr. Hobson) 7 Q To change gears with you a little bit, did 8 you see the Notice that I sent out? 9 A (Witness nods head affirmatively) 10 Q Did you bring what you published - the 11 last ten items? 12 A Yes. I think that's it. (Tendering) It's 13 close, if not exact. 14 Q (Reviewing documents) When is the last 15 time you did any work for the API? 16 A This year. 17 Q Have you continued to get money from them 18 since the last time we had a deposition together? 19 A I don't remember when exactly the last 20 time we met; but I have been funded at various 21 levels more or less continually since then, I 22 believe. 23 Q Well, how much is your current funding 24 level from API? 25 A I suspect this next year it will be on the 48 1 level of $100,000 total. 2 Q And "next year" being '99? 3 A Yes, basically. I'm not exactly sure what 4 the fiscal year is for that, but it's close. 5 Q What about for this year? 6 A I believe it's been 200. 7 Q And the year before? 8 A It would have been the same. 9 Q And the year before? 10 A Now we are getting into -- I believe it 11 was more, but I'm not sure how much more. It might 12 have been 300. I don't recall. 13 Q Has your level of funding from the 14 American Petroleum Institute been more than $300,000 15 a year since you have been in Colorado? 16 A It might have been from 350 at one point, 17 but that would have been total. That would not be 18 what I would see. That would be the total amount of 19 the award, but I wouldn't see all of it. 20 Q The award -- When you say "the award," 21 what do you mean by that? 22 A Well, whatever the total amount is that 23 was part of the grant from API, the University is 24 going to take overhead from that. 25 Q And the overhead -- What's left after 49 1 overhead goes to you? 2 A Goes to my laboratory or to others. 3 But 4 Q And what has the API been getting for its 5 money these last four or five years from you? 6 A Certainly the project that I have been 7 working on for the past year has been focusing on 8 three separate areas of work. One has been looking 9 at the effects of benzene on - and benzene 10 metabolites on lymphoid biology - B and T cell 11 ontogeny, as well as activation. 12 Additional studies we have done have been 13 focusing on the development of a long-term bone 14 marrow culture model system for looking at and 15 integrating various aspects of toxicity. The API's 16 focus is benzene. Ours is benzene, as well as a 17 variety of other substances, but primarily 18 developing a long-term culture model. 19 And another aspect of work we have been 20 doing has been focusing on looking at alterations in 21 metabolism and cell-specific differentiation in bone 22 marrow associated with a variety of factors 23 hydroquinone being one of them, benzene metabolites, 24 but also looking at other environmental factors. 25 In this case we have been looking at 50 1 smokers and evaluating potential alterations in the 2 hematopoietic regulation as a consequence of 3 cigarette smoking. 4 Q And the API has been funding that? 5 A Yes. 6 Q What do you think their interest is? 7 MR. DILLARD: Objection. Calls 8 for speculation. 9 MR. HOBSON: No. I asked what 10 he thinks that they think. 11 A They have been extremely interested in 12 determining whether or not there are other 13 populations of cells in bone marrow that are capable 14 of metabolizing or bioactivating benzene metabolites 15 besides the myeloid series. We have been looking at 16 that for a number of years, and we are reaching a 17 conclusion with respect to those studies. 18 As part of that, I recommended to them 19 that if they were concerned about looking at 20 metabolism they should also focus on looking at 21 altered regulation of differentiation because I 22 think that that is going to impact on metabolism and 23 its susceptibility. And it's my hypothesis that 24 smoking conveys a risk of developing leukemia over 25 and above the contribution it makes to the body 51 1 burden of benzene and benzene metabolites. And this 2 is because the literature is replete with examples 3 of altered hematopoietic parameters in smokers. 4 So, it was basically my suggestion that 5 they fund a pilot study to determine whether, in 6 fact, that is the case. I don't think they are 7 going to be interested in funding that in terms of 8 understanding mechanisms; but if, in fact, we do 9 describe alterations in hematopoietic regulation in 10 smokers, it will form the basis for additional 11 grants to different sponsors besides API. 12 Q What are you doing specifically to test 13 this hypothesis of yours in the laboratory? 14 A We are looking at clonogenic function. We 15 are looking at altered clonogenic response. We are 16 looking at phenotypic changes in surface markers. 17 We are looking at different populations themselves 18 to see whether or not there are shifts in the 19 differentiation paradigm that we see in normal bone 20 marrow compared to that which we see - or in smokers 21 compared to that which we see in nonsmokers. 22 I think that if smoking conveys a risk of 23 leukemia, that's probably the most important 24 contribution that it makes; and, that is, altered 25 differentiation. 52 1 At this point up until the studies we have 2 done, all of the data available on that has been 3 indirect. It's not been bone marrow. It's been 4 peripheral blood data. What we have done is focus 5 in on bone marrow. 6 Q So, you are getting bone marrow from the 7 clinical setting and determining whether it's from a 8 smoker or nonsmoker and making these analyses? 9 A We have designed the study a little bit 10 better and in a little bit more detail than that. 11 We have identified smokers. We have a clinic twice 12 a week in which we take bone marrows. We have been 13 sampling smokers, and we have been matching those 14 individuals with respect to age, gender, and other 15 criteria so that we are looking at relatively 16 comparable groups of individuals. 17 This is a small study. It's a pilot study 18 to see if we, in fact, can observe any changes. 19 Q How do you induce these graduate students 20 to give you bone marrow? 21 A These aren't graduate students. We can't 22 find any graduate students who smoke. But basically 23 ever since I have been in Colorado, we have been 24 recruiting volunteers to give bone marrow; and we 25 pay them a nominal sum of $200. We provide them 53 1 with a great deal of serologic and clinical data on 2 themselves. That is part of the normal workup. And 3 we have never had a dearth of applicants. We 4 usually have a waiting list. 5 The smokers have been a little bit more 6 difficult to recruit because there aren't that many 7 people out there who will readily admit to smoking 8 one- or two-pack days, and that's basically who we 9 have been looking for. 10 Q Tell me how you are progressing with your 11 bone marrow culture model. 12 A The proof is in the pudding for that 13 system. And what we are looking at is whether or 14 not we can provide long-term - and by "long-term" 15 anything over six weeks is considered definitely 16 long-term - bone marrow cultures that will continue 17 to recapitulate progenitor cells and to maintain 18 stem cell activity. At this point I can't tell you 19 whether we are going to be successful or not. 20 Q That's kind of where we were two or three 21 or four years ago when I took your deposition then, 22 isn't it? 23 A We are a little bit further along than 24 that. We definitely -- We can maintain cultures now 25 out for six weeks with clonogenic activity and with 54 1 basically producing a variety of different cell 2 types. We have recently shifted to a model that was 3 originally used to characterize B lymphocyte 4 ontogeny, and I think that's going to prove to be 5 maybe more versatile than the widely-touted what are 6 called long-term cultures today. 7 It's really the conditions and the nature 8 of the cell populations that are seeded that make a 9 difference. 10 Q Can you now start off with what you 11 perceive to be pretty much the stem cell and cause 12 it to divide either in lymphoid line or the myeloid 13 line? 14 A We can give both lymphoid and myeloid 15 differentiation in culture. When I last talked to 16 you, I don't believe we could simultaneously get 17 lymphoid. We can now. 18 Q What made the difference? 19 A Basically the different conditions in the 20 media and the nature of the pattern of cytokines 21 that are used. We have a short-term culture system, 22 a liquid culture system that we published that 23 allows us to look at the myeloid differentiation; 24 and we are just beginning to analyze long-term 25 culture data. Probably within the next six months 55 1 we will have something to say about that. 2 Q It has to do with the change in your 3 culture technique that you were talking about? 4 A Cell husbandry basically. Stem cells 5 don't like to be pushed. 6 Q I wouldn't know. I never met one. 7 I was noticing one of the articles that 8 you brought with you, the Rothman paper. There's 9 quite a long list of co-authors of which you are 10 one. I take it that you know the other co-authors? 11 A I know many of them. 12 Q Would you know if any of the other 13 co-authors are also consultants to the American 14 Petroleum Institute? 15 A Bill Bechtold may have been. I can't 16 speak for him, and I certainly can't speak for him 17 now. I don't see anyone else that I think or that I 18 know for a fact was or is. 19 Q What about any of the other industry trade 20 associations? Do you recognize any of the other 21 co-authors to be affiliated with any of the industry 22 trade associations; for instance, the CMA 23 A Not that I know of. 24 Q -- the Society of Plastics, any of those 25 people? 56 1 A Pardon? 2 Q Society of Plastics and the various trade 3 associations? 4 A I wouldn't - I wouldn't have any 5 information on that. 6 Q What has been your role in this particular 7 study of the Chinese workers? 8 A We have analyzed lymphoid populations at 9 one time or another. In that particular study we 10 were responsible for the analysis of various 11 cytokines and lymphokines, and I have consulted with 12 them in terms of evaluating lymphoid function and 13 monitoring effects on peripheral lymphocytes. 14 Q And I don't notice mention - and I haven't 15 read the whole paper - but I don't notice mention of 16 your work for the industry anywhere in the paper. 17 Do you disclose that to your co-authors? 18 A Of course. That's not - that would not be 19 something that would be relevant to that 20 publication. I was not working -- The work that I 21 did there was funded through the NCI, not through 22 API. 23 Q Without going through each one of these, 24 is any of the published work you have done been paid 25 for by the API's money - in this stack that you have 57 1 handed me here? 2 A I would have to look at it. 3 Q Okay. (Tendering) 4 A (Reviewing documents) They never put these 5 things in the same place. As it happens, no, not 6 any of these. 7 Q I notice that some of those do deal with 8 benzene and hydroquinone benzene metabolite. Did 9 simply none of that information on benzene and 10 benzene metabolites get funded by API? 11 A That's correct. The benzene and benzene 12 metabolite studies you see there were funded 13 predominantly by NIH. 14 Q I'm sorry. By whom? 15 A NIH. 16 Q How do you discern which part of your 17 benzene work is paid for by NIH and what part of it 18 is funded by API? 19 A It depends on the specific nature of the 20 project that we are working on. I have described 21 for you the three major areas we have been working 22 on with respect to studies that are funded by API. 23 Most of those are actually developmental or 24 highly -- They are more risk taking in terms of 25 developing methodology. 58 1 Most of the studies that we have been 2 doing under NIH sponsorship are looking at molecular 3 and cellular mechanisms, leukemogenesis, altered 4 differentiation, and hematopoietic regulation. 5 And, so, those molecular studies and the 6 chromosomal studies, the cytogenetic work we are 7 doing is funded through the National Institute of 8 Environmental Health Sciences. 9 Q So, are you saying that you haven't 10 published anything in the scientific literature that 11 you have attributed funding to the API for? 12 A No, that's not correct. Certainly work 13 You asked for the last ten items. 14 Q Yes. 15 A If I had dug any deeper, I no doubt would 16 have come up with papers that have API sponsorship. 17 We probably have some abstracts that we have 18 published this last year that have API sponsorship; 19 but at this point, I don't have any papers that fall 20 into that category. 21 Q When would you say was the last time that 22 you published work that you attribute sponsorship to 23 the API for? 24 A '95 or '96. I don't know what the last 25 publication there is - whether it is '95. 1 think 59 1 in '95 we probably published one or two papers with 2 API at least co-sponsorship, probably '95. 3 Q And would I find in the text of the 4 publication the funding coming from API? 5 A Yes, in the acknowledgment it would be 6 listed. There are some I have that I know list both 7 NIH and API, and those would be studies where there 8 were aspects of what we were doing that represented 9 the product of both projects. 10 Q Are you funded by any other trade 11 association besides the American Petroleum 12 Institute? 13 A I have a grant from the Chemical 14 Manufacturers Association examining potential 15 mechanisms of butadiene toxicity and interactions 16 between butadiene and other agents of concern with 17 respect to synthetic rubber production. 18 I have a grant from a pharmaceutical 19 company to look at molecular mechanisms of 20 drug-induced aplastic anemia. That's been going for 21 two years and I have reason to believe it will go 22 for a third, but I can't guarantee it. 23 Q Who did you say funded that? 24 A Astra Pharmaceuticals. 25 Q And how long has your CMA funding been 60 1 ongoing? 2 A We had a break of about a year to six 3 months this past year. It's just -- We have just 4 entered into a new three-year - made a proposal, and 5 it was funded to look at the aspects of synthetic 6 rubber production that I just described. So, that's 7 basically a new grant. 8 Q And prior to the gap, how much CMA funding 9 had you received prior to that since leaving CIIT? 10 A Two to three years prior to that was when 11 it started, and I believe it was -- I can't remember 12 the precise amounts on that grant. 13 Q How much is the new grant for? 14 A $189,000 a year; and that's gross. That 15 includes overhead. 16 Q What's your university overhead percentage 17 there? 18 A I believe that the negotiated amount on 19 nongovernment grants is 26 percent, but I could be 20 wrong on that. 21 Q Is it higher or lower on government 22 grants? 23 A It's higher, tends to be. It depends on 24 the nature of the grant. I don't pretend to 25 understand the subtleties of grant administration. 61 Q All right. Have we covered your trade 2 association funding that you have had since you have 3 gone from CIIT? 4 A I believe so. 5 Q One of the things I asked for, too, was 6 anything that you have submitted for publication, 7 but not yet published. Do you have anything in 8 press? 9 A I brought a couple of things that fit that 10 particular criteria. I had two things that are 11 submitted at the present time. 12 Q No title? 13 A One is "Benzene Metabolites, Hydroquinone, 14 and Catechol Act in Synergy to Induce Dose-Dependent 15 Hypoploidy and Minus 5 Q-31 in a Human Cell Line." 16 Q And where did you submit that? A That was submitted to Leukemia Lymphoma. 18 Q And where are you in the publication 19 process? 20 A I'm waiting to -- It's been submitted. I 21 don't have any information on it. 22 I have another one which is entitled, "An 23 Essential Role for NF-kB in Human CD34 Bone Marrow 24 Cell Survival." And that's in submission to Blood. 25 And it's been revised and sent back; so, I'm 62 1 expecting to hear on it shortly. 2 Q And when you say "revised," that means 3 it's gone out for peer review and it's come back 4 with edited - editorial requests? 5 A Yes. 6 Q What else? 7 A In response to the subpoena, I brought 8 manuscripts that have been submitted but not 9 published. 10 Q All right. Let's take the first one of 11 those, and tell me about it. 12 A The first one here was basically this same 13 manuscript that we originally formatted for 14 publication in - I believe it was Science and 15 Nature. And they declined to review it because it 16 didn't meet their criteria for general interest; so, 17 that's basically the same as this. 18 I don't usually keep copies of manuscripts 19 that have not been accepted for publication. I do 20 have a couple of them that I happened to find. 21 Q That missed the knife? 22 A Well, I generally try to keep paper 23 reduction. I would swim in paper if I kept 24 everything that we ever wrote or everything I ever 25 got. I happened to find this in a graduate student 63 1 file. It was a paper that was submitted, rejected 2 for publication; and the graduate student has not 3 rewritten it and I will not rewrite it for her. 4 Q Just the title so that we will have it in 5 the record. 6 A "Hematopoietic Progenitor Cell 7 Proliferation is Altered Following Induced Stress or 8 Glucocorticoid Administration." 9 It requires editorial carving. 10 Q Did you review that prior to the graduate 11 student submitting it? 12 A Sure, but I won't rewrite it for the 13 graduate student; and, therefore, it is their 14 responsibility to -- I mean, I will take it to a 15 certain point; but I'm not going to rewrite it for 16 them. 17 The other one I happen to have in hand is 18 one that we are still working on that basically 19 here's an example of what you were referring to. 20 Here is a paper that the work represents projects 21 co-sponsored by NIH and by API and by NCI that we 22 submitted for publication in Blood and was 23 rejected. And the title is "B Progenitor Cells 24 Express Low Level Myeloperoxidase." 25 Q Were you given an explanation in writing 64 1 as to the reason for rejection? 2 A Oh, yes. We had a number of debates about 3 this submission at the time and decided to send it 4 to Blood in order to determine whether or not a 5 rigorous peer review would support one opinion or 6 the other. And they did. They basically said that 7 the work was fine, but it didn't provide definitive 8 evidence that nonmyeloid cells express 9 myeloperoxidase. 10 This was a study that API wanted us to 11 perform to determine if there were any other 12 populations in bone marrow that were capable of 13 metabolizing benzene metabolites. And it was an 14 exceedingly difficult technological set of 15 experiments and there were mixed opinions on the 16 part of the authors as to what the results showed 17 and the journal helped us come to a consensus on 18 that. 19 Q That you didn't know what it showed? 20 A Well, not really. I mean, basically the 21 journal - the reviewers indicated that while it was 22 clear that the populations we described existed, we 23 could not say that they were B cells and that, 24 therefore, we could not conclude that other than 25 myeloid cells were expressing myeloperoxidase. 65 1 That's part of the peer review process. 2 Q The paper here that you have recently 3 published on dithiocarbamates as potential 4 confounders in butadiene epidemiology, who was the 5 sponsor of that? 6 A The Chemical Manufacturers Association. 7 Q Did I just miss it? I didn't see it 8 listed here. But where would I find that? 9 A Let me see. 10 Q (Tendering) 11 A (Reviewing document) Okay. They are 12 currently sponsoring our studies on this that are 13 based or predicated upon this manuscript. They did 14 not fund this paper. They are currently funding 15 mechanistic studies to evaluate the potential for 16 confounding that we hypothesized might exist in this 17 paper. 18 Q Let me try and keep the piles somewhat 19 together. You slid this across to me awhile ago, 20 but I don't think it's in this. 21 A That's not. 22 Q It should have been in this pile. 23 Let's talk about your expert testimony for 24 awhile, if we could. When was the last time you 25 gave a deposition before today? 66 1 A I'll make it easy on myself. I believe 2 the last deposition I gave was probably in a case 3 called Friloux. It was either Friloux or Murray, 4 but I have given both this year. 5 Q That is a list of appearances that you 6 have got? 7 A Yes. 8 Q What period of time does it cover? 9 A From 1994 to the present. 10 Q And is there a reason why it starts in 11 '94? 12 A I believe you asked for that, but I'm not 13 sure. 14 Q Starting in '94? 15 MR. DILLARD: You asked for four 16 years. 17 Q So, you prepared this specifically just 18 for me? 19 A Not exactly. It coincides with also a 20 list I prepared for presentation in Federal cases. 21 Actually I don't think I edited it in any way for 22 this. 23 Q And what's your current billing rates? 24 A $500 an hour. 25 Q And the $500 an hour - does it go to you 67 1 or the university? 2 A It goes to me. 3 Q So, there is no overhead figure on there 4 for the university? 5 A No. 6 Q How many hours have you got in this case 7 so far? 8 A I have previously billed about 9 approximately - I don't have a record of it 10 approximately 600,060 - excuse me - 6,000 or $6,500, 11 which would represent approximately 12 or 13 hours, 12 something like that. And I probably have an equal 13 amount of time that I have just recently put in 14 preparation. 15 Q What is the most you've ever billed in a 16 case? 17 A Probably $78,000. That was over ten years 18 ago. 19 Q Which one was that? 20 A Skeene. 21 Q Skeene I or Skeene II or both? 22 A Skeene II. 23 Q Do you know what your billing was in 24 Skeene I? 25 A I had no billing in Skeene I. 68 1 Q You weren't there? 2 A I wasn't there. 3 Q Can you give me an estimate of what 4 percentage of your time - I'm sorry - what 5 percentage of your income comes from litigation? 6 A Over the last few years, I would say it's 7 averaged about 50 percent. 8 Q 15? 9 A 50. 10 Q 50? 11 A Yes. 12 Q Is that up or down from what it was 13 earlier? 14 A It varies. It's hard to predict. I'm not 15 sure what it's going to be this year. I know my 16 total time this year will probably be less than it 17 has been in the past years. I don't know what the 18 total amount will be. It depends on basically 19 income from other sources. 20 Q Has your income from litigation been more 21 than 50 percent in the past for a year? 22 A Probably not. I can't say that for 23 certain, but I don't believe so. 24 Q So, it's been rocking right along at 25 50 percent the last few years? 69 1 A Well, you know, it averages. It can go 2 It's been 40 sometimes. When I say "50," I'm 3 basically just stating an average. It's been 35, 4 40. It may have exceeded 50. I don't know that it 5 has. It depends upon my other sources of consulting 6 income, primarily. 7 Q You have, I take it, a salary from the 8 university activities? 9 A That's correct. 10 Q And, so, when you get a grant from the CMA 11 or the API that goes through the university, then 12 does that grant money go to pay part of your salary 13 from the university? 14 A I have -- My salary is fully paid by the 15 university. If I put my time on a research grant, 16 they expect me to defray them through the grant, 17 that cost. So, the amount of salary that I derive 18 as a consequence of my research activities goes to 19 the university; but my salary is paid 100 percent by 20 the university, if that makes sense. 21 Q No, it really didn't; but let me see if I 22 can restate it until I get it right. 23 You get paid a salary from the university? 24 A That's correct. 25 Q If you bring in grant money, some of that 70 1 grant money is used by the university to pay your 2 salary; but your salary doesn't change? 3 A That's correct. 4 THE VIDEOGRAPHER: We need to 5 change the tape. We are off the 6 record at 4:13. 7 8 (A BRIEF RECESS WAS TAKEN.) 9 10 THE VIDEOGRAPHER: We are back 11 on record at 4:14. 12 13 (By Mr. Hobson) 14 Q Does the amount of salary you get vary 15 depending on how successful you are in bringing in I 16 grant money, or is that just considered to be part 17 of the job? 18 A Only very indirectly in the context that 19 my performance is evaluated on the basis of several 20 criteria, one of which is my success in doing 21 research. It's also evaluated on the basis of my 22 teaching, on my service, on my administrative 23 contributions to the university, et cetera, et 24 cetera. 25 Q And then in addition to litigation and 71 1 salary, then, you have consulting? 2 A My consulting income litigation is one 3 part of that. I also derive income from consulting 4 in the pharmaceutical industry that has nothing to 5 do with litigation. 6 Q Tell me how that works. 7 A Just the same as litigation. It's 8 basically consulting. 9 Q And what kinds of things do you do in 10 consulting for pharmaceuticals? 11 A Drug development, designing and evaluating 12 studies in support of registration with FDA or with 13 international or other regulatory agencies around 14 the world, evaluating potential hematopoietic or 15 immunotoxic hazards associated with developmental 16 drugs. 17 Q And you are working there for the 18 pharmaceutical company, not for the agency that is 19 considering the drug? 20 A Usually it's -- That's almost -- It's hard 21 to give that a single answer. Invariably the 22 pharmaceutical company has hired me as a 23 consultant. On occasion that's been at the request 24 of FDA in order to help interpret some of their 25 studies. So, FDA will ask a company to provide my 72 1 services in evaluating their data. 2 Q So, FDA asks specifically for you, but 3 gets the drug company to pick up your fee? 4 A That has happened at least once, yes. 5 Q More often, is it just the agency asking 6 for an evaluation and the drug company picking you 7 to do the work? 8 A Sometimes the agency is asked if I could 9 provide expertise after I already was consulting for 10 the company. That's happened. 11 Q Can you give me some idea of how many 12 different drug companies you consult to? 13 A It varies. That's highly -- I mean, 14 that's a function of who's having trouble with 15 what. Usually if I'm called in, it's because there 16 is a problem or a perceived problem or they're 17 having a problem in interpretation. So, it's 18 usually a Phase III drug. It's usually a drug in 19 the latter stages of development. 20 It's very hard to predict. It can be no 21 activity or tremendous activity, and that's why my 22 income fluctuates rather dramatically. 23 Q If we say this year, how many drug 24 companies have you worked for this year? 25 A One. 73 1 Q And the previous year? 2 A Either last year or the year before, I did 3 a great deal of work for two companies. This year 4 it's one. The year before that, three or four years 5 ago, I think it was probably -- No, there is one 6 there. It varies. It just varies. It's usually 7 And also the nature and intensity of the project 8 varies. 9 Q And the work you have done this year for 10 the one company - has it been much in the way of 11 quantity? 12 A Not much. 13 Q So, this year at least the main source of 14 nonuniversity income has been litigation? 15 A Yes. 16 Q Let's see what you have brought with you 17 here today, if we could. I'm going to set this 18 stack aside and ask the court reporter to mark it as 19 a separate stack. 20 I notice these are reprints. Did you 21 bring these for us to keep, or would you like them 22 back? 23 A You can keep those. 24 Q Okay. 25 A These are the only copies of these in 74 1 existence. 2 Q All right. And you are talking about the 3 ones that were submitted or rejected? 4 A Either that or revised. 5 Q And will you trust our court reporter to 6 keep those for you and return them to you? 7 A (Witness nods head affirmatively) 8 Q What else did you bring in front of you? 9 A A list of cases. 10 Q Okay. 11 A Notes that I have taken in this case. 12 Q That's three ruled notebook pages with 13 handwriting, and it's your handwriting? 14 A Yes, it's my scribble. 15 A copy of the subpoena duces tecum, the 16 list of materials that I reviewed in the case, two 17 letters - submittal letters that accompanied 18 material I received. I don't think these are all of 19 them. I think there must have been another one, but 20 I don't have it with me. It may be buried in the 21 medical records. 22 Papers that I brought in that I reviewed 23 with respect to this case. These are not all 24 inclusive. Some of the others, as I mentioned, have 25 been submitted by other experts in the case; but I 75 1 didn't bring them. I didn't bring Dr. Neal's book. 2 I didn't bring Dr. Aksoy's book and a few references 3 like that, but these are the ones that I wanted to 4 make sure of. 5 Q Can you tell me any of the references that 6 are attached to other depositions that you 7 particularly utilized that you didn't bring? 8 A I would have to review them to give you a 9 responsible answer to that. I looked at most of 10 them 11 Q So 12 A -- if not all of them. 13 Q So, the ones you really planned on using 14 are here today? 15 A Yes. I didn't -- Again, like, I brought 16 an excerpt of Dr. Jandl's book. I didn't bring the 17 book, but clearly that's a reference. Dr. Neal's 18 book. 19 MR. DILLARD: You say 20 "Dr. Neal." You mean Dr. 21 THE WITNESS: I'm sorry. Neal 22 Young. I'm mixing that up. I'm 23 sorry. 24 A I have got one exhibit from Dr. Natelson, 25 which is the most recent or at least a very recent 76 1 peripheral blood analysis of Mr. York. 2 And we have gone through the rest of it. 3 Q I think we have. Let's take a short break 4 here, and maybe we can get the court reporter to 5 mark some of these. I don't care to have some of 6 that stack that's over there. I have forgotten what 7 is there now. The list of things you brought or 8 provided, I don't care for that piece of paper. I 9 don't think -- I guess I will take the transmittal 10 letters because they have dates on there. But there 11 was something else in there that I didn't think I 12 needed. 13 A The subpoena? 14 Q Yes, I don't need that. I have seen it 15 somewhere. That's probably it. 16 So, if we could have the court reporter 17 mark those in a short break, we'll come back and 18 prove those up; and maybe I will be done. 19 THE VIDEOGRAPHER: We are off 20 the record at 4:22. 21 22 (A BRIEF RECESS WAS TAKEN.) 23 24 25 (IRONS EXHIBIT NOS. 1 THROUGH 77 1 41, WERE MARKED FOR IDENTIFICATION. 2 SAME WILL BE FOUND AT THE CONCLUSION 3 OF THIS DEPOSITION.) 4 5 THE VIDEOGRAPHER: We are on the 6 record at 4:37. 7 8 (By Mr. Hobson) 9 Q Dr. Irons, we took a little break here; 10 and we marked the different items. 1 through 10, 11 that's the collection of recently-published articles 12 that you brought for me; is that right? 13 A That's right. 14 Q And then 11 through 32, that would be the 15 list of articles that you primarily are relying upon 16 in this case. Would that be so? 17 A That's correct. 18 Q And then from 33 through 37, that's the 19 publications that you said were offered for 20 publication, but not accepted? 21 A Not entirely. Some of those are currently 22 being considered for publication at the present 23 time. 24 Q That's right. And you went through which 25 one was and which one wasn't? 78 1 A That's correct. 2 Q And then the others are the miscellaneous 3 letters, your handwritten notes, and your list of 4 appearances, correct? 5 A That's correct. 6 Q In the information that you brought for me 7 here today, is your new system, your new model for 8 stem cell development set forth in any of these? 9 A I'm not sure what you are referring to. 10 Q I think you told me that you had changed 11 your model, and I have forgotten exactly what you 12 were saying before. But it somehow involved B 13 lymphocytes so that you could then get 14 differentiation of the myeloid and lymphoid line? 15 A Oh, in terms of an experimental model? 16 Q Yes, sir. 17 A No, because we haven't published anything 18 on that. The proof is in the pudding with that, and 19 there is no value in talking about it. One has to 20 do it. So, until we have the culture system that 21 allows us to do that, I don't have any publications 22 on that. 23 Q And, so, all the information that you have 24 published in the past is really on the earlier 25 system, the earlier model? 79 1 A If you are talking about data derived from 2 different experimental systems, we have the liquid 3 culture system, we have a number of different 4 analytical systems using bone marrow cells and cell 5 lines. If you are talking about a long-term bone 6 marrow culture system, we haven't published on it. 7 Q I'm thinking from our last visit that you 8 were describing for me a model where you were able 9 to take uncommitted stem cells and utilizing either 10 benzene or benzene metabolites be able to create 11 cells in the myeloid direction as opposed to the 12 lymphoid line. 13 Do you remember our discussions about 14 that? 15 A Yes. Well, vaguely. Certainly the liquid 16 culture system I described or that is included here 17 does that. It looks at myeloid differentiation. 18 Q But not lymphoid? 19 A That's correct. 20 Q And, so, the system doesn't really start 21 with an undifferentiated stem cell that you can then 22 direct in another direction, but it starts with a 23 committed myeloid stem cell? 24 A For the -- Certainly for the models that 25 are described - the culture system as described in 80 1 those publications, that's the case. We have 2 published on different isolated effects of benzene 3 metabolites in other substances on lymphoid ontogeny 4 and lymphoid development; but those are looking at 5 specific aspects of the process, not looking at a 6 complete differentiation model. 7 Q Already committed and starting down the 8 line and then you bombard them with some metabolites 9 or benzene? 10 A Or very early effects that may precede a 11 single lineage commitment, but we are looking at 12 isolated cell populations as opposed to a functional 13 differentiated model. 14 Q And I take it your hope is that your new 15 culture models where you can get differentiation 16 down both lines will expand your ability to look at 17 different chemicals and their metabolites and how 18 they affect the blood? 19 A It will make it easier. I think that we 20 can do a lot by looking at the specific - with the 21 specific systems we have, a lot more than we used to 22 be able to because of the technologies that we 23 have. 24 Obviously the hope is that we will be able 25 to monitor effects in both lineages ideally in the 81 1 same system or, if necessary, in separate systems. 2 Q How about in systems that start with the 3 progenitor stem cells? 4 A Well, for the progenitors, that's no 5 problem. We have basically got that fairly well 6 described. I mean, it's consistent with what is 7 seen in both animal models and also in secondary 8 leukemias in humans. 9 Q And the latest paper that you have 10 published in that light would be what? 11 A Well, certainly the - looking at 12 transcriptional regulation in a role of NF-kB in 13 human progenitors, we've described a role for a 14 transcriptional regulatory element that appears to 15 be necessary for stem cell survival and for 16 clonogenic response in bone marrow, certainly in the 17 myeloid lineage. 18 So, that would be the latest; and that's 19 one that has been submitted for publication. 20 Q And not one of the ones you brought here? 21 A Yes, it's one of the manuscripts. 22 Q Is that in this rubber-banded set? 23 A Yes. 24 Q And which number article would it be, 25 please? 82 1 A 35. 2 Q All right, sir. 3 A In addition, we have been able now to 4 analyze actual C34 positive human bone marrow cells 5 for clonogenetic - clonogenic lesions in terms of 6 cytogenetic aberrations in vitro. So, that is also 7 a system that allows us to look at virtually all 8 repopulating cells in terms of the potential for 9 cytogenetic information. 10 Q Not published yet, though? 11 A No. The model has been published, but 12 actually taking it to human bone marrow is something 13 that we have -- The studies are completed, but I 14 haven't analyzed the data. 15 Q And funding for that by? 16 A NIH. 17 Q And which chemicals or chemical 18 metabolites would have been involved there? 19 A Hydroquinone for the first series 20 hydroquinone and catechol. 21 Q In this era of Dolbert and all of its 22 proteges, have you -- I should say projects or 23 proteges. Maybe "proteges" is the right word 24 projects. 25 Has your testimony ever been refused by 83 1 any court? 2 A I have had one court disallow a very 3 narrow aspect of my testimony in a case. It was a 4 very bizarre case. I don't know why he did it. The 5 judge signed an order that was written verbatim by 6 the plaintiff's attorney. It contains numerous 7 errors, falsehoods, misrepresentations. It actually 8 states an opinion I did not make in the case and 9 never have made. The judge disallowed that 10 particular aspect of my testimony. The Supreme 11 Court stayed the case to review that order, and the 12 case was recently settled. 13 Q And where was that pending? 14 A West Virginia. 15 Q Anyplace else? 16 A No. 17 MR. HOBSON: Well, I think 18 that's all I've got. I appreciate 19 your patience. 20 MR. DILLARD: We will reserve 21 all our questions. 22 THE VIDEOGRAPHER: We are off 23 the record at 4:46 p.m. 24 25 (WHEREUPON THE DEPOSITION WAS CONCLUDED.)