Document N2Ye5729LeE2qZ70OG4EXBOLg

1 CAUSE NO. 21916*JG02 2 DANIEL T. MINNEHAN, Individually) IN THE DISTRICT COURT OF and as Next Friend for ) 3 Joshua Stephen Minnehan and ) Kyle Marshal Minnehan ) 4) Plaintiff, ) 5) vs. ) BRAZORIA COUNTY, TEXAS 6) AMERICAN OIL COMPANY, ) 7 Individually and f/k/a Amoco ) Oil Company and Amoco, Inc.; ) 8 et al., ) ) 9 Defendants. ) 239th JUDICIAL DISTRICT 10 11 ********************************************************** 12 ORAL DEPOSITION OF 13 ETHAN NATELSON, MD 14 OCTOBER 15, 2004 15 ********************************************************** 16 ORAL AND DEPOSITION of ETHAN NATELSON, MD, produced 17 as a witness at the instance of the Plaintiff, and duly 18 sworn, was taken in the above-styled and numbered cause on 19 October 15th, 2004, from 11:10 a.m. to 12:40 p.m., before 20 Susan A. Love, Certified Shorthand Reporter in and for the 21 State of Texas, reported by computerized stenotype machine 22 at the Stehlin de Ipolyi Oncology Clinic, P.A., 1315 St. 23 Joseph Parkway, Suite 1800, Houston, Texas, pursuant to 24 the Texas Rules of Civil Procedure and the provisions 25 stated on the record or attached hereto. 1 1 APPEARANCES 2 3 FOR THE PLAINTIFF: 4 Mr. Michael L. Kaeske, Jr. KAESKE LAW FIRM 5 6301 Gaston Avenue, Suite 735 Dallas, Texas 75214 6 7 FOR THE DEFENDANT PHILLIPS PETROLEUM COMPANY, INDIVIDUALLY AND A/K/A PHILLIPS OIL COMPANY, PHILLIPS CHEMICAL COMPANY 8 AND PHILLIPS 66 COMPANY: 9 Mr. Stephen C. Dillard FULBRIGHT & JAWORSKI L.L.P. 10 1301 McKinney, Suite 5100 Houston, Texas 77010 11 12 FOR THE DEFENDANT SHELL OIL COMPANY: 13 Mr. Stan Perry HAYNES and BOONE, LLP 14 One Houston Center 1221 McKinney, Suite 2100 15 Houston, Texas 77010 16 FOR THE DEFENDANTS AMERICAN OIL COMPANY, AMOCO CHEMICAL 17 COMPANY, AMOCO CORPORATION, AMOCO OIL COMPANY, BP AMOCO CORPORATION, BP CHEMICALS, INC.: 18 Mr. James B. Galbraith 19 MCLEOD, ALEXANDER, POWEL & APFFEL, P.C. 802 Rosenberg 20 Galveston, Texas 77550 21 ALSO PRESENT: 22 Dr. Joseph S. Ayoub 23 24 25 2 1 INDEX 2 3 4 PAGE 5 ETHAN NATELSON, MD: 6 Examination by Mr. Kaeske ..................... 4 Signature Page ............................... 60 7 Court Reporter's Certificate .................. 62 8 9 10 11 12 E X H I B I T S 13 14 EXHIBIT NO. DESCRIPTION PAGE 15 1 Black Binder of Articles Produced 58 by Dr. Natelson 16 2 Handwritten Notes by Dr. Natelson and 58 17 Pages from Daniel Minnehan's Medical Records 18 19 20 21 22 23 24 25 3 1 ETHAN NATELSON, MD, 2 having been first duly sworn, testified as follows: 3 EXAMINATION 4 BY MR. KAESKE: 5 Q. Hi, Doctor. 6 A. Good morning. 7 Q. What kind of doctor are you? 8 A. I'm a hematologist. 9 Q. All right. Have you ever diagnosed anyone with 10 benzene-related acute myelogenous leukemia? 11 A. I've diagnosed a person with chemical related. I 12 don't know that it was benzene. He was exposed to many 13 different chemicals. But specifically benzene related, 14 no. 15 Q. All right. So just so I can get a clear question 16 and answer: As far as you can recall, you've never 17 diagnosed anyone with benzene-related acute myelogenous 18 leukemia, correct? 19 A. That would be correct. 20 Q. Have you ever treated anyone with benzene-related 21 acute myelogenous leukemia? 22 A. Again, I've treated one patient that I can think 23 of who had exposure to benzene, in addition to many other 24 chemicals. I don't know that his was benzene related. It 25 was chemical related. But I haven't treated anybody that 4 1 I thought had only benzene and only exposure to 2 benzene-induced leukemia. 3 Q. So as far as you can recall as you sit here 4 today, you've never treated anyone with benzene-related 5 acute myelogenous leukemia, correct? 6 A. Yes, that would be correct. 7 Q. All right. How long have you been practicing in 8 the Houston area? 9 A. I started doing hematology about 35 years ago. 10 But in terms of practice, I began to practice when I got 11 out of the Air Force, which would be around 1972. 12 Q. How many acute myelogenous leukemias do you think 13 you've diagnosed since 1972? 14 A. I would have to speculate. In other words, I 15 don't count them, but I would say probably in the range 16 of -- and this would be real speculation. I would say 17 perhaps four to six a year for all of those years. We'd 18 have to do some calculations. 19 Q. And do you think that the first year that you saw 20 an acute myelogenous leukemia patient in practice was in 21 1972? 22 A. Yes, because that's when I went into practice. 23 Q. When you diagnose someone with -- I presume 24 you're intending to give opinions about the causation of 25 Mr. Minnehan's leukemia; is that correct? 5 1 A. Yes. 2 Q. When you -- and I also presume that you're going 3 to opine that it's not related to benzene exposure, 4 correct? 5 A. I'm going to opine that I don't know the cause 6 for it. 7 Q. Well, are you going to say that it's not related 8 to benzene exposure? 9 A. In all medical probability, yes, that it's not 10 related to benzene exposure. 11 Q. I guess you're going to give the jury the opinion 12 that, in your opinion, Mr. Minnehan's acute myelogenous 13 leukemia is not related to any exposure that he had to 14 benzene, correct? 15 A. I'm going to give what I would say in all medical 16 probability, in any particular case of acute leukemia, 17 it's very difficult to, with certainty, assign a cause. 18 So all one can say is, looking at the case, the milieu it 19 was diagnosed in, the type of leukemia, the circumstances, 20 you can give your best estimate if it was or wasn't. And 21 in my estimate, it would be in all medical probability, it 22 is not caused by benzene. 23 MR. KAESKE: Object as nonresponsive. 24 Q. (BY MR. KAESKE) And that's just for her. 25 A. I understand. 6 1 Q. It's not for you. 2 But I'm just trying to find out if one of 3 the things that you're going to say to the jury is you 4 think his acute myelogenous leukemia was not caused by 5 exposure to benzene. 6 A. I don't believe that it was. 7 Q. And you don't know what caused his acute 8 myelogenous leukemia, correct? 9 A. That's correct. 10 Q. You are not going to give the opinion that 11 smoking caused Mr. Minnehan's acute myelogenous leukemia, 12 correct? 13 A. That's correct. 14 Q. List for me, if you would, all the reasons you 15 believe -- well, let's start with this: You do a 16 differential diagnosis with your own patients, correct -17 A. Yes. 18 Q. -- outside of litigation? When you see a 19 patient, you'll do a differential diagnosis, correct? 20 A. Yes. 21 Q. And part of the purpose in doing a differential 22 diagnosis is to not only diagnose what the disease is but 23 also to figure out if there's a cause, correct? 24 A. Yes. 25 Q. And what you will do to make a differential 7 1 diagnosis in one of your patients is you'll first ask 2 yourself, what is the disease that the patient has, 3 correct? 4 A. Correct. 5 Q. And then the next thing that you will do is you 6 will ask whether or not there are any confounding factors 7 or anything in the background of the individual that might 8 explain the illness, correct? 9 A. Correct. 10 Q. And then the third thing you do is you'll ask 11 yourself, in a case like this one, what's the allegation 12 and is it reasonable, correct? 13 A. Correct. 14 Q. All right. Now, as far as the first question 15 is concerned, what is the disease, you don't have any 16 dispute that Mr. Minnehan has acute myelogenous leukemia, 17 correct? 18 A. Correct. He has acute myeloid leukemia, or what 19 we call AML. 20 Q. And in addition to that, you would agree that 21 there is ample epidemiologic evidence, as well as other 22 scientific evidence, in the form of case reports and 23 scientific studies of the mechanistic methods of 24 benzene-inducing acute myelogenous leukemia that show that 25 benzene does, indeed, cause acute myelogenous leukemia, 8 1 right? 2 A. It is generally accepted that, under certain 3 conditions, benzene may cause AML. 4 MR. KAESKE: Object as nonresponsive. 5 Q. (BY MR. KAESKE) Sorry. My question was really 6 bad. Let me try again. 7 You will agree with me, won't you, that 8 there is ample scientific evidence showing that benzene 9 causes acute myelogenous leukemia, correct? 10 A. Benzene has the capacity to cause acute 11 myelogenous leukemia. 12 Q. All right. Now, as far as any confounding 13 factors are concerned with respect to Mr. Minnehan's 14 disease, and in particular, Mr. Minnehan's case, there are 15 no factors that you would say -- that you can look to as 16 history and say, "These are the things that I think caused 17 his acute myelogenous leukemia," outside of benzene, 18 correct? 19 A. Well, as I said, I don't know the cause of his 20 acute myeloid leukemia. 21 Q. Well, there are no confounding -- if you're doing 22 this differential diagnosis that you would do with one of 23 your own patients, you wouldn't come upon any confounding 24 factors for the cause of his acute myelogenous leukemia, 25 correct? 9 1 A. Well, just as we've said, we recognize that 2 benzene can cause acute myeloid leukemia under certain 3 conditions. Cigarette smoking is a risk factor for acute 4 myeloid leukemia; and he had smoked, at least, at one time 5 in his life. 6 Q. Well, look, you said cigarette smoking is a risk 7 factor for acute myeloid leukemia, right? 8 A. Correct. 9 Q. Now, as far as risk factors are concerned, you 10 have previously testified that in order for you to be 11 comfortable with an epidemiologic study or with causation 12 between a substance and a disease, you need to see a 13 three-times risk, correct? 14 A. That's correct. 15 Q. And you will agree with me that there are no 16 studies published in the peer-reviewed scientific 17 literature that show a three-times risk for smoking and 18 acute myelogenous leukemia, right? 19 A. No, I would disagree with that. In other words, 20 we generally believe that -- or the Surgeon General's 21 report tells us there's a doubling of the risk. But there 22 are studies that show a three-times increase in risk. 23 MR. KAESKE: Object as nonresponsive. 24 Q. (BY MR. KAESKE) Doctor, do you have the Surgeon 25 General's report with you? 10 1 A. Yes, or part of it. 2 Q. And you're convinced that the Surgeon General's 3 report says that there's a doubling of the risk for 4 smoking and acute myelogenous leukemia? 5 A. Well, I have the summary pages of that. We can 6 look at it and see just what they say. He cites a lot of 7 studies, and the conclusion is that cigarette smoking is a 8 risk factor. I don't recall if it says doubling. But 9 that conclusion is that cigarettes are a risk factor. 10 MR. KAESKE: Object as nonresponsive. 11 Q. (BY MR. KAESKE) And I don't mean to niggle with 12 you here. But, look, you just told me that the Surgeon 13 General's report says that there's a doubling of the risk; 14 and we were talking about whether or not there are any 15 studies that show a tripling of the risk, or three-times 16 risk. 17 A. Yes. 18 Q. And so when I said the three-times risk, you said 19 yes, there was a study. And then you pointed me to the 20 Surgeon General's report, which you said was a doubling. 21 So let's deal with that first. Do you believe -- because 22 apparently the Surgeon General's report forms a portion of 23 the basis of your opinion that smoking can increase 24 someone's risk for acute myelogenous leukemia, correct? 25 MR. DILLARD: Object to form. 11 1 A. Yes. The Surgeon General's report, I suppose you 2 could say, validated what we know from the general 3 opinions in the medical literature. 4 MR. KAESKE: Object as nonresponsive. 5 Q. (BY MR. KAESKE) The question was: Does the 6 Surgeon General's report form part of the basis of your 7 opinion that smoking is a risk factor for acute 8 myelogenous leukemia? 9 A. Yes. 10 Q. All right. Now, that report doesn't say anywhere 11 in it that there's a doubling of the risk of AML from 12 smoking, correct? 13 A. We'd have to look at it. I don't recall. It's a 14 long report. I just have the conclusions. We could look 15 at them -- they're in this book -- and see exactly what 16 they are. But it indicates the risk has increased. 17 Q. Fair enough. And we should look at it. 18 A. Yes. 19 Q. But a moment ago when you told us that it showed 20 that there was a doubling of the risk, upon further 21 reflection, you're not sure without looking at it whether 22 or not there's a doubling of the risk. Is that fair? 23 A. That would be fair. 24 Q. Okay. So let's go ahead and pull it out, if 25 you've got it with you, and take a look at it and see what 12 1 it says. 2 A. The final pages cite a number of reports that 3 show varying risk benefits. And he says here: "Among 4 those who smoked more than a pack of cigarettes per day, 5 the risk increased twofold. In 2002 IARC concluded that 6 there's now sufficient evidence for a causal association 7 between cigarette smoking and myeloid leukemia." 8 And then under "Final Conclusions: "The 9 evidence is sufficient to infer a causal relationship 10 between the smoking and acute myeloid leukemia. And, too, 11 the risk for acute myeloid leukemia increases with the 12 number of cigarettes smoked and with duration of smoking." 13 MR. KAESKE: Object to the nonresponsive. 14 Q. (BY MR. KAESKE) Doctor, my question specifically 15 is: Does the Surgeon General's report say that there is a 16 doubling of the risk for acute myelogenous leukemia, not 17 all leukemias, not all myeloid leukemias, but for acute 18 myelogenous leukemia with smoking? 19 A. Well, as I said, among those who smoked more than 20 a pack of cigarettes per day, the risk increased twofold. 21 That's doubling, isn't it? 22 Q. The risk of what, Doctor? 23 A. The risk of acute leukemia is what they're 24 talking about. 25 Q. Can I take a look at that for just a second? 13 1 Maybe I'm -2 A. (Passes document.) 3 Q. Can you cite me to an epidemiologic study that 4 shows a doubling of the risk for acute myelogenous 5 leukemia and smoking? 6 A. This one. This is an article by Pascoletti from 7 1997. And according to the table in this for acute 8 leukemia, he says that for all smokers the O.R. is 2.3; 9 for light smokers, 2.25; and for heavy smokers, 2.30. 10 Q. All right. Can I take a look at that? 11 A. (Passes document.) 12 Q. And this is the article from the British Journal 13 of Hematology for Pascoletti? 14 A. Yes. 15 Q. Now, can you cite me any articles that show a 16 three-times increased risk for smoking and acute 17 myelogenous leukemia? 18 A. Isn't that what I just showed you? The risk is 19 more than three. 20 Q. I'm asking you a different question now. 21 A. I'm sorry. 22 Q. Give me whatever studies you think answer the 23 question, including that one if you think that's one of 24 them. 25 A. I've given you that study. I have many, many 14 1 articles in my files, but I -- and the Surgeon General 2 cites a few, I believe, that increased the risk above 3 three; but I don't have them as we talk here today. 4 Q. What I'd like for you to do for me, if you could, 5 please, sir, is name for me the articles that you can 6 today that show a tripling of the risk for smoking and 7 acute myelogenous leukemia. 8 A. Let's just see here (perusing documents). Well, 9 I can't as we sit here today. I don't have the entirety 10 of the Surgeon General's report, and I don't recall any 11 specific article that would say that. 12 Q. All right. The binder that's on the table in 13 front of you, those are articles that you have pulled 14 specifically for this case; or is that just your benzene 15 file, in general? 16 A. No. That is specific articles for this case. 17 Q. All right. Fair enough. 18 And where did you get those articles? 19 A. Well, these are all articles that I would 20 accumulate, as I accumulate many references in my career. 21 In other words, these references come from various 22 sources. They may be journals that I subscribe to, like 23 Blood or The New England Journal of Medicine. They may be 24 articles that I've ordered through our library here in the 25 hospital. They may come from various sources. 15 1 Q. I guess what I'm getting at is: How did you come 2 upon this particular set of articles? 3 A. Well, the particular set that I selected -4 obviously I can't anticipate what you're going to ask me, 5 so I can't have articles that answer everything. But I 6 picked this set of articles because they address 7 particular points that I think have some potential 8 significance about this case. 9 Q. Yeah. But how did you go find those articles? 10 Or did you go find those articles? 11 A. Oh, I did. In other words, I have several 12 thousand articles in my other office over in the hospital 13 on various subjects, diverse subjects, not necessarily 14 just including benzene literature. But I look through my 15 files, and I pick out the articles that I think might be 16 appropriate for a particular case. 17 Q. And so how did you come about this set? 18 A. Well, for example, one of the features of this 19 particular case is the particular chromosome abnormality 20 present, inversion 16. Well, it wouldn't make sense for 21 me to pick an article that talked about the Philadelphia 22 chromosome. That's a different chromosome. So I picked 23 articles that had to do, at least from the chromosome 24 standpoint, with chromosome inversion 16. 25 Q. And did you already have those articles that are 16 1 in there about the cytogenetics and chromosome 16? Did 2 you already have all those articles in your files before 3 the Daniel Minnehan case came to you? 4 A. I would say probably 95 percent of them I did. 5 Q. And where did you get the other 5 percent of 6 them? 7 A. The other 5 percent would be gotten, for example, 8 if I had a particular article -- or a particular aspect in 9 inversion 16 that I was looking for, I would go into some 10 type of med search file, put in what topic I was after; 11 and if I came up with a particular reference I was 12 interested in on that particular subject and if it wasn't 13 a journal we had in our hospital library, I would get my 14 secretary to order it for me. 15 Q. Did Mr. Dillard first contact you about this 16 case? 17 A. I don't think so. Actually it might have been 18 Mr. Perry. It's been some time ago. I don't remember who 19 the first person was that contacted me about this case. 20 Q. Did any of the lawyers make reference to any 21 articles for you to locate for this case? 22 A. No. 23 Q. Did any of the lawyers provide you with any 24 articles for this case? 25 A. No. 17 1 Q. You've certainly discussed with the lawyers this 2 inversion 16 thing, right? 3 A. Yes. 4 Q. And you know that it's their feeling that that 5 means that it can't be benzene related, right? 6 A. I don't think that that would be a correct 7 statement. 8 Q. What do you think would be a correct statement 9 about inversion 16? 10 A. I think that what would be a correct statement is 11 that when one sees a case of inversion 16, it is far more 12 likely to be de novo leukemia than a chemical-induced 13 leukemia. 14 Q. Are you someone who has personally studied -15 have you conducted any epidemiologic studies on 16 cytogenetics and acute myelogenous leukemia? 17 A. No. I've ordered them occasionally on patients, 18 but I don't do them myself. 19 Q. No. Sorry. 20 Have you conducted any epidemiologic studies 21 on cytogenetics and benzene-related leukemia? 22 A. No. 23 Q. What you know, to the extent that you know 24 something about cytogenetic markers and acute myelogenous 25 leukemia, is what you have read in the literature, 18 1 correct? 2 MR. GALBRAITH: Object to form. 3 A. That would be correct. 4 Q. (BY MR. KAESKE) Have you ever treated a patient 5 with acute myelogenous leukemia M4 inversion 16? 6 A. I don't know. In other words, I have treated a 7 lot of leukemia patients over the years; and I don't 8 recall which particular defect they had. And so I can't 9 tell you that I have or I haven't. 10 Q. You would certainly agree with me that people 11 have been relating acute myelogenous leukemia and benzene 12 exposure since long before we were able to conduct 13 cytogenetic testing on acute myelogenous leukemia 14 patients, correct? 15 A. That is correct. 16 Q. And you would also agree with me that there is no 17 epidemiologic study that shows a statistically significant 18 doubling of the risk for acute myelogenous leukemia with 19 any given cytogenetic marker, correct? 20 A. I'm not sure I understand that question at all. 21 Q. One of the depositions that you've got in your 22 stack of depositions is the deposition of Richard Irons, 23 right? 24 A. Yes. 25 Q. Did you read that deposition? 19 1 A. Yes. 2 Q. You saw where Dr. Irons and I had a discussion 3 about inversion 16, correct? 4 A. I read it. I remember more of the questions you 5 asked about 5 and 7 than inversion 16, but we could look 6 at it. I'm not sure which question you're referring to. 7 Q. Well, here's the point: There isn't any -- first 8 of all, let me see if I can understand what your opinions 9 are about cytogenetic markers. 10 Do you think that there is some cytogenetic 11 marker that is diagnosed of a benzene-induced leukemia? 12 A. No. 13 Q. Do you think that there is some set of 14 cytogenetic markers that you would require to say that 15 within a reasonable degree of medical probability, 16 someone's acute myelogenous leukemia is related to benzene 17 exposure? 18 A. Not as a sole aspect of the case. In other 19 words, certain markers are more common in chemical-induced 20 leukemias than others. But you're looking at the whole of 21 the picture. That's one thing that you look at in terms 22 of opining an opinion. 23 MR. KAESKE: Object as nonresponsive. 24 Q. (BY MR. KAESKE) Maybe you didn't understand my 25 question. 20 1 Are there a set of -- are there any 2 cytogenetic markers or chromosome aberrations that you, in 3 your opinion, need to see, in addition to whatever other 4 things, but that you need to see in order to give the 5 opinion that within a reasonable degree of medical 6 probability, someone's benzene exposure is related to 7 their acute myelogenous leukemia? 8 A. Well, I think, as I said, you can't take an 9 individual case and prove causation, by any means. In 10 other words, we only infer causation by certain things, 11 chromosome abnormalities being one of them. There are 12 certain chromosome abnormalities that are more common than 13 others in a chemical-induced leukemia, but there is no 14 single chromosome abnormality that proves a 15 chemical-induced leukemia. 16 MR. KAESKE: Object as nonresponsive. 17 Q. (BY MR. KAESKE) So I infer from your answer that 18 you believe that cytogenetic markers are something that 19 you use to prove causation, correct? 20 A. They are one aspect of what we look at to try to 21 come to a conclusion on causation. 22 Q. All right. And can you point me to any study 23 published in the peer-reviewed scientific literature that 24 says that -- well, first let me ask you this: Do you 25 think that there is -- that it is generally accepted in 21 1 the scientific community that there are certain chromosome 2 abnormalities that can be used to prove or disprove 3 causation between benzene exposure and an acute 4 myelogenous leukemia? 5 A. Not prove. I don't believe there are any 6 chromosome abnormalities that can prove "yes" or prove 7 "no," as best I'm understanding your question. 8 Q. Well, I think you said in your answer just a 9 moment ago that chromosomal abnormalities are part of your 10 analysis for causation; is that correct? 11 A. Correct. 12 Q. Is there any article in the medical or 13 scientific peer-reviewed literature that says chromosome 14 abnormalities are to be used as a device or piece of 15 information in determining causation for a benzene-related 16 leukemia? 17 A. I don't know if they would state it in that 18 particular language, but there are plenty of articles that 19 say that particular chromosome abnormalities are seen more 20 commonly in benzene-associated leukemia. 21 MR. KAESKE: Object as nonresponsive. 22 Q. (BY MR. KAESKE) And that's certainly not what I 23 asked you. 24 You will agree with me that there is a 25 difference between looking at a bunch of cases and seeing 22 1 what kind of chromosomal abnormalities that they have, and 2 inferring from chromosomal abnormalities that someone has, 3 what the cause of their disease might be, correct? Those 4 are two different things? 5 A. Well, a chromosomal abnormality is one thing; and 6 the causation is another thing. Yes, I agree with that. 7 Q. All right. What I'm asking you for is: Are 8 there any articles published in the peer-reviewed 9 scientific literature that say, in determining the 10 causation of an acute myelogenous leukemia, whether or not 11 it's related to benzene exposure, that what you should do 12 is you should consider the chromosomal abnormalities? 13 A. Well, yes. I think that the articles suggest 14 that that's true. 15 Q. Name one. 16 A. Mauritzson's article, for example, where he looks 17 at chromosome abnormalities in a large number of people 18 and says that certain abnormalities are more suggestive of 19 de novo and other abnormalities are more suggestive of 20 chemical induced. 21 Q. That article that you just said, that's whose 22 article? 23 A. I believe it's Mauritzson. 24 Q. And that's a chemotherapy article? 25 A. Not exactly. In other words, it's sort of a 23 1 statistical analysis of chromosomal abnormalities in 2 myelodysplasia and acute leukemia, with particular 3 attention to what we call therapy related or 4 chemical-induced leukemia or secondary leukemia. 5 MR. KAESKE: Object as nonresponsive. 6 Q. (BY MR. KAESKE) It's not a benzene related -- it 7 doesn't look at benzene-related leukemias, correct? 8 A. Not specifically, no. 9 Q. Right. So my question was about benzene-related 10 leukemias, not about chemotherapy or chemical-induced 11 leukemias. 12 So now that we're clear on that, can you 13 name me an article published in the scientific 14 peer-reviewed literature that says that when you're 15 determining causation for benzene-induced acute 16 myelogenous leukemia, that you look at particular 17 chromosome changes? 18 A. Well, there are numerous articles that cite the 19 fact that chromosome abnormalities of 5 and 7 appear 20 frequently in benzene-related hematologic diseases. 21 That's not a proof, but that's just a statement of 22 frequency. 23 MR. KAESKE: Object as nonresponsive. 24 Q. (BY MR. KAESKE) Sir, I'm talking about 25 methodology. Do you understand that? 24 1 A. I'm totally misunderstanding, obviously, what 2 you're asking me. 3 Q. Let me start with this. And I'm sorry for the 4 confusion. Have you ever seen any articles -- well, I 5 don't want to know if you've ever seen. 6 Can you name for me an article in the 7 peer-reviewed scientific literature discussing the 8 methodology for diagnosing causation in acute myelogenous 9 leukemia, specifically with respect to benzene exposure, 10 that states that chromosome abnormalities are to be used 11 in determining or in helping to determine the causation 12 for an acute myelogenous leukemia with respect to benzene 13 exposure? 14 MR. GALBRAITH: Object to the form. 15 A. The answer would be "no" to that. 16 Q. (BY MR. KAESKE) All right. Thank you. 17 Do you believe that acute myelogenous 18 leukemias that are caused by benzene exposure have a worse 19 prognosis than are acute myelogenous leukemias that are 20 not known what the cause is? 21 A. Yes, that would be true. 22 Q. And when that is the case, that they have a worse 23 prognosis, what does that involve? What does that worse 24 prognosis for benzene-induced leukemia involve? 25 A. Well, generally a benzene-induced leukemia -- 25 1 and in the hematologic literature, we lump benzene-induced 2 leukemia in with chemical-induced leukemia, 3 therapy-induced leukemia, secondary leukemia. We consider 4 all those synonymous. 5 MR. KAESKE: Object as nonresponsive. 6 Q. (BY MR. KAESKE) Sir, I'm just asking you about 7 benzene-related leukemia. 8 A. I understand. And I'm just explaining that when 9 I give my answer, benzene is considered to be the same as 10 these other compounds that we have a great deal of 11 information about. 12 Q. Well, sir, you, at trial, may or may not be able 13 to give that opinion. 14 A. Correct. 15 Q. So right now I'm just asking about benzene, okay? 16 Now, I understand that you haven't specifically treated a 17 benzene-related leukemia; but you seem to have an opinion 18 about -- I mean, I just asked you and you gave me an 19 opinion about benzene-related leukemias and their 20 prognosis; and so I want to focus on that. So if you 21 could, just give me an answer that relates specifically to 22 benzene-related leukemia. 23 MR. DILLARD: Object to form. 24 A. Well, the answer is that in articles on 25 benzene-related leukemia, there is a frequency of 26 1 abnormalities in chromosome 5 and 7. Whenever we see 2 abnormalities in chromosome 5 and 7, they perform badly 3 with treatment. So, therefore, by inference, if I saw a 4 benzene-induced leukemia that had a chromosome 5 and 7 5 abnormality, it would perform badly with treatment. 6 MR. KAESKE: Object as nonresponsive. 7 Q. (BY MR. KAESKE) I guess I didn't ask a good 8 question again. 9 It isn't something about the 5 or 7 10 abnormality itself that makes the person have a bad 11 prognosis, right? It's just a relationship that you're 12 seeing between people that have a particular chromosome 13 abnormality and their prognosis, right? 14 A. Yes, there is a relationship between the type of 15 chromosome abnormality and prognosis, that's correct. 16 Q. Sorry. I gave you two choices, and you said yes. 17 A. Okay. 18 Q. This is what I'm saying: There isn't something 19 about the fact that it's chromosome 5 or that it's 20 chromosome 7 where the damage is that specifically relates 21 to the prognosis, correct? 22 A. Now, say that one again, that question again. 23 I'm not sure I understood that one. I think you said it's 24 not where the specific damage is? I'm not sure exactly 25 how you said that. 27 1 Q. Look, if you've got a chromosome 5 abnormality, 2 it isn't because your chromosome 5 is messed up that you 3 have a bad prognosis, correct? 4 A. I wouldn't know how to answer that. In other 5 words, as I've said, we recognize that a 5 or a 7 6 chromosome abnormality, meaning your 5 or 7 chromosomes 7 are messed up, when you have that, your prognosis is poor. 8 Q. Yeah, but it isn't because you've got that 9 particular chromosome abnormality that your prognosis is 10 poor. It's because of something else that has to do with 11 the disease that your prognosis is poor, right? 12 A. I can't tell you the difference. In other words, 13 the chromosome abnormality relates to the disease 14 directly. And when you see that chromosome abnormality, 15 you imply that whatever mechanism is offered of theirs is 16 making the prognosis worse. 17 Q. Well, it isn't just chromosome 5 and 7 18 abnormalities that have a poor prognosis, is it? 19 A. That's correct. There are others that have a 20 poor prognosis. 21 Q. Yeah, and they are ... 22 A. Well, generally, they're divided up into three 23 general categories of, let's say -- I mean, obviously no 24 leukemia is good. But certain what we call balanced 25 translocations have a better prognosis than, for example, 28 1 multiple chromosome abnormalities, when there are a number 2 of chromosomes abnormal, or chromosomes 5 and 7. And 3 there are some that are so-called good risks; some that 4 are, let's say, intermediate risks; and some that are bad 5 risks. 6 Q. So you can't name me any of the other chromosome 7 abnormalities that are high risk? 8 A. That are high risk? As I just said, multiple -9 Q. That have a bad prognosis. 10 A. Multiple chromosome abnormalities. 11 Q. Among which chromosomes? 12 A. It can be any of them. If I saw four or five 13 different abnormalities in an acute leukemia, that would 14 be a very bad prognosis. 15 Q. All right. What else? What other leukemias have 16 a bad -- what other acute myelogenous leukemias have a bad 17 prognosis? 18 MR. GALBRAITH: Object to form. 19 A. I would have to look at the articles. There may 20 be several. But we could look at those and see which ones 21 are in which category. Generally speaking, the multiple 22 abnormalities in the 5 and 7 are considered to be bad; the 23 balanced translocations, considered to be good; and then 24 there are some that are in the middle that are 25 translocations, let's say, 9 to 11, that are worse than 29 1 some of the translocations but better than others. 2 Q. (BY MR. KAESKE) All right. Now, when we say -3 when you say that the prognosis is poor, what do you mean 4 by that? 5 A. Well, I can give you the exact statement from one 6 of these articles as to what that means. 7 Q. No, I don't want it from an article. You're a 8 clinician, right? 9 A. Yes. 10 Q. So just give me your clinical analysis or give 11 me -- tell me in layman's terms when you say it's a poor 12 prognosis, what can that person expect? 13 A. What that person can expect is to stay in 14 remission -- if you're lucky to get into remission, stay 15 in remission three or four months and probably have about 16 a 10 percent survival at the end of three years. 17 Q. And when you say that they stay in remission for 18 three or four months, then what happens? 19 A. They relapse. 20 Q. Then they relapse? 21 And then what would, if that person -- what 22 would the rest of the clinical course for that person be 23 like? 24 A. Well, generally, when one puts a leukemia into 25 remission with chemotherapy, oftentimes -- not always, but 30 1 oftentimes the first remission is the longest. And as you 2 keep getting into second and third remissions, the 3 interval of time between each remission gets shorter and 4 shorter; and finally the drugs don't seem to work at all. 5 So in a person who is having constant 6 relapses, one might try to proceed with a marrow 7 transplant as an alternate form of treatment. 8 Q. So when you say that someone has -- when we talk 9 about this poor prognosis, what you mean by that is if 10 they achieve relapse [sic], the relapse [sic] will likely 11 not last; is that correct? 12 A. No, the relapse will last. 13 Q. Sorry. 14 A. They won't go back into remission easily. 15 Q. Sorry. I used the wrong word. You saw that. 16 A. Okay. 17 Q. So when you say that someone has a poor 18 prognosis, what you mean by that is if they achieve 19 remission, the remission will likely not last? 20 A. That's correct. 21 Q. And then if someone goes into remission but 22 relapses and their cancer comes back, a choice at that 23 point is transplant, is what you just said, correct? 24 A. Well, one can try alternate drugs; and sometimes 25 you're successful with that. But frequently that tends to 31 1 make you want to try something a little more dramatic, 2 like a transplant. 3 Q. So then if you try a transplant and you have one 4 of these patients and they don't have a related donor, 5 then what does the prognosis look like? 6 A. Well, the best results of a transplant would be 7 with a related donor. Then you go to the so-called 8 national donor match, and you find people who look in the 9 test tube like you but they're not exactly like you. And 10 that's the next best choice to try to do a transplant. 11 Q. Okay. But -- and my question kind of started 12 where you ended. 13 A. Yes. 14 Q. If you're one of those people where you don't 15 have a related donor and so you've got to go into the 16 national matched donor pool, then what's the prognosis 17 like for that kind of transplant? 18 A. Well, it's not as good. In other words, the 19 prognosis for a related transplant is better than an 20 unrelated donor transplant. But it's still better than 21 nothing. 22 Q. But can you not give me any details, any risk 23 analysis, any, "This is the percentage of likelihood," or 24 what's going to happen, what are the possible risk factors 25 for an unrelated donor, that kind of thing? 32 1 A. Well, the situation for acute leukemia, in 2 general -- adult acute leukemia is not great. We 3 typically say that our ability to achieve a cure with 4 chemotherapy alone is probably no better than 20 percent. 5 If we add a transplant to that -- let's assume we got the 6 person in remission and then did a transplant -- they 7 don't always live happily ever after. We might improve 8 that cure rate possibly up to, let's say, 40 percent. But 9 many people that you transplant, and even if the 10 transplant appears successful, ultimately relapses or will 11 die of some other transplant-related complications. So in 12 the end analysis, adult acute leukemia is often fatal. 13 Q. Do you feel like you're familiar with 14 Mr. Minnehan's course up until now? 15 A. Yes. 16 Q. That big huge stack over there (indicating), have 17 you read it all? 18 A. I can't swear that I've studied every page 19 carefully, but I've looked at each one of them, some in 20 more detail and some in a very cursory fashion. And I 21 have an idea of what happened with him. 22 Q. Okay. You'll agree with me, won't you, that the 23 course of his leukemia has been a complicated one, 24 correct? 25 A. Yes. 33 1 Q. And you will agree with me that the course of his 2 leukemia looks like one of those folks that had a poor 3 prognosis, correct? 4 A. No, not exactly. I wouldn't agree with that 5 statement. 6 Q. Why not? 7 A. Because he went into remission fairly promptly 8 and he stayed in remission for an extended period of time, 9 considerably more than three months. And the fact that he 10 ultimately relapsed, people with a great prognosis 11 relapse. People with normal chromosomes relapse. And so 12 the fact that he relapsed is not surprising, whether he 13 had a good risk or a bad risk leukemia. He actually 14 stayed in remission longer than most people with a bad 15 risk leukemia. 16 Q. And can you cite me to an article in the 17 peer-reviewed scientific literature that talks about how 18 long people with a poor risk of acute myelogenous leukemia 19 stay in remission before they relapse? 20 A. We could look out there. There may be some 21 articles that comment about that. 22 Q. Well, why don't you see. 23 A. (Peruses documents) Well, this article which -24 well, let me identify this. It's an article on secondary 25 leukemia, and it's from -- each year the American Society 34 1 of Hematology meets; and a textbook is published, which is 2 the educational booklet; and an expert in that area gives 3 a dissertation. And this is from one of those. It's by 4 Mr. Applebaum, as the lead author. 5 And in talking about people with secondary 6 AML with cytogenetic abnormalities associated with a poor 7 outcome from chemotherapy, he says: "Accordingly, it's 8 not surprising that the overall long-term survival of 9 patients with secondary AML is low. Among 155 patients 10 reported by the MD Anderson group, the median survival was 11 only 3.5 months and fewer than 10 percent were alive in 12 three years." 13 Now, if their median survival was only 14 3.5 months, that meant a lot of them relapsed before 15 3.5 months; so they didn't stay in remission very long. 16 MR. KAESKE: Objection, nonresponsive. 17 Q. (BY MR. KAESKE) That actually doesn't say 18 anything about even achieving remission, does it? That 19 which you just read to us doesn't even talk about 20 achieving remission? 21 A. Well, actually it does, because it goes on to 22 say: "No single form of post-remission chemotherapy has 23 been demonstrated to be superior." In other words, 24 they're talking about the fact that, yes, you can get 25 these people into remission; but you can't keep them 35 1 there. They want to relapse very promptly. 2 Q. So that we're clear, the question that I asked 3 you that prompted you to look for these medical articles 4 was: I'm looking for an article that says what you said, 5 which is that 20 months of remission versus three months 6 of remission is not indicative of a poor prognosis acute 7 myelogenous leukemia. And so we're specifically now 8 looking now about relapse rates. 9 A. Well, let's see if I can find something. These 10 papers are not specifically designed with that in mind, 11 but I may have another that addresses that. Let's see 12 (peruses documents). 13 Okay. This is from Dr. DeVita's textbook, 14 the Sixth Edition, on Cancer: Principles, published in 15 2001. And he says: "AML that occurs as a consequence of 16 prior cytotoxic therapy or that has developed from an 17 antecedent hematologic disorder, for example, 18 myelodyplastic syndrome, has a particularly poor outcome, 19 with a lower incidence of achieving a complete remission 20 and shorter duration of survival than for patients with 21 de novo AML. Multiple studies have demonstrated the 22 prognostic importance of cytogenetic abnormalities in AML, 23 making this the single most important predictor of 24 outcome." And he goes on to say, as you asked me before, 25 which chromosomes have a good prognosis and which ones 36 1 have a bad one. 2 So I believe he's answering your question, 3 that people who have a bad prognosis acute leukemia don't 4 go into remission as easily and they don't stay in 5 remission as long. And the ultimate result is a high 6 incidence of death early on. 7 Q. But what you just read, that doesn't say that 8 they don't stay in remission as long, does it? 9 A. Well, I think -- if it doesn't say it, I think it 10 implies it. I will have to look to see if he says -- he's 11 talking about the ability to go into remission. 12 Q. That's right. And that's why it particularly 13 doesn't answer my question. My question was only, Doctor, 14 in response to one of the things that you said. I'm 15 looking for an article that says, as you have said, that 16 people with these poor prognoses don't stay in remission 17 for as long as 20 months. 18 A. Let me look and see. As I say, I always can't 19 anticipate what I might be asked. And so when I pick 20 articles, I have to pick something general; and so they 21 don't necessarily answer a specific point. But I may have 22 one in here that will get to that. Let's see. I know the 23 one I'm looking for here (perusing documents). 24 Well, I don't think that I can -- most of 25 these articles deal with ability to achieve remission and 37 1 survival. I would have to tell you that I don't have here 2 today articles that show that the length of remission is 3 shorter. Although, I can tell you from 35 years of 4 clinical experience that it is and there are many articles 5 that say that, but I don't have them here today. 6 MR. KAESKE: Objection, nonresponsive. 7 Q. (BY MR. KAESKE) Just as we sit here today, you 8 can't name for me an article in the scientific 9 peer-reviewed literature that shows that length of 10 remission for a poor prognosis for acute myelogenous 11 leukemia is shorter than 20 months? 12 A. That would be true. 13 Q. List for me, if you will, all the reasons you 14 believe that Mr. Minnehan's leukemia is not related to 15 benzene exposure. 16 A. Well, first is if we look at the chromosome 17 abnormality itself. We know that inversion 16 is a rare 18 chromosome abnormality under any circumstances. But in 19 some of these articles, they will look at large numbers of 20 patients with what we call de novo leukemia and what we 21 call therapy-induced or secondary or chemical-induced 22 leukemia, of which I put benzene in that category. 23 The articles suggest that in de novo 24 leukemias, this abnormality appears about some -- around 25 4, let's say 4.3, somewhere around that percent of the 38 1 time. 2 Q. I don't mean to cut you off. I just want an 3 enumeration of the list of reasons. 4 A. Okay. Well, No. 1 is the particular chromosome 5 defect that he has. No. 2 is the fact that it is an 6 isolated chromosome defect, that it is not seen with other 7 chromosome defects, because typically in chemical-induced 8 chromosome defects of inversion 16, they don't appear as 9 an isolated event. You have an inversion 16 plus three or 10 four other things. So when you have an inversion 16 as a 11 sole abnormality, it is much more likely to be caused by 12 de novo as opposed to chemicals. That's No. 1. 13 No. 2 would be the fact that whereas we have 14 extensive literature for 20-plus years on inversion 16 and 15 many, many cases of de novo leukemia with it, there's not 16 a single case in the world's literature of benzene-induced 17 inversion 16. So we have no real basis to think that 18 benzene could do that. Although I would admit that on a 19 theoretical basis it might, we have no actual evidence 20 that it can. 21 So we've got the chromosome defect. We've 22 got the fact that it's never been in an isolated form. 23 We've got the fact that it's never been described after 24 benzene. And then we've got the fact of the occupation 25 and the allegation. 39 1 As best I can determine it, Mr. Minnehan was 2 a refinery worker, a pipefitter, a boilermaker, just like 3 many of his peers in the areas that he worked and just 4 like many of his peers around the country in other 5 refineries. And when you look at epidemiologic studies of 6 refinery workers from around the country, there isn't any 7 increased incidence of acute leukemia and hasn't been for 8 many, many years. So I would have to think that whatever 9 he got exposed to, his fellow workers got exposed to it, 10 too, in the same doses in his refineries and everybody 11 else's refineries. And if that exposure was enough to 12 cause acute leukemia, we would see a high incidence of it 13 in other like-refinery workers; and we don't. So what 14 that tells me is he's not any different than anybody else 15 in his refinery, and there would be no reason for me to 16 think that he had enough exposure to cause acute leukemia. 17 Those would be generally the most important reasons I 18 could cite. 19 Q. So I've got three reasons: One, you've never 20 seen chromosome 16 associated with a secondary leukemia? 21 A. Well, I haven't seen it in the literature -22 excuse me. I've seen chromosome 16 with secondary 23 leukemia, yes; not from benzene. And where we've seen it 24 from secondary leukemia -25 Q. Hold on. So the first thing is you've never seen 40 1 a report of a benzene-related secondary leukemia -- sorry. 2 You've never seen a report of a benzene-related chromosome 3 16 inversion, correct? 4 A. Correct. 5 Q. And so that's the first reason it's not 6 benzene-related? 7 A. You could say one. I don't know which one you'd 8 put the most weight on, but that's a reason. 9 Q. Okay. Then the second reason is because he's 10 only got 16 inversion by itself, not with others -- not 11 with other aberrations, correct? 12 A. Yes. 13 Q. Then the third one is, you don't see there to be 14 an increased incidence of leukemia -- of acute myelogenous 15 leukemia among refinery workers; is that right? 16 A. Of the type that he has, yes, that's correct. 17 Those three, I think, are all important 18 things. And they enabled me to say -- and as I've said 19 before -- in any one case of leukemia, one can never be 20 certain about causation. But one can easily say that more 21 likely than not, it is not caused by chemical exposure 22 because of those reasons. 23 MR. KAESKE: Object as nonresponsive. 24 Q. (BY MR. KAESKE) I just want to make sure that 25 I've got the entire list. 41 1 A. You've got the list. 2 Q. Well, but I need to have the list with the 3 answers to the questions, and then we can proceed. 4 A. Okay. 5 Q. First is that you've never seen a report in the 6 scientific literature of chromosome 16 and benzene 7 exposure, correct? 8 A. Of inversion 16 in benzene exposure, correct. 9 Q. All right. Second is some problem you have with 10 the fact that he's got inversion 16 all by itself, as 11 opposed to with other problems -12 A. Correct. 13 Q. -- with chromosomes, correct? 14 MR. DILLARD: Object to the form. 15 A. Yes. 16 Q. (BY MR. KAESKE) And the third thing is that you 17 haven't seen any increased incidence of acute myelogenous 18 leukemia among refinery workers, correct? 19 A. Well, the bulk of the studies of refinery workers 20 do not suggest an increase. 21 Q. All right. Do you have any particular opinions 22 about Mr. Minnehan's particular exposure? 23 A. You mean how many parts per million or whatever 24 he got exposed to? 25 Q. No, not necessarily. Although if you have an 42 1 opinion about that, then I want to know about it. 2 A. Okay. 3 Q. I presume you do not. 4 A. I do not. I don't know what he was exposed to. 5 Q. Fair enough. 6 What I meant was -- and, look, if I can just 7 kind of speak freely for a second, what I understood your 8 third thing to be was, basically: When you look at 9 like-associated workers, you don't see -- when you look at 10 like occupations, you don't see an increase in acute 11 myelogenous leukemia. That's not an exposure-based 12 statement. It is just a statement about epidemiologic 13 studies in this occupation. 14 And so now my question is: Is there 15 something specific that you're going to say about 16 exposure, or his particular exposure; or are you just 17 going to rely on your understanding of the refinery worker 18 studies? 19 MR. DILLARD: Object to form. 20 A. Just my understanding of the refinery worker 21 studies as they've been published. 22 Q. (BY MR. KAESKE) Okay. Fair enough. 23 And in part, that's because you don't know 24 what Mr. Minnehan's exposure to benzene was, correct? 25 MR. DILLARD: Object to form. 43 1 A. I don't know what his exposure to benzene was. 2 Q. (BY MR. KAESKE) Are there any other reasons that 3 you have for your opinion that Mr. Minnehan's exposure was 4 not benzene -- sorry -- that Mr. Minnehan's acute 5 myelogenous leukemia was not benzene related? 6 A. No. Those would be the important things that I 7 said. 8 Q. You will agree with me, won't you, that all of 9 Mr. Minnehan's treatment since October 24th of the year 10 2000 has been related to his acute myelogenous leukemia, 11 correct, or its effects? 12 MR. DILLARD: Object to form. 13 A. Well, generally speaking, that's true. I mean, 14 you could look at certain specifics. For example, he had 15 to have his spleen removed because he had what we call 16 ITP. That may or may not have been related to his acute 17 leukemia, but he did undergo a splenectomy. 18 Q. (BY MR. KAESKE) Well, he underwent a splenectomy 19 because he had ITP specifically because of the disease 20 process that he's been withstanding since the year 2000, 21 right? 22 A. Not necessarily. I do lots of splenectomies for 23 ITP patients who don't have a acute leukemia. That can 24 occur in many different settings. So I am not a hundred 25 percent certain that it was related to the acute leukemia, 44 1 but it was certainly part of his treatment program. 2 Q. Are you going to give an opinion that ITP and his 3 subsequent splenectomy was not related to his disease 4 process in general, whether it be his acute myelogenous 5 leukemia or his graft-versus-host, or any of the rest of 6 that? 7 A. I can't give an opinion on that because I don't 8 have enough detail. I only have the notes that are in the 9 chart, that they were taking out his spleen because he had 10 a low platelet count and they thought that it would 11 improve. 12 Q. As an answer to my specific question: Are you 13 going to give an opinion in this case that his splenectomy 14 or his ITP were not related to his disease process or his 15 graft-versus-host disease? 16 A. No. 17 Q. Are you going to give an opinion in this case 18 that any of the medical treatments that he has underwent 19 since October 24th, 2004 [sic], are not related to his 20 acute myelogenous leukemia or his graft-versus-host 21 disease? 22 A. No. 23 Q. Have you spoken with any of his treating 24 physicians in this case? 25 A. No. 45 1 Q. Have you spoken with anyone, other than the 2 lawyers, about this case? 3 A. No. 4 Q. All right. Have you seen -- the treatments that 5 you have seen that are in these medical records -- and by 6 the way, have you been given, as far as you know, all of 7 the medical records from Mr. Minnehan from the year 2000 8 until today? 9 A. Well, the records speak for themselves. I'm not 10 sure what the most recent date was on those records. I'm 11 sure that since he's continuing to get care, there would 12 be some records that I don't have there. 13 MR. KAESKE: Do y'all know how up-to-date 14 the medical records are you've given him? 15 MR. PERRY: I don't. 16 MR. KAESKE: When was the last time you sent 17 him medical records? 18 MR. PERRY: I'm not sure. 19 Q. (BY MR. KAESKE) Doctor, when was the last time 20 you received medical records? 21 A. It's been some time ago, and I -- for example, 22 obviously I have records. I made some notes here and I 23 have records up through 4-29-04, but that's six months 24 ago, I guess. And I don't know that I had any notes since 25 that particular time. 46 1 Q. You would agree that all of the treatment that 2 Mr. Minnehan has received over at MD Anderson since 3 October of 2000 has been reasonable and necessary for the 4 treatment of his acute myelogenous leukemia -5 A. Yes. 6 Q. -- and its complications, right? 7 A. Yes. 8 Q. Have you been provided any bills? 9 A. I don't believe there are any bills in that 10 material. 11 Q. Okay. Whatever the bills are that have been 12 associated with the treatments that he had, those costs 13 would also be reasonable and necessary costs associated 14 with the treatments that he's received at MD Anderson for 15 his acute myelogenous leukemia or its complications, 16 correct? 17 MR. PERRY: Object to form. 18 A. Yes. 19 Q. (BY MR. KAESKE) Are you going to give any 20 opinions in this case about -- I just want to ask this one 21 or two last questions about this: Are you going to give 22 any opinions in this case about what exposure levels of 23 benzene are required to cause acute myelogenous leukemia? 24 A. If asked, yes. I can only cite what the 25 literature tells me. 47 1 Q. But you don't have an opinion in this case that 2 Mr. Minnehan's exposure was not enough to have caused his 3 acute myelogenous leukemia, correct? 4 A. I don't know what his exposure was. 5 Q. Okay. So let's see if we can get a "yes" answer 6 to my question, then. 7 A. Okay. 8 Q. You do not have an opinion that Mr. Minnehan's 9 exposure to benzene, whatever it was, was not enough to 10 cause his acute myelogenous leukemia, correct? 11 A. Well, indirectly I think I've said that because I 12 said that were he to have had enough exposure to cause 13 acute leukemia, so would many of his coworkers in his 14 refineries and many other refineries. And because I don't 15 see that, that tells me that whatever exposure he had, it 16 was below those limits. 17 MR. KAESKE: Object as nonresponsive. 18 Q. (BY MR. KAESKE) Are you going to give the 19 opinion that Mr. Minnehan's exposure to benzene, whatever 20 it was, was not enough to cause his acute myelogenous 21 leukemia? 22 A. Yes. 23 Q. Will you agree with me that benzene-induced acute 24 myelogenous leukemia is not a disease that is caused by 25 achieving some amount of cumulative dose to benzene? 48 1 MR. DILLARD: Object to form. 2 A. Well, I'm not certain. Are you asking that one 3 has to achieve a particular dose? Is that what you're 4 asking? 5 Q. (BY MR. KAESKE) Not exactly. 6 A. What -7 Q. Let's take lead, for example. 8 A. All right. 9 Q. You get sick when you get a certain amount of 10 lead in your body, right? 11 A. Yes. 12 Q. Benzene is not that kind of disease where you get 13 sick when you get a -- well, acute myelogenous leukemia 14 and benzene is not that kind of disease where you get a -15 you hit a certain threshold and then you get acute 16 myelogenous leukemia, correct? 17 MR. DILLARD: Object to form. 18 A. Well, it's certainly not akin to lead poisoning. 19 In general, the studies suggest that one can relate the 20 cumulative dose to benzene along with the risk of catching 21 leukemia. 22 MR. KAESKE: Object as nonresponsive. 23 Q. (BY MR. KAESKE) Sir, I'm not talking to you 24 now about -- just so that you're clear, I'm not at all 25 talking to you about risk. I don't even want to know 49 1 about risk. I don't even want to consider risk. 2 A. Okay. 3 Q. I want to talk about biologically how the disease 4 is caused, okay? When we talk about biologically how 5 acute myelogenous leukemia is caused by benzene exposure, 6 it is not a disease that is caused by achieving a certain 7 amount of benzene toxicity in the blood or in the body 8 before you can achieve acute myelogenous leukemia from 9 benzene exposure, correct? 10 MR. DILLARD: Object to form. 11 A. I think that would be true, yes. 12 Q. (BY MR. KAESKE) All right. I want to take a 13 break for a second; and then I want to see whether or not 14 I have any more questions to ask you. Would that be all 15 right? 16 A. Certainly. 17 Q. Thanks. 18 (Ten-minute recess taken) 19 Q. (BY MR. KAESKE) Would you read those notes into 20 the record, please? 21 A. Sure. It starts out: "David Minnehan, 5/30/58, 22 051-54-4729. Oil field worker-pipefitter-boilermaker 23 supervisor. 10/2000 in Alaska, chest pain, pancytopenia." 24 "10/27/2000, bone marrow, AML-M-4. Bone 25 marrow, 64 percent blasts, inversion 16 defect. 50 1 Peroxidase, positive; platelet count, 110,000; white 2 cell count, 3000; hemoglobin, 13.9." 3 "Initial treatment, Fludarabine and Cytosar" 4 -- and that's F-l-u-d-a-r-a-b-i-n-e and Cytosar, 5 C-y-t-o-s-a-r -- "14 courses of chemotherapy. Relapsed 6 summer of 8/2002. Re-induced with Fludarabine, Cytosar." 7 "Deep vein thrombosis of arms, left axillary 8 vein thrombosis. On Lovenox," L-o-v-e-n-o-x. 9 "Normal bone marrow chromosomes 10 post-therapy." 11 "Splenectomy for ITP, 8/7/03." 12 "Note says still smoking in 10/27/03, 13 40-pack history." 14 "2/6/04, normal bone marrow chromosomes." 15 "2/3/04, receiving Tacrolimus," 16 T-a-c-r-o-l-i-m-u-s, "Prednisone, and Rapamycin," 17 R-a-p-a-m-y-c-i-n." 18 "4/29/04, positive Coombs' test." That's 19 C-o-o-m-b-s apostrophe. "LDH, 701 (normal range 313 to 20 618)." 21 Q. Are those all the notes that you've got on that 22 page? 23 A. Yes. 24 Q. Do you have an opinion about Mr. Minnehan's 25 prognosis? 51 1 A. Well, I don't -- I think we would have to say his 2 prognosis is uncertain at this point. That would be the 3 best I could do in terms of the likelihood of his relapse. 4 Q. What about in the terms of the likelihood of his 5 survival from the graft-versus-host disease? 6 A. Well, I think that it's probably unlikely that he 7 will die of graft-versus-host disease. I think his threat 8 would be on a relapse of the leukemia. 9 Q. Do you know what the status of his 10 graft-versus-host disease is now? 11 A. No. 12 Q. You have previously testified, and it's certainly 13 your opinion, that graft-versus-host disease can be a 14 fatal condition, right? 15 A. Yes, it can. 16 Q. Or that it can lead to other fatal conditions? 17 A. Yes. 18 Q. Have you read Dr. Gardner's deposition in this 19 case? 20 A. Yes. 21 Q. Do you have any criticisms of 22 Dr. Gardner's testimony in this case? 23 A. You would have to pick a specific thing. 24 Dr. Gardner said many things in the deposition, and it 25 might well be that there are some things that I don't 52 1 agree with. 2 Q. Did you take any notes when you read his 3 deposition? 4 A. No. I may have scribbled something on the front 5 cover. I believe that was his deposition that I said 6 something because he made a comment about smoking. 7 Q. What does that say? 8 A. It says: "See 43." And let's see what -9 Q. And then what are the words it says after that? 10 A. "Acute phase reactant." 11 And let's see what I was dealing with on 12 page 43. Oh, yes. What that had to do with, his serum 13 ferritin. That's f-e-r-r-i-t-i-n. And the serum ferritin 14 is generally a reflection of how much iron is in the body 15 in most people. But when you have an inflammatory state 16 like graft-versus-host disease, it often goes sky-high and 17 you lose that relationship. And so what he was saying is 18 that his ferritin is 4400 and that that means he's got a 19 lot of iron overload. 20 I don't believe that to be the case because 21 in this setting, it's totally inaccurate for that reason. 22 Rheumatoid arthritis patients may have levels of 15,000 23 and not have high iron levels. So I think that one can't 24 look at his ferritin level and accurately tell his degree 25 of iron overload. You would have to do it by getting a 53 1 CAT scan or MRI and looking at the liver. 2 Q. Do you know whether or not Mr. Minnehan has been 3 treated because of his high iron levels? 4 A. I have no idea. 5 Q. So you don't know what his treating physicians 6 believe about that point that you just made? 7 A. Correct. 8 Q. Any other criticisms of Dr. Gardner? 9 A. He let's see. It says "pages 38 through 39." I 10 think it was the same thing. In other words, he had a 11 liver biopsy and there was no evidence that he had iron 12 overload from that and that led into the discussion on the 13 ferritin levels. So that was part and parcel of that same 14 comment. 15 "Pages 71 through 72, smoking." I don't 16 know why I cited that. I mean, it had to do with smoking; 17 but there's nothing that he said that I notice I would 18 take any issue with on that page. 19 Q. All right. 20 A. And page 80 is the next page. Well, yes, here on 21 page 80, what he is talking about is the fact that in 22 certain leukemias, you don't find any chromosome changes. 23 He states over here: "Now with the FISH you can find 24 abnormalities in almost 90 percent." 25 So it's a moving database. And the 54 1 implication is that, well, if we did FISH studies on 2 people who had normal chromosomes in leukemia, we would 3 find all their abnormalities. And, actually, there's 4 extensive literature on that, some of which I have here, 5 that says that's not true. And so I would disagree with 6 the statement that when we have a person with normal bone 7 marrow chromosomes, we can simply do a FISH analysis and 8 find the defects. 9 Q. Anything else that you disagree with him about? 10 MR. DILLARD: Well, he said you would have 11 to ask him specific questions. 12 A. Yeah. I mean, it's conceivable that there's 13 something else. But, I mean, those -- I made some notes 14 about those things. But I don't know what else -- you 15 know, it's been some time since I read his deposition; and 16 I don't know what else he said in there that I might 17 disagree with him on. 18 Q. (BY MR. KAESKE) Do you agree or disagree with 19 him that Mr. Minnehan is likely to develop or ultimately 20 have osteoporosis? 21 A. I don't know. I wouldn't have any comment about 22 that. I don't know if he will or will not. 23 Q. Do you have an opinion as to whether or not he 24 will ultimately be diagnosed with diabetes? 25 A. I don't have an opinion in the sense that it 55 1 depends on how long he has to remain on these drugs for 2 graft-versus-host disease. And that's an uncertainty 3 because his graft-versus-host disease could get better. 4 It could get worse. It could stay the same. And those 5 kinds of complications -- the osteoporosis, the diabetes, 6 and so on -- all relate to the duration that one has to be 7 on the steroids and the immunosuppressor drugs for 8 graft-versus-host disease, and we don't -- so I can't give 9 an answer to that. 10 Q. Well, has he been on them long enough now to lead 11 to some future problem like we've just discussed? 12 A. I don't think so. 13 Q. What about potential future renal failure? 14 A. Again, that relates to how long you have to stay 15 on these drugs. We know, for example -- and what he's 16 probably referring to is when we use drugs like 17 Cyclosporine, which is often used in graft-versus-host 18 disease. Depending on how much you give and how long you 19 give it, it can be toxic to the kidneys. And so if you 20 monitor the blood levels and the kidney function starts to 21 be impaired, you try to reduce the levels. Again, all of 22 that depends on how long will he need to be on these 23 drugs. So I don't know if he will or won't get any 24 problems with his kidneys. 25 Q. Well, how much longer do you think he needs to be 56 1 on these drugs before he's going to develop these problems 2 that we've talked about? 3 A. I don't -- well, I'm not certain I know the 4 question. I think you're referring to how long does it 5 take to get kidney abnormalities from Cyclosporine or 6 these kinds of drugs? 7 Q. Yeah, or any of these things. You said you don't 8 know whether the duration is long enough. How long of a 9 duration are you looking for? 10 A. Well, I would think that you have to be on it for 11 several years. Of course, you can acutely get damage if 12 you shoot your levels up very high; renal failure can 13 occur very quickly. But in most people, if you're 14 watching the levels and monitoring the kidney function, it 15 would be many years. I have one patient I'm seeing right 16 now who has got a kidney transplant, and she's been on 17 those drugs for about ten years and hasn't had any major 18 complications. But that's one person. In other words, 19 it's different for different people. It certainly has the 20 potential to damage the kidneys. 21 MR. KAESKE: Object as nonresponsive. 22 Q. (BY MR. KAESKE) I don't have any other 23 questions. Thanks. 24 MR. DILLARD: Thank you, sir. 25 MR. PERRY: Reserve all questions. 57 1 (Exhibits 1 and 2 marked) 2 MR. KAESKE: Before we leave, I'd just like 3 to read into the record the depositions that we've got 4 here. This is the deposition of Dr. Raabe, R-a-a-b-e; 5 Dr. Egilman, E-g-i-l-m-a-n; Dr. Mehlman, M-e-h-l-m-a-n; 6 Dr. Irons; Mr. Minnehan; John Spencer. 7 And actually, Doctor, before we leave, I do 8 need to ask you one more question. 9 THE WITNESS: Okay. 10 MR. KAESKE: Dr. Beran, B-e-r-a-n; and 11 Dr. Nicas. And that appears to be it. 12 Q. (BY MR. KAESKE) You don't have any notes in this 13 case other than that one page of handwritten notes that 14 you've got right there? 15 A. That's correct. 16 Q. Is that right? 17 A. And these, of course, copies of particular pages 18 from the medical records. 19 Q. All right. And you haven't taken any notes when 20 you read any of the depositions? 21 A. No. That's correct. 22 And this deposition, do you want it as part 23 of this or back to that? It's Dr. Gardner's. 24 Q. Well, I think you read all the notes on there 25 into the record, didn't you? 58 1 A. Yes. 2 Q. Then that will be fine. Thanks. 3 (Proceedings concluded at 12:40 p.m.) 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 59 1 CHANGES AND SIGNATURE 2 PAGE LINE CHANGE REASON 3 ________________________________________________________ 4 ________________________________________________________ 5 ________________________________________________________ 6 ________________________________________________________ 7 ________________________________________________________ 8 ________________________________________________________ 9 ________________________________________________________ 10 ________________________________________________________ 11 ________________________________________________________ 12 ________________________________________________________ 13 ________________________________________________________ 14 ________________________________________________________ 15 ________________________________________________________ 16 ________________________________________________________ 17 ________________________________________________________ 18 ________________________________________________________ 19 ________________________________________________________ 20 ________________________________________________________ 21 ________________________________________________________ 22 ________________________________________________________ 23 ________________________________________________________ 24 ________________________________________________________ 25 ETHAN NATELSON,MD 60 1 I, ETHAN NATELSON, MD, have read the foregoing 2 deposition and hereby affix my signature that same is true 3 and correct, except as noted above. 4 5 6 ________________________ ETHAN NATELSON, MD 7 8 9 THE STATE OF ______________ ) 10 COUNTY OF _________________ ) 11 12 Before me,_______________________, on this day 13 personally appeared ETHAN NATELSON, MD, known to me or 14 proved to me on the oath of _________________ or through 15 _______________ (description of identity card or other 16 document) to be the person whose name is subscribed to the 17 foregoing instrument and acknowledged to me that he/she 18 executed the same for the purpose and consideration 19 therein expressed. 20 Given under my hand and seal of office on this 21 ______ day of ____________________, ______. 22 23 ________________________ NOTARY PUBLIC IN AND FOR 24 THE STATE OF ___________ 25 My Commission Expires: ___________ 61 1 CAUSE NO. 21916*JG02 2 DANIEL T. MINNEHAN, Individually) IN THE DISTRICT COURT OF and as Next Friend for ) 3 Joshua Stephen Minnehan and ) Kyle Marshal Minnehan ) 4) Plaintiff, ) 5) vs. ) BRAZORIA COUNTY, TEXAS 6) AMERICAN OIL COMPANY, ) 7 Individually and f/k/a Amoco ) Oil Company and Amoco, Inc.; ) 8 et al., ) ) 9 Defendants. ) 239th JUDICIAL DISTRICT 10 11 12 REPORTER'S CERTIFICATE 13 ORAL DEPOSITION OF ETHAN NATELSON, MD 14 OCTOBER 15, 2004 15 16 I, Susan A. Love, Certified Shorthand Reporter in and 17 for the State of Texas, hereby certify to the following: 18 That the witness, ETHAN NATELSON, MD, was duly sworn 19 and that the transcript of the deposition is a true record 20 of the testimony given by the witness; 21 That the deposition transcript was duly submitted on 22 _________________ to the witness or to the attorney for 23 the witness for examination, signature, and return to me 24 by _________________; 25 62 1 That pursuant to information given to the deposition 2 officer at the time said testimony was taken, the 3 following includes the amount of time used by each party 4 at the deposition and all parties of record: 5 Mr. Michael L. Kaeske, Jr., Attorney for Plaintiff, (1:20); 6 Mr. Stephen C. Dillard, Attorney for Defendant Phillips Petroleum Company, Individually and a/k/a 7 Phillips Oil Company, Phillips Chemical Company and Phillips 66 Company, (0:00); 8 Mr. Stan Perry, Attorney for Defendant Shell Oil Company, (0:00); 9 Mr. James B. Galbraith, Attorney for Defendants American Oil Company, Amoco Chemical Company, Amoco 10 Corporation, Amoco Oil Company, BP Amoco Corporation, BP Chemicals, Inc., (0:00); 11 12 That a copy of this certificate was served on all 13 parties shown herein on _____________ and filed with the 14 Clerk. 15 I further certify that I am neither counsel for, 16 related to, nor employed by any of the parties in the 17 action in which this proceeding was taken, and further 18 that I am not financially or otherwise interested in the 19 outcome of this action. 20 Further certification requirements pursuant to 21 Rule 203 of the Texas Code of Civil Procedure will be 22 complied with after they have occurred. 23 24 25 ***** 63 1 Certified to by me on this _____ day of 2 _____________________, _______. 3 4 5 __________________________ Susan A. Love, CSR 6 Texas CSR No. 5183 Expiration: 12/31/2004 7 Henjum Goucher Reporting Services 12621 Featherwood Drive, Suite 140 8 Houston, Texas 77034 Phone: (281) 464-6000 9 Fax: (281) 464-7733 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 64 1 FURTHER CERTIFICATION UNDER TRCP RULE 203 2 3 The original deposition was/was not returned to the 4 deposition officer on __________________. 5 If returned, the attached Changes and Signature 6 page(s) contain(s) any changes and the reasons therefor. 7 If returned, the original deposition was delivered to 8 Mr. Michael L. Kaeske, Jr., Custodial Attorney. 9 That $____________ is the deposition officer's 10 charges to the Plaintiff for preparing the original 11 deposition and any copies of exhibits; 12 The deposition was delivered in accordance with Rule 13 203.3, and a copy of this certificate, served on all 14 parties shown herein, was filed with the Clerk. 15 Certified to by me on this ______ day of 16 ___________________, _______. 17 18 19 __________________________ Susan A. Love, CSR 20 Texas CSR No. 5183 Expiration: 12/31/2004 21 Henjum Goucher Reporting Services 12621 Featherwood Drive, Suite 140 22 Houston, Texas 77034 Phone: (281) 464-6000 23 Fax: (281) 464-7733 24 25 65