Document oeZGOjgGvwyw7zxMroa54Y04X
1 IN THE COURT OF COMMON PLEAS
2 PHILADELPHIA COUNTY, PENNSYLVANIA
3 CIVIL DIVISION
4 ---
5 EUGENE SALMIERI, et al. : APRIL TERM, 2006
6:
7 vs.
:
8:
9 CRC INDUSTRIES, INC., :
10 et al.
: NO. 02439
11 - - -
12 SEPTEMBER 9, 2008
13 - - -
14 ORAL DEPOSITION OF ROBERT R.
15 MONSON, M.D., taken pursuant to notice, was held
16 at the Hyatt Harborside Hotel, 101 Harborside
17 Drive, Boston, MA 02128, commencing at 9:38 a.m.,
18 before Kimberly S. Gordon, a Registered
19 Professional Reporter, Certified Court Reporter
20 and Notary Public.
21
22 * * *
VERITEXT NATIONAL COURT REPORTING COMPANY
23 KNIPES COHEN
1801 Market Street - Suite 1800
24 Philadelphia, PA 19103
1
1 APPEARANCES: 2
LOCKS LAW FIRM LLC 3 BY: ANDREW J. DuPONT, ESQUIRE
The Curtis Center, Suite 720 East 4 601 Walnut Street
Philadelphia, Pennsylvania 19106 5 215.893.0100
adupont@lockslawpa.com 6 Representing the Plaintiffs 7
WOOLF, McCLANE, BRIGHT, ALLEN 8 & CARPENTER, PLLC
BY: LOUIS C. WOOLF, ESQUIRE 9 900 Riverview Tower
900 South Gay Street 10 Knoxville, Tennessee 37902
865.215.1000 11 lwoolf@wmbac.com
Representing the Defendants, 12 Sunoco, Texaco 13
ABRAMS, SCOTT & BICKLEY, LLP 14 BY: ROBERT P. SCOTT, JR., ESQUIRE
Bank of America Center 15 700 Louisiana, Suite 4000
Houston, Texas 77002 16 713.228.6601
rscott@asbtexas.com 17 Representing the Defendant, ExxonMobil 18 19 20 - - 21 22 23 24
2
1 ---
2 INDEX 3 --4
5 Testimony of: Robert R. Monson, M.D.
6
7
8 By Mr. DuPont.................................5 9 10
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12 E X H I B I T S
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14 EXHIBIT NUMBER DESCRIPTION
PAGE MARKED
15 Exhibit-A
Evaluation of Papers
7
by Steinmaus and Smith
16 Exhibit-B
What is Non-Hodgkin
23
Lymphoma?
17 Exhibit-C
11/21/07 Memorandum
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Exhibit-D 18 Exhibit-E
1/14/08 e-mail Chemical Exposures and Risk of Chronic
29 32
19 Lymphocytic Leukaemia
Exhibit-F
Report with attached
34
20 studies relied upon
Exhibit-G 21 22
5/29/08 e-mail with attachments
93
23
24
3
1 ---
2 DEPOSITION SUPPORT INDEX
3 ---
4
5 Direction to Witness Not to Answer
6 Page Line
7 None
8
9
10 Request for Production of Documents
11 Page Line
12 16
6
13 25
15
14 93
11
15 93
19
16 94
11
17
18
19 Stipulations
20 Page Line
21 5
1
22
23
24
4
1 (It is hereby stipulated and 2 agreed by and between counsel for the 3 respective parties that sealing, filing 4 and certification are waived and that all 5 objections, except as to the form of the 6 question, be reserved until the time of 7 trial.) 8 --9 ROBERT R. MONSON, M.D., after 10 having been first duly sworn, was 11 examined and testified as follows: 12 - - 13 EXAMINATION 14 - - 15 BY MR. DuPONT: 16 Q. Good morning, Dr. Monson. Did 17 you bring a copy of your file with you here 18 today? 19 A. Yes. 20 Q. I see there's a box over on the 21 side of the room. Is that it or -22 A. No, it's here. 23 Q. Is there any organization to your 24 file here what you've just handed me?
5
1 A. The beginning stuff is things, 2 plaintiff witnesses and a couple of odds-and-ends 3 of papers and some e-mails between Mr. Woolf and 4 me. And then there's my report in this case, the 5 papers that upon which the report relies. And 6 then there's a later report, I'm sorry, another 7 report on NHL which I added because Mr. Woolf 8 asked me to because of the recent deposition of 9 one of your witnesses. 10 Q. Can you identify for me what the 11 recent report on NHL is that you're referring to? 12 A. It's at the very bottom. It was 13 not done for this case. 14 Q. And that clipped document, the 15 first page is entitled Evaluation of Paper by 16 Steinmaus C et al. Meta-analysis of Benzene 17 Exposure and Non-Hodgkin Lymphoma, -18 A. Yes. 19 Q. -- colon, Biases Could Mask an 20 Important Association. Can you tell me what this 21 document is? 22 A. It's a review of the paper that 23 was written by Steinmaus, et al., as well as the 24 paper by Martin Smith that preceded it.
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1 Q. And who performed the review of 2 the paper? 3 A. I did. 4 Q. When did you perform this review 5 of the Steinmaus and Smith papers? 6 A. The Smith one I did probably a 7 year ago whenever it came -- it came out in 2007. 8 The Steinmaus one I did earlier this year. 9 Q. Why was it that you performed a 10 review of the Steinmaus paper earlier this year? 11 A. Mr. Woolf asked me to. 12 Q. So your review of the Steinmaus 13 paper, was that in conjunction with the benzene 14 litigation? 15 A. It was in junction with the 16 subject NHL and benzene. It wasn't related to 17 any case or anything. 18 MR. DuPONT: Let's go ahead and 19 mark that Evaluation of Paper by 20 Steinmaus and mark that as Exhibit 21 Monson-A. 22 - - 23 (Whereupon the document was marked, for 24 identification purposes, as Monson-A.)
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1 --2 THE WITNESS: The usual question 3 that comes up, are you going to keep 4 these exhibits and what do I get back? 5 How does that work? 6 BY MR. DuPONT: 7 Q. The exhibits will go with the 8 court reporter. The court reporter will make 9 copies. The originals are maintained by our 10 office. 11 A. The papers as well? Scientific 12 papers? 13 Q. We can discuss that. 14 A. I just want to get it back. I 15 don't care how it's done but I don't want to have 16 to go to the library and get all the papers 17 again. 18 Q. I understand. Can you explain to 19 me what it is you did specifically with respect 20 to the Steinmaus paper, how you evaluated it, 21 what your methodology was? 22 A. I read it. I did the Smith one 23 first, and I read it and evaluated it and looked 24 at the original upon which I relied. And I did a
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1 similar thing with the Steinmaus paper and did 2 some similar corrections to the data or 3 re-analysis of the data that Steinmaus did and 4 then I summarized what I did and compared it to 5 what Steinmaus did. 6 Q. I am going to hand Exhibit 7 Monson-A back to you. Were you asked to perform 8 this review of the Steinmaus and the Smith papers 9 on behalf of any defendant to the benzene 10 litigation? 11 A. No. 12 Q. Any petroleum companies? 13 A. No. 14 Q. What were your conclusions with 15 respect to the Steinmaus paper? 16 A. My conclusion states, quote, the 17 weight of the evidence from a review of the 18 epidemiologic literature comprising over 40 19 published papers shows that there's no basis for 20 suggesting that benzene is associated with the 21 occurrence of non-Hodgkin lymphoma. I call it 22 non-Hodgkin without the S. 23 Q. So you went through and looked at 24 the same studies that the Steinmaus article
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1 looked at? 2 A. At the what study? 3 Q. That the Steinmaus article looked 4 at. 5 A. Did you say same? 6 Q. Is that correct? 7 A. Yes. 8 Q. And you provided a separate 9 analysis than Steinmaus, et al. did? 10 A. Yes. He did an extensive 11 statistical analysis. I didn't repeat that. But 12 in terms of summarizing the data, looking at the 13 papers, taking numbers from the papers that 14 relate any association between benzene and NHL. 15 Q. Did you analyze any of the data 16 in the studies cited by the Steinmaus paper for 17 Healthy Worker Effect or any other influence that 18 the methodologies in those studies could have had 19 on their findings of risk? 20 A. Yes. 21 Q. And what did you do? 22 A. The first issue was which data 23 Steinmaus abstracted from the papers, and I 24 looked at that and sometimes I agreed with what
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1 he did and other times I disagreed. He adjusted 2 relative risks based on all cause MR as well as 3 all cancer SMR, and I did the same thing for all 4 cancer SMR, if that's clear. I did the same 5 adjustment that he did or methodologically the 6 same. And then I compared his paper to Smith's 7 paper in terms of overlap or non-overlap as well 8 as papers I had looked at that either of them may 9 not have. 10 Q. Now, you come to a different 11 conclusion on the causal relationship between NHL 12 and benzene exposure based on the review of the 13 same literature than does Steinmaus? 14 A. I couldn't state what Steinmaus' 15 conclusion was with respect to causality. 16 Q. You come to a different 17 conclusion with respect to the risk of 18 contracting NHL from benzene exposure than does 19 Steinmaus? 20 A. I'd have to look at Steinmaus' 21 conclusions to make sure I can answer that 22 correctly. 23 Q. Why don't you take a look at 24 that?
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1 A. I don't have his paper here. It 2 would be somewhere here. 3 I may not have Steinmaus' paper 4 with me. It may just be an oversight. I'm sure 5 one of you has it. I don't see it, I'm sorry. 6 Do you have it? 7 Q. We'll get to that in a moment. 8 A. Okay. I just added this report 9 at the last minute, and I obviously just took my 10 report, my evaluation. 11 Q. Is it your understanding that CLL 12 is a form of non-Hodgkin lymphoma? 13 A. In recent years, that's the way 14 the classification has moved, yes. 15 Q. Do you have with you a list of 16 your previous testimonies, cases in which you've 17 given depositions or -18 A. No. 19 Q. Do you have that information at 20 your office? 21 A. Yes. 22 Q. Doctor, because we have a court 23 reporter here today, I notice that you are 24 predicting what my question is going to be and at
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1 some points beginning the answer before I finish 2 my response. It makes her job a little difficult 3 if we're speaking over each other. So, if you 4 could allow me to finish my question before you 5 begin your response, I would appreciate that. In 6 turn, I will try to allow you to finish your 7 response before beginning my next question. Is 8 that okay? 9 A. Yes. 10 Q. If at any point in time I ask you 11 a question that you do not understand, would you 12 please let me know and I'll do my best to 13 rephrase or re-ask the question? 14 A. Yes. 15 Q. Doctor, who have you been hired 16 to testify on behalf of in this case? 17 A. I've been hired by Mr. Woolf. 18 And frankly, until today, I wasn't sure on whose 19 behalf he was, he and Mr. Scott are representing. 20 I asked them this morning and I've already 21 forgotten, so Mr. Woolf can tell you what it is. 22 Q. Are you testifying on behalf of 23 Sunoco in this case? 24 MR. WOOLF: Do you want me to
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1 answer for him? 2 THE WITNESS: I don't know. 3 MR. WOOLF: If you really don't 4 know who I represent, I'll be more than 5 glad to restate it for the record. But 6 the witness is here on behalf of Exxon, 7 Sunoco and I believe Chevron. 8 THE WITNESS: This hasn't been 9 discussed. 10 BY MR. DuPONT: 11 Q. How many times have you given a 12 deposition in a case where it's been alleged that 13 somebody sustained a disease or an injury from 14 exposure to benzene? 15 A. I would estimate 15 to 20. 16 Q. And on those occasions, have you 17 ever testified on behalf of an individual who had 18 alleged that they contracted an illness? 19 A. No. 20 Q. Were all your depositions given 21 on behalf of companies that either manufactured 22 or sold products that contained benzene? 23 A. When you say all, do you mean all 24 benzene or do you mean --
14
1 Q. Sure. Of those 15 to 20 2 depositions where you've testified in benzene 3 litigation, we'll talk about those cases, -4 A. Yes. 5 Q. -- were you always testifying on 6 behalf of defendants to the benzene litigation? 7 A. You asked me that question 8 before, didn't you? 9 Q. I'm asking it a different way. I 10 want to make sure I understand. 11 A. I don't understand the 12 difference. 13 Q. My question is: In all of your 14 15 to 20 cases in which you've given depositions, 15 they've been on behalf of companies that made or 16 sold benzene-containing products? 17 A. I would say products alleged to 18 contain benzene. 19 Q. Are you able to recall the names 20 of any of those 15 to 20 cases, the names of the 21 plaintiffs? 22 A. No, I don't remember that. 23 Q. Do you have a list at your office 24 or somewhere compiled all those cases that you've
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1 given testimony in? 2 A. Yes. 3 Q. You did not bring that with you 4 today? 5 A. No. 6 Q. Could you provide that to Mr. 7 Woolf so he can give it to us, please? 8 A. Yes. 9 Q. Thank you. Dr. Monson, what is 10 your rate for testifying here today? 11 A. 8,000 a day. 12 Q. And what is your rate for, either 13 on an hourly basis or however you work it, for 14 preparing your report in this case and reviewing 15 the file? 16 A. 600 an hour. The daily rate is 17 prorated, of course. It's not a flat rate. 18 Q. Have you testified in litigation 19 other than allegations of benzene exposure? 20 A. Yes. 21 Q. What other areas of litigation 22 have you testified in? 23 A. Are you talking now about trial 24 testimony or depositions?
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1 Q. Let me be a little broader. Have 2 you been hired by any companies to testify or 3 prepare reports on their behalf in other areas of 4 litigation besides benzene? 5 A. Yes. 6 Q. Which other areas of litigation? 7 A. I hesitate only because if you 8 say prepare a report and there's no deposition I 9 consider that to be confidential. But if you're 10 talking depositions or trials, then I can just go 11 ahead and tell you what I remember. 12 Q. Tell me what you remember. 13 A. I remember welding; Bendectin, 14 which is a drug taken by women during pregnancy; 15 various radiation cases. There's been several 16 environmental cases; several have been for the 17 plaintiff, on behalf of the plaintiff. There's 18 undoubtedly others but that's what I remember. 19 Q. Have you ever testified on behalf 20 of a plaintiff in a welding case? 21 A. No. 22 Q. The second area was Bendectin 23 that you identified. Did you ever testify on 24 behalf of a plaintiff in Bendectin litigation?
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1 A. No. 2 Q. How about radiation, have you 3 ever testified on behalf of a plaintiff in a 4 radiation exposure case? 5 A. Yes. 6 Q. Did you testify on behalf of 7 defendants as well? 8 A. In other cases, yes. 9 Q. The fourth area was environmental 10 litigation. Can you explain for me what you mean 11 by environmental? 12 A. Yes, one was I testified on 13 behalf of the plaintiff for a sick building issue 14 in a courthouse in Chicago where the ventilation 15 system was improperly installed and the air was 16 bad. There was a situation in Alabama or Georgia 17 where creosotes soaked into the ground and was 18 found to be in a ditch surrounding a church. I 19 testified for the defense in terms of the 20 allegation was multiple diseases were caused by 21 this tarring-like substance. 22 Q. Any others that you can remember? 23 A. Not right now, no. There may be 24 others but I don't remember them.
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1 Q. When did you first begin to 2 testify in litigation? 3 A. The first one was in fact another 4 one it was 1989 thereabouts -- or was it 1979? 5 Sorry, I got to think about my timing here. 6 Anyway, it was emergency temporary ban of 245 T, 7 which is a pesticide made by Dow, and Dow was 8 suing the government. They had the emergency 9 temporary ban overturned, and I testified on 10 behalf of EPA saying that I agreed that there was 11 epidemiologic evidence that warranted concern. 12 I'm not sure about whether it was '79 or '89, but 13 let's say it was 1980. 14 Q. And when did you first begin 15 testifying in benzene exposure cases? 16 A. Maybe 15 years ago, 15 or 17 20 years ago. I can't be precise. 18 Q. How much income do you derive in 19 a year, start with 2007, the last full year, from 20 testifying in litigation? 21 A. That would include preparing 22 reports? 23 Q. Yes. 24 A. Not testifying?
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1 Q. Correct. 2 A. It varies from year to year. I 3 would say in the last decade the lowest was 4 30,000, the highest was 150,000. The mean would 5 probably be around 80,000. 6 Q. And do I understand you've 7 testified on behalf of Mr. Woolf's firm before? 8 A. Yes. 9 Q. Approximately how many times? 10 A. Again, depositions and trials, 11 there's been two trials, perhaps 10 or 15 12 depositions. 13 Q. And have all of the trials and 14 depositions that you testified in on behalf of 15 Mr. Woolf's firm, have all of those involved 16 benzene exposure, allegations of benzene 17 exposure? 18 A. To the best of my recollection, 19 yes. 20 Q. And would I be correct in that 21 all those cases you never came to the conclusion 22 that the plaintiff had contracted an illness as a 23 result of exposure to benzene? 24 A. My testimony related to the
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1 epidemiologic literature rather than to the 2 specific individual. 3 Q. And in any of those cases on 4 which you've testified on behalf of Mr. Woolf's 5 firm, did you ever come to the conclusion that 6 the epidemiological literature supported a causal 7 connection between exposure to benzene and the 8 injury that the plaintiff alleged they sustained 9 as a result of benzene exposure? 10 A. No. 11 Q. Can you tell me how much you have 12 charged for your work in this case, the Salmieri 13 case to date? 14 A. I received one payment I think 15 around 6,000. And a second bill is in the mail, 16 again, for about 6,000. 17 Q. And what did the second bill 18 include, up until what date, what portion of your 19 work? 20 A. Probably through July 31st. 21 Q. Have any of your opinions ever 22 been excluded or have you ever been prevented 23 from testifying in a case? 24 A. No.
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1 Q. Let me take another look at your 2 file here. On the top here, you have an article 3 or actually a printout from the Internet called 4 "What is Non-Hodgkin Lymphoma?". Can you tell me 5 what that document is and why you have it in your 6 file? 7 A. The main reason I looked it up 8 was to determine what percent of NHL is either 9 CLL or small lymphocytic leukemia, and the 10 statement in this document is these related 11 diseases account for about one out of four 12 lymphomas. 13 Q. One out of four lymphomas or one 14 out of four non-Hodgkin lymphomas? 15 A. It says lymphomas. 16 Q. Is it your understanding that CLL 17 and SLL are forms of B cell non-Hodgkin lymphoma? 18 A. Yes. 19 Q. Have you ever sought to determine 20 what percentage of non-Hodgkin lymphomas CLLs and 21 SLLs make up? 22 A. That's what I think the 23 one-in-four refers to. My guess is that this one 24 out of four lymphomas really means one out of
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1 four NHLs. I think the ACS probably didn't write 2 this as clear as they might have. 3 Q. When you say ACS, you're 4 referring to the American Cancer Society? 5 A. Yes. 6 Q. Have you looked beyond the 7 document that you have in front of you from the 8 American Cancer Society? 9 A. I had it and I was trying to find 10 it, but it may have been in one of these papers 11 that I reviewed. 12 MR. DuPONT: Let me mark that as 13 Monson-B, please. 14 - - 15 (Whereupon the document was marked, for 16 identification purposes, as Monson-B.) 17 - - 18 BY MR. DuPONT: 19 Q. Then the next thing you have in 20 your file are some communications with Mr. Woolf 21 concerning what, this case? 22 A. Right. This is really a cover 23 sheet for what files, just an e-mail saying, not 24 an e-mail but a letter that says enclosed are --
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1 Q. I see. We'll put that aside. 2 You're referring to the May 29, 2008 e-mail from 3 Ms. JoAnn -4 A. It's a bit out of order. This 5 goes first. These are two e-mails from, I'm 6 sorry, one e-mail from Lou and one memorandum 7 from me about this case. 8 Q. I'm going to mark your memorandum 9 as Monson-C. 10 - - 11 (Whereupon the document was marked, for 12 identification purposes, as Monson-C.) 13 - - 14 BY MR. DuPONT: 15 Q. In the last paragraph of your 16 memorandum, and this is dated November 21, 2007 17 from yourself to Lou Woolf, the last paragraph 18 you refer to a report of September 10, I believe. 19 Do you see that? 20 A. Yes. 21 Q. What report is that that you're 22 referring to? 23 A. I don't remember. It was a 24 report unrelated to this case that I had done,
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1 and I had all the papers in a pile somewhere. It 2 probably had to do with AML but I can't be sure. 3 But I just looked through those papers as sort of 4 preliminary, to get some preliminary impression 5 of what information was available on CLL. 6 Q. The report would have been from 7 September 10, 2007? 8 A. Yes. 9 Q. And was that a report that you 10 prepared in the context of benzene litigation? 11 A. Yes. 12 Q. Do you have a copy of that report 13 in your office? 14 A. Yes. 15 Q. Is that a report that you can 16 give to Mr. Woolf so that he can provide it to 17 us, please? 18 A. Again, I think it depends on 19 whether it was done for a specific case which was 20 not subject to deposition. Therefore, I believe 21 it was confidential. 22 Q. I'm sure your counsel in this 23 case can sort that out for you. But was this a 24 report that was served on a party to --
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1 A. I don't remember what report it 2 was. I looked at it last night and realized I 3 didn't know which report I was referring to. 4 Q. In any of your other work on 5 behalf of Mr. Woolf's firm and benzene cases, 6 have you analyzed the literature as it relates to 7 CLL? 8 A. No. 9 Q. In any of your other work on 10 behalf of Mr. Woolf's firm, have you analyzed the 11 literature as it relates to benzene and NHL? 12 A. Yes. 13 Q. How many other cases? 14 A. I gave you an answer of 10 to 15. 15 That would be the number. 16 Q. I'm sorry, perhaps I wasn't 17 clear. In how many other occasions on behalf of 18 Mr. Woolf's have you analyzed the literature on 19 non-Hodgkin lymphoma and benzene? 20 A. Two or three. I mean, these were 21 done not with respect to any litigation. They 22 were done by request. 23 Q. And did you formulate reports in 24 those cases involving non-Hodgkin lymphoma?
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1 A. Yes. 2 Q. And do you recall what your 3 conclusions were in any of those reports? 4 A. You can look at my report here 5 and that would be my conclusions. Basically, 6 there's no evidence, there's no consistent 7 evidence for an association between exposure to 8 benzene or benzene-containing products and NHL. 9 Q. When you say I can look at your 10 report here, are you referring to the report that 11 you issued in this case, the Salmieri case? 12 A. No, the Steinmaus and the Smith 13 thing that I gave you before which is unrelated 14 to this case. 15 Q. Have you testified on behalf of 16 any other law firms representing defendants in 17 benzene litigation besides Mr. Woolf's firm? 18 A. Yes. 19 Q. How many others? 20 A. I can recall two at the moment. 21 Q. And who are they? 22 A. One was a paint case and I'm not 23 sure who the defendant was. But the lawyer 24 escapes me; he was from Philadelphia. So,
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1 anyway, the allegation was that there was benzene 2 in paint. And I don't recall the illness. 3 And the other attorney was in 4 Chicago and it was an AML case. And the product 5 I don't recall because there were multiple 6 defendants and it wasn't clear, with multiple 7 products, some were distributors, some were 8 manufacturers, some were users. It was very 9 confusing legally. 10 Q. In any of your prior work for 11 companies that are alleged to have sold or 12 manufactured benzene-containing products, did you 13 look at gasoline literature specifically? 14 A. Yes. 15 Q. How many other cases? 16 A. One or two is what I recall. 17 Q. Do you recall the names of those 18 cases? 19 A. No. 20 Q. Did you issue reports in those 21 cases? 22 A. Yes. 23 Q. And did you testify? 24 A. There were depositions, I
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1 believe. Usually, there's a deposition somewhere 2 along the line. 3 Q. Do you remember when those 4 depositions were given? 5 A. No. It would be in my list of 6 depositions, within the last ten years. 7 Q. We'll mark as the next exhibit, 8 Monson-D, the January 14, 2008 e-mail from Mr. 9 Woolf to yourself. 10 - - 11 (Whereupon the document was marked, for 12 identification purposes, as Monson-D.) 13 - - 14 BY MR. DuPONT: 15 Q. In the PS line of this e-mail, 16 Mr. Woolf asks you and it says: I would 17 appreciate it if you would do it for CLL 18 specifically but also with regard to the small 19 cell NHL issue. 20 And he's referring to his request 21 that you do a detailed report with regard to the 22 relationship between gasoline on the one hand and 23 CLL and benzene and CLL. Take a look at that. 24 Did you in fact do a review of
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1 the literature and issue a report as it relates 2 to small cell NHL? 3 A. I looked to see if I could find 4 anything and didn't. 5 Q. When you say small cell NHL, is 6 that small cell lymphocytic leukemia? 7 A. It's what it's called. You 8 called it SLL. That's small lymphocytic 9 lymphoma. Is that what SLL stands for? 10 Q. What's your understanding of what 11 you were asked to do with respect to small cell 12 NHL? 13 A. Small cell lymphoma, yes. It's 14 called small cell -- no, it's called small 15 lymphocytic, I'm sorry. The terminology is very 16 confusing and this has just come along in the 17 last few years. I believe it's called small 18 lymphoma. Is that the correct term? 19 Q. Is that your understanding of it? 20 A. It's the same disease except for 21 location as CLL. There's CLL which is 22 classically a disease of chronic lymphatic 23 leukemia. And then there's this type of NHL 24 which is called small lymphocytic lymphoma.
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1 That's what it is. 2 Q. Those are both types of B cell 3 non-Hodgkin lymphomas? 4 A. They're two different forms of 5 the same disease is my understanding. I'm not a 6 hematologist. I wouldn't want to. I'm not an 7 expert in that area. 8 Q. And you would agree with me that 9 both CLL and SLL fall within the rubric of B cell 10 non-Hodgkin lymphoma? 11 A. To the best of my recollection. 12 I'm not an expert. I believe I just read it 13 there in the American Cancer Society document. 14 Q. Have you spoken with anyone from 15 ExxonMobil or Sunoco or Texaco regarding this 16 case? 17 A. No. 18 Q. Have you ever spoken with Dr. 19 Schnatter? 20 A. I may have met him many years 21 ago. I don't recall. 22 Q. Did you review any depositions 23 given by Dr. Schnatter? 24 A. No.
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1 Q. There's a paper in here by Aaron 2 Blair, and that's part of your file. Can you 3 tell us why it is you reviewed that paper? 4 A. The title is Chemical Exposures 5 and Risk of Chronic Lymphocytic Leukaemia, 6 spelled the British way. 7 Q. And when in your analysis in this 8 case did you review that? Did you review that as 9 part of preparing your report? 10 A. I was trying to think -- I didn't 11 include it in my report and that was either 12 because when I first wrote the report it hadn't 13 been published -- it was published on-line in 14 October 24, 2007, and I'm not sure exactly when I 15 came across it. But on the other hand, it's a 16 review. It's not a specific study. But it has 17 to do with chemicals and CLL. 18 MR. DuPONT: I'm going to go 19 ahead and mark that as E. 20 - - 21 (Whereupon the document was marked, for 22 identification purposes, as Monson-E.) 23 - - 24 BY MR. DuPONT:
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1 Q. The next section of your file I'm 2 going to hand you appears to be your report and 3 the studies that you relied upon? 4 A. Yes. 5 Q. Are those studies that you've 6 cited to in your report all the studies you 7 intend to rely upon in support of your opinions 8 in this case if you were to testify at trial? 9 A. No. 10 Q. Can you tell me what other 11 articles you rely upon in support of your 12 opinions? 13 A. If new articles come along, I 14 would include them. And if there are articles 15 I've missed that are pointed out to me, I may or 16 may not consider them. 17 Q. Up until this point in time, can 18 you tell me all the articles you intend to rely 19 upon in support of your opinions? 20 A. Yes. 21 Q. And which are those? 22 A. I'm sorry? 23 Q. Which are those? Which articles 24 do you intend to rely upon that have been
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1 published up until this point in time? 2 A. The ones here. As I say, there 3 may be others that I missed, and if I find out 4 about them, I may add them. I have no plans to 5 do that, but you never know. 6 Q. I want to get to your methodology 7 here in a little bit. But I'd like to know -8 MR. DuPONT: First of all, 9 Exhibit-F, we'll make that his report 10 along with the studies that he's relied 11 upon. 12 - - 13 (Whereupon the document was marked, for 14 identification purposes, as Monson-F.) 15 - - 16 BY MR. DuPONT: 17 Q. How did you perform your 18 literature review in order to come to your 19 opinion in this case? 20 A. I usually do a PubMed search of 21 either the disease or the exposure or both. And 22 then I read the bibliography of the papers to see 23 if there are other papers that have not turned up 24 in PubMed.
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1 Q. You say that that's how you 2 usually perform your search? 3 A. Yes. 4 Q. I want to know how you did that 5 specifically as part of your methodology in this 6 case. 7 A. That's what I did. I mean, also, 8 my initial review was of papers I had for other 9 cases on AML which I had obtained through PubMed. 10 Q. And how did you come to the 11 decision on which papers to include or which 12 papers to rely upon in support of your opinions? 13 A. Basically, I looked at studies 14 and saw if they had any information on CLL and 15 benzene or benzene-containing products. 16 Q. And did you then include all 17 papers that had information on CLL and exposure 18 to benzene or benzene-containing products within 19 your report? 20 A. There are some papers that were 21 not studies but were reviews or opinion pieces I 22 did not rely upon. 23 Q. Did you include all papers that 24 you felt were studies as opposed to reviews or
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1 opinion pieces in your report? 2 A. Some papers are updates of 3 earlier papers and I include only the latest 4 paper on a given group of people. 5 Q. Other than situations where you 6 have an update of a previous study and you 7 exclude the prior study, have you included all 8 studies that relate to CLL and exposure to 9 benzene or benzene-containing product? 10 A. Yes, all the ones that I've 11 identified. 12 Q. Am I correct that you did not 13 review the literature and report on that as it 14 relates to non-Hodgkin's lymphoma in your report? 15 A. That's correct. 16 Q. And why is that? 17 A. I wasn't asked to. Other than 18 the small lymphocytic request that we've already 19 discussed, I found no papers. 20 Q. Are you familiar with Dr. 21 Schnatter's 1996 article concerning benzene 22 exposures in the Canadian petroleum distribution 23 workers? 24 A. I don't see that I relied upon
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1 it. I know that Schnatter has written a number 2 of papers and I know that he's written papers 3 with other people, so I don't have -- I don't see 4 that I relied upon it. But if you show it to me, 5 I may be able to say yes, I've seen that and go 6 from there. 7 MR. DuPONT: Why don't we take a 8 five-minute break here? 9 --10 (Whereupon there was a recess in the 11 proceedings from 10:31 to 10:39.) 12 - - 13 BY MR. DuPONT: 14 Q. So the first part of your method 15 in this case is that you go through, you perform 16 a literature search using MedLine? 17 A. PubMed. 18 Q. And then you select those cases 19 that you believe deal with CLL and exposure to 20 benzene or products containing benzene, correct? 21 A. Yes. 22 Q. And then once you have that group 23 of documents you divided them up into studies 24 which dealt with exposure to, likely exposure to
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1 gasoline and CLL and exposure to benzene and CLL? 2 A. Yes. 3 Q. How is it that you came to the 4 conclusion whether or not a study dealt with 5 persons likely exposed to gasoline? 6 A. Either it was about either 7 "gasoline" was in the title or the word 8 "gasoline" was used. Petroleum marketing and 9 distribution, it's my understanding that at least 10 some of those people are exposed to gasoline. 11 Then there are people who work in service 12 stations, people who work as vehicle mechanics. 13 That's about it. 14 Q. So you looked either at the title 15 of the study or the body of the study to see if 16 there was mention of gasoline or a job category 17 such as petroleum distribution, vehicle mechanic, 18 gas station attendant that would indicate to you 19 that there was exposure to gasoline? 20 A. Possible exposure. 21 Q. How come you did not include the 22 2003 Glass article -23 A. That's under benzene. 24 Q. Let me finish. How come you did
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1 not include the 2003 Glass article among the 2 Studies of Persons With Likely Exposure to 3 Gasoline? 4 A. Because it's a study of benzene. 5 Q. Do you have an understanding as 6 to whether or not the workers studied by Glass in 7 the 2003 article were exposed to gasoline? 8 A. Again, all I say in my, on Page 7 9 is that they worked in the petroleum industry and 10 they were -- information on benzene was obtained. 11 Q. Do you know whether or not the 12 workers that were involved in the Glass study of 13 2003 were exposed to gasoline? 14 A. I don't know. 15 Q. If they were exposed to gasoline, 16 would you then include them within your listing 17 under Roman Numeral II of Studies of Persons With 18 Likely Exposure to Gasoline? 19 A. I'd have to look at the paper and 20 decide exactly where it should go. I only 21 include it in the paper once. And benzene is a 22 more specific chemical than gasoline is and I 23 tend to group specific chemicals together 24 separate from mixtures of chemicals.
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1 Q. So, if there's a study that deals 2 with both gasoline exposure and benzene exposure, 3 you put that study in the benzene exposure column 4 as opposed to the gasoline column? 5 A. Yes. 6 Q. Why is that? 7 A. As I say, I think it's something 8 that's specific that bonds together. It's a 9 chemical, whereas gasoline is a product which is 10 a mixture of a number of chemicals. 11 Q. Which include benzene, correct? 12 A. Which may include benzene. 13 Q. Do you know if gasoline is made 14 without benzene? 15 A. No, I don't know that. I'm just 16 saying that. You were asking a general question 17 and I was giving you a general answer. 18 Q. So, if Dr. Glass had published 19 that subjects of her nested case-control study 20 had exposure to gasoline, you would not include 21 that within your list of Studies of Persons With 22 Likely Exposure to Gasoline? 23 A. If I had not done benzene as 24 well, then I would have included it. But since I
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1 did both benzene and gasoline, I included it 2 under benzene. 3 Q. I am going to hand you Dr. 4 Schnatter's 1993 article entitled Retrospective 5 Mortality Study Among Canadian Petroleum 6 Marketing and Distribution Workers. I'll ask you 7 is that a study that you reviewed in the course 8 of coming to your opinions in this case? 9 A. I'm certainly aware of the study 10 and I assume I reviewed it. I can't tell you I 11 did for sure. Do you want to point out anything 12 specific? 13 Q. You have no recollection of 14 reviewing this study in the context of preparing 15 your report in this case? 16 A. I would say that that's correct. 17 It's likely I did review it but I don't recall 18 specifically excluding it or reviewing it. I 19 certainly read it in other contexts. 20 Q. And Dr. Schnatter in that study 21 finds a significantly elevated mortality due to 22 leukemia among tank truck drivers and the SMR is 23 3.35. Do you see that? 24 A. Yes.
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1 Q. Would you include that that 2 study, specifically a finding of SMR of 3.35, 3 supports a conclusion that gasoline distribution 4 workers are at an elevated risk for contracting 5 leukemia? 6 A. Yes, leukemia as a general 7 category, not CLL. 8 Q. A finding of elevated risk for 9 leukemia generally among gasoline distribution 10 workers, is that relevant to CLL? 11 A. No. 12 Q. Why not? 13 A. If there's no information on CLL, 14 it's not relevant. From a cursory look here, I 15 don't see any information on CLL. 16 Q. What about lymphocytic leukemias, 17 if there's a finding of elevated risk for 18 lymphocytic leukemias in general, would that be 19 relevant to whether there's a risk for 20 contracting CLL from exposure to gasoline or 21 benzene? 22 A. It may or may not be because it 23 could refer to acute. It could refer to chronic. 24 I believe I included one or two papers that did
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1 just have lymphocytic. 2 Q. How about the 2002 Guenel study, 3 if you turn to Page 7 of your report? 4 A. Okay. 5 Q. Why did you place that underneath 6 the Roman Numeral III, Studies of Persons Exposed 7 to Benzene, as opposed to Studies of Persons With 8 Likely Exposure to Gasoline? 9 A. It says gas. It doesn't say 10 gasoline. 11 Q. So what do you understand gas to 12 be that they're referring to? 13 A. Natural gas. 14 Q. Do you have that report with you? 15 A. Yes. 16 Q. If you look at Page 89 under 17 Benzene Exposure Assessment? 18 A. Yes. 19 Q. If you look at the first sentence 20 under Benzene Exposure Assessment, it says: 21 "Use of solvents" for cleaning or 22 degreasing materials and "exposure to gasoline" 23 from motor vehicles were the two work tasks that 24 may have entailed exposure to benzene. Do you
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1 see that? 2 A. Yes. 3 Q. Do you agree with me that the gas 4 that's being discussed in Guenel is gasoline and 5 not natural gas? 6 A. No. 7 Q. No? 8 A. If you look further in the 9 article, examples of occupations with such 10 exposures include plumbers of the gas 11 distribution network. And that's not clear. 12 Q. He also discusses mechanics, 13 correct? 14 A. In thermic or hydraulic 15 electricity production plants. And then Group 3 16 up above is coal gasification which leads me to 17 believe that the gas is gas produced from coal, 18 which is essentially natural gas. 19 Q. What about the second exposed 20 work task? 21 A. I'm sorry, where are you looking? 22 Q. If you look at the very bottom of 23 Page 89 on the right-hand column, they discuss 24 benzene exposure may also have occurred from
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1 "exposure to gasoline" identified as the second 2 exposed work task. Motor vehicle mechanics 3 working in garages represented the main 4 occupation with such an exposure. Do you see 5 that? 6 A. No, I'm sorry. Just say again 7 where it is. 8 Q. Sure, the very bottom of Page 89 9 on the right-hand column. 10 A. Yes. Okay, fine. So they may 11 have been exposed to gasoline. But I believe the 12 term "gas" refers to natural gas. 13 Q. And if you continue further down, 14 it also says: In addition, gasoline may have 15 been used as a solvent in garages, even though 16 this practice is proscribed. 17 A. Yes. 18 Q. Did you see anywhere in this case 19 that Mr. Salmieri used gasoline as a solvent? 20 A. I know nothing about the case. 21 Q. Would you now agree with me that 22 the subjects of the study Guenel 2002 had 23 exposure to gasoline? 24 A. Yes.
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1 Q. Based on that, would you include 2 the Guenel study within the list of cases under 3 Studies of Persons With Likely Exposure to 4 Gasoline? 5 A. Not in the article -- not the 6 report as I wrote it because benzene is the 7 primary exposure. Had I done a study only of 8 gasoline workers, then I would have included 9 that. 10 Q. But the benzene exposure comes 11 from gasoline, correct? 12 The authors aren't concluding 13 that the individuals are having exposure to pure 14 benzene in this case, are they? 15 A. It says use of solvents for 16 cleaning or degreasing materials that may have 17 entailed exposure to benzene. 18 Q. Correct. Use of solvents and use 19 of gasoline, correct? 20 A. So use of solvents containing 21 benzene was widely used, so it's hard to say 22 whether there was more exposure from solvents or 23 from gasoline. 24 Q. Do you know what the authors
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1 concluded regarding the benzene content of the 2 solvents versus the gasoline being used? 3 A. On Page 89, they talk about the 4 standard which was less than 1 percent in 1969 5 and less than 2 percent weight in 1986. 6 Q. That's actually .2 percent 7 weight, correct? 8 A. Yes. 9 Q. That's with respect to solvents, 10 right? 11 A. Yes. 12 Q. And then the standard referred to 13 with respect to gasoline is 5 percent? 14 A. Yes. 15 Q. And then the author gives a ratio 16 for exposure to gasoline versus use of solvents 17 on Page 90. Do you see that? 18 A. Yes, I'm trying to figure that 19 out. 20 Q. Am I correct in that the authors 21 assign a ratio of two-to-one for exposure to 22 gasoline versus use of solvent pre-1970 and then 23 a ratio of ten or .4 to .04 for gasoline versus 24 use of solvent after 1985?
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1 A. This is an index of benzene 2 exposure intensity. 3 Q. Correct. 4 A. It doesn't refer to the ratio of 5 use of solvents to the ratio of use of gasoline. 6 Q. Now, you've published some 7 studies with respect to the incidence of leukemia 8 amongst rubber workers? 9 A. Yes. 10 Q. Am I correct in some of those 11 studies you found where there was an increased 12 risk of leukemia amongst rubber workers that some 13 of those workers used gasoline as a solvent in 14 the context of the work? 15 A. They used white gas, which is I 16 guess a form of gasoline. 17 Q. Actually, you characterize it as 18 high test gasoline? 19 A. If you say so. You'd have to 20 point that out to me. 21 Q. I'm going to hand you your 22 article Cancer Mortality and Morbidity Among 23 Rubber Workers and point your attention to Page 24 1035.
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1 MR. WOOLF: What's the date? 2 MR. DuPONT: It's 1978. 3 BY MR. DuPONT: 4 Q. I'll apologize, I'm going to look 5 over your shoulder because I don't have another 6 copy with me. But you write here in 1978 that 7 the most common solvents used in this company 8 were fine petroleum solvents, principally high 9 test gasoline and varnish makers naphtha. Is 10 that correct? 11 A. Yes. 12 Q. You did not include that study 13 within your review of literature in your report 14 in this case, did you? 15 A. No. 16 Q. And that study shows an elevated 17 risk of leukemia among those workers who used 18 gasoline as a solvent? 19 A. Yes. There's no information on 20 CLL. 21 Q. There's 19 cases lymphatic 22 leukemia? 23 A. There's 21 mortality deaths and 24 27 cases.
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1 Q. Did that study in 1978 find 19 2 workers who were diagnosed with lymphatic 3 leukemia? 4 A. No, found 27. 5 Q. 27 with lymphatic leukemia? 6 A. Yes. 7 Q. And then it also found workers 8 with lymphosarcoma? 9 A. Yes. 10 Q. Do you know where the information 11 is today on which those diagnoses were based on? 12 In other words, are there still records that can 13 tell us what forms of lymphatic leukemia those 27 14 workers had? 15 A. No, I don't know. 16 Q. You state in your paper that you 17 hesitate to attribute the excess of leukemia 18 solely to benzene. Do you see that? 19 A. Yes. 20 Q. If you can turn to Page 7 of your 21 report, please? 22 A. Go ahead. 23 Q. At the bottom, you have your 24 discussion of the Glass 2003 study?
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1 A. Right. 2 MR. WOOLF: While you're doing 3 that, let me see Monson '78. 4 MR. DuPONT: Sure. 5 BY MR. DuPONT: 6 Q. Now, your principal comment with 7 respect to the Glass study is that it has a 8 potential flaw and that the cases were identified 9 by self-report rather as part of the standard 10 system of follow-up. Is that correct? 11 A. Yes. 12 Q. And am I correct in that your 13 concern with that is that cases of CLL may have 14 been omitted because they were not reported? 15 A. No. It's more that cases of CLL 16 may have self-identified if they were concerned 17 about benzene exposure. 18 Q. Have you reviewed Dr. Glass' 19 response to critiques of the 2003 article and the 20 use of self-reporting? 21 A. I believe so. There's two or 22 three subsequent articles dealing with the 23 exposure assessment, and the self-reporting, I 24 don't have it in my mind.
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1 Q. Are you familiar with the 2 Institute of Occupational Medicine? 3 A. Can you say more about it? 4 Q. Sure. In July of 2005, Institute 5 of Occupational Medicine authored a study 6 entitled A Review of the Data Quality and 7 Comparability of Case-Control Studies With Low 8 Level Exposure to Benzene in the Petroleum 9 Industry. The principal author was B.G. Miller. 10 A. Can I see it? 11 Q. Sure. 12 A. No, I haven't seen this. 13 Q. Do you agree with Dr. Glass' 14 response to the criticism and the use of 15 self-reporting that essentially it does not 16 affect the validity of the study because there's 17 an over 90 percent participation rate of the 18 members of the cohort? 19 A. Can I see that, please? 20 Q. Sure. 21 A. I don't see the 90 percent. I 22 suspect it's in here somewhere. Was it on this 23 page? 24 Q. Were you aware that there was an
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1 over 90 percent participation rate? 2 A. I know I've read that paper. 3 That's all I can say. 4 Q. So you're not aware that there 5 was an over 90 percent participation rate? 6 A. If I had read the paper, I 7 undoubtedly read that statement. I don't recall 8 that statement. 9 Q. If there was an over 90 percent 10 participation rate in that cohort examined by Dr. 11 Glass in 2003, would you agree with me that that 12 would eliminate any concern with respect to any 13 selection bias or reporting bias? 14 A. It wouldn't eliminate anything 15 because that's an overall percentage. It's not 16 specific for people with CLL or for benzene 17 exposure. 18 Q. If you had no information to 19 suggest that there was a different percentage of 20 reporting rate or inclusion rate for CLLs -21 A. It doesn't eliminate it. It's 22 better to have a 90 percent inclusion rate than a 23 50 percent inclusion rate. 24 Q. Would you agree with me that it
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1 would eliminate any cause for concern with 2 respect to the reporting bias? 3 A. It wouldn't eliminate it. It 4 would minimize it. 5 Q. If Dr. Schnatter wrote that there 6 were no obvious design flaws in the 2003 7 Schnatter study, would you agree with him? 8 A. I'm sorry? 9 Q. If Dr. Schnatter concluded that 10 there were no obvious design flaws in Deborah 11 Glass' 2003 study, would you agree with his 12 conclusion? 13 A. I wouldn't disagree with it. I 14 haven't read that. The main concern about the 15 health watch study in general is comparing Glass 16 to Gun, overall excess of CLL in the entire 17 cohort. And when you do a case-control 18 evaluation of benzene which goes beyond the basic 19 data in the follow-up study, you find this 20 excess. So it's an ambiguous study. 21 Q. The Glass 2003 is a nested 22 case-control? 23 A. Within the Gun cohort. 24 Q. Correct.
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1 A. In addition, she identifies other 2 cases that are not included in it. 3 Q. So, with Gun and Glass, in 4 certain respects, you're looking at different 5 cohort members? 6 A. The Gun study is the cohort. The 7 Glass study includes Gun plus other people. And 8 it's not clear to me that they belong to 9 different cohorts. 10 Is Gun a mortality or -- Gun has 11 cancer incidence as well so it's -- there's 12 ambiguity into how those studies were done 13 because they were done by different people at 14 different institutions. 15 Q. So you can't necessarily relate 16 the findings of one to the other, can you? 17 A. They should be consistent with 18 each other and they're not, and that raises a 19 general concern of what's going on and I can't 20 answer that question. 21 Q. But the Gun study doesn't 22 invalidate the findings of Glass' 2003 study, 23 does it? 24 A. It's not consistent with it.
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1 Q. But it does not invalidate the 2 findings, does it? 3 A. Not by itself. But one has to 4 present both sets of findings in attempting to 5 evaluate that study in general. 6 Q. You mentioned that you used a 7 weight of the evidence approach in your report. 8 Can you describe that for me what your weight of 9 the evidence -10 A. Can you point out where I say 11 that? 12 Q. Sure. Do you in fact use a 13 weight of the evidence approach? 14 A. That term is a bit loaded and I 15 -- okay. It's on Page 2. The term "weight of 16 the evidence" is used in describing or in 17 discussing the Bradford-Hill criteria. 18 Q. So do you use a weight of the 19 evidence approach in coming to your opinions in 20 your report? 21 A. I would say that that is part of 22 what I do, yes. 23 Q. Could you describe for me what 24 your methodology is for your weight of the
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1 evidence approach? 2 A. If you look at the summarization 3 of the papers, just start out on Page 10 which 4 contains Studies of Persons With Likely Exposure 5 to Gasoline, one way to summarize the weight of 6 the evidence is to summarize the data and that 7 would be under or in the line titled Sums. 8 Another way to describe the 9 weight of the evidence is to compare the 10 distribution of observed over expected ratios, 11 whether they're less than .9, .9 to 1.1 or 12 greater than 1.1. So those are two different 13 ways of summarizing the weight of the evidence. 14 Q. Your weight of the evidence 15 approach is limited to looking at epidemiology 16 studies. Is that correct? 17 A. Yes. 18 Q. And specifically it's limited to 19 those epidemiology studies which you felt were 20 properly included within either benzene-exposed 21 populations and likely exposure to gasoline as it 22 related to CLL? 23 A. Yes. I include all leukemia as 24 well.
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1 Q. So you include all leukemia? 2 A. In this particular review, I 3 included all leukemia as well as CLL. 4 Q. So findings relating to all 5 leukemia in your review are relevant to CLL? 6 A. No. 7 Q. But you included them? 8 A. I included them for comparison 9 purposes. 10 Q. On Page 10, you have your summary 11 of the data and you have a table for the Studies 12 of Persons With Likely Exposure to Gasoline, 13 correct? 14 A. Yes. 15 Q. And there you look at six 16 studies; Schwartz, Wong, Hunting, Lynge, Milham 17 and Sorahan? 18 A. Yes. 19 Q. And you provide the observed and 20 expected numbers of leukemia in one column and 21 then CLL in another and then what the ratios are? 22 A. Yes. 23 Q. And then you provide the sums of 24 all the observed, all the expected and all the
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1 ratios? 2 A. It's not the sum of the ratios. 3 It's the ratio of the sums. 4 Q. Again, in that chart, you did not 5 include, on Page 10, you did not include the 6 Guenel or the Glass study? 7 A. No. 8 Q. And you did not include 9 Schnatter's 1996 study? 10 A. No. 11 Q. And then on the next page you do 12 the same thing for what you've chosen to be 13 Studies of Populations Exposed to Benzene? 14 A. Yes. 15 Q. And there you also did not 16 include the Glass study. Is that correct? 17 A. Yes. 18 Q. And you did not include Dr. 19 Schnatter's 1996 paper either? 20 A. Right. 21 Q. Are you familiar with Wendy 22 Huebner's 2004 study looking at Baton Rouge and 23 Baytown Mobil refineries? 24 A. Yes.
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1 Q. I'm correct, am I not, that 2 refinery workers are exposed to gasoline? 3 A. I would say there's potential 4 exposure. I don't know the nature of refinery 5 workers in general. 6 Q. Wouldn't that be important for 7 you to know in order to assign a study such as 8 Dr. Huebner's study to benzene exposure or likely 9 gasoline exposure category? 10 A. Yes. 11 Q. And am I correct that you did not 12 include Dr. Huebner's 2004 study in your review 13 and your report, did you? 14 A. No. 15 Q. You did not do that? 16 A. I don't see it. 17 Q. How come you didn't include her 18 study? 19 A. I'd have to look at it and see. 20 Q. While you're doing that, can I 21 have your copy of the Glass study, please? 22 A. (Witness complies.) 23 Q. Thank you, Doctor. 24 A. This is included in a group of
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1 petroleum workers that I did not review because 2 there was little or no information on specific 3 exposures. 4 Q. That study found an SMR of 2.42 5 for chronic lymphocytic leukemia within the Baton 6 Rouge finding, didn't it? 7 A. I believe so, yes. 8 Q. Would you agree with me that 9 refinery workers are a population of workers that 10 are exposed to gasoline and benzene? 11 A. As I say, I don't know that. I 12 notice that it says during the war there was use 13 of or production of high something, aviation 14 gasoline. But it doesn't say how many people 15 were exposed or how long this was done. And the 16 paper doesn't talk about gasoline beyond that 17 that I can see. 18 Q. So gasoline exposure was one of 19 the exposures that the authors considered? 20 A. They mentioned it. I can't say 21 that they considered it. 22 Q. Doctor, if you look to Page 12 of 23 your report in the Conclusions section? 24 A. Go on.
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1 Q. Under Studies of Persons Exposed 2 to Benzene, second paragraph, you say there is no 3 consistency among the 12 studies of persons 4 exposed to benzene that there is a positive 5 association between benzene and CLL. Do you see 6 that? 7 A. Yes. 8 Q. Which of the 12 studies are you 9 referring to? 10 A. The inverse studies would be 11 Decoufle -- I'm sorry. 1983 Tsai, Rinsky, 12 Collins, Ji. 13 Q. You say six show a positive 14 association. Those would be Linos, Arp -- which 15 ones are they that show positive association, the 16 six? 17 A. Linos, Arp, Bernard, Malone, 18 Guenel, Sorahan. 19 Q. Again, you're not including 20 Glass? 21 A. The problem with Glass is that 22 this is -- I didn't include Gun either. I agree 23 that Glass shows a positive association on an 24 internal analysis. But the external analysis
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1 shows no excess. And so it's an ambiguous 2 situation that by itself provides little 3 information to base an opinion. I don't deny the 4 existence of the Glass study nor its conclusions. 5 Q. You don't consider them in your 6 analysis of the -7 A. It's not a study of a population. 8 It's a case-control study within a cohort. 9 Q. That makes it a nested 10 case-control study, right? 11 A. It's more than that. That's the 12 problem. To some extent, it's nested but then it 13 goes beyond that. It's a combination of a nested 14 case-control and a non-population-based 15 case-control study. 16 Q. Certainly, in 2003, what were the 17 expected number of CLLs for Glass' 2003 study? 18 There's 11 observed, correct? How many expected? 19 A. I should have the Gun paper to 20 put it in context. 21 MR. WOOLF: I have a copy of the 22 Gun article with me if you want to see it 23 in conjunction with what you're looking 24 at.
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1 THE WITNESS: All right. 2 BY MR. DuPONT: 3 Q. My question is is with respect to 4 the Glass 2003 study. Do you know what the 5 expected number of CLLs were? 6 A. The observed number was 11. 7 Q. Correct. 8 A. You said expected? And then the 9 analysis was internal by cumulative lifetime 10 benzene exposure. That's Table 6 and that's the 11 relevant data in this article. So that under 12 four cumulative lifetime -- under four PPM years 13 by definition the relative risk is 1; between 4 14 and 8 is 2.8; and above 8 it's 4.5. It doesn't 15 break it down by the numbers. 16 Q. So your answer is no, you don't 17 know what the expected number of CLLs was? 18 A. No, because it isn't -- it's 11 19 in this particular analysis. Observed is 11 and 20 expected is 11. And within that, she looks at 21 the distribution but doesn't say how many 22 observed cases there are in the three categories. 23 And the intervals are extremely wide, so it's 24 quite possible that the observed number in the
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1 higher categories is 1 each or something like 2 that. 3 Q. I respectfully move to strike 4 your response. It was not a response. 5 My question was: Do you know 6 what the expected number of CLLs was? 7 A. No, except as I said in this 8 table the observed number and the expected number 9 are the same. That's what I responded. 10 Q. Turn to Page 9 of your report. 11 You provide your analysis of the 2007 ATSDR 12 toxicological profile for benzene? 13 A. I'm sorry, let me just -- is this 14 mine or yours? 15 Q. It's yours. 16 A. Did you write on it? 17 Q. I did not. 18 A. I'm sorry, go back to your 19 question. 20 Q. Sure. Turn to Page 9 of your 21 report. 22 A. Okay. 23 Q. At the bottom of the page, you 24 provide your analysis of the ATSDR's
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1 toxicological profile for benzene in 2007? 2 A. I provide a statement from the 3 ATSDR report. 4 Q. You state that CLL is not 5 discussed, correct? 6 A. Yes. 7 Q. Had the ATSDR found that there 8 was suggestive evidence of association between 9 benzene and CLL, would that have influenced your 10 consideration? 11 A. I would have looked to see why 12 they made that statement. 13 Q. Would a finding by the ATSDR that 14 there was suggestive evidence that benzene causes 15 CLL, would that influence your weight of the 16 evidence analysis towards a more consistent 17 finding of elevated risk for CLL from benzene 18 exposure? 19 A. You're giving me a hypothetical 20 and I can't answer that. 21 Q. Do you give credence to the fact 22 that the ATSDR or other government agencies find 23 suggestive evidence of the link between CLL 24 exposure and benzene -- I misspoke. I'll
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1 rephrase the question. 2 Is a conclusion of an agency of 3 the federal government such as the ATSDR that 4 there's suggestive evidence or causal association 5 between benzene exposure and CLL, is that 6 important in your consideration or weight of the 7 evidence? 8 A. It's relevant but then I have to 9 look at what the basis for that conclusion is. 10 Q. What would you want to look at? 11 A. I'd want to look at why they make 12 that statement, which there should be a reference 13 to the scientific literature. 14 MR. WOOLF: Counsel, since you've 15 asked him about ATSDR, if you have a 16 reference from the ATSDR that there is a 17 suggestive basis that benzene causes CLL, 18 I'd appreciate it if you would show it to 19 the witness so he might comment on it. 20 BY MR. DuPONT: 21 Q. Would your answer be the same if 22 the EPA concluded that there was suggestive 23 evidence that exposure to benzene causes CLL? 24 A. Yes.
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1 Q. So you would find that relevant 2 and important to your analysis, correct? 3 A. I didn't say important. I said I 4 would consider it as relevant to look at. 5 Q. If the EPA concluded that there's 6 suggestive evidence of a causal association 7 between CLL and benzene exposure, would that 8 influence your decision that the weight of the 9 evidence is stronger that benzene exposure causes 10 CLL? 11 A. Not by itself. I'd have to look 12 at the basis for that conclusion. 13 Q. Doctor, are you familiar with the 14 Shanghai studies? 15 A. Are these the Chinese benzene 16 studies? 17 Q. Right, being done by your 18 clients. 19 A. No. 20 Q. You're not familiar with them? 21 A. No. My clients? 22 Q. ExxonMobil, Chevron, Texaco. 23 A. No. You're not talking about the 24 NCI studies is what I'm asking?
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1 Q. No, the ones that are being 2 conducted by the American Petroleum Institute and 3 some of the oil companies. 4 A. No, I'm not. 5 Q. So you wouldn't know whether 6 those studies made any findings with respect to 7 CLL? 8 A. No. 9 Q. Do you agree that the 10 epidemiological findings as they relate to NHL 11 are applicable to CLL? 12 A. No. 13 Q. If Dr. Schnatter testified that 14 the epidemiological findings as they relate to B 15 cell NHLs are applicable to CLL, would you 16 disagree with him? 17 A. I don't know enough about the 18 types of NHL to make a comment. 19 Q. Would you disagree with him? 20 Would you think he's wrong? 21 MR. SCOTT: Object to form. 22 THE WITNESS: No, I can't make a 23 comment. 24 BY MR. DuPONT:
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1 Q. Doctor, you accept that benzene 2 causes leukemia, correct? 3 A. I accept that at certain levels 4 it causes myelogenous leukemia. 5 Q. And if you accept that benzene 6 causes, as you say, acute myelogenous leukemia at 7 certain levels, is what's the determinant for you 8 is then the amount of exposure that the person 9 sustains in order to link the benzene exposure to 10 AML, correct? 11 A. In essence, yes. 12 Q. So all you're really looking at 13 is the dose of benzene that the person intakes 14 into their body, correct? 15 A. Specifically a measure that is 16 used is parts per million years, which is an 17 exposure measure. 18 Q. Correct. 19 A. Not a dose measure. 20 Q. And what's important is how much 21 benzene exposure there is, correct, in your 22 analysis? 23 A. How much there is for how long. 24 Q. No matter where that benzene
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1 exposure comes from as long as you have that 2 amount of benzene exposure for what you say is 3 the correct length of period of time? 4 A. Can I just get a cup of coffee 5 since I see it over there? Then I'll answer your 6 question. 7 Q. I'll get you the cup of coffee, 8 if you can answer the question? 9 A. With a little bit of milk. I was 10 distracted by seeing the coffee, I'm sorry. 11 - - 12 (Whereupon the court reporter read back 13 the pertinent testimony.) 14 - - 15 THE WITNESS: Yes. 16 BY MR. DuPONT: 17 Q. So, in your analysis, it's 18 relevant not where the exposure to benzene comes 19 from; what's important is the amount of exposure? 20 A. Yes. 21 Q. Doctor, the IARC, their monograph 22 on gasoline was published in 1989. Is that 23 correct? 24 A. Yes.
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1 Q. So that predates Dr. Schnatter's 2 1996 study? 3 A. Yes. 4 Q. And it predates Guenel's study in 5 2002, correct? 6 A. Yes. 7 Q. Would you agree with me that a 8 lot has happened with respect to benzene research 9 since 1989? 10 A. Yes. 11 Q. Would you also agree with me a 12 lot has happened with respect to gasoline 13 research since 1989? 14 A. A lot is -- I'm not sure I would 15 agree with that gasoline per se. 16 Q. I guess what I'm getting at is: 17 Isn't the 1989 IARC monograph on gasoline a 18 little outdated? 19 A. Yes. 20 Q. The risk in contracting leukemia 21 from benzene exposure, is that supralinear at low 22 doses? 23 A. At low doses? You have to define 24 low.
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1 Q. Is the risk in contracting 2 leukemia supralinear at any point? 3 A. I have no information to that 4 effect. 5 Q. Do you agree that benzene is a 6 carcinogen by all routes of exposure? 7 A. Are you talking about human or 8 animal? 9 Q. Human. 10 A. I don't know that. The only 11 information that is in the epidemiologic 12 literature to the best of my knowledge is 13 inhalation. 14 Q. Now, are you familiar with how 15 the EPA performs its weight of the analysis? 16 A. No. 17 Q. Strike that. That was a poorly 18 phrased question. 19 Do you know how the EPA performs 20 its weight of the evidence analysis as it relates 21 to benzene? 22 A. No. 23 Q. Do you know how epidemiology 24 studies rank in comparison to things such as
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1 mechanistic studies or chromosomal studies or 2 bioassays in the weight of analysis approach? 3 A. For EPA? 4 Q. Correct. 5 A. No. 6 Q. Why is it that epidemiologists 7 use nested case-control studies as opposed to 8 cohort studies? 9 A. Ordinarily, when one does a 10 cohort study, one has only limited information on 11 exposure either work area or substances. So, if 12 they find an excess or if there's a disease that 13 is of interest, they then go back and collect 14 further exposure information on the cases of 15 disease of interest and the comparison group. 16 Q. So would it then be an advantage 17 of the nested case-control study that you have 18 better information concerning exposure? 19 A. Theoretical advantage. 20 Q. Is it also an advantage of the 21 nested case-control study that you have a better 22 understanding of what the comparison population 23 is? 24 A. I don't understand that question.
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1 Q. When you have a nested 2 case-control study, you're taking cases within a 3 larger cohort and comparing them to the cohort as 4 a total? 5 A. No, you're comparing them to a 6 subset of the cohort. 7 Q. And the subset that you're 8 comparing them to, is that generally better 9 defined in other forms of cohort studies? 10 A. I still don't understand -11 better defined with respect to what? 12 Q. With respect to what the 13 comparison population is. Are you able as an 14 epidemiologist to assure yourself or have a more 15 better understanding of what the comparison 16 population is? 17 A. You're talking about two 18 different things. In the cohort study, usually 19 the comparison population is external. 20 Q. Correct. 21 A. Either another company, another 22 area within the same company or general 23 population statistics. 24 Q. Correct.
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1 A. In a case-control, a nested 2 case-control study, the comparison group -- I 3 call them a group rather than a population 4 because they're selected on some basis from the 5 overall non-case population. 6 Q. And because the comparison group 7 in a nested case-control study is internal as 8 opposed to external in the cohort study, you have 9 a better defined comparison group for nested 10 case-control studies? 11 A. See, that's what I have trouble 12 with. You're saying "better defined". With 13 respect to what? 14 Q. You have a more certain 15 understanding of what exactly the comparison 16 group is? 17 A. I don't think that that follows. 18 Q. You're familiar with the 19 Bradford-Hill factors? 20 A. Yes. The term usually uses 21 criteria but I wouldn't object to your using 22 factors. 23 Q. In order to use the Bradford-Hill 24 factors, you don't necessarily have to satisfy
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1 all the different factors in order to come to a 2 conclusion concerning causation, do you? 3 A. No. 4 Q. So they're not really criteria; 5 they're just different things you want to look 6 at? 7 A. Yes. The word "criteria" is used 8 but it doesn't mean it's the best word. 9 Q. Sometimes, for example, the 10 biological plausibility of a causal association 11 will be stronger than say the consistency of the 12 evidence? 13 A. You better rephrase that, please. 14 Q. Are there circumstances wherein 15 reviewing the Bradford-Hill factors the 16 biological plausibility of the causal association 17 is stronger or more relevant than the consistency 18 of the evidence? 19 A. You mean epidemiologic evidence? 20 Q. Yes. 21 A. Thank you. Would you repeat the 22 question? 23 - - 24 (Whereupon the court reporter read back
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1 the pertinent testimony.) 2 --3 THE WITNESS: I'm aware of one 4 situation, and there may be a second, 5 where IARC has considered mechanistic 6 factors, which are biologic factors, if 7 you will, in animals, to be sufficient to 8 judge that the substance is a carcinogen 9 in humans. That's ethylene oxide. 10 There's very little human evidence on 11 ethylene oxide. 12 BY MR. DuPONT: 13 Q. So where there is little human 14 evidence, looking at the biological plausibility 15 is more important? 16 A. There has in situations where 17 that is correct. In general, it's not the usual 18 way of making judgments. 19 I believe the reason that they 20 came to that conclusion is they understand the 21 mechanism that causes ethylene oxide to cause 22 cancer in animals and they understand that the 23 mechanism is the same in humans. 24 Q. You'd agree with me epidemiology
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1 studies cannot rule out causal association? 2 A. Whether an association is causal 3 or not is a matter of judgment. No study can 4 either rule out or rule in the judgment of the 5 causal association. 6 Q. Then it also would be true that 7 epidemiology studies cannot rule out an elevated 8 risk as a result of exposure of a particular 9 chemical? In other words, if you have a negative 10 finding in an epidemiology study, that doesn't 11 mean that there's no risk to exposure to that 12 agent, does it? 13 A. Single study, no. But if you got 14 100 studies which shows an elevated risk, I would 15 say that's sufficient evidence to come to a 16 judgment that there is no elevated risk. 17 Q. Are you familiar with the terms 18 Type 1 error and Type 2 error as they relate to 19 biases in epidemiology? 20 A. You say bias and I'm trying to 21 think what I learned in statistics. I wouldn't 22 call them biases. I would call them what 23 statisticians call them, which is errors. And 24 I'm familiar with the terms.
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1 Q. The term Type 1 error, does that 2 often refer to a finding that there is an 3 association when none is actually present due to 4 chance? 5 A. I'm sorry, I never remember which 6 is one or two. One of them is that way and one 7 is the other way. One is failure to find an 8 association when in fact there is one. 9 Q. When you design an epidemiology 10 study as an epidemiologist, do you design the 11 study so it's more likely you're going to have an 12 error of not finding an association than you 13 would of actually finding association when it's 14 actually by chance? In other words, do you try 15 and design the study to avoid what I'll term the 16 Type 1 error? 17 A. In most of the studies I've done, 18 I haven't considered Type 1 or Type 2 errors 19 because I study everyone available in a given 20 population, so there's no issue as to is it too 21 large, too small, whatever. You study everybody. 22 Q. When an epidemiologist sits down 23 and designs a cohort study or other type of 24 epidemiology study, is it the general practice to
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1 design the study so that you're avoiding the 2 error of finding a risk by chance? 3 A. That's done much more in clinical 4 trials, how big a clinical trial should one do 5 based on what one already knows. 6 In epidemiology, if you know 7 nothing, you can't do a power calculation. And 8 if you have a population of limited size, either 9 you make a judgment is this population large 10 enough to study. And in the absence of any 11 information, there's no answer other than yes, 12 it's large enough to study. 13 Q. In your analysis in this case, in 14 your report as part of your methodology, do you 15 make any kind of accounting for any biases that 16 were present in studies that you reviewed? 17 A. Only to the extent if I felt the 18 study was totally wrong, bad that I would not 19 include it. 20 Q. For example, did you consider 21 whether in any of your studies that you've listed 22 in the report there is a misclassification of 23 exposure or misclassification of disease? 24 A. No.
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1 Q. Did you consider the Healthy 2 Worker Effect in analyzing any of the studies 3 that you relied upon? 4 A. On this report, no. 5 Q. Essentially, what you've done is 6 a small meta-analysis of the CLL and leukemia 7 literature? 8 A. No. I did a description. 9 Q. A description? 10 A. A meta-analysis makes a number of 11 assumptions with respect to the papers that are 12 being reviewed, and they wouldn't be met by a 13 review of the literature. Meta-analysis, again, 14 are much more relevant to clinical trials. 15 MR. DuPONT: Let's take a 16 five-minute break. 17 - - 18 (Whereupon there was a recess in the 19 proceedings from 12:11 to 12:24.) 20 - - 21 BY MR. DuPONT: 22 Q. Doctor, I have before me what's 23 marked as Monson-A. It's your Evaluation of 24 Papers by Steinmaus and then also your Evaluation
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1 of Martin Smith's Paper on NHL. And the 2 Steinmaus evaluation, if I'm correct, is dated 3 July 7, 2008 at the bottom of the paper and then 4 on your signature line it's also dated July 7, 5 2008. And the analysis of Martin Smith's paper 6 is dated June 30, 2008. 7 When did you start the project 8 that culminated in these two evaluations? 9 A. The Martin Smith one would have 10 been sometime in 2007. I just, I put the date on 11 when I printed it out. The Steinmaus one, again, 12 was just after it came out, probably the 13 beginning of this year. 14 Q. How much were you paid for your 15 work to analyze the Steinmaus and Smith papers? 16 A. I really don't have any 17 recollection. I can make a guess but I don't 18 really know. Ten to 15,000 I'd say. 19 Q. Did you submit an invoice to Mr. 20 Woolf for that? 21 A. Yes. 22 Q. You included in your evaluations 23 discussion of Glass' 2003 article, correct? 24 A. If you say so, yes.
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1 Q. Which study design or data 2 collection biases did you analyze in your report 3 in this case with respect to the literature that 4 you cited? 5 A. Are you talking about Smith or 6 Steinmaus? 7 Q. I'm sorry, I wasn't clear. Let's 8 talk about Steinmaus first. 9 A. Why don't you give me your copy? 10 Can you repeat the question, please? 11 - - 12 (Whereupon the court reporter read back 13 the pertinent testimony.) 14 - - 15 THE WITNESS: First, I compared 16 my reading of the literature to Steinmaus 17 and either agreed or disagreed with his 18 abstracting of data from the literature. 19 So I did that for case-control studies of 20 benzene exposure and NHL; cohort studies 21 of benzene exposure and NHL; cohort 22 studies of refinery work and NHL. 23 Next, I adjusted the relative 24 risks that's similar to what Steinmaus
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1 did in Tables 3 and 4 based on the all 2 cancer SMR. And then I compared papers 3 that Steinmaus either referenced, cited, 4 or not referenced in Smith. Smith's 5 paper had a lot of papers that he cited 6 in his tables but didn't give references, 7 whereas if I say referenced that means 8 that Smith gave a reference with a 9 number. 10 And there were some papers in 11 Steinmaus but not in Smith, and there 12 were some papers in Smith that were not 13 in Steinmaus. 14 BY MR. DuPONT: 15 Q. And where do you provide your 16 analysis of any design bias in the studies or any 17 data collection bias in the studies? 18 A. I don't think I mentioned design 19 bias per se. On Pages 4 through 6, I note where 20 I agreed with what Steinmaus took out of the 21 paper in terms of numbers and then when I 22 disagreed. 23 Q. But I want to talk about design 24 biases specifically for these various studies.
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1 Did you look at and try and ascertain whether 2 there were any design biases for any of these 3 studies? 4 A. If I did it, it was implicit, not 5 explicit. 6 Q. What do you mean by that? 7 A. I didn't go into it with that 8 term in my mind. 9 Q. What types of design biases are 10 there that you would be looking for? 11 A. I don't know. I didn't do it. I 12 haven't thought about it. I don't want to make 13 up something on the spur of the moment. 14 Q. So you didn't look at this 15 literature that you cited in your analysis of 16 Steinmaus for any design biases? 17 A. When I go through literature, the 18 first thing I do is, as I said before, if I feel 19 it's a paper that is of no value, I exclude it as 20 a design bias. But I don't keep a list of such 21 papers. Otherwise, if the paper is of reasonable 22 scientific merit, I include it. There still may 23 be design biases in it but I don't discuss them 24 when I summarize the literature.
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1 Q. So is there any way for me to 2 know which studies you excluded because of a 3 design bias as opposed to for some other reason? 4 A. No, I wouldn't say there were a 5 lot. 6 Q. Is there any way for me to know 7 which ones you excluded? 8 A. No. 9 Q. Did you find design biases in any 10 of the studies that you included in your 11 evaluation of Steinmaus? 12 A. As I say, I didn't look for 13 design bias. 14 Q. How about data collection biases, 15 did you evaluate any of the studies that you 16 analyzed with respect to the Steinmaus report for 17 data collection biases? 18 A. Not by the authors. 19 Q. What do you mean by that? 20 A. I didn't look to see whether an 21 author, whether there was data collection bias in 22 the paper itself. 23 Q. You mean the Steinmaus paper 24 itself?
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1 A. No, the paper that Steinmaus 2 cited. 3 Q. What are the relevant design 4 biases that an epidemiologist would consider in 5 evaluating literature? 6 A. As I said, I haven't considered 7 that at all in this report and I don't want to 8 make things up on the spur of the moment. 9 Q. I understand that. Putting this 10 report aside, generally, what are the various 11 design biases that an epidemiologist would want 12 to consider when analyzing the literature? 13 A. Mainly, the most common one is 14 studies where an author selects people who have 15 both exposure and the disease and then mills a 16 study around it which guarantees an association. 17 Q. And what's the term for that type 18 of bias? 19 A. Selection bias. 20 Q. Any other forms of design biases? 21 A. There's observation bias where 22 either the disease is misclassified because of 23 knowledge of the exposure or the exposure is 24 misclassified because of knowledge of the
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1 disease. Then there is a term "confounding" 2 which is not a design bias but which is a 3 characteristic of all scientific studies. 4 Q. Any other design biases besides 5 selection? 6 A. Those are the three that I use. 7 Q. How about data collection biases? 8 A. I included that in what I was 9 just saying. 10 Q. So data collection bias is a part 11 of -12 A. Design bias would be selection 13 bias, data collection bias, and there would be 14 observation bias. 15 Q. What about Healthy Worker Effect, 16 where does that fall? 17 A. I call it confounded. Other 18 people call it selection bias, and I disagree 19 with them. 20 Q. Why do you call it confounding? 21 A. Because it's a characteristic of 22 the individuals in the population and there is a 23 potential for having knowledge of both health 24 status and disease outcome and, therefore, you
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1 have the ability to control for it. 2 Q. Did you do anything to determine 3 how classification of disease may have influenced 4 the findings? 5 A. No. 6 Q. Did you do anything to determine 7 how classification of exposure in the various 8 articles cited and referenced by Steinmaus 9 influenced the findings? 10 A. No. 11 Q. If you go to Page 12 of the 12 evaluation of Steinmaus that you've done? 13 A. All right. 14 Q. Under Title B, Evaluation of 15 Papers Cited by Steinmaus, and then No. 1, 16 Citations in Table 2, you say you disagree with 17 eight of the authors' citations from these 16 18 papers. You say two of the papers include 19 solvents other than benzene. 20 A. Right. 21 Q. Why do you disagree with their 22 use of those studies that include solvents, as 23 you characterize them, to be other than benzene? 24 A. It doesn't say that it's benzene
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1 that's in the paper. One says all solvents. 2 Q. Did you do anything to determine 3 whether or not benzene was in the solvents that 4 the papers were referring to? 5 A. No. 6 Q. Did you do anything to determine 7 that benzene was not in the solvents the paper 8 was referring to? 9 A. No. I read the paper and if it 10 said -- I read the paper. And if it didn't say 11 this is exposure to benzene, I wouldn't include 12 it. 13 Q. So am I correct in that what 14 you're doing here in your evaluation of Steinmaus 15 is you're evaluating the paper and either 16 agreeing or disagreeing with the authors on, A, 17 whether they chose to include a particular study 18 or, B, how they characterized the study? 19 A. Yes, which includes abstracting 20 data from the study. 21 Q. Lymphosarcoma, by the way, that's 22 a form of NHL? 23 A. Yes. 24 MR. DuPONT: Why don't we take a
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1 break for lunch? 2 As a matter of housekeeping, 3 Doctor, this is the last portion of your 4 file that hasn't been marked and I'll 5 mark it as Exhibit-G. This is the 6 May 29, 2008 e-mail from Ms. JoAnn 7 Niedens on behalf of Louis C. Woolf to 8 yourself enclosing the report of Paul 9 Roda, report of Dr. Robert Laumbach. And 10 then there are two articles, the Mehlman 11 2004 article from European Journal of 12 Oncology, and Dr. Peter Infante's article 13 Benzene: An Historical Perspective on 14 the American and European Occupational 15 Setting. 16 BY MR. DuPONT: 17 Q. Do these two articles go with 18 Exhibit-G in that they're articles cited by Dr. 19 Roda and Dr. Laumbach? 20 A. Yes. 21 Q. Then we'll group those with 22 Exhibit-G. So then do we have the entirety of 23 your file here? 24 A. Yes.
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1 --2 (Whereupon the document was marked, for 3 identification purposes, as Monson-G.) 4 --5 BY MR. DuPONT: 6 Q. Do you have invoices that you 7 prepared for your work to date? 8 A. Once it's paid, I throw it away. 9 I know I have at least one because it hasn't been 10 paid. 11 Q. If I could ask you to provide 12 that to your counsel and he can give me a copy of 13 that, I would appreciate it? 14 A. Just to be clear, which invoices 15 are you talking about? 16 Q. That's a good point, your invoice 17 for your work on the Salmieri case. 18 A. Fine. 19 Q. I'd also like invoices for your 20 work in preparing your evaluation of the paper by 21 Steinmaus and Smith that we've marked as 22 Monson-A. 23 A. Is that acceptable to Mr. Woolf? 24 MR. WOOLF: He'll just ask you
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1 and then I'll take care of whether it's 2 acceptable or not. I'll let you know. 3 THE WITNESS: Fine. 4 BY MR. DuPONT: 5 Q. And additionally, with respect to 6 your requests to prepare this evaluation of 7 Steinmaus and Smith, were there any written 8 communications that set forth for you what it was 9 that Mr. Woolf wanted? 10 A. If there were, I don't have them. 11 Q. If there are any, if I could ask 12 you to provide those to your counsel as well? 13 I'd appreciate it. 14 A. Fine. 15 - - 16 (Whereupon there was a recess in the 17 proceedings from 12:45 to 1:39.) 18 - - 19 BY MR. DuPONT: 20 Q. Could you turn to your Summaries 21 and Conclusions starting on Page 12 with respect 22 to the Steinmaus? 23 A. Okay. 24 Q. First of all, do you agree that
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1 the study power of an epidemiology study is 2 higher when the relative risks are higher? 3 A. Power is generally used to -4 when it's used in an epi study, it's used to 5 decide what theoretical relative risk could be 6 observed so that it's statistically significant. 7 It's a predictive thing, not a descriptive thing. 8 Do you understand the difference? 9 Q. Right. Go ahead. 10 A. So that the way one states it is 11 that, if in fact there is an association in the 12 data irrespective of causality, we're just 13 talking about data now, if there is in fact a 14 relative risk greater than one, if the relative 15 risk is higher, it is more likely to be found to 16 be statistically significant than if the relative 17 risk is lower. I'm talking about relative risk 18 above one now. 19 Q. Right. 20 A. So, in that sense, statisticians 21 say something like you said that the study has 22 more or only has the power to detect a relative 23 risk of whatever, say five. It doesn't have 24 enough power to detect one of three, even though
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1 they may observe a relative risk of three. 2 Q. But, generally, the higher your 3 relative risk gets, there's a corollary that the 4 higher the power the study is? 5 A. Again, I want to be careful about 6 prediction versus description. The confidence 7 interval is the description of the data, whereas 8 the power is something that's used in designing 9 studies. 10 Q. Right. 11 A. It's not used in interpreting 12 studies. 13 Q. Independent of classifying 14 whether it's descriptive or interpretative -15 A. Predictive. Interpretative is 16 entirely different. 17 Q. Independent of the 18 classifications, would you agree with me that 19 when you see studies with higher relative risks 20 that studies also have a higher power? 21 A. I don't use that type of 22 statement. That's a description of a study 23 that's already been done. Power is used before 24 the study is done.
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1 Q. Regardless of whether you use 2 that type of statement, is that true -3 A. If I don't use it, it's 4 irrelevant. I don't comment on that situation. 5 Q. How can you say it's irrelevant 6 just because you don't comment on it? 7 A. Because I think it's incorrect to 8 say that. 9 Q. So you think it's incorrect that 10 when you have a higher relative risk there's 11 usually a corollary that the study power is 12 higher as well? 13 A. You stated that differently than 14 you did before. See, I don't use the term 15 "power" hardly at all. I don't want to go beyond 16 that. I don't want to make something up. 17 Q. What do you use instead of 18 "power"? 19 A. Confidence interval. 20 Q. Would it then be true that the 21 higher relative risks are found in a study the 22 narrower confidence intervals are? 23 A. No. Confidence intervals has to 24 do with both the relative risk and the size of
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1 the study. 2 Q. Do you agree with the proposition 3 that higher relative risks are less likely to be 4 due to confounding factors? 5 A. I've written that, so I agree 6 with it in general. It's not an absolute 7 statement. 8 Q. Do you agree that studies where 9 you have an internal comparison, such as nested 10 case-control studies, that those types of studies 11 are not subject to the Healthy Worker Effect? 12 A. In general, yes. 13 Q. Turning to your paper under 14 Summaries and Conclusions on Page 12, you say 15 that the authors' methods do not accord with 16 methods recommended by other authors. In other 17 words, Steinmaus, their methods don't accord with 18 methods recommended by other authors. Do you see 19 that at the bottom of the second paragraph under 20 Comment? 21 A. Yes. 22 Q. Which authors are you referring 23 to? Which other authors are you referring to? 24 A. Bottom of Page 2, Checkoway, et
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1 al.; top of Page 3, Breslow and Dade and 2 Greenberg, et al., as well as Checkoway again. 3 Q. How are the Steinmaus methods 4 different than those recommended by Checkoway and 5 Breslow? 6 A. The specific issue had to do with 7 how one measures exposure and all the papers -- I 8 shouldn't say all. Many of the papers use 9 different methods. 10 You can use peak exposure. You 11 can use duration of exposure. You can use 12 average exposure. You can use length of work. 13 Anyway, there's different ways to describe 14 exposure which industrial hygienists use. But 15 the standard way and the one that these authors 16 recommend is use of what I said, PPM years, which 17 is in essence cumulative exposure. And that's 18 what I used. 19 Q. So one of your disagreements with 20 Steinmaus is that they do not use or they do not 21 solely use cumulative exposures? 22 A. That's right. They seem to pick 23 the one that they like the best. 24 Q. And you believe that Checkoway
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1 and Breslow in their articles recommend the use 2 of cumulative exposures? 3 A. Yes. 4 Q. Then you say that the rules used 5 by Steinmaus are arbitrary. Do you see that 6 under Results on Page 12 of your report? 7 A. Yes. 8 Q. Which rules do you believe 9 Steinmaus used that are arbitrary? 10 A. There's, as I said, there's a 11 fair amount of, fair number of papers that 12 Steinmaus either uses that Smith doesn't or vice 13 versa and it's not clear why. So, if it's not 14 clear, it's arbitrary as far as I'm concerned. 15 Q. So, because you don't understand 16 why they selected, Steinmaus selected to use 17 certain papers that Smith either did or did not 18 use, that's what you believe is arbitrary about 19 the rules? 20 A. Yes. Some of them clearly were 21 incorrect in Smith. Steinmaus was correct in not 22 including them for a variety of reasons. But 23 there are others that it wasn't clear why they 24 were in Steinmaus, and that's on Page 11.
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1 Q. So which are the papers that you 2 believe it's not clear why Steinmaus decided to 3 use them? 4 A. I can't. I don't have that 5 listed and I don't remember. 6 Q. Besides selecting papers to use 7 without clear reasons for doing so, are there any 8 other rules used by Steinmaus that you believe 9 are arbitrary? 10 A. There were two things I pointed 11 out, one is the one-sided P value, but that 12 doesn't enter into any of what I did so we'll 13 just let it go. I don't believe in one-sided P 14 values. 15 The other thing is the Healthy 16 Worker Effect. I would say it's generally 17 accepted that the Healthy Worker Effect for 18 cancer is less than that for all causes and 19 that's just safer -- for example, if the Healthy 20 Worker Effect for all causes is .8, then for 21 cancer it would be .9. It's just to illustrate 22 what I mean. 23 Q. Okay. 24 A. So that one should really correct
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1 for it comparing it to the SMR for all cancer 2 rather than for all causes. 3 Q. And why is that? What's your 4 basis -5 A. Because if you got a cancer, you 6 should compare it to other cancers. Most of the 7 Healthy Worker Effect is due to non-cancers which 8 can be detected at the time people start working, 9 whereas cancer cannot be predicted at that time. 10 Q. Isn't the Healthy Worker Effect 11 the result of a judgment of a person when they 12 first start to work? 13 A. The Healthy Worker Effect is an 14 observation that studies of workers compared to 15 general population shows a lower than expected 16 mortality. And that is because of selection at 17 the time people search for it. But it's 18 different for different causes. 19 Q. Do you have a greater power or 20 greater ability to determine the Healthy Worker 21 Effect by looking at all causes as opposed to 22 cancers because there are more cases of all 23 causes than there are of cancers? 24 A. No. All causes includes diseases
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1 that, as I said, people tend to develop before 2 they're say age 20, which is sort of an average 3 year of starting work; chronic respiratory 4 disease, chronic GI disease, chronic cardiac 5 disease. Many chronic diseases that develop in 6 younger people lead to the Healthy Worker Effect. 7 Q. I guess my question is: If 8 you're looking at two populations, you're looking 9 at cancers and you're looking at all causes of 10 death? 11 A. Those aren't two populations. 12 Those are two types of outcome. 13 Q. Right. If you're looking at a 14 group of workers and trying to determine whether 15 or not there's a Healthy Worker Effect, those 16 workers who died of cancer, there's going to be 17 less of those workers dying of cancer than there 18 are going to be of workers dying of all causes, 19 correct? 20 A. Yes. 21 Q. So that you have a greater power 22 to determine the Healthy Worker Effect by looking 23 at all causes? 24 A. You don't use it in that context.
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1 You use the confidence interval. You'd have a 2 narrower confidence interval for all causes than 3 for cancer, but you'd have a higher relative risk 4 that's closer to 1 for cancer than for all 5 causes. So they work in opposite directions, so 6 I can't answer the question. 7 Q. You also say the data selected by 8 Steinmaus is arbitrary? 9 A. That's where I'm talking about 10 the various measures of exposure to benzene. In 11 a paper where there are different ways of doing 12 it, he tends to pick the one that gives the 13 highest relative risk. 14 Q. Have you reviewed any literature 15 that suggests that peak exposures and other 16 models of benzene exposure are more important in 17 the causation analysis -18 A. I'm aware that such literature 19 exists, and I'm sure I've read snip-its of it. 20 Q. Do you disagree? 21 A. I'm not convinced that there's a 22 strong case that can be made for it. 23 Q. But do you disagree that that's 24 true?
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1 A. I don't disagree and I don't 2 agree. I'm aware that some people hold that 3 view, and I believe that it differs for different 4 chemicals or physical agents. 5 Q. By the way, have you ever 6 testified in tobacco litigation? 7 A. No. 8 Q. Have you done any work in the 9 context of tobacco litigation? 10 A. I wrote a report once for a 11 tobacco lawyer. He didn't like it. 12 Q. Going back to Page 12, under 13 Title B, Evaluation of Papers Cited by Steinmaus, 14 et al., Subpart 1, Citations of Table 2, we 15 discussed the two papers that includes solvents 16 other than benzene. Which two papers are those 17 you're referring to? 18 A. Sorry, I lost my place. 19 Q. Page 12. 20 A. No, but I refer to one of the 21 tables. 22 Q. I'm sorry. 23 A. Citations in Table 3, so it's 24 Page 5 -- that's not correct. I'm sorry, which
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1 question did you just ask me? 2 Q. There's Citations in Table 2. 3 A. Okay, 2. You say two of the 4 papers includes solvents other than benzene. 5 Q. My question is which papers are 6 you referring to? 7 A. Yes, Dryver and Franceschi. 8 Q. What are the solvents that are 9 included in Dryver? 10 A. Aromatic, all aromatic. 11 Q. Aromatic solvents containing 12 benzene. Is that correct? 13 A. Benzene is an aromatic solvent. 14 Q. Do aromatic solvents contain 15 benzene? 16 A. Some do and some don't. If the 17 classification is all aromatic solvents, then 18 benzene would be included. 19 Q. Do you recall how Dryver defines 20 aromatic solvents? 21 A. No. 22 Q. Incidentally, did Dryver find an 23 increased risk of NHL from exposure to gasoline? 24 A. I don't know, unless it's in my
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1 other report. It's not in this report. On NHL, 2 I don't know. 3 Q. Look at Table 2 of the Dryver 4 study. I point your attention to the category 5 for Gasoline Greater Than Five Years Versus Less 6 Than Five Years. You find an OR of 1.92. 7 A. Okay. 8 Q. Is that correct? 9 A. Yes. 10 Q. And that's statistically 11 significant? 12 A. Yes. 13 Q. Why do you disagree with the 14 selection of Franceschi? 15 A. Again, it says all solvents. 16 Q. What type of solvents were being 17 used in the Franceschi study? 18 A. I don't know. 19 Q. Which study from this Table 2 do 20 you say was used in a misleading way? 21 A. Is there only one? 22 Q. I believe you say in your 23 commentary that there was one. 24 A. I say two.
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1 Q. Do you? Then I apologize. 2 A. Fritschi 2005, she reported a 3 relative risk of 0.3 based on two cases with 4 substantial exposure. But if you look at all 5 exposure, you get a relative risk of 1.1. So the 6 substantial group is so small to be meaningless. 7 And your other one that's 8 misleading is Glass. There's no dose response 9 relationship, and when you do a post hoc division 10 of PPM years, you usually cut the line where the 11 data leads you to and that's not appropriate. 12 Again, if you use all 20 cases, 13 the odds ratio is .9. If you use only two cases, 14 it's 1.5. It's a similar criticism to Fritschi. 15 Q. You say that there are cases that 16 are incorrectly cited out of this Table 2. 17 A. Fabbro-Peray, I say not final 18 analysis. I don't know specifically. I think 19 that probably corrected for confounding or 20 something. 21 Schnatter, it's hard for me to 22 decipher exactly what I meant. But it didn't 23 change relative risk very much, .9 to .8. Even 24 that, that's a guess.
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1 And in Seidler, there were 2 actually 12 cases and not 11. There's one other 3 case that was sort of in another table. Again, 4 it doesn't change the relative risk 5 substantially. 6 Q. So, in Seidler, there are 7 12 cases because there's one case reported in a 8 separate table? 9 A. It's either in a separate table 10 or a separate section, yes. There is the 11 but 11 then there's one somewhere else and you just 12 missed it. 13 Q. Anything else? 14 A. No. 15 Q. Then you have a discussion of 16 Citations in Table 3 and you say you disagree 17 with two of the citations. Those would be the 18 Bloeman 2004 and Wong 1987? 19 A. Right. 20 Q. Why do you disagree with Bloeman? 21 A. It's highly selected data of 22 15-years lag. The Bloeman citation is based on 23 two cases with a 15-year lag with exposure 24 greater than 28 PPM years, which gives a relative
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1 risk of 2.2. But if you use all three cases and 2 no selection in terms of follow-up, you get a 3 relative risk of .7. So major differences based 4 on very small numbers. 5 Q. Why do you disagree with Wong? 6 A. It's based on only one case. And 7 Steinmaus states the relative risk is 1.5, but in 8 Table 11 on Wong, the relative risk is 0.7. And 9 I can't go beyond that. That's what I wrote. 10 Q. You say in Citations in Table 4 11 you disagree with eight of the citations. The 12 first is Collingwood 1996. That's at the 13 Paulsboro, New Jersey refinery? 14 A. Right. Again, there's only two 15 cases and you can pick and choose. Steinmaus 16 used Table 7 and I used Table 5, which I assume I 17 thought was a more relevant table. 18 Q. Why is that? Why did you use 5 19 instead of 7? 20 A. I don't know. It's the same 21 number of cases and it doesn't change the 22 relative risk that much. But I didn't go through 23 these papers at all in preparation for this, so I 24 don't know.
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1 Q. You disagree with the Dagg 1992 2 El Segundo and Richmond studies? 3 A. Right, superceded my Satin. 4 Q. So, since Satin later published 5 on the same cohorts, -6 A. Right. 7 Q. -- you disagree with their use? 8 A. Right. 9 Q. You disagree with the use of the 10 Gun 2006? 11 A. Only because they used mortality 12 and not incidence. 13 Q. Why is that? 14 A. Incidence, if you have it, it's 15 better information because it includes non-fatal 16 cases. 17 Q. Next is Thomas 1982. 18 A. Right. This is one of a whole 19 bunch of studies that were superceded by later 20 papers. 21 Q. You say disagree, data likely 22 included in Divine and Satin? 23 A. Right. 24 Q. What makes you think it was
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1 likely included? 2 A. There's other papers that, 3 there's at least two other papers that I didn't 4 put in because I don't think Steinmaus did. But 5 they were members of the OCAW, Oil, Chemical and 6 Atomic Workers. They were case-control studies. 7 And they were in companies that were later, in 8 which cohort studies were later conducted during 9 the same time period. 10 Q. What information do you have to 11 show you that the Thomas data was included in 12 Divine and Satin? 13 A. As I say, I believe they belong 14 to the union in the plants that were studied by 15 Satin and by Divine. 16 Q. And then next is Tsai 1993. Is 17 that the same reason? You say you disagreed 18 because it did not include the Wilmington plant. 19 A. Yes. I guess Martinez is one 20 plant and Wilmington is another. And the paper 21 includes both plants, but Steinmaus only picked 22 the one where there was slight excess. 23 Q. And then the last two that you 24 disagree with is Wong 2001a and Wong 2001b. And
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1 A related to Beaumont and B to Torrance. 2 A. Here, Steinmaus chose to put in 3 people who had been exposed for 30 or more years 4 which gave higher relative risk than those. I 5 tried to include all data in these tables. 6 Q. When you say three citations from 7 this table are outdated, are you referring to the 8 two Dagg and the Thomas 1982 which you believe 9 were superceded? 10 A. I think that's right, yes. 11 Q. When you say four are cited in an 12 arbitrary and misleading manner, which ones are 13 you referring to? 14 A. What page are you on now? 15 Q. Still under discussion of 16 Citations in Table 4. 17 A. So you're up here? 18 Q. Page 13. 19 A. Yes, I see. So Collingwood would 20 be arbitrary, Gun and the two Wong papers. 21 Q. One of the main things you focus 22 on is there's six papers on NHL not included by 23 Steinmaus that were apparently included in Smith, 24 and you point to the appendix on the Smith
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1 evaluation to identify which papers those were. 2 Which appendix are you referring to? 3 A. It would be Appendix A of this 4 report. I only have -- did I get this from you 5 or I got this from Lou? You should have the 6 appendix. It starts with A. It would be Page A1 7 or A16; I'm not sure. 8 Q. Let me hand back Exhibit-A to you 9 and ask you to refer me which appendix you're 10 referring to. 11 A. That was a separate report that I 12 included in the appendix to this report because 13 the whole thing is very confusing. 14 Q. Which of the six studies that you 15 say were not included within Steinmaus that were 16 included within Smith? 17 A. I can just read these. 18 Q. What page are you reading from? 19 A. On Table 8. 20 What I'm questioning is you say 21 that these were included in Smith and I just want 22 to make sure that that's correct. Where do you 23 read that? 24 Q. If you look to the last page of
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1 your report or your summary of Steinmaus above 2 where you give conclusions, -3 A. Right. 4 Q. -- under Comment, it says of 5 special interest are the six papers cited by 6 Smith but not mentioned by Steinmaus. 7 A. Okay. 8 MR. WOOLF: If you guys will look 9 at Page 11, it's talking about the same 10 six studies. 11 MR. DuPONT: Okay. 12 THE WITNESS: I guess that's it 13 then, okay, because there's another table 14 with six studies and that's on Page 8 and 15 they're the same six studies. Okay, so 16 we're clear on that. 17 MR. WOOLF: No, they're not. 18 THE WITNESS: They're not? 19 MR. WOOLF: No. If you'll turn 20 to Page 11? 21 THE WITNESS: I'm turning to Page 22 8 and Page 5. They're the same. 23 MR. WOOLF: Yes. 24 THE WITNESS: Thank you.
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1 BY MR. DuPONT: 2 Q. So the six studies listed on Page 3 5 and the six studies listed on Page 8 are the 4 studies you claim were omitted by -5 A. That's what I'm uncertain about. 6 MR. WOOLF: Dr. Monson, if you 7 look at Page 11 of the critique and 8 refresh your recollection? 9 THE WITNESS: Thank you. That's 10 the different six studies. Thank you 11 very much. 12 All right, so these would be the 13 papers that are not included in Steinmaus 14 but are included in Smith on Page 11. 15 BY MR. DuPONT: 16 Q. And why do you think they should 17 have been included in Steinmaus or not? 18 A. I didn't say I think they should. 19 I'm saying they weren't even though they were 20 included in Smith. And since Smith is the 21 co-author, obviously they were working together. 22 I don't know why Steinmaus didn't include them. 23 Q. Why do you critique the fact that 24 Steinmaus didn't include them?
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1 A. Steinmaus? 2 Q. It is Steinmaus. 3 A. Then I spelled it wrong. Because 4 I think they're relevant papers. 5 Q. Do you disagree with the ATSDR's 6 evaluation that there's suggestive evidence for 7 benzene causing NHL? 8 A. Did I put that in my report? 9 Q. I believe you did. 10 A. I wouldn't have done it in my CLL 11 report, and I don't think it's in this report 12 either. 13 Q. Turn to Page 9 of your report in 14 this case, Salmieri. You quote the ATSDR's 2007 15 toxicological profile for benzene, Page 223, 16 including the quote that there is suggestive 17 evidence of associations between benzene and 18 non-Hodgkin's lymphoma and multiple myeloma. Do 19 you disagree with that statement? 20 A. I agree the ATSDR stated that. 21 Q. Do you agree with their position? 22 A. I wouldn't go so far as to say 23 suggestive evidence. I believe that's an 24 overstatement. I would agree that there are
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1 papers that show positive associations. But the 2 weight of the evidence does not support anything 3 beyond saying that some studies show a positive 4 association, some show a negative association and 5 there's no consistency among the studies. 6 Q. So the ATSDR has it wrong but 7 you're right? 8 A. They're not wrong. I'm saying 9 the word "suggestive" is too strong to me. 10 Q. If you were to rank it on a scale 11 of one to ten, what does the term "suggestive" 12 mean with ten being the highest and one being the 13 lowest? 14 A. I don't have any number in mind. 15 Q. But suggestive, you used the word 16 "suggestive" causation is strong? 17 A. I don't quantitate a substantive, 18 a descriptive term. 19 Q. Nonetheless, you believe it's a 20 strong description of the causal association? 21 A. I'm sorry? 22 Q. To say that there's suggestive 23 evidence, you believe that -24 A. I didn't say it's strong. I said
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1 it's stronger than I would say it. I would say 2 it's weak. Suggestive means weak to me. But I 3 would make an even weaker statement. 4 Q. Are you familiar with Lewis' 2003 5 study where he found a relative risk of 1.81 for 6 CLL? 7 A. I'm familiar with several studies 8 by Lewis but I don't have any recollection of the 9 specific ones, if you can show it to me. 10 Q. I will show you the cover page 11 with the citation. 12 MR. WOOLF: What's the year of 13 that? 14 MR. DuPONT: 2003, Lou. It's 15 Mortality and Cancer Morbidity in Cohort 16 of Canadian Petroleum Workers. 17 THE WITNESS: I've seen it but I 18 don't know of any specifics on it. 19 BY MR. DuPONT: 20 Q. Are you able to tell me why you 21 didn't include it within your review? 22 A. It's a petroleum study and I 23 didn't include petroleum studies per se. 24 MR. WOOLF: What was that, Lewis?
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1 MR. DuPONT: 2003. 2 THE WITNESS: Occupational and 3 Environmental Medicine, OEM. 4 MR. DuPONT: That's all I have. 5 --6 (Witness excused.) 7 (Deposition concluded at 8 approximately 2:27 p.m.) 9 --10 11 12 13 14 15 16 17 18 19 20 21 22 23 24
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1 ACKNOWLEDGMENT OF DEPONENT
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4 hereby certify that I have read the foregoing
5 pages, 1 - 125 , and that the same is a correct
6 transcription of the answers given by me to the
7 questions therein propounded, except for the
8 corrections or changes in form or substance, if
9 any, noted in the attached Errata Sheet.
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1 2 CERTIFICATE 3 4 5 I HEREBY CERTIFY that the witness 6 was duly sworn by me and that the deposition is a 7 true record of the testimony given by the 8 witness. 9 10 11 12 13 Kimberly S. Gordon, a 14 Registered Professional Reporter, 15 Certified Court Reporter 16 and Notary Public 17 Dated: SEPTEMBER 22, 2008 18 19 20 (The foregoing certification of this 21 transcript does not apply to any reproduction of 22 the same by any means, unless under the direct 23 control and/or supervision of the certifying 24 reporter.)
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